Approved by the FDA on May 28, 2021, olanzapine-samidorphan combination (OSC) (Lybalvi, manufactured and distributed by Alkermes, Inc. Waltham, MA USA) is intended to help mitigate some of the weight gain that can be anticipated with the use of olanzapine alone (Table).^1-3 Olanzapine (Zyprexa, originally manufactured and distributed by Eli Lilly and Company/Lilly USA, LLC, Indianapolis, IN USA) is a second-generation antipsychotic that has been available for a quarter century.⁴ Although highly efficacious,^5,6 olanzapine has been associated with weight gain, at times substantial, as well as disturbances in glucose and lipid metabolism.⁷ The addition of samidorphan, an opioid antagonist, to olanzapine in a single tablet may act to decrease the amount of long-term weight gain that can be expected for some patients taking olanzapine alone, consequently minimizing the anticipated increase in waist circumference (a proxy for the measurement of burden imposed by metabolically active adipose tissue). Approval of OSC for the treatment of schizophrenia was based on 2 pivotal randomized controlled trials and their extension studies.^8-11 Approval of OSC for bipolar I disorder (acute treatment of manic/mixed episodes as a monotherapy or adjunctive to lithium or valproate, and as a monotherapy maintenance treatment) was based on legacy studies conducted with olanzapine, after establishing that samidorphan does not alter the pharmacokinetics of olanzapine, including in combination with lithium or valproate.^3,12,13 OSC should be distinguished from a different combination product, olanzapine-fluoxetine combination (Symbyax, originally manufactured and distributed by Eli Lilly and Company/Lilly USA, LLC, Indianapolis, IN USA), approved for acute depressive episodes associated with bipolar I disorder and for treatment-resistant depression.¹⁴

OSC offers the potential to consider olanzapine earlier in the treatment of schizophrenia or bipolar I disorder, especially among practitioners who might otherwise be hesitant to prescribe this agent because of concerns over the risk of excessive weight gain.

OSC is available in 4 dosage strengths containing 5 mg, 10 mg, 15 mg, or 20 mg of olanzapine; all tablets contain 10 mg of samidorphan.² The recommended starting dose for OSC mirrors the language contained in the legacy olanzapine product label.⁴ For schizophrenia, the recommended initial dose (olanzapine/samidorphan) is 5 mg/10 mg or 10 mg/10 mg once daily. For bipolar I manic or mixed episodes, the recommended starting dose for monotherapy is 10 mg/10 mg or 15 mg/10 mg, and for use with lithium or valproate, 10 mg/10 mg. For all indications, the recommended target dose can be 10 mg/10 mg, 15 mg/10 mg, or 20 mg/10 mg, with 5 mg/10 mg as an additional potential dose for maintenance monotherapy of bipolar I disorder. The maximum dose is 20 mg/10 mg once daily. Because the amount of samidorphan in each tablet is fixed at 10 mg, combining tablets of OSC, or cutting OSC tablets in half, is not advisable.

Continue to: How it works...

Product labeling notes that olanzapine is an atypical antipsychotic, that its efficacy in schizophrenia or bipolar I disorder could be mediated through a combination of dopamine and serotonin type 2 (5HT2) antagonism, and that the mechanism of action of samidorphan could be mediated through opioid receptor antagonism.²

The pharmacodynamic profile of olanzapine is complex.² It binds with high affinity to the following receptors: serotonin 5HT2A/2C, 5HT6 (Ki = 4, 11, and 5 nM, respectively), dopamine D1-4 (Ki = 11-31 nM), histamine H1 (Ki = 7 nM), and adrenergic alpha-1 receptors (Ki = 19 nM). Olanzapine is an antagonist with moderate affinity binding for serotonin 5HT3 (Ki = 57 nM) and muscarinic M1-5 (Ki = 73, 96, 132, 32, and 48 nM, respectively). Olanzapine binds with low affinity to gamma aminobutyric acid type A (GABA-A), benzodiazepine, and beta-adrenergic receptors (Ki >10 µM). Olanzapine’s muscarinic receptor affinity can explain why olanzapine can be associated with constipation, dry mouth, and tachycardia, all adverse reactions possibly related to cholinergic antagonism. Thus, OSC should be used with caution in patients with a current diagnosis or prior history of urinary retention, clinically significant prostatic hypertrophy, constipation, or a history of paralytic ileus or related conditions; a potential drug-drug interaction can be anticipated with concomitant use of anticholinergic medications.² Other pharmacodynamic drug-drug interactions that can occur with the olanzapine component of OSC include the possibility that diazepam, alcohol, or other CNS-acting drugs may potentiate orthostatic hypotension, and there may be a need to reduce the dosage of concomitantly prescribed antihypertensive drugs in patients being treated for hypertension. Moreover, OSC is not recommended in patients receiving levodopa and dopamine agonists.

Samidorphan binds to the mu-, kappa-, and delta-opioid receptors (Ki = .052, .23, and 2.7 nM, respectively).² Samidorphan is an antagonist at the mu-opioid receptors with partial agonist activity at kappa- and delta-opioid receptors. A major human metabolite of samidorphan (N-dealkylated) binds to the mu-, kappa-, and delta-opioid receptors (Ki = .26, 23, and 56 nM, respectively), and functions as a mu-opioid receptor agonist. The N-oxide major human metabolite binds to mu-, kappa-, and delta-opioid receptors (Ki = 8, 110, and 280 nM, respectively) and functions as a mu-opioid receptor antagonist. This profile differs from that of other opioid antagonists such as naltrexone.^15,16

OSC is not a scheduled drug subject to the Controlled Substances Act. Because samidorphan functions as an opioid antagonist, OSC is contraindicated in patients using opioids or undergoing acute opioid withdrawal.² To avoid precipitating opioid withdrawal, there should be at least a 7-day opioid-free interval from the last use of short-acting opioids, and at least a 14-day opioid-free interval from the last use of long-acting opioids, before initiating OSC. In emergency situations when an opioid is required, OSC should be discontinued. Patients who attempt to overcome opioid blockade while receiving OSC by using high or repeated doses of exogenous opioids could experience life-threatening or fatal opioid intoxication. Likewise, patients may have decreased tolerance to opioids if OSC therapy is interrupted or discontinued.

Regarding cardiac electrophysiology, OSC was not observed to prolong the electrocardiogram QTc interval to any clinically relevant extent when tested at doses up to 30 mg/30 mg (1.5 times and 3 times the maximum recommended daily dosage of olanzapine and samidorphan, respectively).¹⁷

Clinical pharmacokinetics

The pharmacokinetics of both olanzapine and samidorphan are linear over the clinical dose range and there is no pharmacokinetic interaction between olanzapine and samidorphan after oral administration of OSC.² Coadministration of OSC with lithium or valproate does not have a clinically significant effect on systemic exposure of lithium or valproate.¹³ OSC steady-state concentrations of olanzapine and samidorphan are reached within 7 days, with accumulation at steady state being 2-fold for olanzapine and 1.3-fold for samidorphan (at 5 days). Elimination half-life for olanzapine is 35 to 52 hours, and for samidorphan, 7 to 11 hours. Olanzapine is metabolized primarily via UGT1A4 and CYP1A2, whereas samidorphan is primarily metabolized by CYP3A4. Consequently, concomitant use of OSC with strong CYP3A4 inducers is not recommended. The recommendation regarding CYP1A2 modulators and OSC are similar to those for olanzapine^2,4: consider reducing the dosage of the olanzapine component in OSC when used concomitantly with strong CYP1A2 inhibitors, and consider increasing the dosage of the olanzapine component in OSC when used concomitantly with CYP1A2 inducers. Because cigarette smoke contains polycyclic aromatic hydrocarbons that act as CYP1A2 inducers,¹⁸ olanzapine clearance is much higher in smokers than in nonsmokers.² This translates to potentially clinically relevant differences when optimizing the dose. In a study of patients with schizophrenia, olanzapine concentrations were lower in self-reported smokers (16.5, 34.2, and 60.9 ng/mL) than in self-reported nonsmokers (25.6, 43.4, and 113.2 ng/mL) for dosages of 10, 20, and 40 mg/d, respectively.¹⁹ In contrast, samidorphan pharmacokinetics are not affected by smoking status.²

No dose adjustment of OSC is needed in patients with hepatic or renal impairment; however, OSC is not recommended for patients with end-stage renal disease because this has not been specifically studied.²

Continue to: Efficacy...

The efficacy of OSC in the treatment of schizophrenia in adults is supported, in part, by the extensive legacy of studies of orally administered olanzapine.² For OSC specifically, acute efficacy was primarily demonstrated in a randomized, double-blind, phase 3, 4-week study establishing superiority vs placebo in acutely exacerbated patients with schizophrenia.⁸ Mitigation of weight gain was assessed separately in a randomized, double-blind, phase 3, 24-week study comparing OSC with olanzapine in non-acute outpatients with schizophrenia.¹⁰ Both of these 2 trials were accompanied by 52-week open-label extension studies.^9,11

The 4-week study evaluated the antipsychotic efficacy of OSC in 401 patients experiencing an acute exacerbation or relapse of schizophrenia who required inpatient treatment.⁸ Patients were required to have a Positive and Negative Syndrome Scale (PANSS) total score ≥80, with a score ≥4 on at least 3 of selected positive symptoms, and a Clinical Global Impression-Severity (CGI-S) score ≥4 at baseline and screening. Patients were required to be inpatients for the first 2 weeks of the study, and were encouraged to remain as inpatients for all 4 weeks. Patients were randomized to receive OSC, olanzapine, or placebo. Dosing was once-daily and flexible based on clinical response and tolerability for the first 2 weeks of the study, and fixed thereafter. Patients assigned to OSC could receive 10 mg/10 mg or 20 mg/10 mg, and patients randomized to olanzapine could receive 10 mg or 20 mg. The study compared OSC with placebo, with olanzapine serving as an active control. Treatment with OSC resulted in significant improvements in symptoms compared with placebo at Week 4, as measured by changes in PANSS total scores from baseline. Improvement in PANSS scores with OSC relative to placebo was similar to that observed with olanzapine. The antipsychotic efficacy of OSC relative to placebo was also supported by improvements in CGI-S scores. Thus, the inclusion of samidorphan in OSC did not negatively impact the antipsychotic efficacy of olanzapine.

In the 24-week study, 561 patients were randomized to OSC or olanzapine.¹⁰ There was no placebo control. Patients were treated with doses of OSC 10 mg/10 mg or 20 mg/10 mg, or with doses of olanzapine 10 mg or 20 mg. Dosing was flexible for the first 4 weeks of the study and fixed thereafter. Eligible patients were age 18 to 55 years (younger than the 4-week study, where the maximum age was 70 years), with a body mass index of 18 to 30 kg/m² (lower than the upper limit of 40 kg/m² used in the 4-week study). In contrast to the acutely exacerbated patients in the 4-week study, patients were required to have a PANSS total score of 50 to 90, CGI-S score ≤4, and symptoms suitable for outpatient treatment. The co-primary endpoints were percent change from baseline in body weight and proportion of patients who gained ≥10% body weight at Week 24. Treatment with OSC or olanzapine resulted in similar improvements in PANSS total and CGI-S scores, but treatment with OSC was associated with statistically significantly less weight gain than treatment with olanzapine, and with a smaller proportion of patients who gained ≥10% body weight. The least squares mean percent weight change from baseline to the end of treatment was 4.2% with OSC vs 6.6% with olanzapine. Although patients treated with OSC or olanzapine had similar weight gain for the first 4 weeks of treatment, OSC weight gain stabilized after approximately the 6th week, whereas patients who received olanzapine continued to gain weight throughout the remainder of the treatment period. The risk of gaining ≥10% body weight from baseline was reduced by 50% with OSC compared with olanzapine. Moreover, the odds of gaining ≥7% body weight from baseline at Week 24 were also reduced by 50% for OSC compared with olanzapine. OSC was also associated with smaller increases in waist circumference compared with olanzapine, which was observable as early as Week 1. The risk of experiencing a 5-cm increase in waist circumference was 50% lower for patients treated with OSC vs olanzapine, a relevant threshold in assessing risk of all-cause mortality and cardiovascular disease.²⁰ However, changes in metabolic laboratory parameters in patients treated with OSC or olanzapine were generally small and were similar between groups. In addition, there were little differences between the 2 treatment groups in metabolic parameter changes considered to be of potential clinical significance, based on commonly used thresholds.

Patients on stable, chronic olanzapine therapy were not specifically studied, so the weight effect of switching from olanzapine to OSC is unknown.For bipolar I manic or mixed episodes, the use of OSC as monotherapy or in combination with lithium or valproate, as well as for maintenance monotherapy, was approved based on legacy clinical trials with olanzapine, as described in product labeling,^2,4 as well as pharmacokinetic data evidencing that OSC did not have a clinically significant effect on the pharmacokinetics of lithium or valproate.¹³ A study is in progress to evaluate the effect of OSC compared with olanzapine on body weight in young adults with schizophrenia, schizophreniform, or bipolar I disorder who are early in their illness (ClinicalTrials.gov identifier: NCT03187769).

Overall tolerability and safety

The systemic safety and tolerability profile for OSC would be expected to be similar to that for olanzapine, unless there are adverse events that are specifically related to the samidorphan component. In the 4-week acute study described above,⁸ adverse events that occurred at least twice the rate of placebo with OSC included increased weight (18.7%, 14.3%, 3.0%, for OSC, olanzapine, and placebo, respectively), somnolence (9.0%, 9.8%, 2.2%), dry mouth (7.5%, 5.3%, 0.7%), and headache (6.0%, 5.3%, 3.0%). In the 24-week study,¹⁰ which did not have a placebo control, the most commonly reported adverse events (≥10% of patients) were increased weight (24.8% vs 36.2% for OSC vs olanzapine), somnolence (21.2% vs 18.1%), dry mouth (12.8% vs 8.0%), and increased appetite (10.9% vs 12.3%). In both studies, rates of discontinuation due to adverse events were low and similar between groups (in the 4-week study, 1.5% for OSC, 2.3% for olanzapine, and 5.2% for placebo; in the 24-week study, 12.0% for OSC and 9.8% for olanzapine).

In the 2 open-label, phase 3, 52-week extension studies,^9,11 long-term tolerability was evidenced by low rates discontinuation due to adverse events (≤6%). Neither extension study reported any clinically meaningful changes over time in hematology, biochemistry, vital signs, or electrocardiogram parameters.³ In addition to durability of antipsychotic response as evidenced by sustained improvements in PANSS and CGI-S scores over time, waist circumference and weight remained stable, and the observed long-term changes in weight were consistent with weight changes observed with other second-generation antipsychotics.³ Long-term changes in metabolic laboratory parameter values were small and remained stable, and there was little change in glycosylated hemoglobin (hemoglobin A1c) values, which suggests that glycemic control was maintained with long-term OSC treatment.³ Caveats to consider are that the extension studies were open label without comparators, and they may have selected for patients who responded favorably to OSC treatment in the preceding studies.³Warnings and precautions in OSC product labeling are generally similar to those for other second-generation antipsychotics,²¹ other than warnings and precautions specifically related to samidorphan being an opioid antagonist, and special mention of “Drug Reaction with Eosinophilia and Systemic Symptoms” and “Anticholinergic (Antimuscarinic) Effects” warnings, which also are contained in the olanzapine legacy label.^2,4

Summary

Olanzapine has a plethora of evidence supporting its robust efficacy profile^5,6; however, its use is stymied by an unfavorable weight and metabolic profile.⁷ OSC may help mitigate at least some of the weight gain that would be expected with the use of olanzapine alone in the long-term treatment of patients with schizophrenia or bipolar I disorder. The addition of samidorphan does not deleteriously affect the efficacy of olanzapine, but decreases the risk of gaining ≥10% or ≥7% of baseline body weight by approximately 50% compared with olanzapine alone. Increase in waist circumference, a proxy for how much metabolically active fat one has, is lower with OSC than it is with olanzapine. Because samidorphan is an opioid receptor antagonist, OSC is contraindicated in patients using opioids and in those undergoing acute opioid withdrawal. Dosage strengths available for OSC parallel those for olanzapine, and all strengths including the same fixed dose of samidorphan—10 mg—so advise patients not to double up on the tablets, and to not split them.

Related Resource

• Olanzapine and samidorphan (Lybalvi) prescribing information. https://www.lybalvi.com/lybalvi-prescribing-information.pdf

Drug Brand Names

Diazepam • Valium

Lithium • Eskalith, Lithobid

Olanzapine • Zyprexa

Olanzapine-fluoxetine combination • Symbyax

Olanzapine-samidorphan combination • Lybalvi

Valproate • Depakote, Depakene

Bottom Line

Olanzapine-samidorphan combination (OSC) is intended to mitigate some of the weight gain anticipated when using olanzapine alone. For clinicians who have prescribed olanzapine and have seen its therapeutic benefits, OSC will be a welcome addition to the therapeutic armamentarium. For practitioners who may have avoided olanzapine entirely, OSC can provide another means of offering this therapeutic option and counter “olanzapine hesitancy.”

Approved by the FDA on May 28, 2021, olanzapine-samidorphan combination (OSC) (Lybalvi, manufactured and distributed by Alkermes, Inc. Waltham, MA USA) is intended to help mitigate some of the weight gain that can be anticipated with the use of olanzapine alone (Table).^1-3 Olanzapine (Zyprexa, originally manufactured and distributed by Eli Lilly and Company/Lilly USA, LLC, Indianapolis, IN USA) is a second-generation antipsychotic that has been available for a quarter century.⁴ Although highly efficacious,^5,6 olanzapine has been associated with weight gain, at times substantial, as well as disturbances in glucose and lipid metabolism.⁷ The addition of samidorphan, an opioid antagonist, to olanzapine in a single tablet may act to decrease the amount of long-term weight gain that can be expected for some patients taking olanzapine alone, consequently minimizing the anticipated increase in waist circumference (a proxy for the measurement of burden imposed by metabolically active adipose tissue). Approval of OSC for the treatment of schizophrenia was based on 2 pivotal randomized controlled trials and their extension studies.^8-11 Approval of OSC for bipolar I disorder (acute treatment of manic/mixed episodes as a monotherapy or adjunctive to lithium or valproate, and as a monotherapy maintenance treatment) was based on legacy studies conducted with olanzapine, after establishing that samidorphan does not alter the pharmacokinetics of olanzapine, including in combination with lithium or valproate.^3,12,13 OSC should be distinguished from a different combination product, olanzapine-fluoxetine combination (Symbyax, originally manufactured and distributed by Eli Lilly and Company/Lilly USA, LLC, Indianapolis, IN USA), approved for acute depressive episodes associated with bipolar I disorder and for treatment-resistant depression.¹⁴

OSC offers the potential to consider olanzapine earlier in the treatment of schizophrenia or bipolar I disorder, especially among practitioners who might otherwise be hesitant to prescribe this agent because of concerns over the risk of excessive weight gain.

OSC is available in 4 dosage strengths containing 5 mg, 10 mg, 15 mg, or 20 mg of olanzapine; all tablets contain 10 mg of samidorphan.² The recommended starting dose for OSC mirrors the language contained in the legacy olanzapine product label.⁴ For schizophrenia, the recommended initial dose (olanzapine/samidorphan) is 5 mg/10 mg or 10 mg/10 mg once daily. For bipolar I manic or mixed episodes, the recommended starting dose for monotherapy is 10 mg/10 mg or 15 mg/10 mg, and for use with lithium or valproate, 10 mg/10 mg. For all indications, the recommended target dose can be 10 mg/10 mg, 15 mg/10 mg, or 20 mg/10 mg, with 5 mg/10 mg as an additional potential dose for maintenance monotherapy of bipolar I disorder. The maximum dose is 20 mg/10 mg once daily. Because the amount of samidorphan in each tablet is fixed at 10 mg, combining tablets of OSC, or cutting OSC tablets in half, is not advisable.

Continue to: How it works...

Product labeling notes that olanzapine is an atypical antipsychotic, that its efficacy in schizophrenia or bipolar I disorder could be mediated through a combination of dopamine and serotonin type 2 (5HT2) antagonism, and that the mechanism of action of samidorphan could be mediated through opioid receptor antagonism.²

The pharmacodynamic profile of olanzapine is complex.² It binds with high affinity to the following receptors: serotonin 5HT2A/2C, 5HT6 (Ki = 4, 11, and 5 nM, respectively), dopamine D1-4 (Ki = 11-31 nM), histamine H1 (Ki = 7 nM), and adrenergic alpha-1 receptors (Ki = 19 nM). Olanzapine is an antagonist with moderate affinity binding for serotonin 5HT3 (Ki = 57 nM) and muscarinic M1-5 (Ki = 73, 96, 132, 32, and 48 nM, respectively). Olanzapine binds with low affinity to gamma aminobutyric acid type A (GABA-A), benzodiazepine, and beta-adrenergic receptors (Ki >10 µM). Olanzapine’s muscarinic receptor affinity can explain why olanzapine can be associated with constipation, dry mouth, and tachycardia, all adverse reactions possibly related to cholinergic antagonism. Thus, OSC should be used with caution in patients with a current diagnosis or prior history of urinary retention, clinically significant prostatic hypertrophy, constipation, or a history of paralytic ileus or related conditions; a potential drug-drug interaction can be anticipated with concomitant use of anticholinergic medications.² Other pharmacodynamic drug-drug interactions that can occur with the olanzapine component of OSC include the possibility that diazepam, alcohol, or other CNS-acting drugs may potentiate orthostatic hypotension, and there may be a need to reduce the dosage of concomitantly prescribed antihypertensive drugs in patients being treated for hypertension. Moreover, OSC is not recommended in patients receiving levodopa and dopamine agonists.

Samidorphan binds to the mu-, kappa-, and delta-opioid receptors (Ki = .052, .23, and 2.7 nM, respectively).² Samidorphan is an antagonist at the mu-opioid receptors with partial agonist activity at kappa- and delta-opioid receptors. A major human metabolite of samidorphan (N-dealkylated) binds to the mu-, kappa-, and delta-opioid receptors (Ki = .26, 23, and 56 nM, respectively), and functions as a mu-opioid receptor agonist. The N-oxide major human metabolite binds to mu-, kappa-, and delta-opioid receptors (Ki = 8, 110, and 280 nM, respectively) and functions as a mu-opioid receptor antagonist. This profile differs from that of other opioid antagonists such as naltrexone.^15,16

OSC is not a scheduled drug subject to the Controlled Substances Act. Because samidorphan functions as an opioid antagonist, OSC is contraindicated in patients using opioids or undergoing acute opioid withdrawal.² To avoid precipitating opioid withdrawal, there should be at least a 7-day opioid-free interval from the last use of short-acting opioids, and at least a 14-day opioid-free interval from the last use of long-acting opioids, before initiating OSC. In emergency situations when an opioid is required, OSC should be discontinued. Patients who attempt to overcome opioid blockade while receiving OSC by using high or repeated doses of exogenous opioids could experience life-threatening or fatal opioid intoxication. Likewise, patients may have decreased tolerance to opioids if OSC therapy is interrupted or discontinued.

Regarding cardiac electrophysiology, OSC was not observed to prolong the electrocardiogram QTc interval to any clinically relevant extent when tested at doses up to 30 mg/30 mg (1.5 times and 3 times the maximum recommended daily dosage of olanzapine and samidorphan, respectively).¹⁷

Clinical pharmacokinetics

The pharmacokinetics of both olanzapine and samidorphan are linear over the clinical dose range and there is no pharmacokinetic interaction between olanzapine and samidorphan after oral administration of OSC.² Coadministration of OSC with lithium or valproate does not have a clinically significant effect on systemic exposure of lithium or valproate.¹³ OSC steady-state concentrations of olanzapine and samidorphan are reached within 7 days, with accumulation at steady state being 2-fold for olanzapine and 1.3-fold for samidorphan (at 5 days). Elimination half-life for olanzapine is 35 to 52 hours, and for samidorphan, 7 to 11 hours. Olanzapine is metabolized primarily via UGT1A4 and CYP1A2, whereas samidorphan is primarily metabolized by CYP3A4. Consequently, concomitant use of OSC with strong CYP3A4 inducers is not recommended. The recommendation regarding CYP1A2 modulators and OSC are similar to those for olanzapine^2,4: consider reducing the dosage of the olanzapine component in OSC when used concomitantly with strong CYP1A2 inhibitors, and consider increasing the dosage of the olanzapine component in OSC when used concomitantly with CYP1A2 inducers. Because cigarette smoke contains polycyclic aromatic hydrocarbons that act as CYP1A2 inducers,¹⁸ olanzapine clearance is much higher in smokers than in nonsmokers.² This translates to potentially clinically relevant differences when optimizing the dose. In a study of patients with schizophrenia, olanzapine concentrations were lower in self-reported smokers (16.5, 34.2, and 60.9 ng/mL) than in self-reported nonsmokers (25.6, 43.4, and 113.2 ng/mL) for dosages of 10, 20, and 40 mg/d, respectively.¹⁹ In contrast, samidorphan pharmacokinetics are not affected by smoking status.²

No dose adjustment of OSC is needed in patients with hepatic or renal impairment; however, OSC is not recommended for patients with end-stage renal disease because this has not been specifically studied.²

Continue to: Efficacy...

The efficacy of OSC in the treatment of schizophrenia in adults is supported, in part, by the extensive legacy of studies of orally administered olanzapine.² For OSC specifically, acute efficacy was primarily demonstrated in a randomized, double-blind, phase 3, 4-week study establishing superiority vs placebo in acutely exacerbated patients with schizophrenia.⁸ Mitigation of weight gain was assessed separately in a randomized, double-blind, phase 3, 24-week study comparing OSC with olanzapine in non-acute outpatients with schizophrenia.¹⁰ Both of these 2 trials were accompanied by 52-week open-label extension studies.^9,11

The 4-week study evaluated the antipsychotic efficacy of OSC in 401 patients experiencing an acute exacerbation or relapse of schizophrenia who required inpatient treatment.⁸ Patients were required to have a Positive and Negative Syndrome Scale (PANSS) total score ≥80, with a score ≥4 on at least 3 of selected positive symptoms, and a Clinical Global Impression-Severity (CGI-S) score ≥4 at baseline and screening. Patients were required to be inpatients for the first 2 weeks of the study, and were encouraged to remain as inpatients for all 4 weeks. Patients were randomized to receive OSC, olanzapine, or placebo. Dosing was once-daily and flexible based on clinical response and tolerability for the first 2 weeks of the study, and fixed thereafter. Patients assigned to OSC could receive 10 mg/10 mg or 20 mg/10 mg, and patients randomized to olanzapine could receive 10 mg or 20 mg. The study compared OSC with placebo, with olanzapine serving as an active control. Treatment with OSC resulted in significant improvements in symptoms compared with placebo at Week 4, as measured by changes in PANSS total scores from baseline. Improvement in PANSS scores with OSC relative to placebo was similar to that observed with olanzapine. The antipsychotic efficacy of OSC relative to placebo was also supported by improvements in CGI-S scores. Thus, the inclusion of samidorphan in OSC did not negatively impact the antipsychotic efficacy of olanzapine.

In the 24-week study, 561 patients were randomized to OSC or olanzapine.¹⁰ There was no placebo control. Patients were treated with doses of OSC 10 mg/10 mg or 20 mg/10 mg, or with doses of olanzapine 10 mg or 20 mg. Dosing was flexible for the first 4 weeks of the study and fixed thereafter. Eligible patients were age 18 to 55 years (younger than the 4-week study, where the maximum age was 70 years), with a body mass index of 18 to 30 kg/m² (lower than the upper limit of 40 kg/m² used in the 4-week study). In contrast to the acutely exacerbated patients in the 4-week study, patients were required to have a PANSS total score of 50 to 90, CGI-S score ≤4, and symptoms suitable for outpatient treatment. The co-primary endpoints were percent change from baseline in body weight and proportion of patients who gained ≥10% body weight at Week 24. Treatment with OSC or olanzapine resulted in similar improvements in PANSS total and CGI-S scores, but treatment with OSC was associated with statistically significantly less weight gain than treatment with olanzapine, and with a smaller proportion of patients who gained ≥10% body weight. The least squares mean percent weight change from baseline to the end of treatment was 4.2% with OSC vs 6.6% with olanzapine. Although patients treated with OSC or olanzapine had similar weight gain for the first 4 weeks of treatment, OSC weight gain stabilized after approximately the 6th week, whereas patients who received olanzapine continued to gain weight throughout the remainder of the treatment period. The risk of gaining ≥10% body weight from baseline was reduced by 50% with OSC compared with olanzapine. Moreover, the odds of gaining ≥7% body weight from baseline at Week 24 were also reduced by 50% for OSC compared with olanzapine. OSC was also associated with smaller increases in waist circumference compared with olanzapine, which was observable as early as Week 1. The risk of experiencing a 5-cm increase in waist circumference was 50% lower for patients treated with OSC vs olanzapine, a relevant threshold in assessing risk of all-cause mortality and cardiovascular disease.²⁰ However, changes in metabolic laboratory parameters in patients treated with OSC or olanzapine were generally small and were similar between groups. In addition, there were little differences between the 2 treatment groups in metabolic parameter changes considered to be of potential clinical significance, based on commonly used thresholds.

Patients on stable, chronic olanzapine therapy were not specifically studied, so the weight effect of switching from olanzapine to OSC is unknown.For bipolar I manic or mixed episodes, the use of OSC as monotherapy or in combination with lithium or valproate, as well as for maintenance monotherapy, was approved based on legacy clinical trials with olanzapine, as described in product labeling,^2,4 as well as pharmacokinetic data evidencing that OSC did not have a clinically significant effect on the pharmacokinetics of lithium or valproate.¹³ A study is in progress to evaluate the effect of OSC compared with olanzapine on body weight in young adults with schizophrenia, schizophreniform, or bipolar I disorder who are early in their illness (ClinicalTrials.gov identifier: NCT03187769).

Overall tolerability and safety

The systemic safety and tolerability profile for OSC would be expected to be similar to that for olanzapine, unless there are adverse events that are specifically related to the samidorphan component. In the 4-week acute study described above,⁸ adverse events that occurred at least twice the rate of placebo with OSC included increased weight (18.7%, 14.3%, 3.0%, for OSC, olanzapine, and placebo, respectively), somnolence (9.0%, 9.8%, 2.2%), dry mouth (7.5%, 5.3%, 0.7%), and headache (6.0%, 5.3%, 3.0%). In the 24-week study,¹⁰ which did not have a placebo control, the most commonly reported adverse events (≥10% of patients) were increased weight (24.8% vs 36.2% for OSC vs olanzapine), somnolence (21.2% vs 18.1%), dry mouth (12.8% vs 8.0%), and increased appetite (10.9% vs 12.3%). In both studies, rates of discontinuation due to adverse events were low and similar between groups (in the 4-week study, 1.5% for OSC, 2.3% for olanzapine, and 5.2% for placebo; in the 24-week study, 12.0% for OSC and 9.8% for olanzapine).

In the 2 open-label, phase 3, 52-week extension studies,^9,11 long-term tolerability was evidenced by low rates discontinuation due to adverse events (≤6%). Neither extension study reported any clinically meaningful changes over time in hematology, biochemistry, vital signs, or electrocardiogram parameters.³ In addition to durability of antipsychotic response as evidenced by sustained improvements in PANSS and CGI-S scores over time, waist circumference and weight remained stable, and the observed long-term changes in weight were consistent with weight changes observed with other second-generation antipsychotics.³ Long-term changes in metabolic laboratory parameter values were small and remained stable, and there was little change in glycosylated hemoglobin (hemoglobin A1c) values, which suggests that glycemic control was maintained with long-term OSC treatment.³ Caveats to consider are that the extension studies were open label without comparators, and they may have selected for patients who responded favorably to OSC treatment in the preceding studies.³Warnings and precautions in OSC product labeling are generally similar to those for other second-generation antipsychotics,²¹ other than warnings and precautions specifically related to samidorphan being an opioid antagonist, and special mention of “Drug Reaction with Eosinophilia and Systemic Symptoms” and “Anticholinergic (Antimuscarinic) Effects” warnings, which also are contained in the olanzapine legacy label.^2,4

Summary

Olanzapine has a plethora of evidence supporting its robust efficacy profile^5,6; however, its use is stymied by an unfavorable weight and metabolic profile.⁷ OSC may help mitigate at least some of the weight gain that would be expected with the use of olanzapine alone in the long-term treatment of patients with schizophrenia or bipolar I disorder. The addition of samidorphan does not deleteriously affect the efficacy of olanzapine, but decreases the risk of gaining ≥10% or ≥7% of baseline body weight by approximately 50% compared with olanzapine alone. Increase in waist circumference, a proxy for how much metabolically active fat one has, is lower with OSC than it is with olanzapine. Because samidorphan is an opioid receptor antagonist, OSC is contraindicated in patients using opioids and in those undergoing acute opioid withdrawal. Dosage strengths available for OSC parallel those for olanzapine, and all strengths including the same fixed dose of samidorphan—10 mg—so advise patients not to double up on the tablets, and to not split them.

Related Resource

• Olanzapine and samidorphan (Lybalvi) prescribing information. https://www.lybalvi.com/lybalvi-prescribing-information.pdf

Drug Brand Names

Diazepam • Valium

Lithium • Eskalith, Lithobid

Olanzapine • Zyprexa

Olanzapine-fluoxetine combination • Symbyax

Olanzapine-samidorphan combination • Lybalvi

Valproate • Depakote, Depakene

Bottom Line

Olanzapine-samidorphan combination (OSC) is intended to mitigate some of the weight gain anticipated when using olanzapine alone. For clinicians who have prescribed olanzapine and have seen its therapeutic benefits, OSC will be a welcome addition to the therapeutic armamentarium. For practitioners who may have avoided olanzapine entirely, OSC can provide another means of offering this therapeutic option and counter “olanzapine hesitancy.”

Approved by the FDA on May 28, 2021, olanzapine-samidorphan combination (OSC) (Lybalvi, manufactured and distributed by Alkermes, Inc. Waltham, MA USA) is intended to help mitigate some of the weight gain that can be anticipated with the use of olanzapine alone (Table).^1-3 Olanzapine (Zyprexa, originally manufactured and distributed by Eli Lilly and Company/Lilly USA, LLC, Indianapolis, IN USA) is a second-generation antipsychotic that has been available for a quarter century.⁴ Although highly efficacious,^5,6 olanzapine has been associated with weight gain, at times substantial, as well as disturbances in glucose and lipid metabolism.⁷ The addition of samidorphan, an opioid antagonist, to olanzapine in a single tablet may act to decrease the amount of long-term weight gain that can be expected for some patients taking olanzapine alone, consequently minimizing the anticipated increase in waist circumference (a proxy for the measurement of burden imposed by metabolically active adipose tissue). Approval of OSC for the treatment of schizophrenia was based on 2 pivotal randomized controlled trials and their extension studies.^8-11 Approval of OSC for bipolar I disorder (acute treatment of manic/mixed episodes as a monotherapy or adjunctive to lithium or valproate, and as a monotherapy maintenance treatment) was based on legacy studies conducted with olanzapine, after establishing that samidorphan does not alter the pharmacokinetics of olanzapine, including in combination with lithium or valproate.^3,12,13 OSC should be distinguished from a different combination product, olanzapine-fluoxetine combination (Symbyax, originally manufactured and distributed by Eli Lilly and Company/Lilly USA, LLC, Indianapolis, IN USA), approved for acute depressive episodes associated with bipolar I disorder and for treatment-resistant depression.¹⁴

OSC offers the potential to consider olanzapine earlier in the treatment of schizophrenia or bipolar I disorder, especially among practitioners who might otherwise be hesitant to prescribe this agent because of concerns over the risk of excessive weight gain.

OSC is available in 4 dosage strengths containing 5 mg, 10 mg, 15 mg, or 20 mg of olanzapine; all tablets contain 10 mg of samidorphan.² The recommended starting dose for OSC mirrors the language contained in the legacy olanzapine product label.⁴ For schizophrenia, the recommended initial dose (olanzapine/samidorphan) is 5 mg/10 mg or 10 mg/10 mg once daily. For bipolar I manic or mixed episodes, the recommended starting dose for monotherapy is 10 mg/10 mg or 15 mg/10 mg, and for use with lithium or valproate, 10 mg/10 mg. For all indications, the recommended target dose can be 10 mg/10 mg, 15 mg/10 mg, or 20 mg/10 mg, with 5 mg/10 mg as an additional potential dose for maintenance monotherapy of bipolar I disorder. The maximum dose is 20 mg/10 mg once daily. Because the amount of samidorphan in each tablet is fixed at 10 mg, combining tablets of OSC, or cutting OSC tablets in half, is not advisable.

Continue to: How it works...

Product labeling notes that olanzapine is an atypical antipsychotic, that its efficacy in schizophrenia or bipolar I disorder could be mediated through a combination of dopamine and serotonin type 2 (5HT2) antagonism, and that the mechanism of action of samidorphan could be mediated through opioid receptor antagonism.²

The pharmacodynamic profile of olanzapine is complex.² It binds with high affinity to the following receptors: serotonin 5HT2A/2C, 5HT6 (Ki = 4, 11, and 5 nM, respectively), dopamine D1-4 (Ki = 11-31 nM), histamine H1 (Ki = 7 nM), and adrenergic alpha-1 receptors (Ki = 19 nM). Olanzapine is an antagonist with moderate affinity binding for serotonin 5HT3 (Ki = 57 nM) and muscarinic M1-5 (Ki = 73, 96, 132, 32, and 48 nM, respectively). Olanzapine binds with low affinity to gamma aminobutyric acid type A (GABA-A), benzodiazepine, and beta-adrenergic receptors (Ki >10 µM). Olanzapine’s muscarinic receptor affinity can explain why olanzapine can be associated with constipation, dry mouth, and tachycardia, all adverse reactions possibly related to cholinergic antagonism. Thus, OSC should be used with caution in patients with a current diagnosis or prior history of urinary retention, clinically significant prostatic hypertrophy, constipation, or a history of paralytic ileus or related conditions; a potential drug-drug interaction can be anticipated with concomitant use of anticholinergic medications.² Other pharmacodynamic drug-drug interactions that can occur with the olanzapine component of OSC include the possibility that diazepam, alcohol, or other CNS-acting drugs may potentiate orthostatic hypotension, and there may be a need to reduce the dosage of concomitantly prescribed antihypertensive drugs in patients being treated for hypertension. Moreover, OSC is not recommended in patients receiving levodopa and dopamine agonists.

Samidorphan binds to the mu-, kappa-, and delta-opioid receptors (Ki = .052, .23, and 2.7 nM, respectively).² Samidorphan is an antagonist at the mu-opioid receptors with partial agonist activity at kappa- and delta-opioid receptors. A major human metabolite of samidorphan (N-dealkylated) binds to the mu-, kappa-, and delta-opioid receptors (Ki = .26, 23, and 56 nM, respectively), and functions as a mu-opioid receptor agonist. The N-oxide major human metabolite binds to mu-, kappa-, and delta-opioid receptors (Ki = 8, 110, and 280 nM, respectively) and functions as a mu-opioid receptor antagonist. This profile differs from that of other opioid antagonists such as naltrexone.^15,16

OSC is not a scheduled drug subject to the Controlled Substances Act. Because samidorphan functions as an opioid antagonist, OSC is contraindicated in patients using opioids or undergoing acute opioid withdrawal.² To avoid precipitating opioid withdrawal, there should be at least a 7-day opioid-free interval from the last use of short-acting opioids, and at least a 14-day opioid-free interval from the last use of long-acting opioids, before initiating OSC. In emergency situations when an opioid is required, OSC should be discontinued. Patients who attempt to overcome opioid blockade while receiving OSC by using high or repeated doses of exogenous opioids could experience life-threatening or fatal opioid intoxication. Likewise, patients may have decreased tolerance to opioids if OSC therapy is interrupted or discontinued.

Regarding cardiac electrophysiology, OSC was not observed to prolong the electrocardiogram QTc interval to any clinically relevant extent when tested at doses up to 30 mg/30 mg (1.5 times and 3 times the maximum recommended daily dosage of olanzapine and samidorphan, respectively).¹⁷

Clinical pharmacokinetics

The pharmacokinetics of both olanzapine and samidorphan are linear over the clinical dose range and there is no pharmacokinetic interaction between olanzapine and samidorphan after oral administration of OSC.² Coadministration of OSC with lithium or valproate does not have a clinically significant effect on systemic exposure of lithium or valproate.¹³ OSC steady-state concentrations of olanzapine and samidorphan are reached within 7 days, with accumulation at steady state being 2-fold for olanzapine and 1.3-fold for samidorphan (at 5 days). Elimination half-life for olanzapine is 35 to 52 hours, and for samidorphan, 7 to 11 hours. Olanzapine is metabolized primarily via UGT1A4 and CYP1A2, whereas samidorphan is primarily metabolized by CYP3A4. Consequently, concomitant use of OSC with strong CYP3A4 inducers is not recommended. The recommendation regarding CYP1A2 modulators and OSC are similar to those for olanzapine^2,4: consider reducing the dosage of the olanzapine component in OSC when used concomitantly with strong CYP1A2 inhibitors, and consider increasing the dosage of the olanzapine component in OSC when used concomitantly with CYP1A2 inducers. Because cigarette smoke contains polycyclic aromatic hydrocarbons that act as CYP1A2 inducers,¹⁸ olanzapine clearance is much higher in smokers than in nonsmokers.² This translates to potentially clinically relevant differences when optimizing the dose. In a study of patients with schizophrenia, olanzapine concentrations were lower in self-reported smokers (16.5, 34.2, and 60.9 ng/mL) than in self-reported nonsmokers (25.6, 43.4, and 113.2 ng/mL) for dosages of 10, 20, and 40 mg/d, respectively.¹⁹ In contrast, samidorphan pharmacokinetics are not affected by smoking status.²

No dose adjustment of OSC is needed in patients with hepatic or renal impairment; however, OSC is not recommended for patients with end-stage renal disease because this has not been specifically studied.²

Continue to: Efficacy...

The efficacy of OSC in the treatment of schizophrenia in adults is supported, in part, by the extensive legacy of studies of orally administered olanzapine.² For OSC specifically, acute efficacy was primarily demonstrated in a randomized, double-blind, phase 3, 4-week study establishing superiority vs placebo in acutely exacerbated patients with schizophrenia.⁸ Mitigation of weight gain was assessed separately in a randomized, double-blind, phase 3, 24-week study comparing OSC with olanzapine in non-acute outpatients with schizophrenia.¹⁰ Both of these 2 trials were accompanied by 52-week open-label extension studies.^9,11

The 4-week study evaluated the antipsychotic efficacy of OSC in 401 patients experiencing an acute exacerbation or relapse of schizophrenia who required inpatient treatment.⁸ Patients were required to have a Positive and Negative Syndrome Scale (PANSS) total score ≥80, with a score ≥4 on at least 3 of selected positive symptoms, and a Clinical Global Impression-Severity (CGI-S) score ≥4 at baseline and screening. Patients were required to be inpatients for the first 2 weeks of the study, and were encouraged to remain as inpatients for all 4 weeks. Patients were randomized to receive OSC, olanzapine, or placebo. Dosing was once-daily and flexible based on clinical response and tolerability for the first 2 weeks of the study, and fixed thereafter. Patients assigned to OSC could receive 10 mg/10 mg or 20 mg/10 mg, and patients randomized to olanzapine could receive 10 mg or 20 mg. The study compared OSC with placebo, with olanzapine serving as an active control. Treatment with OSC resulted in significant improvements in symptoms compared with placebo at Week 4, as measured by changes in PANSS total scores from baseline. Improvement in PANSS scores with OSC relative to placebo was similar to that observed with olanzapine. The antipsychotic efficacy of OSC relative to placebo was also supported by improvements in CGI-S scores. Thus, the inclusion of samidorphan in OSC did not negatively impact the antipsychotic efficacy of olanzapine.

In the 24-week study, 561 patients were randomized to OSC or olanzapine.¹⁰ There was no placebo control. Patients were treated with doses of OSC 10 mg/10 mg or 20 mg/10 mg, or with doses of olanzapine 10 mg or 20 mg. Dosing was flexible for the first 4 weeks of the study and fixed thereafter. Eligible patients were age 18 to 55 years (younger than the 4-week study, where the maximum age was 70 years), with a body mass index of 18 to 30 kg/m² (lower than the upper limit of 40 kg/m² used in the 4-week study). In contrast to the acutely exacerbated patients in the 4-week study, patients were required to have a PANSS total score of 50 to 90, CGI-S score ≤4, and symptoms suitable for outpatient treatment. The co-primary endpoints were percent change from baseline in body weight and proportion of patients who gained ≥10% body weight at Week 24. Treatment with OSC or olanzapine resulted in similar improvements in PANSS total and CGI-S scores, but treatment with OSC was associated with statistically significantly less weight gain than treatment with olanzapine, and with a smaller proportion of patients who gained ≥10% body weight. The least squares mean percent weight change from baseline to the end of treatment was 4.2% with OSC vs 6.6% with olanzapine. Although patients treated with OSC or olanzapine had similar weight gain for the first 4 weeks of treatment, OSC weight gain stabilized after approximately the 6th week, whereas patients who received olanzapine continued to gain weight throughout the remainder of the treatment period. The risk of gaining ≥10% body weight from baseline was reduced by 50% with OSC compared with olanzapine. Moreover, the odds of gaining ≥7% body weight from baseline at Week 24 were also reduced by 50% for OSC compared with olanzapine. OSC was also associated with smaller increases in waist circumference compared with olanzapine, which was observable as early as Week 1. The risk of experiencing a 5-cm increase in waist circumference was 50% lower for patients treated with OSC vs olanzapine, a relevant threshold in assessing risk of all-cause mortality and cardiovascular disease.²⁰ However, changes in metabolic laboratory parameters in patients treated with OSC or olanzapine were generally small and were similar between groups. In addition, there were little differences between the 2 treatment groups in metabolic parameter changes considered to be of potential clinical significance, based on commonly used thresholds.

Patients on stable, chronic olanzapine therapy were not specifically studied, so the weight effect of switching from olanzapine to OSC is unknown.For bipolar I manic or mixed episodes, the use of OSC as monotherapy or in combination with lithium or valproate, as well as for maintenance monotherapy, was approved based on legacy clinical trials with olanzapine, as described in product labeling,^2,4 as well as pharmacokinetic data evidencing that OSC did not have a clinically significant effect on the pharmacokinetics of lithium or valproate.¹³ A study is in progress to evaluate the effect of OSC compared with olanzapine on body weight in young adults with schizophrenia, schizophreniform, or bipolar I disorder who are early in their illness (ClinicalTrials.gov identifier: NCT03187769).

Overall tolerability and safety

The systemic safety and tolerability profile for OSC would be expected to be similar to that for olanzapine, unless there are adverse events that are specifically related to the samidorphan component. In the 4-week acute study described above,⁸ adverse events that occurred at least twice the rate of placebo with OSC included increased weight (18.7%, 14.3%, 3.0%, for OSC, olanzapine, and placebo, respectively), somnolence (9.0%, 9.8%, 2.2%), dry mouth (7.5%, 5.3%, 0.7%), and headache (6.0%, 5.3%, 3.0%). In the 24-week study,¹⁰ which did not have a placebo control, the most commonly reported adverse events (≥10% of patients) were increased weight (24.8% vs 36.2% for OSC vs olanzapine), somnolence (21.2% vs 18.1%), dry mouth (12.8% vs 8.0%), and increased appetite (10.9% vs 12.3%). In both studies, rates of discontinuation due to adverse events were low and similar between groups (in the 4-week study, 1.5% for OSC, 2.3% for olanzapine, and 5.2% for placebo; in the 24-week study, 12.0% for OSC and 9.8% for olanzapine).

In the 2 open-label, phase 3, 52-week extension studies,^9,11 long-term tolerability was evidenced by low rates discontinuation due to adverse events (≤6%). Neither extension study reported any clinically meaningful changes over time in hematology, biochemistry, vital signs, or electrocardiogram parameters.³ In addition to durability of antipsychotic response as evidenced by sustained improvements in PANSS and CGI-S scores over time, waist circumference and weight remained stable, and the observed long-term changes in weight were consistent with weight changes observed with other second-generation antipsychotics.³ Long-term changes in metabolic laboratory parameter values were small and remained stable, and there was little change in glycosylated hemoglobin (hemoglobin A1c) values, which suggests that glycemic control was maintained with long-term OSC treatment.³ Caveats to consider are that the extension studies were open label without comparators, and they may have selected for patients who responded favorably to OSC treatment in the preceding studies.³Warnings and precautions in OSC product labeling are generally similar to those for other second-generation antipsychotics,²¹ other than warnings and precautions specifically related to samidorphan being an opioid antagonist, and special mention of “Drug Reaction with Eosinophilia and Systemic Symptoms” and “Anticholinergic (Antimuscarinic) Effects” warnings, which also are contained in the olanzapine legacy label.^2,4

Summary

Olanzapine has a plethora of evidence supporting its robust efficacy profile^5,6; however, its use is stymied by an unfavorable weight and metabolic profile.⁷ OSC may help mitigate at least some of the weight gain that would be expected with the use of olanzapine alone in the long-term treatment of patients with schizophrenia or bipolar I disorder. The addition of samidorphan does not deleteriously affect the efficacy of olanzapine, but decreases the risk of gaining ≥10% or ≥7% of baseline body weight by approximately 50% compared with olanzapine alone. Increase in waist circumference, a proxy for how much metabolically active fat one has, is lower with OSC than it is with olanzapine. Because samidorphan is an opioid receptor antagonist, OSC is contraindicated in patients using opioids and in those undergoing acute opioid withdrawal. Dosage strengths available for OSC parallel those for olanzapine, and all strengths including the same fixed dose of samidorphan—10 mg—so advise patients not to double up on the tablets, and to not split them.

Related Resource

• Olanzapine and samidorphan (Lybalvi) prescribing information. https://www.lybalvi.com/lybalvi-prescribing-information.pdf

Drug Brand Names

Diazepam • Valium

Lithium • Eskalith, Lithobid

Olanzapine • Zyprexa

Olanzapine-fluoxetine combination • Symbyax

Olanzapine-samidorphan combination • Lybalvi

Valproate • Depakote, Depakene

Bottom Line

Olanzapine-samidorphan combination (OSC) is intended to mitigate some of the weight gain anticipated when using olanzapine alone. For clinicians who have prescribed olanzapine and have seen its therapeutic benefits, OSC will be a welcome addition to the therapeutic armamentarium. For practitioners who may have avoided olanzapine entirely, OSC can provide another means of offering this therapeutic option and counter “olanzapine hesitancy.”

Researchers have identified a risk locus on chromosome 7 containing DNA variations that increase the risk that an individual will attempt suicide, even in the absence of a psychiatric disorder.

This finding suggests the genetic underpinnings of suicide attempts are partially shared and partially distinct from those of related psychiatric disorders, the investigators note.

“This study brings us a step closer to understanding the neurobiology of suicidality, with the ultimate goal of developing new treatments and prevention strategies,” Niamh Mullins, PhD, department of psychiatry, department of genetics and genomic sciences, Icahn School of Medicine at Mount Sinai in New York, said in an interview.

The study was published online in Biological Psychiatry.

Largest study to date

In the largest genetic association study of suicide attempt published to date, the researchers conducted a genome-wide association study (GWAS) of 29,782 suicide attempt cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC).

Two loci reached genome-wide significance for suicide attempt – the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with suicide attempt after conditioning on psychiatric disorders and was replicated in an independent cohort of over 14,000 veterans in the Million Veteran Program.

“This is the first replicated genetic locus that contributes more to suicide attempt than related psychiatric disorders,” Dr. Mullins said.

“The study found overlap in the genetic basis of suicide attempt and that of related psychiatric disorders, particularly major depression, but also with that of nonpsychiatric risk factors such as smoking, pain, risk-taking behavior, sleep disturbances, and poorer general health,” Dr. Mullins said.

“These genetic relationships between suicide attempt and nonpsychiatric risk factors were not a by-product of comorbid psychiatric illness, suggesting that there is some shared biological basis between suicide attempt and nonpsychiatric risk factors,” she added.

Dr. Mullins cautioned that the findings do not have any immediate impact on patient care.

“The ultimate goal of this research is to gain insight into the underlying biological pathways involved in suicide attempts or suicidal thoughts, providing potential avenues to treatments and prevention strategies,” she said.

“The study findings also point to the importance of studying the potential direct causal paths between these risk factors and suicide attempt in patients with and without psychiatric illness,” Douglas Ruderfer, PhD, of Vanderbilt University Medical Center, Nashville, Tenn., cofounder and cochair of the consortium and senior author of the paper, added in a news release.

A version of this article first appeared on Medscape.com.

Researchers have identified a risk locus on chromosome 7 containing DNA variations that increase the risk that an individual will attempt suicide, even in the absence of a psychiatric disorder.

This finding suggests the genetic underpinnings of suicide attempts are partially shared and partially distinct from those of related psychiatric disorders, the investigators note.

“This study brings us a step closer to understanding the neurobiology of suicidality, with the ultimate goal of developing new treatments and prevention strategies,” Niamh Mullins, PhD, department of psychiatry, department of genetics and genomic sciences, Icahn School of Medicine at Mount Sinai in New York, said in an interview.

The study was published online in Biological Psychiatry.

Largest study to date

In the largest genetic association study of suicide attempt published to date, the researchers conducted a genome-wide association study (GWAS) of 29,782 suicide attempt cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC).

Two loci reached genome-wide significance for suicide attempt – the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with suicide attempt after conditioning on psychiatric disorders and was replicated in an independent cohort of over 14,000 veterans in the Million Veteran Program.

“This is the first replicated genetic locus that contributes more to suicide attempt than related psychiatric disorders,” Dr. Mullins said.

“The study found overlap in the genetic basis of suicide attempt and that of related psychiatric disorders, particularly major depression, but also with that of nonpsychiatric risk factors such as smoking, pain, risk-taking behavior, sleep disturbances, and poorer general health,” Dr. Mullins said.

“These genetic relationships between suicide attempt and nonpsychiatric risk factors were not a by-product of comorbid psychiatric illness, suggesting that there is some shared biological basis between suicide attempt and nonpsychiatric risk factors,” she added.

Dr. Mullins cautioned that the findings do not have any immediate impact on patient care.

“The ultimate goal of this research is to gain insight into the underlying biological pathways involved in suicide attempts or suicidal thoughts, providing potential avenues to treatments and prevention strategies,” she said.

“The study findings also point to the importance of studying the potential direct causal paths between these risk factors and suicide attempt in patients with and without psychiatric illness,” Douglas Ruderfer, PhD, of Vanderbilt University Medical Center, Nashville, Tenn., cofounder and cochair of the consortium and senior author of the paper, added in a news release.

A version of this article first appeared on Medscape.com.

Researchers have identified a risk locus on chromosome 7 containing DNA variations that increase the risk that an individual will attempt suicide, even in the absence of a psychiatric disorder.

This finding suggests the genetic underpinnings of suicide attempts are partially shared and partially distinct from those of related psychiatric disorders, the investigators note.

“This study brings us a step closer to understanding the neurobiology of suicidality, with the ultimate goal of developing new treatments and prevention strategies,” Niamh Mullins, PhD, department of psychiatry, department of genetics and genomic sciences, Icahn School of Medicine at Mount Sinai in New York, said in an interview.

The study was published online in Biological Psychiatry.

Largest study to date

In the largest genetic association study of suicide attempt published to date, the researchers conducted a genome-wide association study (GWAS) of 29,782 suicide attempt cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC).

Two loci reached genome-wide significance for suicide attempt – the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with suicide attempt after conditioning on psychiatric disorders and was replicated in an independent cohort of over 14,000 veterans in the Million Veteran Program.

“This is the first replicated genetic locus that contributes more to suicide attempt than related psychiatric disorders,” Dr. Mullins said.

“The study found overlap in the genetic basis of suicide attempt and that of related psychiatric disorders, particularly major depression, but also with that of nonpsychiatric risk factors such as smoking, pain, risk-taking behavior, sleep disturbances, and poorer general health,” Dr. Mullins said.

“These genetic relationships between suicide attempt and nonpsychiatric risk factors were not a by-product of comorbid psychiatric illness, suggesting that there is some shared biological basis between suicide attempt and nonpsychiatric risk factors,” she added.

Dr. Mullins cautioned that the findings do not have any immediate impact on patient care.

“The ultimate goal of this research is to gain insight into the underlying biological pathways involved in suicide attempts or suicidal thoughts, providing potential avenues to treatments and prevention strategies,” she said.

“The study findings also point to the importance of studying the potential direct causal paths between these risk factors and suicide attempt in patients with and without psychiatric illness,” Douglas Ruderfer, PhD, of Vanderbilt University Medical Center, Nashville, Tenn., cofounder and cochair of the consortium and senior author of the paper, added in a news release.

A version of this article first appeared on Medscape.com.

For this Psychiatry Leaders’ Perspectives, Awais Aftab, MD, interviewed Alan F. Schatzberg, MD. Dr. Schatzberg is the Kenneth T. Norris, Jr., Professor of Psychiatry and Behavioral Sciences at Stanford University. He served as the Chair of the Department at Stanford until 2010 and currently directs the Stanford Mood Disorders Center. He was the 136th president of the American Psychiatric Association (APA) (2009-2010). He has been an active investigator in the biology and psycho­pharmacology of depressive disorders, and has authored more than 700 publications and abstracts, including Schatzberg’s Manual of Clinical Psychopharmacology. Dr. Schatzberg is also the coeditor of the Textbook of Psychopharmacology with Charles B. Nemeroff, MD, PhD. He is a Past President of the American College of Neuropsychopharmacology (ACNP) and the Society of Biological Psychiatry, and was also the Secretary-General of the International Society of Psychoneuroendocrinology (ISPNE). In 2003, he was elected to the Institute of Medicine of the National Academy of Sciences (National Academy of Medicine). He has received numerous prestigious awards, including the 2005 Distinguished Service in Psychiatry Award from the American College of Psychiatrists, the 2005 Falcone Award from the National Alliance for Research in Schizophrenia and Affective Disorders, the 2014 Kraepelin Gold Medal from the Max Planck Institute of Psychiatry, the 2015 Gold Medal from the Society of Biological Psychiatry, the 2015 Lifetime Achievement Award of the ISPNE, the 2017 Julius Axelrod Mentorship Award from the ACNP, the 2018 Donald Klein, MD, Lifetime Achievement Award from the American Society of Clinical Psychopharmacology, and the 2018 Jules Marmor, MD, Award for Biopsychosocial Research from the APA.

Dr. Aftab: You have devoted much of your career to the development of psychopharmacology. What is your perspective on where the field of psychopharmacology stands at present, especially amid the widespread recognition of “treatment resistance” as a pervasive phenomenon and the scarcity of validated neurobiologic etiological models for psychiatric disorders?

Dr. Schatzberg: We have made considerable progress in the development of new classes of agents for major depression, but as we develop new agents, we still see a large percentage of patients who do not seem to demonstrate adequate responses, particularly in major depressive disorder. This has driven us to look for agents that work differently than previous ones. Although we have some new agents with seeming efficacy and newer mechanisms of action, eg, esketamine, these have largely been derived from clinical, often serendipitous, observations of antidepressant effects rather than from prospective development based on a known pharmacological effect or a biological construct of the disorder. Another intriguing and possibly effective anxiolytic and antidepressive agent is psilocybin, whose potential use is largely derived from clinicians who found it helpful in their practices in combination with psychotherapy. These 2 demonstrate how as we branch out into new territory, we find ourselves moving more and more toward drugs of known clinical risk; eg, mind-altering agents or drugs of abuse. These agents may offer risk-benefit ratios that can ultimately prove to be less attractive than what we might have wanted when we ventured on the journey. Unfortunately, there has been little dialogue about the limitations of several of these agents.

In the case of esketamine, the notion has been that the drug is a blocker of the N-methyl-d-aspartate (NMDA) glutamate receptor, suggesting it is relatively safe. However, we and others have now clearly demonstrated that the antidepressant effect in humans and the antidepressant behavioral effects in rodents are mediated via the mu opioid receptor.^1-3 This implies an abuse and dependence risk, and it is concerning that there has been much emphasis on ketamine’s effect on the NMDA glutamate receptor and not enough on this opioid effect, even though the very active enantiomer esketamine demonstrates relatively equal micromolar binding to both mu and NMDA receptors. Understanding the biology of major depression better and elucidating the key mechanisms of action of agents are both needed if we are to develop more effective and still safe agents.

One approach that has been applied recently is target validation that purports to use functional MRI to assess behavioral and cognitive effects of drugs to allow inferences regarding efficacy in specific disorders. As we have discussed in a recent paper published in the American Journal of Psychiatry,⁴ this can be quite misleading and may provide both false positive and negative information. From my perspective, these tests do not appear sensitive enough to screen for patients having a disorder, nor for assessing possible drug effects in those patients. Thus, it is unclear if they can provide answers today that we can be confident in.

Continue to: Dr. Aftab...

For this Psychiatry Leaders’ Perspectives, Awais Aftab, MD, interviewed Alan F. Schatzberg, MD. Dr. Schatzberg is the Kenneth T. Norris, Jr., Professor of Psychiatry and Behavioral Sciences at Stanford University. He served as the Chair of the Department at Stanford until 2010 and currently directs the Stanford Mood Disorders Center. He was the 136th president of the American Psychiatric Association (APA) (2009-2010). He has been an active investigator in the biology and psycho­pharmacology of depressive disorders, and has authored more than 700 publications and abstracts, including Schatzberg’s Manual of Clinical Psychopharmacology. Dr. Schatzberg is also the coeditor of the Textbook of Psychopharmacology with Charles B. Nemeroff, MD, PhD. He is a Past President of the American College of Neuropsychopharmacology (ACNP) and the Society of Biological Psychiatry, and was also the Secretary-General of the International Society of Psychoneuroendocrinology (ISPNE). In 2003, he was elected to the Institute of Medicine of the National Academy of Sciences (National Academy of Medicine). He has received numerous prestigious awards, including the 2005 Distinguished Service in Psychiatry Award from the American College of Psychiatrists, the 2005 Falcone Award from the National Alliance for Research in Schizophrenia and Affective Disorders, the 2014 Kraepelin Gold Medal from the Max Planck Institute of Psychiatry, the 2015 Gold Medal from the Society of Biological Psychiatry, the 2015 Lifetime Achievement Award of the ISPNE, the 2017 Julius Axelrod Mentorship Award from the ACNP, the 2018 Donald Klein, MD, Lifetime Achievement Award from the American Society of Clinical Psychopharmacology, and the 2018 Jules Marmor, MD, Award for Biopsychosocial Research from the APA.

Dr. Aftab: You have devoted much of your career to the development of psychopharmacology. What is your perspective on where the field of psychopharmacology stands at present, especially amid the widespread recognition of “treatment resistance” as a pervasive phenomenon and the scarcity of validated neurobiologic etiological models for psychiatric disorders?

Dr. Schatzberg: We have made considerable progress in the development of new classes of agents for major depression, but as we develop new agents, we still see a large percentage of patients who do not seem to demonstrate adequate responses, particularly in major depressive disorder. This has driven us to look for agents that work differently than previous ones. Although we have some new agents with seeming efficacy and newer mechanisms of action, eg, esketamine, these have largely been derived from clinical, often serendipitous, observations of antidepressant effects rather than from prospective development based on a known pharmacological effect or a biological construct of the disorder. Another intriguing and possibly effective anxiolytic and antidepressive agent is psilocybin, whose potential use is largely derived from clinicians who found it helpful in their practices in combination with psychotherapy. These 2 demonstrate how as we branch out into new territory, we find ourselves moving more and more toward drugs of known clinical risk; eg, mind-altering agents or drugs of abuse. These agents may offer risk-benefit ratios that can ultimately prove to be less attractive than what we might have wanted when we ventured on the journey. Unfortunately, there has been little dialogue about the limitations of several of these agents.

In the case of esketamine, the notion has been that the drug is a blocker of the N-methyl-d-aspartate (NMDA) glutamate receptor, suggesting it is relatively safe. However, we and others have now clearly demonstrated that the antidepressant effect in humans and the antidepressant behavioral effects in rodents are mediated via the mu opioid receptor.^1-3 This implies an abuse and dependence risk, and it is concerning that there has been much emphasis on ketamine’s effect on the NMDA glutamate receptor and not enough on this opioid effect, even though the very active enantiomer esketamine demonstrates relatively equal micromolar binding to both mu and NMDA receptors. Understanding the biology of major depression better and elucidating the key mechanisms of action of agents are both needed if we are to develop more effective and still safe agents.

One approach that has been applied recently is target validation that purports to use functional MRI to assess behavioral and cognitive effects of drugs to allow inferences regarding efficacy in specific disorders. As we have discussed in a recent paper published in the American Journal of Psychiatry,⁴ this can be quite misleading and may provide both false positive and negative information. From my perspective, these tests do not appear sensitive enough to screen for patients having a disorder, nor for assessing possible drug effects in those patients. Thus, it is unclear if they can provide answers today that we can be confident in.

Continue to: Dr. Aftab...

For this Psychiatry Leaders’ Perspectives, Awais Aftab, MD, interviewed Alan F. Schatzberg, MD. Dr. Schatzberg is the Kenneth T. Norris, Jr., Professor of Psychiatry and Behavioral Sciences at Stanford University. He served as the Chair of the Department at Stanford until 2010 and currently directs the Stanford Mood Disorders Center. He was the 136th president of the American Psychiatric Association (APA) (2009-2010). He has been an active investigator in the biology and psycho­pharmacology of depressive disorders, and has authored more than 700 publications and abstracts, including Schatzberg’s Manual of Clinical Psychopharmacology. Dr. Schatzberg is also the coeditor of the Textbook of Psychopharmacology with Charles B. Nemeroff, MD, PhD. He is a Past President of the American College of Neuropsychopharmacology (ACNP) and the Society of Biological Psychiatry, and was also the Secretary-General of the International Society of Psychoneuroendocrinology (ISPNE). In 2003, he was elected to the Institute of Medicine of the National Academy of Sciences (National Academy of Medicine). He has received numerous prestigious awards, including the 2005 Distinguished Service in Psychiatry Award from the American College of Psychiatrists, the 2005 Falcone Award from the National Alliance for Research in Schizophrenia and Affective Disorders, the 2014 Kraepelin Gold Medal from the Max Planck Institute of Psychiatry, the 2015 Gold Medal from the Society of Biological Psychiatry, the 2015 Lifetime Achievement Award of the ISPNE, the 2017 Julius Axelrod Mentorship Award from the ACNP, the 2018 Donald Klein, MD, Lifetime Achievement Award from the American Society of Clinical Psychopharmacology, and the 2018 Jules Marmor, MD, Award for Biopsychosocial Research from the APA.

Dr. Aftab: You have devoted much of your career to the development of psychopharmacology. What is your perspective on where the field of psychopharmacology stands at present, especially amid the widespread recognition of “treatment resistance” as a pervasive phenomenon and the scarcity of validated neurobiologic etiological models for psychiatric disorders?

Dr. Schatzberg: We have made considerable progress in the development of new classes of agents for major depression, but as we develop new agents, we still see a large percentage of patients who do not seem to demonstrate adequate responses, particularly in major depressive disorder. This has driven us to look for agents that work differently than previous ones. Although we have some new agents with seeming efficacy and newer mechanisms of action, eg, esketamine, these have largely been derived from clinical, often serendipitous, observations of antidepressant effects rather than from prospective development based on a known pharmacological effect or a biological construct of the disorder. Another intriguing and possibly effective anxiolytic and antidepressive agent is psilocybin, whose potential use is largely derived from clinicians who found it helpful in their practices in combination with psychotherapy. These 2 demonstrate how as we branch out into new territory, we find ourselves moving more and more toward drugs of known clinical risk; eg, mind-altering agents or drugs of abuse. These agents may offer risk-benefit ratios that can ultimately prove to be less attractive than what we might have wanted when we ventured on the journey. Unfortunately, there has been little dialogue about the limitations of several of these agents.

In the case of esketamine, the notion has been that the drug is a blocker of the N-methyl-d-aspartate (NMDA) glutamate receptor, suggesting it is relatively safe. However, we and others have now clearly demonstrated that the antidepressant effect in humans and the antidepressant behavioral effects in rodents are mediated via the mu opioid receptor.^1-3 This implies an abuse and dependence risk, and it is concerning that there has been much emphasis on ketamine’s effect on the NMDA glutamate receptor and not enough on this opioid effect, even though the very active enantiomer esketamine demonstrates relatively equal micromolar binding to both mu and NMDA receptors. Understanding the biology of major depression better and elucidating the key mechanisms of action of agents are both needed if we are to develop more effective and still safe agents.

One approach that has been applied recently is target validation that purports to use functional MRI to assess behavioral and cognitive effects of drugs to allow inferences regarding efficacy in specific disorders. As we have discussed in a recent paper published in the American Journal of Psychiatry,⁴ this can be quite misleading and may provide both false positive and negative information. From my perspective, these tests do not appear sensitive enough to screen for patients having a disorder, nor for assessing possible drug effects in those patients. Thus, it is unclear if they can provide answers today that we can be confident in.

Continue to: Dr. Aftab...

The ongoing COVID-19 pandemic was the biggest medical news or event of 2021, according to an overwhelming 84% of 987 of our readers who answered a recent Medscape Medical News poll. Perhaps no surprise there.

Coming in distant second, at 26%, was the new law requiring that patients be granted electronic access to clinical notes. The controversial Food and Drug Administration approval of aducanumab (Aduhelm, Biogen/Eisai) to treat Alzheimer’s disease was next, cited by almost 16% when asked what they would remember most about 2021.

Coming in at 10% or less were the permanent end to the Step 2 Clinical Skills test, the JAMA deputy editor resignation over controversial comments, and an “other” option that allowed for write-in responses.

It should be noted respondents could choose up to three answers to this and other questions in this survey, except for questions about profession and specialty.
 

Exciting news in 2021

Widespread availability of COVID-19 vaccines was the No. 1 response – chosen by 85% – when asked what medical news or events excited them in 2021.

FDA clearance of a 5-minute test for early dementia was selected by 22%, followed by almost 16% citing approval in October 2021 of abemaciclib (Verzenio, Lilly) “described as the first advance for early breast cancer in 20 years.”

The resignation of JAMA editors over a podcast on race rounded out the list of exciting medical news or events – coming in fourth at 11%. A total 5% of readers chose “other” and were asked to specify what news or events excited them in 2021.
 

A frustrating year?

Medscape also asked readers what medical news or events frustrated them in 2021. A majority, 81%, chose COVID-19 vaccine hesitancy or refusal. Almost one-third, 31%, chose the effect of climate change on health worldwide.

Some of the most memorable news or events of 2021 were also selected as frustrating by readers. For example, 22% were frustrated by the law requiring that patients be granted electronic access to clinical notes, followed by 19% who referred to the aducanumab approval in June. Furthermore, about 12% selected the JAMA resignations.
 

A shocking survey question

Asked what medical news or event from 2021 shocked readers, COVID-19 vaccine hesitancy or refusal was the most common answer, at 69%.

The U.S. Preventive Services Task Force ruling out aspirin in people over age 60 for primary prevention of cardiovascular disease shocked 36% of respondents.

Coming in third and fourth on the survey were the two JAMA editors resigning after a podcast on race, chosen by 19%, and the demise of the Step 2 Clinical Skills test, selected by 18%.

Interestingly, almost 96% of respondents were physicians. Less than 1% were residents, physician assistants, or nurses. Respondents also represented a wide range of specialties. From a list of 29 possible specialties, including “other,” family medicine, internal medicine, and psychiatry were the most common.

For more on the year that was 2021, see the Medscape Year in Medicine 2021: News That Made a Difference slideshow. Read Medscape’s full Year in Medicine report.

Wondering what stood out most to our readers in 2020? Here is a story about the results of a similar survey 1 year ago.

A version of this article first appeared on Medscape.com.

The ongoing COVID-19 pandemic was the biggest medical news or event of 2021, according to an overwhelming 84% of 987 of our readers who answered a recent Medscape Medical News poll. Perhaps no surprise there.

Coming in distant second, at 26%, was the new law requiring that patients be granted electronic access to clinical notes. The controversial Food and Drug Administration approval of aducanumab (Aduhelm, Biogen/Eisai) to treat Alzheimer’s disease was next, cited by almost 16% when asked what they would remember most about 2021.

Coming in at 10% or less were the permanent end to the Step 2 Clinical Skills test, the JAMA deputy editor resignation over controversial comments, and an “other” option that allowed for write-in responses.

It should be noted respondents could choose up to three answers to this and other questions in this survey, except for questions about profession and specialty.
 

Exciting news in 2021

Widespread availability of COVID-19 vaccines was the No. 1 response – chosen by 85% – when asked what medical news or events excited them in 2021.

FDA clearance of a 5-minute test for early dementia was selected by 22%, followed by almost 16% citing approval in October 2021 of abemaciclib (Verzenio, Lilly) “described as the first advance for early breast cancer in 20 years.”

The resignation of JAMA editors over a podcast on race rounded out the list of exciting medical news or events – coming in fourth at 11%. A total 5% of readers chose “other” and were asked to specify what news or events excited them in 2021.
 

A frustrating year?

Medscape also asked readers what medical news or events frustrated them in 2021. A majority, 81%, chose COVID-19 vaccine hesitancy or refusal. Almost one-third, 31%, chose the effect of climate change on health worldwide.

Some of the most memorable news or events of 2021 were also selected as frustrating by readers. For example, 22% were frustrated by the law requiring that patients be granted electronic access to clinical notes, followed by 19% who referred to the aducanumab approval in June. Furthermore, about 12% selected the JAMA resignations.
 

A shocking survey question

Asked what medical news or event from 2021 shocked readers, COVID-19 vaccine hesitancy or refusal was the most common answer, at 69%.

The U.S. Preventive Services Task Force ruling out aspirin in people over age 60 for primary prevention of cardiovascular disease shocked 36% of respondents.

Coming in third and fourth on the survey were the two JAMA editors resigning after a podcast on race, chosen by 19%, and the demise of the Step 2 Clinical Skills test, selected by 18%.

Interestingly, almost 96% of respondents were physicians. Less than 1% were residents, physician assistants, or nurses. Respondents also represented a wide range of specialties. From a list of 29 possible specialties, including “other,” family medicine, internal medicine, and psychiatry were the most common.

For more on the year that was 2021, see the Medscape Year in Medicine 2021: News That Made a Difference slideshow. Read Medscape’s full Year in Medicine report.

Wondering what stood out most to our readers in 2020? Here is a story about the results of a similar survey 1 year ago.

A version of this article first appeared on Medscape.com.

The ongoing COVID-19 pandemic was the biggest medical news or event of 2021, according to an overwhelming 84% of 987 of our readers who answered a recent Medscape Medical News poll. Perhaps no surprise there.

Coming in distant second, at 26%, was the new law requiring that patients be granted electronic access to clinical notes. The controversial Food and Drug Administration approval of aducanumab (Aduhelm, Biogen/Eisai) to treat Alzheimer’s disease was next, cited by almost 16% when asked what they would remember most about 2021.

Coming in at 10% or less were the permanent end to the Step 2 Clinical Skills test, the JAMA deputy editor resignation over controversial comments, and an “other” option that allowed for write-in responses.

It should be noted respondents could choose up to three answers to this and other questions in this survey, except for questions about profession and specialty.
 

Exciting news in 2021

Widespread availability of COVID-19 vaccines was the No. 1 response – chosen by 85% – when asked what medical news or events excited them in 2021.

FDA clearance of a 5-minute test for early dementia was selected by 22%, followed by almost 16% citing approval in October 2021 of abemaciclib (Verzenio, Lilly) “described as the first advance for early breast cancer in 20 years.”

The resignation of JAMA editors over a podcast on race rounded out the list of exciting medical news or events – coming in fourth at 11%. A total 5% of readers chose “other” and were asked to specify what news or events excited them in 2021.
 

A frustrating year?

Medscape also asked readers what medical news or events frustrated them in 2021. A majority, 81%, chose COVID-19 vaccine hesitancy or refusal. Almost one-third, 31%, chose the effect of climate change on health worldwide.

Some of the most memorable news or events of 2021 were also selected as frustrating by readers. For example, 22% were frustrated by the law requiring that patients be granted electronic access to clinical notes, followed by 19% who referred to the aducanumab approval in June. Furthermore, about 12% selected the JAMA resignations.
 

A shocking survey question

Asked what medical news or event from 2021 shocked readers, COVID-19 vaccine hesitancy or refusal was the most common answer, at 69%.

The U.S. Preventive Services Task Force ruling out aspirin in people over age 60 for primary prevention of cardiovascular disease shocked 36% of respondents.

Coming in third and fourth on the survey were the two JAMA editors resigning after a podcast on race, chosen by 19%, and the demise of the Step 2 Clinical Skills test, selected by 18%.

Interestingly, almost 96% of respondents were physicians. Less than 1% were residents, physician assistants, or nurses. Respondents also represented a wide range of specialties. From a list of 29 possible specialties, including “other,” family medicine, internal medicine, and psychiatry were the most common.

For more on the year that was 2021, see the Medscape Year in Medicine 2021: News That Made a Difference slideshow. Read Medscape’s full Year in Medicine report.

Wondering what stood out most to our readers in 2020? Here is a story about the results of a similar survey 1 year ago.

A version of this article first appeared on Medscape.com.

Inpatient violence is a significant problem for psychiatric facilities because it can have serious physical and psychological consequences for both staff and patients.¹ Victimized staff can experience decreased productivity and emotional distress, while victimized patients can experience disrupted treatment and delayed discharge.¹ Twenty-five to 35% of psychiatric inpatients display violent behavior during their hospitalization.¹ A subset are extreme offenders.^1,2 This small group of violent patients accounts for the majority of inpatient violence and the most serious injuries.^1,2

Reducing inpatient violence starts with conducting a targeted violence risk assessment to identify patients who are at elevated risk of being violent. Although conducting a targeted violence risk assessment is beyond the scope of this article, here I outline practical steps that clinicians can take to reduce the risk of inpatient violence. These steps complement and overlap with those I described in “Workplace violence: Enhance your safety in outpatient settings” (Pearls, Current Psychiatry, August 2021, p. 37-38). These approaches should be customized for your setting with the possible assistance and input of legal counsel, risk management, and law enforcement.³

Identify underlying motives. Inpatient violence is often a result of 3 primary psychiatric etiologies: difficulty with impulse control, symptoms of psychosis, or predatory traits.¹ Impulsivity drives most of the violence on inpatient units, followed by predatory violence and symptoms of psychosis.¹ Once you identify the psychiatric motive, you can develop an individualized, tailored treatment plan to reduce the risk of violence. The treatment plan can include using de-escalation techniques, administering scheduled and as-needed medications to target underlying symptoms, having patients assume responsibility for their behaviors, holding patients accountable for their behaviors, and other psychosocial interventions.¹ Use seclusion and restraint only when it is the least restrictive means of providing safety.^1,4

Develop plans and policies. As you would do in an outpatient setting, assess for hazards within the inpatient unit. Plan for the possible types of violence that may occur on the unit (eg, physical violence against hospital personnel and/or other patients, verbal harassment, etc).³ Develop policies and procedures to identify, communicate, track, and document patients’ concerning behaviors (eg, posting a safety board where staff can record aggressive behaviors and other safety issues).^3,4 When developing these plans and policies, include patients by creating patient/staff workgroups to develop expectations for civil behavior that apply to both patients and staff, as well as training patients to co-lead groups dealing with accepting responsibility for their own recovery.⁵ These plans and policies should include informing patients that threats and violence will not be tolerated. Frequently review these plans and policies with patients and staff.

Provide communication and education. Maintain strong psychiatric leadership on the unit that encourages open lines of communication. Encourage staff to promptly report incidents. Frequently ask staff if they have any safety concerns, and solicit their opinions on how to reduce risks.⁴ Include discussions about safety during staff and community meetings. Communicate patients’ behaviors that are distressing or undesired (eg, threats, harassment, etc) to all unit personnel.³ Notify staff when you plan to interact with a patient who is at risk for violence or is acutely agitated.⁴ Teach staff how to recognize the nonverbal warning signs of behavior escalation and provide training on proper de-escalation and response.^3,4 Also train staff on how to develop strong therapeutic alliances with patients.¹ After a violent incident, use the postincident debriefing session to gather information that can be used to develop additional interventions and reduce the risk of subsequent violence.¹

Implement common-sense strategies. Ensure that there are adequate numbers of nursing staff during each shift.¹ Avoid overcrowded units, hallways, and common areas. Consider additional monitoring during unit transition times, such as during shift changes, meals, and medication administration.¹ Avoid excessive noise.¹ Employ one-to-one staff observation as clinically indicated.¹ Avoid taking an authoritarian stance when explaining to patients why their requests have been denied⁴; if possible, when you are unable to meet a patient’s demands, offer them choices.^1,4 If feasible, accompany patients to a calmer space where they can de-escalate.¹ Install video surveillance cameras at entrances, exits, and other strategic locations and post signs signaling their presence.³ Install panic buttons at the nursing station and other areas (eg, restrooms).³

Ensure your personal safety. As mentioned previously, do not interact with a patient who has recently been aggressive or has voiced threats without adequate staff support.⁴ During the patient encounter, leave space between you and the patient.¹ Avoid having your back to the exit of the room,^3,4 and make sure the patient is not blocking the exit and that you can leave the room quickly if needed. Don’t wear anything that could be used as a weapon against you (eg, ties or necklaces) or could impede your escape.⁴ Avoid wearing valuables that might be damaged during a “take down.”⁴ If feasible, wear an audible alarm.³

Inpatient violence is a significant problem for psychiatric facilities because it can have serious physical and psychological consequences for both staff and patients.¹ Victimized staff can experience decreased productivity and emotional distress, while victimized patients can experience disrupted treatment and delayed discharge.¹ Twenty-five to 35% of psychiatric inpatients display violent behavior during their hospitalization.¹ A subset are extreme offenders.^1,2 This small group of violent patients accounts for the majority of inpatient violence and the most serious injuries.^1,2

Reducing inpatient violence starts with conducting a targeted violence risk assessment to identify patients who are at elevated risk of being violent. Although conducting a targeted violence risk assessment is beyond the scope of this article, here I outline practical steps that clinicians can take to reduce the risk of inpatient violence. These steps complement and overlap with those I described in “Workplace violence: Enhance your safety in outpatient settings” (Pearls, Current Psychiatry, August 2021, p. 37-38). These approaches should be customized for your setting with the possible assistance and input of legal counsel, risk management, and law enforcement.³

Identify underlying motives. Inpatient violence is often a result of 3 primary psychiatric etiologies: difficulty with impulse control, symptoms of psychosis, or predatory traits.¹ Impulsivity drives most of the violence on inpatient units, followed by predatory violence and symptoms of psychosis.¹ Once you identify the psychiatric motive, you can develop an individualized, tailored treatment plan to reduce the risk of violence. The treatment plan can include using de-escalation techniques, administering scheduled and as-needed medications to target underlying symptoms, having patients assume responsibility for their behaviors, holding patients accountable for their behaviors, and other psychosocial interventions.¹ Use seclusion and restraint only when it is the least restrictive means of providing safety.^1,4

Develop plans and policies. As you would do in an outpatient setting, assess for hazards within the inpatient unit. Plan for the possible types of violence that may occur on the unit (eg, physical violence against hospital personnel and/or other patients, verbal harassment, etc).³ Develop policies and procedures to identify, communicate, track, and document patients’ concerning behaviors (eg, posting a safety board where staff can record aggressive behaviors and other safety issues).^3,4 When developing these plans and policies, include patients by creating patient/staff workgroups to develop expectations for civil behavior that apply to both patients and staff, as well as training patients to co-lead groups dealing with accepting responsibility for their own recovery.⁵ These plans and policies should include informing patients that threats and violence will not be tolerated. Frequently review these plans and policies with patients and staff.

Provide communication and education. Maintain strong psychiatric leadership on the unit that encourages open lines of communication. Encourage staff to promptly report incidents. Frequently ask staff if they have any safety concerns, and solicit their opinions on how to reduce risks.⁴ Include discussions about safety during staff and community meetings. Communicate patients’ behaviors that are distressing or undesired (eg, threats, harassment, etc) to all unit personnel.³ Notify staff when you plan to interact with a patient who is at risk for violence or is acutely agitated.⁴ Teach staff how to recognize the nonverbal warning signs of behavior escalation and provide training on proper de-escalation and response.^3,4 Also train staff on how to develop strong therapeutic alliances with patients.¹ After a violent incident, use the postincident debriefing session to gather information that can be used to develop additional interventions and reduce the risk of subsequent violence.¹

Implement common-sense strategies. Ensure that there are adequate numbers of nursing staff during each shift.¹ Avoid overcrowded units, hallways, and common areas. Consider additional monitoring during unit transition times, such as during shift changes, meals, and medication administration.¹ Avoid excessive noise.¹ Employ one-to-one staff observation as clinically indicated.¹ Avoid taking an authoritarian stance when explaining to patients why their requests have been denied⁴; if possible, when you are unable to meet a patient’s demands, offer them choices.^1,4 If feasible, accompany patients to a calmer space where they can de-escalate.¹ Install video surveillance cameras at entrances, exits, and other strategic locations and post signs signaling their presence.³ Install panic buttons at the nursing station and other areas (eg, restrooms).³

Ensure your personal safety. As mentioned previously, do not interact with a patient who has recently been aggressive or has voiced threats without adequate staff support.⁴ During the patient encounter, leave space between you and the patient.¹ Avoid having your back to the exit of the room,^3,4 and make sure the patient is not blocking the exit and that you can leave the room quickly if needed. Don’t wear anything that could be used as a weapon against you (eg, ties or necklaces) or could impede your escape.⁴ Avoid wearing valuables that might be damaged during a “take down.”⁴ If feasible, wear an audible alarm.³

Inpatient violence is a significant problem for psychiatric facilities because it can have serious physical and psychological consequences for both staff and patients.¹ Victimized staff can experience decreased productivity and emotional distress, while victimized patients can experience disrupted treatment and delayed discharge.¹ Twenty-five to 35% of psychiatric inpatients display violent behavior during their hospitalization.¹ A subset are extreme offenders.^1,2 This small group of violent patients accounts for the majority of inpatient violence and the most serious injuries.^1,2

Reducing inpatient violence starts with conducting a targeted violence risk assessment to identify patients who are at elevated risk of being violent. Although conducting a targeted violence risk assessment is beyond the scope of this article, here I outline practical steps that clinicians can take to reduce the risk of inpatient violence. These steps complement and overlap with those I described in “Workplace violence: Enhance your safety in outpatient settings” (Pearls, Current Psychiatry, August 2021, p. 37-38). These approaches should be customized for your setting with the possible assistance and input of legal counsel, risk management, and law enforcement.³

Identify underlying motives. Inpatient violence is often a result of 3 primary psychiatric etiologies: difficulty with impulse control, symptoms of psychosis, or predatory traits.¹ Impulsivity drives most of the violence on inpatient units, followed by predatory violence and symptoms of psychosis.¹ Once you identify the psychiatric motive, you can develop an individualized, tailored treatment plan to reduce the risk of violence. The treatment plan can include using de-escalation techniques, administering scheduled and as-needed medications to target underlying symptoms, having patients assume responsibility for their behaviors, holding patients accountable for their behaviors, and other psychosocial interventions.¹ Use seclusion and restraint only when it is the least restrictive means of providing safety.^1,4

Develop plans and policies. As you would do in an outpatient setting, assess for hazards within the inpatient unit. Plan for the possible types of violence that may occur on the unit (eg, physical violence against hospital personnel and/or other patients, verbal harassment, etc).³ Develop policies and procedures to identify, communicate, track, and document patients’ concerning behaviors (eg, posting a safety board where staff can record aggressive behaviors and other safety issues).^3,4 When developing these plans and policies, include patients by creating patient/staff workgroups to develop expectations for civil behavior that apply to both patients and staff, as well as training patients to co-lead groups dealing with accepting responsibility for their own recovery.⁵ These plans and policies should include informing patients that threats and violence will not be tolerated. Frequently review these plans and policies with patients and staff.

Provide communication and education. Maintain strong psychiatric leadership on the unit that encourages open lines of communication. Encourage staff to promptly report incidents. Frequently ask staff if they have any safety concerns, and solicit their opinions on how to reduce risks.⁴ Include discussions about safety during staff and community meetings. Communicate patients’ behaviors that are distressing or undesired (eg, threats, harassment, etc) to all unit personnel.³ Notify staff when you plan to interact with a patient who is at risk for violence or is acutely agitated.⁴ Teach staff how to recognize the nonverbal warning signs of behavior escalation and provide training on proper de-escalation and response.^3,4 Also train staff on how to develop strong therapeutic alliances with patients.¹ After a violent incident, use the postincident debriefing session to gather information that can be used to develop additional interventions and reduce the risk of subsequent violence.¹

Implement common-sense strategies. Ensure that there are adequate numbers of nursing staff during each shift.¹ Avoid overcrowded units, hallways, and common areas. Consider additional monitoring during unit transition times, such as during shift changes, meals, and medication administration.¹ Avoid excessive noise.¹ Employ one-to-one staff observation as clinically indicated.¹ Avoid taking an authoritarian stance when explaining to patients why their requests have been denied⁴; if possible, when you are unable to meet a patient’s demands, offer them choices.^1,4 If feasible, accompany patients to a calmer space where they can de-escalate.¹ Install video surveillance cameras at entrances, exits, and other strategic locations and post signs signaling their presence.³ Install panic buttons at the nursing station and other areas (eg, restrooms).³

Ensure your personal safety. As mentioned previously, do not interact with a patient who has recently been aggressive or has voiced threats without adequate staff support.⁴ During the patient encounter, leave space between you and the patient.¹ Avoid having your back to the exit of the room,^3,4 and make sure the patient is not blocking the exit and that you can leave the room quickly if needed. Don’t wear anything that could be used as a weapon against you (eg, ties or necklaces) or could impede your escape.⁴ Avoid wearing valuables that might be damaged during a “take down.”⁴ If feasible, wear an audible alarm.³

Perinatal mental health disorders such as perinatal depression are common complications of pregnancy¹ and cause significant disability in mothers and children.² Yet despite facing higher 12-month rates of depression than White women,³ Black and Hispanic women are less likely than White women to be diagnosed with and receive treatment for postpartum depression.⁴

In addition to leading to >800,000 deaths in the United States alone (as of mid-December 2021),⁵ COVID-19 has disrupted health care delivery, including perinatal mental health services.⁶ Emerging data also describe neuropsychiatric effects of COVID-19 on both infected and uninfected individuals.⁷ Because Black and Hispanic individuals bear a disproportionate burden of COVID-19,⁸ compared to White women, women of color stand to be more adversely impacted by the direct effects of the disease as well as by related disruptions in perinatal psychiatry services.

Reasons for perinatal health disparities are multifactorial, complex, and interrelated. Disparities, which can be seen as proportionate differences in access by members of minority groups compared with groups in the majority, are related to differences in mental health screening, health care accessibility, and decisions to initiate treatment. In this commentary, we define “women of color” as non-White women, and focus on how traditional barriers to perinatal mental health treatment in women of color are exacerbated in the era of COVID-19. We focus primarily on postpartum depression because it is the peripartum mental health disorder with the highest likelihood of uptake in screening and treatment practices; however, disparities may be present in other mental health disorders during this period.

Gaps in screening and identification

Postpartum depression is a source of mitigatable risk for mother and neonate in the peripartum period, and the topic of screening for its presence arises in educational and best practices materials for primary care, OB-GYN, and pediatric care clinicians. Despite considerable evidence demonstrating better outcomes (for mother and child) with early detection and treatment of perinatal mental health disorders, racial and ethnic disparities persist in the screening process. At baseline, Black, Asian, and American Indian and Alaska Native women are less likely than White women to be screened for depression.⁹ Research shows that screening practices differ based on type of clinic, with one study noting that patients of family physicians were more likely to be screened for perinatal depression than were patients of OB-GYNs or nursing midwives.⁹ Even after adjusting for clinic type, racial differences in screening persist, with fewer women of color screened than their White counterparts.⁹ The literature consistently shows that within the same care settings, physicians deliver less information, less supportive talk, and less evidence-based treatment to Black and Hispanic patients and patients of lower economic status.^10-12 Patient-clinician ethnic concordance is shown to positively impact the therapeutic relationship; at present, depressive symptoms are underrecognized in people of color, for whom referral to psychiatric care may be further compounded by inadequate knowledge of psychiatric resources.^10-13

Data from Medicaid programs reveal that compared to White women, Black women are less likely to attend postpartum visits, which leads to a downstream effect on the ability to identify Black women with mental health disorders during the postpartum period.¹⁴ In addition to experiencing fewer opportunities for detection, women of color are more likely to report somatic symptoms of depression, which may not be detected in routinely employed perinatal depression screening tools.¹⁵

Continue to: Disparities in accessibility and treatment...

Disparities in accessibility and treatment

Black women are more likely to present in crisis and, hence, to acute care settings, which is likely related to disparities in screening and early detection.^16,17 In a recent study investigating racial and ethnic differences in postpartum depression care, Chan et al¹⁶ found that Black women experience higher rates of hospital-based care compared with other racial groups. This study highlights the unavailability or inaccessibility of primary preventive measures to women in racial minority groups, which supports earlier studies that reported a correlation between access to care and severity of illness.¹⁶ Women in crisis may experience magnified disparities in access to high-quality care as they encounter institutional racism, potential loss of parental rights, and barriers due to insurance status.^17,18 Furthermore, access to care for patients who are members of racial minority groups is limited in settings where culturally competent practices are absent or diminished, or discriminatory procedures are implicitly accepted and prevalent.^12,19-22 The adverse impact of language constraints on accessibility of care is also well-documented, with recommendations such as ready access to interpreters to mitigate against miscommunications.²³

Black and Hispanic women also experience significant delays between the time of delivery and treatment initiation.⁴ Studies of postpartum depression detection and treatment in specialty and primary care clinics show that, even when they desire treatment, women of color are less likely than White women to be offered treatment for postpartum depression.²⁴ In terms of treatment options, research suggests women of color prefer psychotherapy over medication management.^25,26 However, studies show that White women are more likely to be referred to psychotherapy.²⁷ Research also reveals that Black and Hispanic women who are receptive to psychotropic medications have reduced rates of medication refills,⁴ which suggests that in these patients, counseling and monitoring adverse effects is suboptimal. In terms of treatment for substance use disorders (SUDs), after adjusting for maternal characteristics, Black and Hispanic women are significantly less likely to receive medication-assisted treatment (MAT) in pregnancy,²⁸ and MAT is significantly less likely to be available in neighborhoods more densely populated by individuals of color.^29,30

Several studies have explored possible explanations for discrepancies in treatment, including cultural expectations, differences in socioeconomic class, and racism. The stigma associated with psychiatric illness, misinformation about psychiatric treatments, and financial limitations have a substantial bearing on a patient’s willingness or ability to engage in psychiatric care.²⁵ Regarding SUDs, a fear of legal reprisal is likely to deter women of color from seeking care.³¹ Such fears are not unfounded; research has demonstrated that interactions with Child Protective Services are increased among women of color compared to White women in similar situations.³²

Furthermore, there is evidence that women of color receive less practical support, such as childcare, breastfeeding support, and transportation, during the postpartum period. Despite the preponderance of literature demonstrating the psychological benefits of breastfeeding,^33,34 structural and psychosocial barriers appear to disproportionately affect breastfeeding rates in Hispanic, Black, American Indian, and Native women, with Black women experiencing the lowest rates of breastfeeding overall.³⁵ Women in minority groups additionally experience disproportionate uncertainty about employment-based breastfeeding regulations.^35,36 Specifically, many low-income jobs are not covered under the Family and Medical Leave Act, and compared to White women, Black women return to work on average 2 weeks earlier to jobs that are less welcoming to breastfeeding.³⁵ In addition, insufficient education and support from health care settings and counselors play significant roles in disincentivizing women in minority groups from engaging in recommended breastfeeding and childcare practices.^37,38

Continue to: COVID-19’s influence on these disparities...

COVID-19’s influence on these disparities

The COVID-19 pandemic has disproportionately impacted individuals of color. Black communities have experienced a higher rate of COVID-19 infection and a higher rate of death attributed to COVID-19, even after adjusting for age, poverty, medical comorbidities, and epidemic duration.³⁹ The reasons for the disproportionate effects of the pandemic are complex and deeply ingrained in society.³⁹ Emerging data indicate that COVID-19 might also lead to increased levels of psychological distress, anxiety, and depression in pregnant women^33,40,41 and in Black women in particular.⁴² A survey of 913 pregnant women in Philadelphia conducted in May 2020 found significantly higher rates of anxiety and depression among Black women compared with White women, even after controlling for maternal age, gestational age, socioeconomic status, and marital status.⁴² A cross-sectional study of 163 women found that during the perinatal period, women of color were more likely than their White counterparts to experience negative changes in their mental health.⁴³ These differences are concerning because pregnant women who experience high levels of stress during the pandemic are at high risk for preterm delivery and perinatal complications.⁴⁴

Women of color may be disproportionately excluded by models of care that have become commonplace during the pandemic. Remote obstetric care became more common during the COVID-19 pandemic⁴⁵; however, Black and Hispanic patients have been less likely than White patients to use telehealth services.⁴⁶ Whether the differences are related to a lower likelihood of having a usual source of care, less access to digital resources, decreased awareness of the availability of telehealth, or less familiarity with digital technology, the common factor in all of the hypothesized reasons is structural racism.⁴⁶ This is despite the fact that pregnant Black women report higher rates of concern than their White peers regarding the quality of their prenatal care during the pandemic.⁴² In a small study that surveyed 100 women about their preference for obstetric care, a significantly higher proportion of White women preferred virtual visits, with non-White women preferring in-person visits.⁴⁷ Reasons cited for preferring virtual visits included convenience, safety with respect to viral transmission, compatibility with working from home, and less time waiting for the clinician; reasons cited for preferring in-person visits included a feeling of missing out on important parts of care, receiving less clinician attention, and having less of a connection with their clinician during virtual visits.⁴⁷ Women of color have lower rates of perinatal depression screening than their White counterparts,⁹ and less frequent telehealth visits might lead to a further reduction in the detection and treatment of depression and other mental health conditions in this population.

Along with increasing telehealth services during the pandemic, many hospitals implemented stricter visitation policies for patients, including women giving birth, with the potential for greater detrimental impact on women of color. Before the pandemic, a survey of >2,500 women found that up to 10% of Black women reported experiencing racism during hospitalization for obstetrics-related care.⁴⁸ These women also reported barriers to open and supportive communication with their clinicians.⁴⁸ A recent study by Gur et al⁴² found that pregnant Black women reported more worries about the birthing experience during the pandemic than White women. In a setting with restricted visitors, all women are at risk for having a lonelier birth experience, but women of color who are already concerned about barriers to communication and racist care practices also must contend with their lived experience of systemic inequity, barriers to communication, and concerns about frank racism, without the support and potential advocacy they may usually rely upon to get them through medical experiences. Furthermore, pregnant women with mental illness are at greater risk for pregnancy complications. Together, these data suggest that women in minority groups who are pregnant and have mental illness are particularly vulnerable and are at greater risk without social support and advocacy during hospitalization.

The postpartum period is accompanied by unique concerns in terms of breastfeeding and social support for women of color. Women in minority groups had lower breastfeeding rates before the pandemic. Several studies looked at the impact of COVID-19 and associated restrictions on breastfeeding. In the United Kingdom, women in minority groups were more likely to stop breastfeeding due to the challenges of COVID-19–related restrictions.⁴⁹ Compared with White women, these women were also more likely to report less practical support for breastfeeding during the pandemic.⁴⁹ Other factors associated with low breastfeeding rates include lower levels of education and stressful living conditions.⁴⁹ Though these factors were present before COVID-19, the pandemic has exacerbated these differences. Taken together, the evidence points to a role of long-standing structural and systemic inequity and racism in the health and wellbeing of women in minority groups.

A look towards solutions

Although perinatal mental health racial disparities predate the COVID-19 pandemic, differences in access to screening, identification, and treatment for mental health disorders place pregnant women of color and their children at heightened risk for poor health outcomes compared to their White counterparts during and after the pandemic. Despite the advent and progression of telehealth, existing race-based differences appear to have been maintained or exacerbated. The reasons for disparities are multifactorial and interrelated, and some of the outcomes perpetuate certain drivers of racism, which in turn drive continued inequity. Given the symptoms of depression, it is especially worrisome that clinicians may expect vulnerable women with illness-induced amotivation, anhedonia, and apathy to advocate for their own care.

Overall, the evidence confirms an imperative need—before, during, and after the COVID-19 pandemic—to provide education in mental health and cultural competency to clinicians such as obstetricians and pediatricians, who are more likely to have the first contact with women with perinatal depression. Health systems and government agencies also bear a responsibility to provide avenues for perinatal care clinicians to receive training and to increase access to culturally appropriate treatments through policy and structural changes.

Bottom Line

Racial disparities in perinatal mental health care persist despite widespread incorporation of telehealth into psychiatric services. Until causal factors are appropriately addressed through education, implementation, and structural changes, the benefits that have accompanied expanded psychiatric services via telehealth may only serve to exacerbate these differences.

Perinatal mental health disorders such as perinatal depression are common complications of pregnancy¹ and cause significant disability in mothers and children.² Yet despite facing higher 12-month rates of depression than White women,³ Black and Hispanic women are less likely than White women to be diagnosed with and receive treatment for postpartum depression.⁴

In addition to leading to >800,000 deaths in the United States alone (as of mid-December 2021),⁵ COVID-19 has disrupted health care delivery, including perinatal mental health services.⁶ Emerging data also describe neuropsychiatric effects of COVID-19 on both infected and uninfected individuals.⁷ Because Black and Hispanic individuals bear a disproportionate burden of COVID-19,⁸ compared to White women, women of color stand to be more adversely impacted by the direct effects of the disease as well as by related disruptions in perinatal psychiatry services.

Reasons for perinatal health disparities are multifactorial, complex, and interrelated. Disparities, which can be seen as proportionate differences in access by members of minority groups compared with groups in the majority, are related to differences in mental health screening, health care accessibility, and decisions to initiate treatment. In this commentary, we define “women of color” as non-White women, and focus on how traditional barriers to perinatal mental health treatment in women of color are exacerbated in the era of COVID-19. We focus primarily on postpartum depression because it is the peripartum mental health disorder with the highest likelihood of uptake in screening and treatment practices; however, disparities may be present in other mental health disorders during this period.

Gaps in screening and identification

Postpartum depression is a source of mitigatable risk for mother and neonate in the peripartum period, and the topic of screening for its presence arises in educational and best practices materials for primary care, OB-GYN, and pediatric care clinicians. Despite considerable evidence demonstrating better outcomes (for mother and child) with early detection and treatment of perinatal mental health disorders, racial and ethnic disparities persist in the screening process. At baseline, Black, Asian, and American Indian and Alaska Native women are less likely than White women to be screened for depression.⁹ Research shows that screening practices differ based on type of clinic, with one study noting that patients of family physicians were more likely to be screened for perinatal depression than were patients of OB-GYNs or nursing midwives.⁹ Even after adjusting for clinic type, racial differences in screening persist, with fewer women of color screened than their White counterparts.⁹ The literature consistently shows that within the same care settings, physicians deliver less information, less supportive talk, and less evidence-based treatment to Black and Hispanic patients and patients of lower economic status.^10-12 Patient-clinician ethnic concordance is shown to positively impact the therapeutic relationship; at present, depressive symptoms are underrecognized in people of color, for whom referral to psychiatric care may be further compounded by inadequate knowledge of psychiatric resources.^10-13

Data from Medicaid programs reveal that compared to White women, Black women are less likely to attend postpartum visits, which leads to a downstream effect on the ability to identify Black women with mental health disorders during the postpartum period.¹⁴ In addition to experiencing fewer opportunities for detection, women of color are more likely to report somatic symptoms of depression, which may not be detected in routinely employed perinatal depression screening tools.¹⁵

Continue to: Disparities in accessibility and treatment...

Disparities in accessibility and treatment

Black women are more likely to present in crisis and, hence, to acute care settings, which is likely related to disparities in screening and early detection.^16,17 In a recent study investigating racial and ethnic differences in postpartum depression care, Chan et al¹⁶ found that Black women experience higher rates of hospital-based care compared with other racial groups. This study highlights the unavailability or inaccessibility of primary preventive measures to women in racial minority groups, which supports earlier studies that reported a correlation between access to care and severity of illness.¹⁶ Women in crisis may experience magnified disparities in access to high-quality care as they encounter institutional racism, potential loss of parental rights, and barriers due to insurance status.^17,18 Furthermore, access to care for patients who are members of racial minority groups is limited in settings where culturally competent practices are absent or diminished, or discriminatory procedures are implicitly accepted and prevalent.^12,19-22 The adverse impact of language constraints on accessibility of care is also well-documented, with recommendations such as ready access to interpreters to mitigate against miscommunications.²³

Black and Hispanic women also experience significant delays between the time of delivery and treatment initiation.⁴ Studies of postpartum depression detection and treatment in specialty and primary care clinics show that, even when they desire treatment, women of color are less likely than White women to be offered treatment for postpartum depression.²⁴ In terms of treatment options, research suggests women of color prefer psychotherapy over medication management.^25,26 However, studies show that White women are more likely to be referred to psychotherapy.²⁷ Research also reveals that Black and Hispanic women who are receptive to psychotropic medications have reduced rates of medication refills,⁴ which suggests that in these patients, counseling and monitoring adverse effects is suboptimal. In terms of treatment for substance use disorders (SUDs), after adjusting for maternal characteristics, Black and Hispanic women are significantly less likely to receive medication-assisted treatment (MAT) in pregnancy,²⁸ and MAT is significantly less likely to be available in neighborhoods more densely populated by individuals of color.^29,30

Several studies have explored possible explanations for discrepancies in treatment, including cultural expectations, differences in socioeconomic class, and racism. The stigma associated with psychiatric illness, misinformation about psychiatric treatments, and financial limitations have a substantial bearing on a patient’s willingness or ability to engage in psychiatric care.²⁵ Regarding SUDs, a fear of legal reprisal is likely to deter women of color from seeking care.³¹ Such fears are not unfounded; research has demonstrated that interactions with Child Protective Services are increased among women of color compared to White women in similar situations.³²

Furthermore, there is evidence that women of color receive less practical support, such as childcare, breastfeeding support, and transportation, during the postpartum period. Despite the preponderance of literature demonstrating the psychological benefits of breastfeeding,^33,34 structural and psychosocial barriers appear to disproportionately affect breastfeeding rates in Hispanic, Black, American Indian, and Native women, with Black women experiencing the lowest rates of breastfeeding overall.³⁵ Women in minority groups additionally experience disproportionate uncertainty about employment-based breastfeeding regulations.^35,36 Specifically, many low-income jobs are not covered under the Family and Medical Leave Act, and compared to White women, Black women return to work on average 2 weeks earlier to jobs that are less welcoming to breastfeeding.³⁵ In addition, insufficient education and support from health care settings and counselors play significant roles in disincentivizing women in minority groups from engaging in recommended breastfeeding and childcare practices.^37,38

Continue to: COVID-19’s influence on these disparities...

COVID-19’s influence on these disparities

The COVID-19 pandemic has disproportionately impacted individuals of color. Black communities have experienced a higher rate of COVID-19 infection and a higher rate of death attributed to COVID-19, even after adjusting for age, poverty, medical comorbidities, and epidemic duration.³⁹ The reasons for the disproportionate effects of the pandemic are complex and deeply ingrained in society.³⁹ Emerging data indicate that COVID-19 might also lead to increased levels of psychological distress, anxiety, and depression in pregnant women^33,40,41 and in Black women in particular.⁴² A survey of 913 pregnant women in Philadelphia conducted in May 2020 found significantly higher rates of anxiety and depression among Black women compared with White women, even after controlling for maternal age, gestational age, socioeconomic status, and marital status.⁴² A cross-sectional study of 163 women found that during the perinatal period, women of color were more likely than their White counterparts to experience negative changes in their mental health.⁴³ These differences are concerning because pregnant women who experience high levels of stress during the pandemic are at high risk for preterm delivery and perinatal complications.⁴⁴

Women of color may be disproportionately excluded by models of care that have become commonplace during the pandemic. Remote obstetric care became more common during the COVID-19 pandemic⁴⁵; however, Black and Hispanic patients have been less likely than White patients to use telehealth services.⁴⁶ Whether the differences are related to a lower likelihood of having a usual source of care, less access to digital resources, decreased awareness of the availability of telehealth, or less familiarity with digital technology, the common factor in all of the hypothesized reasons is structural racism.⁴⁶ This is despite the fact that pregnant Black women report higher rates of concern than their White peers regarding the quality of their prenatal care during the pandemic.⁴² In a small study that surveyed 100 women about their preference for obstetric care, a significantly higher proportion of White women preferred virtual visits, with non-White women preferring in-person visits.⁴⁷ Reasons cited for preferring virtual visits included convenience, safety with respect to viral transmission, compatibility with working from home, and less time waiting for the clinician; reasons cited for preferring in-person visits included a feeling of missing out on important parts of care, receiving less clinician attention, and having less of a connection with their clinician during virtual visits.⁴⁷ Women of color have lower rates of perinatal depression screening than their White counterparts,⁹ and less frequent telehealth visits might lead to a further reduction in the detection and treatment of depression and other mental health conditions in this population.

Along with increasing telehealth services during the pandemic, many hospitals implemented stricter visitation policies for patients, including women giving birth, with the potential for greater detrimental impact on women of color. Before the pandemic, a survey of >2,500 women found that up to 10% of Black women reported experiencing racism during hospitalization for obstetrics-related care.⁴⁸ These women also reported barriers to open and supportive communication with their clinicians.⁴⁸ A recent study by Gur et al⁴² found that pregnant Black women reported more worries about the birthing experience during the pandemic than White women. In a setting with restricted visitors, all women are at risk for having a lonelier birth experience, but women of color who are already concerned about barriers to communication and racist care practices also must contend with their lived experience of systemic inequity, barriers to communication, and concerns about frank racism, without the support and potential advocacy they may usually rely upon to get them through medical experiences. Furthermore, pregnant women with mental illness are at greater risk for pregnancy complications. Together, these data suggest that women in minority groups who are pregnant and have mental illness are particularly vulnerable and are at greater risk without social support and advocacy during hospitalization.

The postpartum period is accompanied by unique concerns in terms of breastfeeding and social support for women of color. Women in minority groups had lower breastfeeding rates before the pandemic. Several studies looked at the impact of COVID-19 and associated restrictions on breastfeeding. In the United Kingdom, women in minority groups were more likely to stop breastfeeding due to the challenges of COVID-19–related restrictions.⁴⁹ Compared with White women, these women were also more likely to report less practical support for breastfeeding during the pandemic.⁴⁹ Other factors associated with low breastfeeding rates include lower levels of education and stressful living conditions.⁴⁹ Though these factors were present before COVID-19, the pandemic has exacerbated these differences. Taken together, the evidence points to a role of long-standing structural and systemic inequity and racism in the health and wellbeing of women in minority groups.

A look towards solutions

Although perinatal mental health racial disparities predate the COVID-19 pandemic, differences in access to screening, identification, and treatment for mental health disorders place pregnant women of color and their children at heightened risk for poor health outcomes compared to their White counterparts during and after the pandemic. Despite the advent and progression of telehealth, existing race-based differences appear to have been maintained or exacerbated. The reasons for disparities are multifactorial and interrelated, and some of the outcomes perpetuate certain drivers of racism, which in turn drive continued inequity. Given the symptoms of depression, it is especially worrisome that clinicians may expect vulnerable women with illness-induced amotivation, anhedonia, and apathy to advocate for their own care.

Overall, the evidence confirms an imperative need—before, during, and after the COVID-19 pandemic—to provide education in mental health and cultural competency to clinicians such as obstetricians and pediatricians, who are more likely to have the first contact with women with perinatal depression. Health systems and government agencies also bear a responsibility to provide avenues for perinatal care clinicians to receive training and to increase access to culturally appropriate treatments through policy and structural changes.

Bottom Line

Racial disparities in perinatal mental health care persist despite widespread incorporation of telehealth into psychiatric services. Until causal factors are appropriately addressed through education, implementation, and structural changes, the benefits that have accompanied expanded psychiatric services via telehealth may only serve to exacerbate these differences.

Perinatal mental health disorders such as perinatal depression are common complications of pregnancy¹ and cause significant disability in mothers and children.² Yet despite facing higher 12-month rates of depression than White women,³ Black and Hispanic women are less likely than White women to be diagnosed with and receive treatment for postpartum depression.⁴

In addition to leading to >800,000 deaths in the United States alone (as of mid-December 2021),⁵ COVID-19 has disrupted health care delivery, including perinatal mental health services.⁶ Emerging data also describe neuropsychiatric effects of COVID-19 on both infected and uninfected individuals.⁷ Because Black and Hispanic individuals bear a disproportionate burden of COVID-19,⁸ compared to White women, women of color stand to be more adversely impacted by the direct effects of the disease as well as by related disruptions in perinatal psychiatry services.

Reasons for perinatal health disparities are multifactorial, complex, and interrelated. Disparities, which can be seen as proportionate differences in access by members of minority groups compared with groups in the majority, are related to differences in mental health screening, health care accessibility, and decisions to initiate treatment. In this commentary, we define “women of color” as non-White women, and focus on how traditional barriers to perinatal mental health treatment in women of color are exacerbated in the era of COVID-19. We focus primarily on postpartum depression because it is the peripartum mental health disorder with the highest likelihood of uptake in screening and treatment practices; however, disparities may be present in other mental health disorders during this period.

Gaps in screening and identification

Postpartum depression is a source of mitigatable risk for mother and neonate in the peripartum period, and the topic of screening for its presence arises in educational and best practices materials for primary care, OB-GYN, and pediatric care clinicians. Despite considerable evidence demonstrating better outcomes (for mother and child) with early detection and treatment of perinatal mental health disorders, racial and ethnic disparities persist in the screening process. At baseline, Black, Asian, and American Indian and Alaska Native women are less likely than White women to be screened for depression.⁹ Research shows that screening practices differ based on type of clinic, with one study noting that patients of family physicians were more likely to be screened for perinatal depression than were patients of OB-GYNs or nursing midwives.⁹ Even after adjusting for clinic type, racial differences in screening persist, with fewer women of color screened than their White counterparts.⁹ The literature consistently shows that within the same care settings, physicians deliver less information, less supportive talk, and less evidence-based treatment to Black and Hispanic patients and patients of lower economic status.^10-12 Patient-clinician ethnic concordance is shown to positively impact the therapeutic relationship; at present, depressive symptoms are underrecognized in people of color, for whom referral to psychiatric care may be further compounded by inadequate knowledge of psychiatric resources.^10-13

Data from Medicaid programs reveal that compared to White women, Black women are less likely to attend postpartum visits, which leads to a downstream effect on the ability to identify Black women with mental health disorders during the postpartum period.¹⁴ In addition to experiencing fewer opportunities for detection, women of color are more likely to report somatic symptoms of depression, which may not be detected in routinely employed perinatal depression screening tools.¹⁵

Continue to: Disparities in accessibility and treatment...

Disparities in accessibility and treatment

Black women are more likely to present in crisis and, hence, to acute care settings, which is likely related to disparities in screening and early detection.^16,17 In a recent study investigating racial and ethnic differences in postpartum depression care, Chan et al¹⁶ found that Black women experience higher rates of hospital-based care compared with other racial groups. This study highlights the unavailability or inaccessibility of primary preventive measures to women in racial minority groups, which supports earlier studies that reported a correlation between access to care and severity of illness.¹⁶ Women in crisis may experience magnified disparities in access to high-quality care as they encounter institutional racism, potential loss of parental rights, and barriers due to insurance status.^17,18 Furthermore, access to care for patients who are members of racial minority groups is limited in settings where culturally competent practices are absent or diminished, or discriminatory procedures are implicitly accepted and prevalent.^12,19-22 The adverse impact of language constraints on accessibility of care is also well-documented, with recommendations such as ready access to interpreters to mitigate against miscommunications.²³

Black and Hispanic women also experience significant delays between the time of delivery and treatment initiation.⁴ Studies of postpartum depression detection and treatment in specialty and primary care clinics show that, even when they desire treatment, women of color are less likely than White women to be offered treatment for postpartum depression.²⁴ In terms of treatment options, research suggests women of color prefer psychotherapy over medication management.^25,26 However, studies show that White women are more likely to be referred to psychotherapy.²⁷ Research also reveals that Black and Hispanic women who are receptive to psychotropic medications have reduced rates of medication refills,⁴ which suggests that in these patients, counseling and monitoring adverse effects is suboptimal. In terms of treatment for substance use disorders (SUDs), after adjusting for maternal characteristics, Black and Hispanic women are significantly less likely to receive medication-assisted treatment (MAT) in pregnancy,²⁸ and MAT is significantly less likely to be available in neighborhoods more densely populated by individuals of color.^29,30

Several studies have explored possible explanations for discrepancies in treatment, including cultural expectations, differences in socioeconomic class, and racism. The stigma associated with psychiatric illness, misinformation about psychiatric treatments, and financial limitations have a substantial bearing on a patient’s willingness or ability to engage in psychiatric care.²⁵ Regarding SUDs, a fear of legal reprisal is likely to deter women of color from seeking care.³¹ Such fears are not unfounded; research has demonstrated that interactions with Child Protective Services are increased among women of color compared to White women in similar situations.³²

Furthermore, there is evidence that women of color receive less practical support, such as childcare, breastfeeding support, and transportation, during the postpartum period. Despite the preponderance of literature demonstrating the psychological benefits of breastfeeding,^33,34 structural and psychosocial barriers appear to disproportionately affect breastfeeding rates in Hispanic, Black, American Indian, and Native women, with Black women experiencing the lowest rates of breastfeeding overall.³⁵ Women in minority groups additionally experience disproportionate uncertainty about employment-based breastfeeding regulations.^35,36 Specifically, many low-income jobs are not covered under the Family and Medical Leave Act, and compared to White women, Black women return to work on average 2 weeks earlier to jobs that are less welcoming to breastfeeding.³⁵ In addition, insufficient education and support from health care settings and counselors play significant roles in disincentivizing women in minority groups from engaging in recommended breastfeeding and childcare practices.^37,38

Continue to: COVID-19’s influence on these disparities...

COVID-19’s influence on these disparities

The COVID-19 pandemic has disproportionately impacted individuals of color. Black communities have experienced a higher rate of COVID-19 infection and a higher rate of death attributed to COVID-19, even after adjusting for age, poverty, medical comorbidities, and epidemic duration.³⁹ The reasons for the disproportionate effects of the pandemic are complex and deeply ingrained in society.³⁹ Emerging data indicate that COVID-19 might also lead to increased levels of psychological distress, anxiety, and depression in pregnant women^33,40,41 and in Black women in particular.⁴² A survey of 913 pregnant women in Philadelphia conducted in May 2020 found significantly higher rates of anxiety and depression among Black women compared with White women, even after controlling for maternal age, gestational age, socioeconomic status, and marital status.⁴² A cross-sectional study of 163 women found that during the perinatal period, women of color were more likely than their White counterparts to experience negative changes in their mental health.⁴³ These differences are concerning because pregnant women who experience high levels of stress during the pandemic are at high risk for preterm delivery and perinatal complications.⁴⁴

Women of color may be disproportionately excluded by models of care that have become commonplace during the pandemic. Remote obstetric care became more common during the COVID-19 pandemic⁴⁵; however, Black and Hispanic patients have been less likely than White patients to use telehealth services.⁴⁶ Whether the differences are related to a lower likelihood of having a usual source of care, less access to digital resources, decreased awareness of the availability of telehealth, or less familiarity with digital technology, the common factor in all of the hypothesized reasons is structural racism.⁴⁶ This is despite the fact that pregnant Black women report higher rates of concern than their White peers regarding the quality of their prenatal care during the pandemic.⁴² In a small study that surveyed 100 women about their preference for obstetric care, a significantly higher proportion of White women preferred virtual visits, with non-White women preferring in-person visits.⁴⁷ Reasons cited for preferring virtual visits included convenience, safety with respect to viral transmission, compatibility with working from home, and less time waiting for the clinician; reasons cited for preferring in-person visits included a feeling of missing out on important parts of care, receiving less clinician attention, and having less of a connection with their clinician during virtual visits.⁴⁷ Women of color have lower rates of perinatal depression screening than their White counterparts,⁹ and less frequent telehealth visits might lead to a further reduction in the detection and treatment of depression and other mental health conditions in this population.

Along with increasing telehealth services during the pandemic, many hospitals implemented stricter visitation policies for patients, including women giving birth, with the potential for greater detrimental impact on women of color. Before the pandemic, a survey of >2,500 women found that up to 10% of Black women reported experiencing racism during hospitalization for obstetrics-related care.⁴⁸ These women also reported barriers to open and supportive communication with their clinicians.⁴⁸ A recent study by Gur et al⁴² found that pregnant Black women reported more worries about the birthing experience during the pandemic than White women. In a setting with restricted visitors, all women are at risk for having a lonelier birth experience, but women of color who are already concerned about barriers to communication and racist care practices also must contend with their lived experience of systemic inequity, barriers to communication, and concerns about frank racism, without the support and potential advocacy they may usually rely upon to get them through medical experiences. Furthermore, pregnant women with mental illness are at greater risk for pregnancy complications. Together, these data suggest that women in minority groups who are pregnant and have mental illness are particularly vulnerable and are at greater risk without social support and advocacy during hospitalization.

The postpartum period is accompanied by unique concerns in terms of breastfeeding and social support for women of color. Women in minority groups had lower breastfeeding rates before the pandemic. Several studies looked at the impact of COVID-19 and associated restrictions on breastfeeding. In the United Kingdom, women in minority groups were more likely to stop breastfeeding due to the challenges of COVID-19–related restrictions.⁴⁹ Compared with White women, these women were also more likely to report less practical support for breastfeeding during the pandemic.⁴⁹ Other factors associated with low breastfeeding rates include lower levels of education and stressful living conditions.⁴⁹ Though these factors were present before COVID-19, the pandemic has exacerbated these differences. Taken together, the evidence points to a role of long-standing structural and systemic inequity and racism in the health and wellbeing of women in minority groups.

A look towards solutions

Although perinatal mental health racial disparities predate the COVID-19 pandemic, differences in access to screening, identification, and treatment for mental health disorders place pregnant women of color and their children at heightened risk for poor health outcomes compared to their White counterparts during and after the pandemic. Despite the advent and progression of telehealth, existing race-based differences appear to have been maintained or exacerbated. The reasons for disparities are multifactorial and interrelated, and some of the outcomes perpetuate certain drivers of racism, which in turn drive continued inequity. Given the symptoms of depression, it is especially worrisome that clinicians may expect vulnerable women with illness-induced amotivation, anhedonia, and apathy to advocate for their own care.

Overall, the evidence confirms an imperative need—before, during, and after the COVID-19 pandemic—to provide education in mental health and cultural competency to clinicians such as obstetricians and pediatricians, who are more likely to have the first contact with women with perinatal depression. Health systems and government agencies also bear a responsibility to provide avenues for perinatal care clinicians to receive training and to increase access to culturally appropriate treatments through policy and structural changes.

Bottom Line

Racial disparities in perinatal mental health care persist despite widespread incorporation of telehealth into psychiatric services. Until causal factors are appropriately addressed through education, implementation, and structural changes, the benefits that have accompanied expanded psychiatric services via telehealth may only serve to exacerbate these differences.

For uncomplicated gonorrhea in a pregnant woman, what is the most appropriate treatment?

Continue to the answer...

The current recommendation from the Centers for Disease Control and Prevention for treatment of uncomplicated gonorrhea is a single 500-mg intramuscular dose of ceftriaxone. For the patient who is opposed to an intramuscular injection, an alternative treatment is cefixime 800 mg orally. With either of these regimens, if chlamydia infection cannot be excluded, the pregnant patient also should receive azithromycin 1,000 mg orally in a single dose. In a nonpregnant patient, doxycycline 100 mg orally twice daily for 7 days should be used to cover for concurrent chlamydia infection.

In a patient with an allergy to β-lactam antibiotics, an alternative regimen for treatment of uncomplicated gonorrhea is intramuscular gentamicin 240 mg plus a single 2,000-mg dose of oral azithromycin. (St Cyr S, Barbee L, Workowski KA, et al. Update to CDC’s treatment guidelines for gonococcal infection, 2020. MMWR Morbid Mortal Wkly Rep. 2020;69:1911-1916.)

For uncomplicated gonorrhea in a pregnant woman, what is the most appropriate treatment?

Continue to the answer...

The current recommendation from the Centers for Disease Control and Prevention for treatment of uncomplicated gonorrhea is a single 500-mg intramuscular dose of ceftriaxone. For the patient who is opposed to an intramuscular injection, an alternative treatment is cefixime 800 mg orally. With either of these regimens, if chlamydia infection cannot be excluded, the pregnant patient also should receive azithromycin 1,000 mg orally in a single dose. In a nonpregnant patient, doxycycline 100 mg orally twice daily for 7 days should be used to cover for concurrent chlamydia infection.

In a patient with an allergy to β-lactam antibiotics, an alternative regimen for treatment of uncomplicated gonorrhea is intramuscular gentamicin 240 mg plus a single 2,000-mg dose of oral azithromycin. (St Cyr S, Barbee L, Workowski KA, et al. Update to CDC’s treatment guidelines for gonococcal infection, 2020. MMWR Morbid Mortal Wkly Rep. 2020;69:1911-1916.)

For uncomplicated gonorrhea in a pregnant woman, what is the most appropriate treatment?

Continue to the answer...

The current recommendation from the Centers for Disease Control and Prevention for treatment of uncomplicated gonorrhea is a single 500-mg intramuscular dose of ceftriaxone. For the patient who is opposed to an intramuscular injection, an alternative treatment is cefixime 800 mg orally. With either of these regimens, if chlamydia infection cannot be excluded, the pregnant patient also should receive azithromycin 1,000 mg orally in a single dose. In a nonpregnant patient, doxycycline 100 mg orally twice daily for 7 days should be used to cover for concurrent chlamydia infection.

In a patient with an allergy to β-lactam antibiotics, an alternative regimen for treatment of uncomplicated gonorrhea is intramuscular gentamicin 240 mg plus a single 2,000-mg dose of oral azithromycin. (St Cyr S, Barbee L, Workowski KA, et al. Update to CDC’s treatment guidelines for gonococcal infection, 2020. MMWR Morbid Mortal Wkly Rep. 2020;69:1911-1916.)

Are you still wearing a cloth face mask?

Amid the rapidly spreading Omicron variant, experts stress that we all should swap cloth masks for N95 respirators or 3-ply surgical masks.

For background: N95 respirators are tightly fitting masks that cover your mouth and nose and help prevent contact with droplets and tiny particles in the air from people talking, coughing, sneezing, and spreading in other ways. Usually worn by health care workers and first responders, these masks can filter up to 95% of air droplets and particles, according to the CDC.

KN95 and KN94 masks are similar but are designed to meet international standards, unlike N95s that are approved by the Centers for Disease Control and Prevention’s National Institute for Occupational Safety and Health.

Meanwhile, a 3-ply surgical mask is a looser-fitting mask that can help prevent contact with infected droplets in the air.

But recommendations to opt for N95 and 3-ply surgical masks over cloth masks are nothing new, says Leana Wen, MD, an emergency doctor and public health professor at George Washington University, Washington.

In fact, public health experts have been urging stronger mask protection for months.

“It’s not just with Omicron that we need better masks, it was with Delta, it was with Alpha before that,” Dr. Wen said. “We have known for many months that COVID-19 is airborne, and therefore, a simple cloth mask is not going to cut it.”

Here’s what to know about these protective masks.
 

They’re necessary

Omicron is spreading much faster than previous COVID-19 variants. As it’s up to three times as likely to spread as the Delta variant, mask-wearing is paramount right now, says Anita Gupta, DO, an adjunct assistant professor of anesthesiology and critical care medicine and pain medicine at Johns Hopkins University, Baltimore.

The quality of a mask also matters a lot, said Dr. Wen.

“Double masking, including a well-fitting cloth mask on top of a surgical mask, adds additional protection,” she said. “Ideally, though, people should be wearing an N95, KN95, or KF94 when in indoor settings around other people with unknown vaccination status.”

If wearing an N95 mask causes extreme discomfort, wear it in high-risk settings where there are lots of people, like crowded restaurants and busy commuter trains, says Dr. Wen. “If you’re in a grocery store, there’s plenty of space and ventilation. You may not need an N95. I recommend that people obtain different masks and practice with them in low-risk settings before they go out in public in a high-risk setting.”

But people should wear a 3-ply surgical mask at the very least.
 

Three-ply surgical and N95 mask qualities

With 3-ply surgical masks, the fit of the mask is often more of an issue than its comfort, Dr. Wen said. But there are ways to adjust these masks, especially for those who have smaller heads.

“You can put a rubber band around the ear loops and make them a bit tighter,” said Dr. Wen. “Some people have found that using pins in their hair, that’s another way of keeping the loops in place.”

Another important tip on 3-ply surgical masks and N95s: These masks are reusable.

But how many times you should use them varies, Dr. Wen said. “As an example, if you are sweating a lot, and the mask is now really damp. Or putting it in your purse or backpack, and now it’s misshapen, and you cannot get it back to fit on your face, then it’s time to throw it away.”
 

Protection first

For some, cloth masks became somewhat of a statement, with people sporting logos of their favorite NFL team, or maybe even a fun animal print.

But you should always keep in mind the purpose of wearing a mask, Dr. Wen said. “Mask wearing is very functional and is about reducing your likelihood of contracting COVID. People should also use whatever methods inspire them, too, but for me, it’s purely a functional exercise.”

Mask wearing is not always enjoyable, but it remains critical in keeping people safe from COVID-19, especially the elderly and other high-risk people, Gupta says.

“There is lots of research and experts working hard to stop COVID-19,” she says. “It is important for all of us to remember that wearing a mask alone doesn’t make us safe.”

“We all need to keep washing our hands frequently and maintaining a distance from people, as well.”

For more information on where to find 3-ply surgical masks and N95s, check here or here to start.

A version of this article first appeared on WebMD.com.

Are you still wearing a cloth face mask?

Amid the rapidly spreading Omicron variant, experts stress that we all should swap cloth masks for N95 respirators or 3-ply surgical masks.

For background: N95 respirators are tightly fitting masks that cover your mouth and nose and help prevent contact with droplets and tiny particles in the air from people talking, coughing, sneezing, and spreading in other ways. Usually worn by health care workers and first responders, these masks can filter up to 95% of air droplets and particles, according to the CDC.

KN95 and KN94 masks are similar but are designed to meet international standards, unlike N95s that are approved by the Centers for Disease Control and Prevention’s National Institute for Occupational Safety and Health.

Meanwhile, a 3-ply surgical mask is a looser-fitting mask that can help prevent contact with infected droplets in the air.

But recommendations to opt for N95 and 3-ply surgical masks over cloth masks are nothing new, says Leana Wen, MD, an emergency doctor and public health professor at George Washington University, Washington.

In fact, public health experts have been urging stronger mask protection for months.

“It’s not just with Omicron that we need better masks, it was with Delta, it was with Alpha before that,” Dr. Wen said. “We have known for many months that COVID-19 is airborne, and therefore, a simple cloth mask is not going to cut it.”

Here’s what to know about these protective masks.
 

They’re necessary

Omicron is spreading much faster than previous COVID-19 variants. As it’s up to three times as likely to spread as the Delta variant, mask-wearing is paramount right now, says Anita Gupta, DO, an adjunct assistant professor of anesthesiology and critical care medicine and pain medicine at Johns Hopkins University, Baltimore.

The quality of a mask also matters a lot, said Dr. Wen.

“Double masking, including a well-fitting cloth mask on top of a surgical mask, adds additional protection,” she said. “Ideally, though, people should be wearing an N95, KN95, or KF94 when in indoor settings around other people with unknown vaccination status.”

If wearing an N95 mask causes extreme discomfort, wear it in high-risk settings where there are lots of people, like crowded restaurants and busy commuter trains, says Dr. Wen. “If you’re in a grocery store, there’s plenty of space and ventilation. You may not need an N95. I recommend that people obtain different masks and practice with them in low-risk settings before they go out in public in a high-risk setting.”

But people should wear a 3-ply surgical mask at the very least.
 

Three-ply surgical and N95 mask qualities

With 3-ply surgical masks, the fit of the mask is often more of an issue than its comfort, Dr. Wen said. But there are ways to adjust these masks, especially for those who have smaller heads.

“You can put a rubber band around the ear loops and make them a bit tighter,” said Dr. Wen. “Some people have found that using pins in their hair, that’s another way of keeping the loops in place.”

Another important tip on 3-ply surgical masks and N95s: These masks are reusable.

But how many times you should use them varies, Dr. Wen said. “As an example, if you are sweating a lot, and the mask is now really damp. Or putting it in your purse or backpack, and now it’s misshapen, and you cannot get it back to fit on your face, then it’s time to throw it away.”
 

Protection first

For some, cloth masks became somewhat of a statement, with people sporting logos of their favorite NFL team, or maybe even a fun animal print.

But you should always keep in mind the purpose of wearing a mask, Dr. Wen said. “Mask wearing is very functional and is about reducing your likelihood of contracting COVID. People should also use whatever methods inspire them, too, but for me, it’s purely a functional exercise.”

Mask wearing is not always enjoyable, but it remains critical in keeping people safe from COVID-19, especially the elderly and other high-risk people, Gupta says.

“There is lots of research and experts working hard to stop COVID-19,” she says. “It is important for all of us to remember that wearing a mask alone doesn’t make us safe.”

“We all need to keep washing our hands frequently and maintaining a distance from people, as well.”

For more information on where to find 3-ply surgical masks and N95s, check here or here to start.

A version of this article first appeared on WebMD.com.

Are you still wearing a cloth face mask?

Amid the rapidly spreading Omicron variant, experts stress that we all should swap cloth masks for N95 respirators or 3-ply surgical masks.

For background: N95 respirators are tightly fitting masks that cover your mouth and nose and help prevent contact with droplets and tiny particles in the air from people talking, coughing, sneezing, and spreading in other ways. Usually worn by health care workers and first responders, these masks can filter up to 95% of air droplets and particles, according to the CDC.

KN95 and KN94 masks are similar but are designed to meet international standards, unlike N95s that are approved by the Centers for Disease Control and Prevention’s National Institute for Occupational Safety and Health.

Meanwhile, a 3-ply surgical mask is a looser-fitting mask that can help prevent contact with infected droplets in the air.

But recommendations to opt for N95 and 3-ply surgical masks over cloth masks are nothing new, says Leana Wen, MD, an emergency doctor and public health professor at George Washington University, Washington.

In fact, public health experts have been urging stronger mask protection for months.

“It’s not just with Omicron that we need better masks, it was with Delta, it was with Alpha before that,” Dr. Wen said. “We have known for many months that COVID-19 is airborne, and therefore, a simple cloth mask is not going to cut it.”

Here’s what to know about these protective masks.
 

They’re necessary

Omicron is spreading much faster than previous COVID-19 variants. As it’s up to three times as likely to spread as the Delta variant, mask-wearing is paramount right now, says Anita Gupta, DO, an adjunct assistant professor of anesthesiology and critical care medicine and pain medicine at Johns Hopkins University, Baltimore.

The quality of a mask also matters a lot, said Dr. Wen.

“Double masking, including a well-fitting cloth mask on top of a surgical mask, adds additional protection,” she said. “Ideally, though, people should be wearing an N95, KN95, or KF94 when in indoor settings around other people with unknown vaccination status.”

If wearing an N95 mask causes extreme discomfort, wear it in high-risk settings where there are lots of people, like crowded restaurants and busy commuter trains, says Dr. Wen. “If you’re in a grocery store, there’s plenty of space and ventilation. You may not need an N95. I recommend that people obtain different masks and practice with them in low-risk settings before they go out in public in a high-risk setting.”

But people should wear a 3-ply surgical mask at the very least.
 

Three-ply surgical and N95 mask qualities

With 3-ply surgical masks, the fit of the mask is often more of an issue than its comfort, Dr. Wen said. But there are ways to adjust these masks, especially for those who have smaller heads.

“You can put a rubber band around the ear loops and make them a bit tighter,” said Dr. Wen. “Some people have found that using pins in their hair, that’s another way of keeping the loops in place.”

Another important tip on 3-ply surgical masks and N95s: These masks are reusable.

But how many times you should use them varies, Dr. Wen said. “As an example, if you are sweating a lot, and the mask is now really damp. Or putting it in your purse or backpack, and now it’s misshapen, and you cannot get it back to fit on your face, then it’s time to throw it away.”
 

Protection first

For some, cloth masks became somewhat of a statement, with people sporting logos of their favorite NFL team, or maybe even a fun animal print.

But you should always keep in mind the purpose of wearing a mask, Dr. Wen said. “Mask wearing is very functional and is about reducing your likelihood of contracting COVID. People should also use whatever methods inspire them, too, but for me, it’s purely a functional exercise.”

Mask wearing is not always enjoyable, but it remains critical in keeping people safe from COVID-19, especially the elderly and other high-risk people, Gupta says.

“There is lots of research and experts working hard to stop COVID-19,” she says. “It is important for all of us to remember that wearing a mask alone doesn’t make us safe.”

“We all need to keep washing our hands frequently and maintaining a distance from people, as well.”

For more information on where to find 3-ply surgical masks and N95s, check here or here to start.

A version of this article first appeared on WebMD.com.

With new cases of COVID-19 skyrocketing to more than 240,000 a day recently in the U.S., many people are facing the same situation: A family member or friend tests positive or was exposed to someone who did, and the holiday gathering, visit, or return to work is just days or hours away. Now what?

New guidance issued Dec. 27 by the Centers for Disease Control and Prevention shortens the recommended isolation and quarantine period for the general population, coming after the agency shortened the isolation period for health care workers.

This news organization reached out to two infectious disease specialists to get answers to questions that are frequently asked in these situations.
 

If you have tested positive for COVID-19, what do you do next?

“If you have tested positive, you are infected. At the moment, you are [either] symptomatically affected or presymptomatically infected,’’ said Paul A. Offit, MD, director of the Vaccine Education Center and professor of pediatrics at Children’s Hospital of Philadelphia. At that point, you need to isolate for 5 days, according to the new CDC guidance. (That period has been shortened from 10 days.)

Isolation means separating the infected person from others. Quarantine refers to things you should do if you’re exposed to the virus or you have a close contact infected with COVID-19.

Under the new CDC guidelines, after the 5-day isolation, if the infected person then has no symptoms, he or she can leave isolation and then wear a mask for 5  days.

Those who test positive also need to tell their close contacts they are positive, said Amesh Adalja, MD, a senior scholar at the Johns Hopkins Center for Health Security.  

According to the CDC, the change to a shortened quarantine time is motivated by science ‘’demonstrating that the majority of SARS-CoV-2 transmission occurs early in the course of the illness, generally in the 1-2 days prior to onset of symptoms and the 2-3 days after.”
 

If you have been exposed to someone with COVID-19, what do you do next?

“If they are vaccinated and boosted, the guidance says there is no need to quarantine,” Dr. Adalja said. But the CDC guidance does recommend these people wear a well-fitting mask at all times when around others for 10 days after exposure.

For everyone else, including the unvaccinated and those who are more than 6 months out from their second Pfizer or Moderna vaccine dose, or more than 2 months from their J&J dose, the CDC recommends a quarantine for 5 days – and wearing a mask for the 5 days after that.

On a practical level, Dr. Adalja said he thinks those who are vaccinated but not boosted could also skip the quarantine and wear a mask for 10 days. Dr. Offit agrees. Because many people exposed have trouble quarantining, Dr. Offit advises those exposed who can’t follow that guidance to be sure to wear a mask for 10 days when indoors. The CDC guidance also offers that as another strategy – that if a 5-day quarantine is not feasible, the exposed person should wear a mask for 10 days when around others.

But if  someone who was exposed gets symptoms, that person then enters the infected category and follows that guidance, Dr. Offit said.
 

When should the person who has been exposed get tested?

After the exposure, ‘’you should probably wait 2-3 days,” Dr. Offit said. “The virus has to reproduce itself.”

Testing should be done by those exposed at least once, Dr. Adalja said.

“But there’s data to support daily testing to guide their activities, but this is not CDC guidance. Home tests are sufficient for this purpose.”
 

At what point can the infected person mingle safely with others?

“Technically, if asymptomatic, 10 days without a mask, 5 days with a mask,” said Dr. Adalja. “I think this could also be guided with home test negativity being a gauge [as to whether to mingle].”

A version of this article first appeared on WebMD.com.

With new cases of COVID-19 skyrocketing to more than 240,000 a day recently in the U.S., many people are facing the same situation: A family member or friend tests positive or was exposed to someone who did, and the holiday gathering, visit, or return to work is just days or hours away. Now what?

New guidance issued Dec. 27 by the Centers for Disease Control and Prevention shortens the recommended isolation and quarantine period for the general population, coming after the agency shortened the isolation period for health care workers.

This news organization reached out to two infectious disease specialists to get answers to questions that are frequently asked in these situations.
 

If you have tested positive for COVID-19, what do you do next?

“If you have tested positive, you are infected. At the moment, you are [either] symptomatically affected or presymptomatically infected,’’ said Paul A. Offit, MD, director of the Vaccine Education Center and professor of pediatrics at Children’s Hospital of Philadelphia. At that point, you need to isolate for 5 days, according to the new CDC guidance. (That period has been shortened from 10 days.)

Isolation means separating the infected person from others. Quarantine refers to things you should do if you’re exposed to the virus or you have a close contact infected with COVID-19.

Under the new CDC guidelines, after the 5-day isolation, if the infected person then has no symptoms, he or she can leave isolation and then wear a mask for 5  days.

Those who test positive also need to tell their close contacts they are positive, said Amesh Adalja, MD, a senior scholar at the Johns Hopkins Center for Health Security.  

According to the CDC, the change to a shortened quarantine time is motivated by science ‘’demonstrating that the majority of SARS-CoV-2 transmission occurs early in the course of the illness, generally in the 1-2 days prior to onset of symptoms and the 2-3 days after.”
 

If you have been exposed to someone with COVID-19, what do you do next?

“If they are vaccinated and boosted, the guidance says there is no need to quarantine,” Dr. Adalja said. But the CDC guidance does recommend these people wear a well-fitting mask at all times when around others for 10 days after exposure.

For everyone else, including the unvaccinated and those who are more than 6 months out from their second Pfizer or Moderna vaccine dose, or more than 2 months from their J&J dose, the CDC recommends a quarantine for 5 days – and wearing a mask for the 5 days after that.

On a practical level, Dr. Adalja said he thinks those who are vaccinated but not boosted could also skip the quarantine and wear a mask for 10 days. Dr. Offit agrees. Because many people exposed have trouble quarantining, Dr. Offit advises those exposed who can’t follow that guidance to be sure to wear a mask for 10 days when indoors. The CDC guidance also offers that as another strategy – that if a 5-day quarantine is not feasible, the exposed person should wear a mask for 10 days when around others.

But if  someone who was exposed gets symptoms, that person then enters the infected category and follows that guidance, Dr. Offit said.
 

When should the person who has been exposed get tested?

After the exposure, ‘’you should probably wait 2-3 days,” Dr. Offit said. “The virus has to reproduce itself.”

Testing should be done by those exposed at least once, Dr. Adalja said.

“But there’s data to support daily testing to guide their activities, but this is not CDC guidance. Home tests are sufficient for this purpose.”
 

At what point can the infected person mingle safely with others?

“Technically, if asymptomatic, 10 days without a mask, 5 days with a mask,” said Dr. Adalja. “I think this could also be guided with home test negativity being a gauge [as to whether to mingle].”

A version of this article first appeared on WebMD.com.

With new cases of COVID-19 skyrocketing to more than 240,000 a day recently in the U.S., many people are facing the same situation: A family member or friend tests positive or was exposed to someone who did, and the holiday gathering, visit, or return to work is just days or hours away. Now what?

New guidance issued Dec. 27 by the Centers for Disease Control and Prevention shortens the recommended isolation and quarantine period for the general population, coming after the agency shortened the isolation period for health care workers.

This news organization reached out to two infectious disease specialists to get answers to questions that are frequently asked in these situations.
 

If you have tested positive for COVID-19, what do you do next?

“If you have tested positive, you are infected. At the moment, you are [either] symptomatically affected or presymptomatically infected,’’ said Paul A. Offit, MD, director of the Vaccine Education Center and professor of pediatrics at Children’s Hospital of Philadelphia. At that point, you need to isolate for 5 days, according to the new CDC guidance. (That period has been shortened from 10 days.)

Isolation means separating the infected person from others. Quarantine refers to things you should do if you’re exposed to the virus or you have a close contact infected with COVID-19.

Under the new CDC guidelines, after the 5-day isolation, if the infected person then has no symptoms, he or she can leave isolation and then wear a mask for 5  days.

Those who test positive also need to tell their close contacts they are positive, said Amesh Adalja, MD, a senior scholar at the Johns Hopkins Center for Health Security.  

According to the CDC, the change to a shortened quarantine time is motivated by science ‘’demonstrating that the majority of SARS-CoV-2 transmission occurs early in the course of the illness, generally in the 1-2 days prior to onset of symptoms and the 2-3 days after.”
 

If you have been exposed to someone with COVID-19, what do you do next?

“If they are vaccinated and boosted, the guidance says there is no need to quarantine,” Dr. Adalja said. But the CDC guidance does recommend these people wear a well-fitting mask at all times when around others for 10 days after exposure.

For everyone else, including the unvaccinated and those who are more than 6 months out from their second Pfizer or Moderna vaccine dose, or more than 2 months from their J&J dose, the CDC recommends a quarantine for 5 days – and wearing a mask for the 5 days after that.

On a practical level, Dr. Adalja said he thinks those who are vaccinated but not boosted could also skip the quarantine and wear a mask for 10 days. Dr. Offit agrees. Because many people exposed have trouble quarantining, Dr. Offit advises those exposed who can’t follow that guidance to be sure to wear a mask for 10 days when indoors. The CDC guidance also offers that as another strategy – that if a 5-day quarantine is not feasible, the exposed person should wear a mask for 10 days when around others.

But if  someone who was exposed gets symptoms, that person then enters the infected category and follows that guidance, Dr. Offit said.
 

When should the person who has been exposed get tested?

After the exposure, ‘’you should probably wait 2-3 days,” Dr. Offit said. “The virus has to reproduce itself.”

Testing should be done by those exposed at least once, Dr. Adalja said.

“But there’s data to support daily testing to guide their activities, but this is not CDC guidance. Home tests are sufficient for this purpose.”
 

At what point can the infected person mingle safely with others?

“Technically, if asymptomatic, 10 days without a mask, 5 days with a mask,” said Dr. Adalja. “I think this could also be guided with home test negativity being a gauge [as to whether to mingle].”

A version of this article first appeared on WebMD.com.

Rapid antigen tests for COVID-19 might be less effective at detecting the Omicron variant that is spreading rapidly across the United States, according to the Food and Drug Administration.

Early data suggest that COVID-19 antigen tests “do detect the Omicron variant but may have reduced sensitivity,” the FDA said in a statement posted Dec. 28 on its website.

The FDA is working with the National Institutes of Health’s Rapid Acceleration of Diagnostics (RADx) initiative to assess the performance of antigen tests with patient samples that have the Omicron variant.

The potential for antigen tests to be less sensitive for the Omicron variant emerged in tests using patient samples containing live virus, “which represents the best way to evaluate true test performance in the short term,” the FDA said.

Initial laboratory tests using heat-activated (killed) virus samples found that antigen tests were able to detect the Omicron variant.

“It is important to note that these laboratory data are not a replacement for clinical study evaluations using patient samples with live virus, which are ongoing. The FDA and RADx are continuing to further evaluate the performance of antigen tests using patient samples with live virus,” the FDA said.
 

Testing still important

The agency continues to recommend use of antigen tests as directed in the authorized labeling and in accordance with the instructions included with the tests.

They note that antigen tests are generally less sensitive and less likely to pick up very early infections, compared with molecular tests.

The FDA continues to recommend that an individual with a negative antigen test who has symptoms or a high likelihood of infection because of exposure follow-up with a molecular test to determine if they have COVID-19.

An individual with a positive antigen test should self-isolate and seek follow-up care with a health care provider to determine the next steps.

The FDA, with partners and test developers, are continuing to evaluate test sensitivity, as well as the best timing and frequency of antigen testing.

The agency said that it will provide updated information and any needed recommendations when appropriate.

A version of this article first appeared on Medscape.com.

Rapid antigen tests for COVID-19 might be less effective at detecting the Omicron variant that is spreading rapidly across the United States, according to the Food and Drug Administration.

Early data suggest that COVID-19 antigen tests “do detect the Omicron variant but may have reduced sensitivity,” the FDA said in a statement posted Dec. 28 on its website.

The FDA is working with the National Institutes of Health’s Rapid Acceleration of Diagnostics (RADx) initiative to assess the performance of antigen tests with patient samples that have the Omicron variant.

The potential for antigen tests to be less sensitive for the Omicron variant emerged in tests using patient samples containing live virus, “which represents the best way to evaluate true test performance in the short term,” the FDA said.

Initial laboratory tests using heat-activated (killed) virus samples found that antigen tests were able to detect the Omicron variant.

“It is important to note that these laboratory data are not a replacement for clinical study evaluations using patient samples with live virus, which are ongoing. The FDA and RADx are continuing to further evaluate the performance of antigen tests using patient samples with live virus,” the FDA said.
 

Testing still important

The agency continues to recommend use of antigen tests as directed in the authorized labeling and in accordance with the instructions included with the tests.

They note that antigen tests are generally less sensitive and less likely to pick up very early infections, compared with molecular tests.

The FDA continues to recommend that an individual with a negative antigen test who has symptoms or a high likelihood of infection because of exposure follow-up with a molecular test to determine if they have COVID-19.

An individual with a positive antigen test should self-isolate and seek follow-up care with a health care provider to determine the next steps.

The FDA, with partners and test developers, are continuing to evaluate test sensitivity, as well as the best timing and frequency of antigen testing.

The agency said that it will provide updated information and any needed recommendations when appropriate.

A version of this article first appeared on Medscape.com.

Rapid antigen tests for COVID-19 might be less effective at detecting the Omicron variant that is spreading rapidly across the United States, according to the Food and Drug Administration.

Early data suggest that COVID-19 antigen tests “do detect the Omicron variant but may have reduced sensitivity,” the FDA said in a statement posted Dec. 28 on its website.

The FDA is working with the National Institutes of Health’s Rapid Acceleration of Diagnostics (RADx) initiative to assess the performance of antigen tests with patient samples that have the Omicron variant.

The potential for antigen tests to be less sensitive for the Omicron variant emerged in tests using patient samples containing live virus, “which represents the best way to evaluate true test performance in the short term,” the FDA said.

Initial laboratory tests using heat-activated (killed) virus samples found that antigen tests were able to detect the Omicron variant.

“It is important to note that these laboratory data are not a replacement for clinical study evaluations using patient samples with live virus, which are ongoing. The FDA and RADx are continuing to further evaluate the performance of antigen tests using patient samples with live virus,” the FDA said.
 

Testing still important

The agency continues to recommend use of antigen tests as directed in the authorized labeling and in accordance with the instructions included with the tests.

They note that antigen tests are generally less sensitive and less likely to pick up very early infections, compared with molecular tests.

The FDA continues to recommend that an individual with a negative antigen test who has symptoms or a high likelihood of infection because of exposure follow-up with a molecular test to determine if they have COVID-19.

An individual with a positive antigen test should self-isolate and seek follow-up care with a health care provider to determine the next steps.

The FDA, with partners and test developers, are continuing to evaluate test sensitivity, as well as the best timing and frequency of antigen testing.

The agency said that it will provide updated information and any needed recommendations when appropriate.

A version of this article first appeared on Medscape.com.