Commentary

Acne during pregnancy and lactation is common and poses a considerable treatment challenge for dermatologists. It is a disease that often is trivialized, viewed by the ill informed as cosmetic in nature. Combined with fetal and neonatal health concerns plus a healthy dose of medicolegal overlay, treatment of acne in this patient population may be complicated.

Pregnant and lactating women have been summarily orphaned from advances in drug therapy. Due to, in no small part, the pervasive litigious atmosphere surrounding birth defects in pregnancy, many health care providers have defaulted to avoiding all medications in this patient population to be “on the safe side,” and many have convinced pregnant women that taking medication to relieve pain and discomfort while pregnant is selfish and vain, especially where acne is concerned. However, erring on the safe side is not always safe. Drug avoidance can lead to increased physical and psychiatric morbidity.

Numerous studies have shown that acne is not trivial or inconsequential and may even be associated with suicidal ideations.^1,2 In one study, female gender and acne were both jointly and independently associated with the risk for major depression and suicide.³ The traditional notion that pregnancy is a time of joy and emotional well-being is not supported by data. There is a marked increase of mood instability during pregnancy. According to the American Psychological Association, the incidence of true clinical postpartum depression in the United States is 1 in 7 pregnancies but is likely much higher, as it often remains undiagnosed.⁴ These women may consider suicide and may even harm their children. Therefore, “first, do no harm” might indeed involve aggressive therapy in this patient population; at the very least, it warrants a thorough consideration of the risks and benefits rather than a knee-jerk “wait until you stop breastfeeding” default. Without adequate knowledge of true drug risks and with the stakes so high, we find ourselves in medicolegal quicksand. As clinicians, we understand the concept of weighing risks and benefits, but the balance of the scale cannot be determined when no evidence exists regarding the relative weight of the risk side.

Most drug risks in pregnancy are noted after market approval and are obtained from published case reports and retrospective birth defect registries. Reported problems likely represent a small fraction of actual cases. The absence of direct information regarding drug use during pregnancy is exacerbated by the knowledge that there are large gender differences in drug pharmacokinetics. This dichotomy would be expected to be especially pronounced between men and pregnant women in whom drug absorption, distribution, and elimination are all notably altered. A poorly publicized aberration in the drug approval process is that gender information is not required from generic medication bioequivalence studies. Although studies for drugs indicated for both sexes need to include male and female participants, resulting data showing gender differences are not required to be disclosed, which means that it is theoretically possible for a generic drug to be approved based on results in men only.

The pregnancy categories for drugs (A, B, C, D, and X), which were initially defined in 1979, have been our only aid in risk assessment but have little clinical relevance beyond defining the level of medicolegal risk. Furthermore, these drug categories are poised to disappear before the publication of this editorial, as new guidelines for labeling human prescription drugs are mandated to begin on June 30, 2015.⁵ Although guaranteed to be confusing at first, it seems the new labeling guidelines will be much more helpful for clinicians. One of the most important changes is the inclusion of the following statement in pregnancy and lactation subsections on drug labels: “All pregnancies have a background risk of birth defect, loss, or other adverse outcome regardless of drug exposure. The fetal risk summary below describes (name of drug)’s potential to increase the risk of developmental abnormalities above the background risk.”⁵ In the absence of concerning human data, efforts will be made to put positive animal data into perspective. In the absence of systemic exposure the label will state: “(Name of drug) is not absorbed systemically from (part of body) and cannot be detected in the blood. Maternal use is not expected to result in fetal exposure to the drug.”⁵ This final rule includes virtually all topical acne products, including topical retinoids.

As weak as the evidence-based risk information is for drugs in pregnancy, it is worse for lactation. It is a commonly mistaken belief among practitioners that the safety, or lack thereof, of medications during pregnancy indicates safety during lactation. In actuality, decisions should instead be based on safety data on the drug during the neonatal period. Levels of neonatal drug exposure through breast milk is 5- to 10-fold less than fetal exposure in utero.⁶ Therefore, it generally is safer for women to take drugs during lactation than during pregnancy. For the most part, medications enter the breast milk by passive diffusion from the maternal bloodstream. Several hours after a medication is taken, maternal blood levels fall and drug from the breast milk flows back along the concentration gradient into the maternal circulation. Therefore, safety is maximized by administering maternal medications immediately after the last feed and just prior to the longest sleep period of the child, usually at night.

In the lactation section of the new labeling guidelines ruling, the verbiage is completely different and highly clinically relevant. If the data demonstrate that a drug does not affect the quantity and/or quality of human breast milk, the product label must state: “The use of (name of drug) is compatible with breastfeeding.”⁵ If the drug is not systemically absorbed, the label will state simply and clearly, “Breastfeeding is not expected to result in fetal exposure to the drug.” Therefore, if these labeling guidelines are followed, it appears that all topical acne medications will be interpreted as safe during lactation under the new guidelines.

Dermatologists have taken an oath to “first, do no harm,” but in the case of acne in pregnancy and especially in lactation, we may need to treat aggressively and push the envelope beyond our current category B medications. Erring on the side of caution may be the wrong approach, especially in lactation where psychological consequences are high and neonatal exposure is minimal. The new US Food and Drug Administration guidelines should be helpful in the process of risk assessment and aid us in discussing rational, thoughtful, practical approaches with our patients.

Acne during pregnancy and lactation is common and poses a considerable treatment challenge for dermatologists. It is a disease that often is trivialized, viewed by the ill informed as cosmetic in nature. Combined with fetal and neonatal health concerns plus a healthy dose of medicolegal overlay, treatment of acne in this patient population may be complicated.

Pregnant and lactating women have been summarily orphaned from advances in drug therapy. Due to, in no small part, the pervasive litigious atmosphere surrounding birth defects in pregnancy, many health care providers have defaulted to avoiding all medications in this patient population to be “on the safe side,” and many have convinced pregnant women that taking medication to relieve pain and discomfort while pregnant is selfish and vain, especially where acne is concerned. However, erring on the safe side is not always safe. Drug avoidance can lead to increased physical and psychiatric morbidity.

Numerous studies have shown that acne is not trivial or inconsequential and may even be associated with suicidal ideations.^1,2 In one study, female gender and acne were both jointly and independently associated with the risk for major depression and suicide.³ The traditional notion that pregnancy is a time of joy and emotional well-being is not supported by data. There is a marked increase of mood instability during pregnancy. According to the American Psychological Association, the incidence of true clinical postpartum depression in the United States is 1 in 7 pregnancies but is likely much higher, as it often remains undiagnosed.⁴ These women may consider suicide and may even harm their children. Therefore, “first, do no harm” might indeed involve aggressive therapy in this patient population; at the very least, it warrants a thorough consideration of the risks and benefits rather than a knee-jerk “wait until you stop breastfeeding” default. Without adequate knowledge of true drug risks and with the stakes so high, we find ourselves in medicolegal quicksand. As clinicians, we understand the concept of weighing risks and benefits, but the balance of the scale cannot be determined when no evidence exists regarding the relative weight of the risk side.

Most drug risks in pregnancy are noted after market approval and are obtained from published case reports and retrospective birth defect registries. Reported problems likely represent a small fraction of actual cases. The absence of direct information regarding drug use during pregnancy is exacerbated by the knowledge that there are large gender differences in drug pharmacokinetics. This dichotomy would be expected to be especially pronounced between men and pregnant women in whom drug absorption, distribution, and elimination are all notably altered. A poorly publicized aberration in the drug approval process is that gender information is not required from generic medication bioequivalence studies. Although studies for drugs indicated for both sexes need to include male and female participants, resulting data showing gender differences are not required to be disclosed, which means that it is theoretically possible for a generic drug to be approved based on results in men only.

The pregnancy categories for drugs (A, B, C, D, and X), which were initially defined in 1979, have been our only aid in risk assessment but have little clinical relevance beyond defining the level of medicolegal risk. Furthermore, these drug categories are poised to disappear before the publication of this editorial, as new guidelines for labeling human prescription drugs are mandated to begin on June 30, 2015.⁵ Although guaranteed to be confusing at first, it seems the new labeling guidelines will be much more helpful for clinicians. One of the most important changes is the inclusion of the following statement in pregnancy and lactation subsections on drug labels: “All pregnancies have a background risk of birth defect, loss, or other adverse outcome regardless of drug exposure. The fetal risk summary below describes (name of drug)’s potential to increase the risk of developmental abnormalities above the background risk.”⁵ In the absence of concerning human data, efforts will be made to put positive animal data into perspective. In the absence of systemic exposure the label will state: “(Name of drug) is not absorbed systemically from (part of body) and cannot be detected in the blood. Maternal use is not expected to result in fetal exposure to the drug.”⁵ This final rule includes virtually all topical acne products, including topical retinoids.

As weak as the evidence-based risk information is for drugs in pregnancy, it is worse for lactation. It is a commonly mistaken belief among practitioners that the safety, or lack thereof, of medications during pregnancy indicates safety during lactation. In actuality, decisions should instead be based on safety data on the drug during the neonatal period. Levels of neonatal drug exposure through breast milk is 5- to 10-fold less than fetal exposure in utero.⁶ Therefore, it generally is safer for women to take drugs during lactation than during pregnancy. For the most part, medications enter the breast milk by passive diffusion from the maternal bloodstream. Several hours after a medication is taken, maternal blood levels fall and drug from the breast milk flows back along the concentration gradient into the maternal circulation. Therefore, safety is maximized by administering maternal medications immediately after the last feed and just prior to the longest sleep period of the child, usually at night.

In the lactation section of the new labeling guidelines ruling, the verbiage is completely different and highly clinically relevant. If the data demonstrate that a drug does not affect the quantity and/or quality of human breast milk, the product label must state: “The use of (name of drug) is compatible with breastfeeding.”⁵ If the drug is not systemically absorbed, the label will state simply and clearly, “Breastfeeding is not expected to result in fetal exposure to the drug.” Therefore, if these labeling guidelines are followed, it appears that all topical acne medications will be interpreted as safe during lactation under the new guidelines.

Dermatologists have taken an oath to “first, do no harm,” but in the case of acne in pregnancy and especially in lactation, we may need to treat aggressively and push the envelope beyond our current category B medications. Erring on the side of caution may be the wrong approach, especially in lactation where psychological consequences are high and neonatal exposure is minimal. The new US Food and Drug Administration guidelines should be helpful in the process of risk assessment and aid us in discussing rational, thoughtful, practical approaches with our patients.

Acne during pregnancy and lactation is common and poses a considerable treatment challenge for dermatologists. It is a disease that often is trivialized, viewed by the ill informed as cosmetic in nature. Combined with fetal and neonatal health concerns plus a healthy dose of medicolegal overlay, treatment of acne in this patient population may be complicated.

Pregnant and lactating women have been summarily orphaned from advances in drug therapy. Due to, in no small part, the pervasive litigious atmosphere surrounding birth defects in pregnancy, many health care providers have defaulted to avoiding all medications in this patient population to be “on the safe side,” and many have convinced pregnant women that taking medication to relieve pain and discomfort while pregnant is selfish and vain, especially where acne is concerned. However, erring on the safe side is not always safe. Drug avoidance can lead to increased physical and psychiatric morbidity.

Numerous studies have shown that acne is not trivial or inconsequential and may even be associated with suicidal ideations.^1,2 In one study, female gender and acne were both jointly and independently associated with the risk for major depression and suicide.³ The traditional notion that pregnancy is a time of joy and emotional well-being is not supported by data. There is a marked increase of mood instability during pregnancy. According to the American Psychological Association, the incidence of true clinical postpartum depression in the United States is 1 in 7 pregnancies but is likely much higher, as it often remains undiagnosed.⁴ These women may consider suicide and may even harm their children. Therefore, “first, do no harm” might indeed involve aggressive therapy in this patient population; at the very least, it warrants a thorough consideration of the risks and benefits rather than a knee-jerk “wait until you stop breastfeeding” default. Without adequate knowledge of true drug risks and with the stakes so high, we find ourselves in medicolegal quicksand. As clinicians, we understand the concept of weighing risks and benefits, but the balance of the scale cannot be determined when no evidence exists regarding the relative weight of the risk side.

Most drug risks in pregnancy are noted after market approval and are obtained from published case reports and retrospective birth defect registries. Reported problems likely represent a small fraction of actual cases. The absence of direct information regarding drug use during pregnancy is exacerbated by the knowledge that there are large gender differences in drug pharmacokinetics. This dichotomy would be expected to be especially pronounced between men and pregnant women in whom drug absorption, distribution, and elimination are all notably altered. A poorly publicized aberration in the drug approval process is that gender information is not required from generic medication bioequivalence studies. Although studies for drugs indicated for both sexes need to include male and female participants, resulting data showing gender differences are not required to be disclosed, which means that it is theoretically possible for a generic drug to be approved based on results in men only.

The pregnancy categories for drugs (A, B, C, D, and X), which were initially defined in 1979, have been our only aid in risk assessment but have little clinical relevance beyond defining the level of medicolegal risk. Furthermore, these drug categories are poised to disappear before the publication of this editorial, as new guidelines for labeling human prescription drugs are mandated to begin on June 30, 2015.⁵ Although guaranteed to be confusing at first, it seems the new labeling guidelines will be much more helpful for clinicians. One of the most important changes is the inclusion of the following statement in pregnancy and lactation subsections on drug labels: “All pregnancies have a background risk of birth defect, loss, or other adverse outcome regardless of drug exposure. The fetal risk summary below describes (name of drug)’s potential to increase the risk of developmental abnormalities above the background risk.”⁵ In the absence of concerning human data, efforts will be made to put positive animal data into perspective. In the absence of systemic exposure the label will state: “(Name of drug) is not absorbed systemically from (part of body) and cannot be detected in the blood. Maternal use is not expected to result in fetal exposure to the drug.”⁵ This final rule includes virtually all topical acne products, including topical retinoids.

As weak as the evidence-based risk information is for drugs in pregnancy, it is worse for lactation. It is a commonly mistaken belief among practitioners that the safety, or lack thereof, of medications during pregnancy indicates safety during lactation. In actuality, decisions should instead be based on safety data on the drug during the neonatal period. Levels of neonatal drug exposure through breast milk is 5- to 10-fold less than fetal exposure in utero.⁶ Therefore, it generally is safer for women to take drugs during lactation than during pregnancy. For the most part, medications enter the breast milk by passive diffusion from the maternal bloodstream. Several hours after a medication is taken, maternal blood levels fall and drug from the breast milk flows back along the concentration gradient into the maternal circulation. Therefore, safety is maximized by administering maternal medications immediately after the last feed and just prior to the longest sleep period of the child, usually at night.

In the lactation section of the new labeling guidelines ruling, the verbiage is completely different and highly clinically relevant. If the data demonstrate that a drug does not affect the quantity and/or quality of human breast milk, the product label must state: “The use of (name of drug) is compatible with breastfeeding.”⁵ If the drug is not systemically absorbed, the label will state simply and clearly, “Breastfeeding is not expected to result in fetal exposure to the drug.” Therefore, if these labeling guidelines are followed, it appears that all topical acne medications will be interpreted as safe during lactation under the new guidelines.

Dermatologists have taken an oath to “first, do no harm,” but in the case of acne in pregnancy and especially in lactation, we may need to treat aggressively and push the envelope beyond our current category B medications. Erring on the side of caution may be the wrong approach, especially in lactation where psychological consequences are high and neonatal exposure is minimal. The new US Food and Drug Administration guidelines should be helpful in the process of risk assessment and aid us in discussing rational, thoughtful, practical approaches with our patients.

A 56-year-old woman presents with hypertension. Her blood pressures have been about 160/100 mm Hg. Past medical history includes depression, GERD, and hypothyroidism, and the patient has an allergy to sulfamethoxazole (rash).

She receives a prescription for hydrochlorothiazide. The pharmacist calls later to report that the pharmacy did not fill the prescription because the patient has a sulfa allergy.

What would you recommend?

A. Call in a prescription for a calcium channel blocker.

B. Call in a prescription for an ACE inhibitor.

C. Call in a prescription for a beta-blocker.

D. Call and ask the pharmacist to fill the hydrochlorothiazide prescription.

I have received this call from pharmacies many times. The patients are usually very frustrated because they could not pick up their medications. Is this the right call from the pharmacist? Does the fact that the patient has a sulfa allergy make prescribing hydrochlorothiazide wrong?

Allergies to sulfonamide antibiotics occur in about 3% of patients who are prescribed the drugs. Sulfa-containing antibiotics contain a five- or six-member nitrogen-containing ring attached to the N1 nitrogen of the sulfonamide group and an arylamine group (H₂N) at the N4 position of the sulfonamide group (Pharmacotherapy 2004;24:856-70). Sulfa-containing nonantibiotics – including thiazides and loop diuretics, as well as COX-2 inhibitors – do not contain these same features.

There has always been concern that there is a possibility of increased risk of drug reactions in patients who receive a sulfa nonantibiotic, and frequently prescriptions for these medicines are not filled by pharmacies without directly confirming the intent by speaking with the prescriber.

Brian Hemstreet, Pharm.D., and Robert Page II, Pharm.D., did a prospective, observational study of patients admitted to a hospital with a history of sulfa allergy (Pharmacotherapy 2006;26:551-7). A total of 94 patients were studied who had a reported sulfa allergy. Forty of these patients were taking a sulfonamide nonantibiotic at the time of admission (most commonly furosemide). Nine of the patients received a sulfonamide nonantibiotic during their hospitalization. None of the patients had a drug reaction, either while receiving a sulfonamide nonantibiotic in the hospital, or previously while receiving one as an outpatient.

Dr. Pilar Tornero and colleagues used patch testing and control oral challenge in patients with previous fixed drug eruptions to trimethoprim-sulfamethoxazole or an unknown sulfonamide (Contact Dermatitis 2004;51:57-62). All patients received low doses of oral sulfonamide antibiotics (trimethoprim-sulfamethoxazole, sulfadiazine, or sulfamethizole). All patients also received furosemide.

Every patient with previous known sulfa reaction had a positive oral challenge test when given sulfamethoxazole. There was cross reactivity with other sulfa antibiotics: Seven of 18 patients with prior sulfamethoxazole allergy reacted to oral challenge with sulfadiazine, and 4 of 9 patients with prior allergy with sulfamethoxazole reacted to challenge with sulfamethazine. All 28 patients in the study were challenged with furosemide (a sulfa nonantibiotic) with no allergic reactions.

Dr. Brian Strom and colleagues conducted a retrospective cohort study using general practice research database, looking at risk of allergic reactions within 30 days of receipt of a sulfonamide nonantibiotic (N. Engl. J. Med. 2003;349:1628-35).

Patients who had a history of prior hypersensitivity to a sulfonamide antibiotic were compared with those with no previous history of allergy. Analyses were also performed in patients with a prior penicillin allergy. A total of 969 patients who had an allergic reaction after a sulfonamide antibiotic were evaluated.

Of those patients, 9.1% had an allergic reaction after receiving a sulfonamide nonantibiotic. In those patients without a sulfa antibiotic allergy, only 1.6% had a reaction to a sulfa nonantibiotic. Interestingly, in patients with a prior history of penicillin reaction, 14.6% had an allergic reaction when receiving a sulfa nonantibiotic.

Patients with a history of sulfa allergy to a sulfa antibiotic are more likely to have a reaction to a sulfa nonantibiotic than are those without a previous allergy history. But this appears to be due to overall increased reactiveness and not a cross reactivity, because those with history of penicillin allergy had an even higher allergy rate to sulfa nonantibiotics than did patients with a prior sulfa allergy.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

A 56-year-old woman presents with hypertension. Her blood pressures have been about 160/100 mm Hg. Past medical history includes depression, GERD, and hypothyroidism, and the patient has an allergy to sulfamethoxazole (rash).

She receives a prescription for hydrochlorothiazide. The pharmacist calls later to report that the pharmacy did not fill the prescription because the patient has a sulfa allergy.

What would you recommend?

A. Call in a prescription for a calcium channel blocker.

B. Call in a prescription for an ACE inhibitor.

C. Call in a prescription for a beta-blocker.

D. Call and ask the pharmacist to fill the hydrochlorothiazide prescription.

I have received this call from pharmacies many times. The patients are usually very frustrated because they could not pick up their medications. Is this the right call from the pharmacist? Does the fact that the patient has a sulfa allergy make prescribing hydrochlorothiazide wrong?

Allergies to sulfonamide antibiotics occur in about 3% of patients who are prescribed the drugs. Sulfa-containing antibiotics contain a five- or six-member nitrogen-containing ring attached to the N1 nitrogen of the sulfonamide group and an arylamine group (H₂N) at the N4 position of the sulfonamide group (Pharmacotherapy 2004;24:856-70). Sulfa-containing nonantibiotics – including thiazides and loop diuretics, as well as COX-2 inhibitors – do not contain these same features.

There has always been concern that there is a possibility of increased risk of drug reactions in patients who receive a sulfa nonantibiotic, and frequently prescriptions for these medicines are not filled by pharmacies without directly confirming the intent by speaking with the prescriber.

Brian Hemstreet, Pharm.D., and Robert Page II, Pharm.D., did a prospective, observational study of patients admitted to a hospital with a history of sulfa allergy (Pharmacotherapy 2006;26:551-7). A total of 94 patients were studied who had a reported sulfa allergy. Forty of these patients were taking a sulfonamide nonantibiotic at the time of admission (most commonly furosemide). Nine of the patients received a sulfonamide nonantibiotic during their hospitalization. None of the patients had a drug reaction, either while receiving a sulfonamide nonantibiotic in the hospital, or previously while receiving one as an outpatient.

Dr. Pilar Tornero and colleagues used patch testing and control oral challenge in patients with previous fixed drug eruptions to trimethoprim-sulfamethoxazole or an unknown sulfonamide (Contact Dermatitis 2004;51:57-62). All patients received low doses of oral sulfonamide antibiotics (trimethoprim-sulfamethoxazole, sulfadiazine, or sulfamethizole). All patients also received furosemide.

Every patient with previous known sulfa reaction had a positive oral challenge test when given sulfamethoxazole. There was cross reactivity with other sulfa antibiotics: Seven of 18 patients with prior sulfamethoxazole allergy reacted to oral challenge with sulfadiazine, and 4 of 9 patients with prior allergy with sulfamethoxazole reacted to challenge with sulfamethazine. All 28 patients in the study were challenged with furosemide (a sulfa nonantibiotic) with no allergic reactions.

Dr. Brian Strom and colleagues conducted a retrospective cohort study using general practice research database, looking at risk of allergic reactions within 30 days of receipt of a sulfonamide nonantibiotic (N. Engl. J. Med. 2003;349:1628-35).

Patients who had a history of prior hypersensitivity to a sulfonamide antibiotic were compared with those with no previous history of allergy. Analyses were also performed in patients with a prior penicillin allergy. A total of 969 patients who had an allergic reaction after a sulfonamide antibiotic were evaluated.

Of those patients, 9.1% had an allergic reaction after receiving a sulfonamide nonantibiotic. In those patients without a sulfa antibiotic allergy, only 1.6% had a reaction to a sulfa nonantibiotic. Interestingly, in patients with a prior history of penicillin reaction, 14.6% had an allergic reaction when receiving a sulfa nonantibiotic.

Patients with a history of sulfa allergy to a sulfa antibiotic are more likely to have a reaction to a sulfa nonantibiotic than are those without a previous allergy history. But this appears to be due to overall increased reactiveness and not a cross reactivity, because those with history of penicillin allergy had an even higher allergy rate to sulfa nonantibiotics than did patients with a prior sulfa allergy.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

A 56-year-old woman presents with hypertension. Her blood pressures have been about 160/100 mm Hg. Past medical history includes depression, GERD, and hypothyroidism, and the patient has an allergy to sulfamethoxazole (rash).

She receives a prescription for hydrochlorothiazide. The pharmacist calls later to report that the pharmacy did not fill the prescription because the patient has a sulfa allergy.

What would you recommend?

A. Call in a prescription for a calcium channel blocker.

B. Call in a prescription for an ACE inhibitor.

C. Call in a prescription for a beta-blocker.

D. Call and ask the pharmacist to fill the hydrochlorothiazide prescription.

I have received this call from pharmacies many times. The patients are usually very frustrated because they could not pick up their medications. Is this the right call from the pharmacist? Does the fact that the patient has a sulfa allergy make prescribing hydrochlorothiazide wrong?

Allergies to sulfonamide antibiotics occur in about 3% of patients who are prescribed the drugs. Sulfa-containing antibiotics contain a five- or six-member nitrogen-containing ring attached to the N1 nitrogen of the sulfonamide group and an arylamine group (H₂N) at the N4 position of the sulfonamide group (Pharmacotherapy 2004;24:856-70). Sulfa-containing nonantibiotics – including thiazides and loop diuretics, as well as COX-2 inhibitors – do not contain these same features.

There has always been concern that there is a possibility of increased risk of drug reactions in patients who receive a sulfa nonantibiotic, and frequently prescriptions for these medicines are not filled by pharmacies without directly confirming the intent by speaking with the prescriber.

Brian Hemstreet, Pharm.D., and Robert Page II, Pharm.D., did a prospective, observational study of patients admitted to a hospital with a history of sulfa allergy (Pharmacotherapy 2006;26:551-7). A total of 94 patients were studied who had a reported sulfa allergy. Forty of these patients were taking a sulfonamide nonantibiotic at the time of admission (most commonly furosemide). Nine of the patients received a sulfonamide nonantibiotic during their hospitalization. None of the patients had a drug reaction, either while receiving a sulfonamide nonantibiotic in the hospital, or previously while receiving one as an outpatient.

Dr. Pilar Tornero and colleagues used patch testing and control oral challenge in patients with previous fixed drug eruptions to trimethoprim-sulfamethoxazole or an unknown sulfonamide (Contact Dermatitis 2004;51:57-62). All patients received low doses of oral sulfonamide antibiotics (trimethoprim-sulfamethoxazole, sulfadiazine, or sulfamethizole). All patients also received furosemide.

Every patient with previous known sulfa reaction had a positive oral challenge test when given sulfamethoxazole. There was cross reactivity with other sulfa antibiotics: Seven of 18 patients with prior sulfamethoxazole allergy reacted to oral challenge with sulfadiazine, and 4 of 9 patients with prior allergy with sulfamethoxazole reacted to challenge with sulfamethazine. All 28 patients in the study were challenged with furosemide (a sulfa nonantibiotic) with no allergic reactions.

Dr. Brian Strom and colleagues conducted a retrospective cohort study using general practice research database, looking at risk of allergic reactions within 30 days of receipt of a sulfonamide nonantibiotic (N. Engl. J. Med. 2003;349:1628-35).

Patients who had a history of prior hypersensitivity to a sulfonamide antibiotic were compared with those with no previous history of allergy. Analyses were also performed in patients with a prior penicillin allergy. A total of 969 patients who had an allergic reaction after a sulfonamide antibiotic were evaluated.

Of those patients, 9.1% had an allergic reaction after receiving a sulfonamide nonantibiotic. In those patients without a sulfa antibiotic allergy, only 1.6% had a reaction to a sulfa nonantibiotic. Interestingly, in patients with a prior history of penicillin reaction, 14.6% had an allergic reaction when receiving a sulfa nonantibiotic.

Patients with a history of sulfa allergy to a sulfa antibiotic are more likely to have a reaction to a sulfa nonantibiotic than are those without a previous allergy history. But this appears to be due to overall increased reactiveness and not a cross reactivity, because those with history of penicillin allergy had an even higher allergy rate to sulfa nonantibiotics than did patients with a prior sulfa allergy.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

Last week, one of my patients presented with a BMI of 49 and two canes. Knee x-ray shows marked medial compartment narrowing bilaterally. We will inject her knees with steroids, but this will be temporary.

As the obesity epidemic continues to rage, native joints are rapidly being replaced with metal ones. Our pitiful homegrown joints were not designed to carry all this human weight. Joint forces in the hip and knee have been estimated to be 3 times body weight when walking on level ground and 6-10 times body weight when stooping or bending. Combine this with all the ‘screen time’ (average 8 hours a day for U.S. adults) and all the trips to the bathroom from the poorly controlled diabetes, and we are set up for needing a lot more orthopedic surgeons.

So should we push for surgery?

I am reluctant to immediately and eagerly pursue surgery based upon data from Ward et al. elucidating the increased risk for complications after joint surgery among patients with a BMI > 40 (J.Arthroplasty. 2015 Jun 3. pii: S0883-5403(15)00474-X. doi: 10.1016/j.arth.2015.03.045. [Epub ahead of print]). Data from the bariatric literature suggest that the risk of complications following joint replacement is lower if bariatric surgery is performed first. Weight loss as we look toward joint replacement is a good idea for both our orthopedic colleagues and our patients.

So we will work on weight loss first

In patients with osteoarthritis, a moderate amount of weight loss can significantly improve knee function. The short term efficacy of weight loss is comparable to joint replacement. But clinicians need to be wary of the “pain-exercise block”: patients telling us they cannot lose weight because the pain prevents them from exercising. I tell my patients that weight loss and weight maintenance can be managed effectively through dietary modification and that they do not have to run a marathon, they just need to walk if they can. But patients do not always want to hear this. Caloric restriction is psychologically painful for many. I remind them that 30 minutes of exercise can be undone in 30 seconds with a bar of chocolate, so we need to skip the chocolate bar if we do light exercise or forgo exercise altogether. Exercise is important for a million other reasons, but many of our patients can’t engage, especially when presenting with gait assist devices.

My patient and I started the discussion of bariatric surgery. In the meantime, we are going to try a trial of lorcaserin and hope the knees hold out. We are likely going to need more steroids.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter: @jonebbert.

Last week, one of my patients presented with a BMI of 49 and two canes. Knee x-ray shows marked medial compartment narrowing bilaterally. We will inject her knees with steroids, but this will be temporary.

As the obesity epidemic continues to rage, native joints are rapidly being replaced with metal ones. Our pitiful homegrown joints were not designed to carry all this human weight. Joint forces in the hip and knee have been estimated to be 3 times body weight when walking on level ground and 6-10 times body weight when stooping or bending. Combine this with all the ‘screen time’ (average 8 hours a day for U.S. adults) and all the trips to the bathroom from the poorly controlled diabetes, and we are set up for needing a lot more orthopedic surgeons.

So should we push for surgery?

I am reluctant to immediately and eagerly pursue surgery based upon data from Ward et al. elucidating the increased risk for complications after joint surgery among patients with a BMI > 40 (J.Arthroplasty. 2015 Jun 3. pii: S0883-5403(15)00474-X. doi: 10.1016/j.arth.2015.03.045. [Epub ahead of print]). Data from the bariatric literature suggest that the risk of complications following joint replacement is lower if bariatric surgery is performed first. Weight loss as we look toward joint replacement is a good idea for both our orthopedic colleagues and our patients.

So we will work on weight loss first

In patients with osteoarthritis, a moderate amount of weight loss can significantly improve knee function. The short term efficacy of weight loss is comparable to joint replacement. But clinicians need to be wary of the “pain-exercise block”: patients telling us they cannot lose weight because the pain prevents them from exercising. I tell my patients that weight loss and weight maintenance can be managed effectively through dietary modification and that they do not have to run a marathon, they just need to walk if they can. But patients do not always want to hear this. Caloric restriction is psychologically painful for many. I remind them that 30 minutes of exercise can be undone in 30 seconds with a bar of chocolate, so we need to skip the chocolate bar if we do light exercise or forgo exercise altogether. Exercise is important for a million other reasons, but many of our patients can’t engage, especially when presenting with gait assist devices.

My patient and I started the discussion of bariatric surgery. In the meantime, we are going to try a trial of lorcaserin and hope the knees hold out. We are likely going to need more steroids.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter: @jonebbert.

Last week, one of my patients presented with a BMI of 49 and two canes. Knee x-ray shows marked medial compartment narrowing bilaterally. We will inject her knees with steroids, but this will be temporary.

As the obesity epidemic continues to rage, native joints are rapidly being replaced with metal ones. Our pitiful homegrown joints were not designed to carry all this human weight. Joint forces in the hip and knee have been estimated to be 3 times body weight when walking on level ground and 6-10 times body weight when stooping or bending. Combine this with all the ‘screen time’ (average 8 hours a day for U.S. adults) and all the trips to the bathroom from the poorly controlled diabetes, and we are set up for needing a lot more orthopedic surgeons.

So should we push for surgery?

I am reluctant to immediately and eagerly pursue surgery based upon data from Ward et al. elucidating the increased risk for complications after joint surgery among patients with a BMI > 40 (J.Arthroplasty. 2015 Jun 3. pii: S0883-5403(15)00474-X. doi: 10.1016/j.arth.2015.03.045. [Epub ahead of print]). Data from the bariatric literature suggest that the risk of complications following joint replacement is lower if bariatric surgery is performed first. Weight loss as we look toward joint replacement is a good idea for both our orthopedic colleagues and our patients.

So we will work on weight loss first

In patients with osteoarthritis, a moderate amount of weight loss can significantly improve knee function. The short term efficacy of weight loss is comparable to joint replacement. But clinicians need to be wary of the “pain-exercise block”: patients telling us they cannot lose weight because the pain prevents them from exercising. I tell my patients that weight loss and weight maintenance can be managed effectively through dietary modification and that they do not have to run a marathon, they just need to walk if they can. But patients do not always want to hear this. Caloric restriction is psychologically painful for many. I remind them that 30 minutes of exercise can be undone in 30 seconds with a bar of chocolate, so we need to skip the chocolate bar if we do light exercise or forgo exercise altogether. Exercise is important for a million other reasons, but many of our patients can’t engage, especially when presenting with gait assist devices.

My patient and I started the discussion of bariatric surgery. In the meantime, we are going to try a trial of lorcaserin and hope the knees hold out. We are likely going to need more steroids.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter: @jonebbert.

Recently, the West Virginia Supreme Court ruled that patients can sue doctors if they became addicted to a medication the doctors prescribed even if the patients have committed crimes, such as doctor shopping, to get there.

Apparently, no one can be held responsible for their own actions anymore.

-Oxford-/iStockphotos.com

This is a serious catch-22 for doctors. On the one hand, we have ethical considerations, and oaths, to help others and relieve suffering. Now, on the flip side, doing just that can open us to legal action.

I prescribe narcotics. I try to use them judiciously, and only in people for whom other options have failed or are contraindicated. I suspect most doctors are the same. Every drug has its risks and benefits, and we try to make a calculated decision for each patient. I ask for the patient’s input, too, since he or she is the one who’ll be taking it.

I also have to depend on patients’ honesty. Patients who sell drugs to others, take more than I’ve prescribed, or use other methods of getting them (doctor shopping, buying them off the street) are all committing serious offenses. The development of monitoring databases where I can check on such behaviors has helped me catch those who’ve abused the medications.

One person quoted in an article about the court decision said, “I lied to everybody. I would steal. I pawned my grandma’s wedding rings. I was breaking into houses, doing anything and everything to stay high.”

So, obviously, that was all the doctor’s fault. He was trying to help her, and apparently led her to commit theft and burglary. I suppose the next step in such insanity is that he could be charged as an accomplice in her crimes. After all, it’s not her fault that she decided to steal from others.

This opens up a gold mine. Crooks obtaining narcotics through illicit means can now sue the doctors who were originally trying to help them.

How will it affect me?

I’ll likely further decrease my writing for controlled pain meds. I really can’t give up my DEA number entirely, because I need it to write for several epilepsy medications. But the use of narcotics in my practice will decline. Other docs will probably do the same.

Sadly, this only hurts those who legitimately need pain relief. It will be harder for them to find doctors willing to prescribe narcotics, and even if they do, it’s possible those physicians won’t take their insurance.

Some will say my reaction to the ruling means I don’t care, which isn’t true. I do care. I signed up for this job to help people. But I also have a family to support and protect, and have to think of them, too.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Recently, the West Virginia Supreme Court ruled that patients can sue doctors if they became addicted to a medication the doctors prescribed even if the patients have committed crimes, such as doctor shopping, to get there.

Apparently, no one can be held responsible for their own actions anymore.

-Oxford-/iStockphotos.com

This is a serious catch-22 for doctors. On the one hand, we have ethical considerations, and oaths, to help others and relieve suffering. Now, on the flip side, doing just that can open us to legal action.

I prescribe narcotics. I try to use them judiciously, and only in people for whom other options have failed or are contraindicated. I suspect most doctors are the same. Every drug has its risks and benefits, and we try to make a calculated decision for each patient. I ask for the patient’s input, too, since he or she is the one who’ll be taking it.

I also have to depend on patients’ honesty. Patients who sell drugs to others, take more than I’ve prescribed, or use other methods of getting them (doctor shopping, buying them off the street) are all committing serious offenses. The development of monitoring databases where I can check on such behaviors has helped me catch those who’ve abused the medications.

One person quoted in an article about the court decision said, “I lied to everybody. I would steal. I pawned my grandma’s wedding rings. I was breaking into houses, doing anything and everything to stay high.”

So, obviously, that was all the doctor’s fault. He was trying to help her, and apparently led her to commit theft and burglary. I suppose the next step in such insanity is that he could be charged as an accomplice in her crimes. After all, it’s not her fault that she decided to steal from others.

This opens up a gold mine. Crooks obtaining narcotics through illicit means can now sue the doctors who were originally trying to help them.

How will it affect me?

I’ll likely further decrease my writing for controlled pain meds. I really can’t give up my DEA number entirely, because I need it to write for several epilepsy medications. But the use of narcotics in my practice will decline. Other docs will probably do the same.

Sadly, this only hurts those who legitimately need pain relief. It will be harder for them to find doctors willing to prescribe narcotics, and even if they do, it’s possible those physicians won’t take their insurance.

Some will say my reaction to the ruling means I don’t care, which isn’t true. I do care. I signed up for this job to help people. But I also have a family to support and protect, and have to think of them, too.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Recently, the West Virginia Supreme Court ruled that patients can sue doctors if they became addicted to a medication the doctors prescribed even if the patients have committed crimes, such as doctor shopping, to get there.

Apparently, no one can be held responsible for their own actions anymore.

-Oxford-/iStockphotos.com

This is a serious catch-22 for doctors. On the one hand, we have ethical considerations, and oaths, to help others and relieve suffering. Now, on the flip side, doing just that can open us to legal action.

I prescribe narcotics. I try to use them judiciously, and only in people for whom other options have failed or are contraindicated. I suspect most doctors are the same. Every drug has its risks and benefits, and we try to make a calculated decision for each patient. I ask for the patient’s input, too, since he or she is the one who’ll be taking it.

I also have to depend on patients’ honesty. Patients who sell drugs to others, take more than I’ve prescribed, or use other methods of getting them (doctor shopping, buying them off the street) are all committing serious offenses. The development of monitoring databases where I can check on such behaviors has helped me catch those who’ve abused the medications.

One person quoted in an article about the court decision said, “I lied to everybody. I would steal. I pawned my grandma’s wedding rings. I was breaking into houses, doing anything and everything to stay high.”

So, obviously, that was all the doctor’s fault. He was trying to help her, and apparently led her to commit theft and burglary. I suppose the next step in such insanity is that he could be charged as an accomplice in her crimes. After all, it’s not her fault that she decided to steal from others.

This opens up a gold mine. Crooks obtaining narcotics through illicit means can now sue the doctors who were originally trying to help them.

How will it affect me?

I’ll likely further decrease my writing for controlled pain meds. I really can’t give up my DEA number entirely, because I need it to write for several epilepsy medications. But the use of narcotics in my practice will decline. Other docs will probably do the same.

Sadly, this only hurts those who legitimately need pain relief. It will be harder for them to find doctors willing to prescribe narcotics, and even if they do, it’s possible those physicians won’t take their insurance.

Some will say my reaction to the ruling means I don’t care, which isn’t true. I do care. I signed up for this job to help people. But I also have a family to support and protect, and have to think of them, too.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Patient choice, contraceptive effectiveness, and medical eligibility all need to be incorporated into the contraceptive counseling for reproductive-age women who have cancer or are in remission. Based on these principles, women can minimize the risk of an unintended pregnancy, continue to receive necessary adjuvant or preventive therapy, and maintain high levels of contraception satisfaction.

The Centers for Disease Control and Prevention (CDC) has published medical eligibility criteria (MEC) to assist providers in selecting medically appropriate contraception for women with various health conditions, including cancer (MMWR Recomm. Rep. 2010;59(RR-4):1-6).

Certain classes of hormonal contraception are contraindicated in specific cancer types. It is important to note that the copper intrauterine device (ParaGard) is very effective (with a first-year failure rate of 0.8%) and has no cancer-related contraindications. Any contraceptive with estrogen or progesterone is relatively contraindicated in hormonally mediated cancers, including breast, endometrial, or other cancers that have estrogen (ER) or progesterone (PR) positive receptors. Combined hormonal contraception is contraindicated even in breast cancers that are ER/PR negative for the first 5 years, after which they are CDC MEC category 3 (risks likely outweigh the benefits).

Venous thromboembolism (VTE) is an important cancer-related morbidity. Active cancer increases the risk of VTE by fourfold, which is further increased if the patient is on chemotherapy (Arch. Intern. Med. 2000;160:809-15). Estrogen is known to increase thrombotic risk, and therefore it is contraindicated in any patient at risk for VTE or with a history of a VTE. There is some debate about the use of progestin-only contraceptives in those at risk of (or with a history of) VTE. The best evidence and CDC guidelines indicate that progestin-only methods can be used in patients with cancer or with a history of VTE. Importantly, no known association exists between emergency contraception and VTE (Obstet. Gynecol. 2010;115:1100-9).

Other cancer-specific problems that may impact contraception include thrombocytopenia, gastrointestinal side effects, and drug interactions. Thrombocytopenia may exacerbate or cause abnormal uterine bleeding. Therefore, menstrual suppression with continuous combined hormonal contraception or progestin-only methods, including the hormonal IUD and implant, may be ideal. Regarding gastrointestinal side effects, emesis and mucositis from cancer and treatment may reduce absorption of oral contraceptives, so alternatives should be considered. Antacids, analgesics, antifungals, anticonvulsants, and antiretrovirals are all known to affect hepatic metabolism and may affect oral contraceptive efficacy.

Given the possibility of chemotherapy-induced immunosuppression, there is a theoretical concern about the infectious risk of an indwelling foreign body such as an IUD or implant. The best evidence to date, however, does not support an increased risk, even in the setting of neutropenia. Chemotherapy also increases osteoporosis. Gynecologists should use caution with depot medroxyprogesterone acetate (DMPA), although there is no absolute contraindication, especially for shorter durations of use.

Many breast cancer patients are prescribed tamoxifen as adjuvant therapy, but the antiestrogenic effects of tamoxifen may not prevent pregnancy (Cancer Imaging 2008;8:135-45). Therefore, it is critical for reproductive-age women taking tamoxifen to be given effective contraception. Experts have not reached a consensus on the use of levonorgestrel intrauterine systems (LNG-IUS, Mirena, or Skyla) in the setting of breast cancer.

On the one hand, patients on long-term tamoxifen may benefit from the endometrial protective effect of an LNG-IUS (Lancet 2000;356:1711-7). It is uncertain if women with an LNG-IUS in place at the time of breast cancer diagnosis should have the device removed. Placing a LNG-IUS is contraindicated in all cases of active cancer, but if the patient has no evidence of disease for more than 5 years, the CDC lists the LNG-IUS as category 3. Expert consensus is that studies are needed with LNG-IUS use in women with breast cancer and that use of the LNG-IUS in this population should be made with careful consideration of the risks and benefits (Fertil. Steril. 2008;90:17-22; Contraception 2012;86:191-8).

Physicians should consider the contraceptive needs of women who are actively being or have recently been treated for cancer, as 17% of female cancers occur in women of reproductive age. The copper IUD is a highly effective option with very few contraindications. In patients with a history of non–hormonal related cancer (and without any history of VTE), all contraceptive options can be considered, including those containing estrogen. Estrogen-containing contraceptives should be avoided in those with a history of hormonally related cancers. Those not familiar with the wide array of options should consider referring early, and family planning specialists should consider medical eligibility while counseling women about the most effective contraceptive options.

Dr. Zerden is a family planning fellow in the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill. He reported having no financial disclosures. E-mail Dr. Zerden at [email protected].

Patient choice, contraceptive effectiveness, and medical eligibility all need to be incorporated into the contraceptive counseling for reproductive-age women who have cancer or are in remission. Based on these principles, women can minimize the risk of an unintended pregnancy, continue to receive necessary adjuvant or preventive therapy, and maintain high levels of contraception satisfaction.

The Centers for Disease Control and Prevention (CDC) has published medical eligibility criteria (MEC) to assist providers in selecting medically appropriate contraception for women with various health conditions, including cancer (MMWR Recomm. Rep. 2010;59(RR-4):1-6).

Certain classes of hormonal contraception are contraindicated in specific cancer types. It is important to note that the copper intrauterine device (ParaGard) is very effective (with a first-year failure rate of 0.8%) and has no cancer-related contraindications. Any contraceptive with estrogen or progesterone is relatively contraindicated in hormonally mediated cancers, including breast, endometrial, or other cancers that have estrogen (ER) or progesterone (PR) positive receptors. Combined hormonal contraception is contraindicated even in breast cancers that are ER/PR negative for the first 5 years, after which they are CDC MEC category 3 (risks likely outweigh the benefits).

Venous thromboembolism (VTE) is an important cancer-related morbidity. Active cancer increases the risk of VTE by fourfold, which is further increased if the patient is on chemotherapy (Arch. Intern. Med. 2000;160:809-15). Estrogen is known to increase thrombotic risk, and therefore it is contraindicated in any patient at risk for VTE or with a history of a VTE. There is some debate about the use of progestin-only contraceptives in those at risk of (or with a history of) VTE. The best evidence and CDC guidelines indicate that progestin-only methods can be used in patients with cancer or with a history of VTE. Importantly, no known association exists between emergency contraception and VTE (Obstet. Gynecol. 2010;115:1100-9).

Other cancer-specific problems that may impact contraception include thrombocytopenia, gastrointestinal side effects, and drug interactions. Thrombocytopenia may exacerbate or cause abnormal uterine bleeding. Therefore, menstrual suppression with continuous combined hormonal contraception or progestin-only methods, including the hormonal IUD and implant, may be ideal. Regarding gastrointestinal side effects, emesis and mucositis from cancer and treatment may reduce absorption of oral contraceptives, so alternatives should be considered. Antacids, analgesics, antifungals, anticonvulsants, and antiretrovirals are all known to affect hepatic metabolism and may affect oral contraceptive efficacy.

Given the possibility of chemotherapy-induced immunosuppression, there is a theoretical concern about the infectious risk of an indwelling foreign body such as an IUD or implant. The best evidence to date, however, does not support an increased risk, even in the setting of neutropenia. Chemotherapy also increases osteoporosis. Gynecologists should use caution with depot medroxyprogesterone acetate (DMPA), although there is no absolute contraindication, especially for shorter durations of use.

Many breast cancer patients are prescribed tamoxifen as adjuvant therapy, but the antiestrogenic effects of tamoxifen may not prevent pregnancy (Cancer Imaging 2008;8:135-45). Therefore, it is critical for reproductive-age women taking tamoxifen to be given effective contraception. Experts have not reached a consensus on the use of levonorgestrel intrauterine systems (LNG-IUS, Mirena, or Skyla) in the setting of breast cancer.

On the one hand, patients on long-term tamoxifen may benefit from the endometrial protective effect of an LNG-IUS (Lancet 2000;356:1711-7). It is uncertain if women with an LNG-IUS in place at the time of breast cancer diagnosis should have the device removed. Placing a LNG-IUS is contraindicated in all cases of active cancer, but if the patient has no evidence of disease for more than 5 years, the CDC lists the LNG-IUS as category 3. Expert consensus is that studies are needed with LNG-IUS use in women with breast cancer and that use of the LNG-IUS in this population should be made with careful consideration of the risks and benefits (Fertil. Steril. 2008;90:17-22; Contraception 2012;86:191-8).

Physicians should consider the contraceptive needs of women who are actively being or have recently been treated for cancer, as 17% of female cancers occur in women of reproductive age. The copper IUD is a highly effective option with very few contraindications. In patients with a history of non–hormonal related cancer (and without any history of VTE), all contraceptive options can be considered, including those containing estrogen. Estrogen-containing contraceptives should be avoided in those with a history of hormonally related cancers. Those not familiar with the wide array of options should consider referring early, and family planning specialists should consider medical eligibility while counseling women about the most effective contraceptive options.

Dr. Zerden is a family planning fellow in the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill. He reported having no financial disclosures. E-mail Dr. Zerden at [email protected].

Patient choice, contraceptive effectiveness, and medical eligibility all need to be incorporated into the contraceptive counseling for reproductive-age women who have cancer or are in remission. Based on these principles, women can minimize the risk of an unintended pregnancy, continue to receive necessary adjuvant or preventive therapy, and maintain high levels of contraception satisfaction.

The Centers for Disease Control and Prevention (CDC) has published medical eligibility criteria (MEC) to assist providers in selecting medically appropriate contraception for women with various health conditions, including cancer (MMWR Recomm. Rep. 2010;59(RR-4):1-6).

Certain classes of hormonal contraception are contraindicated in specific cancer types. It is important to note that the copper intrauterine device (ParaGard) is very effective (with a first-year failure rate of 0.8%) and has no cancer-related contraindications. Any contraceptive with estrogen or progesterone is relatively contraindicated in hormonally mediated cancers, including breast, endometrial, or other cancers that have estrogen (ER) or progesterone (PR) positive receptors. Combined hormonal contraception is contraindicated even in breast cancers that are ER/PR negative for the first 5 years, after which they are CDC MEC category 3 (risks likely outweigh the benefits).

Venous thromboembolism (VTE) is an important cancer-related morbidity. Active cancer increases the risk of VTE by fourfold, which is further increased if the patient is on chemotherapy (Arch. Intern. Med. 2000;160:809-15). Estrogen is known to increase thrombotic risk, and therefore it is contraindicated in any patient at risk for VTE or with a history of a VTE. There is some debate about the use of progestin-only contraceptives in those at risk of (or with a history of) VTE. The best evidence and CDC guidelines indicate that progestin-only methods can be used in patients with cancer or with a history of VTE. Importantly, no known association exists between emergency contraception and VTE (Obstet. Gynecol. 2010;115:1100-9).

Other cancer-specific problems that may impact contraception include thrombocytopenia, gastrointestinal side effects, and drug interactions. Thrombocytopenia may exacerbate or cause abnormal uterine bleeding. Therefore, menstrual suppression with continuous combined hormonal contraception or progestin-only methods, including the hormonal IUD and implant, may be ideal. Regarding gastrointestinal side effects, emesis and mucositis from cancer and treatment may reduce absorption of oral contraceptives, so alternatives should be considered. Antacids, analgesics, antifungals, anticonvulsants, and antiretrovirals are all known to affect hepatic metabolism and may affect oral contraceptive efficacy.

Given the possibility of chemotherapy-induced immunosuppression, there is a theoretical concern about the infectious risk of an indwelling foreign body such as an IUD or implant. The best evidence to date, however, does not support an increased risk, even in the setting of neutropenia. Chemotherapy also increases osteoporosis. Gynecologists should use caution with depot medroxyprogesterone acetate (DMPA), although there is no absolute contraindication, especially for shorter durations of use.

Many breast cancer patients are prescribed tamoxifen as adjuvant therapy, but the antiestrogenic effects of tamoxifen may not prevent pregnancy (Cancer Imaging 2008;8:135-45). Therefore, it is critical for reproductive-age women taking tamoxifen to be given effective contraception. Experts have not reached a consensus on the use of levonorgestrel intrauterine systems (LNG-IUS, Mirena, or Skyla) in the setting of breast cancer.

On the one hand, patients on long-term tamoxifen may benefit from the endometrial protective effect of an LNG-IUS (Lancet 2000;356:1711-7). It is uncertain if women with an LNG-IUS in place at the time of breast cancer diagnosis should have the device removed. Placing a LNG-IUS is contraindicated in all cases of active cancer, but if the patient has no evidence of disease for more than 5 years, the CDC lists the LNG-IUS as category 3. Expert consensus is that studies are needed with LNG-IUS use in women with breast cancer and that use of the LNG-IUS in this population should be made with careful consideration of the risks and benefits (Fertil. Steril. 2008;90:17-22; Contraception 2012;86:191-8).

Physicians should consider the contraceptive needs of women who are actively being or have recently been treated for cancer, as 17% of female cancers occur in women of reproductive age. The copper IUD is a highly effective option with very few contraindications. In patients with a history of non–hormonal related cancer (and without any history of VTE), all contraceptive options can be considered, including those containing estrogen. Estrogen-containing contraceptives should be avoided in those with a history of hormonally related cancers. Those not familiar with the wide array of options should consider referring early, and family planning specialists should consider medical eligibility while counseling women about the most effective contraceptive options.

Dr. Zerden is a family planning fellow in the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill. He reported having no financial disclosures. E-mail Dr. Zerden at [email protected].