Testicular cancer is noted to be the most common malignant cancer among men aged 15-44 years.¹ Despite its being the most common, studies show testicular cancer accounts for only 1% of cancers among men over all. Although several risk factors have been identified, there are no clear direct causes of testicular cancer, and its incidence is on the rise.

In 2004 and again in 2010, the United States Preventive Services Task Force (USPSTF) determined that routine screening in asymptomatic males for testicular cancer either by self-exam or ultrasound did not yield better health outcomes.¹ A 2015 study found that testicular cancer incidence in males over 15 years in the United States rose from 5.7/100,000 in 1992 to 6.8/100,000 in 2009, with a significant annual percentage change of 1.1% (P less than .001).² Thankfully, mortality rates have declined since the 1970s because of the improvements made in chemotherapy regimens.³Why are we seeing increased rates of testicular cancer?

Although several studies have investigated this issue, few have been able to determine an exact cause and effect, but several theories have been put forth as likely causes in the rising rates. Most of the established risk factors – such as cryptorchidism, age, race, and exposure to estrogen-mimicking chemicals in utero – have been well described in the literature, but what other factors are affecting our youth?

Increase in sedentary lifestyle is believed to play a role, mostly in relationship to the increase in heat exposure.⁴ As with cryptorchidism, the elevated temperatures associated with internal body temperatures and testicular exposure to it for extended time periods makes this association reasonable.

Dietary factors have shown a strong relationship to development of testicular cancer, as well. High-fat diets and large intake of dairy products were particularly implicated and correlated regionally with the highest incidences.⁵ Highest rates of testicular cancer are noted to be in Denmark and other European countries in which there is a high intake of dairy products.

Physical activity such as horseback riding, bicycle riding, and motorcycle riding had varied results when studied, but repeated low-level trauma has been associated with an increased risk of testicular cancer.⁶

Occupations that have repeated exposure to high-heat environments, such as fireman and factory workers, also showed elevated incidences. Aircraft maintenance and handling of heavy metal and pesticides also have showed a correlation. A substantial amount of evidence indicates that environmental pollutants with estrogenic or antiandrogenic activity are associated with increasing incidence of testicular cancer.⁴

Genetics have the strongest correlation as a risk factor. It has been well documented that there is an eight- to tenfold increase in risk if a brother has been diagnosed with testicular cancer and a four- to sixfold in risk for the son if a father had testicular cancer. Down syndrome also showed increased genetic risk for testicular cancer.³

Although mortality rates are declining and screening for testicular cancer is not indicated, it is important to remember the risk factors and consider it in the differential diagnosis of a symptomatic male given 26%-56% of newly diagnosed testicular cancer patients were wrongly diagnosed initially.¹ Dietary guidance also can be helpful for patients who do have increased risk factors; have them avoid high fat diets and excessive dairy intake. Make patients aware that testicular cancer is most common in younger men, and if they note any changes in their testicle, they should seek medical attention.
 

Dr. Pearce is a pediatrician in Frankfort, Ill. She said she had no relevant financial disclosures. Email her at [email protected].

References

1. Ann Intern Med. 2010;153:396-9.

2. World J Urol. 2015 May;33(5):623-31.

3. N Engl J Med. 2014;371:2005-16.

4. CMAJ. 1999 Jan 26;160(2):213-4.

5. Nat Rev Urol. 2012;9(6):339-49.

6. Int J Cancer. 2005 Sep 1;116(3):331-9.

Testicular cancer is noted to be the most common malignant cancer among men aged 15-44 years.¹ Despite its being the most common, studies show testicular cancer accounts for only 1% of cancers among men over all. Although several risk factors have been identified, there are no clear direct causes of testicular cancer, and its incidence is on the rise.

In 2004 and again in 2010, the United States Preventive Services Task Force (USPSTF) determined that routine screening in asymptomatic males for testicular cancer either by self-exam or ultrasound did not yield better health outcomes.¹ A 2015 study found that testicular cancer incidence in males over 15 years in the United States rose from 5.7/100,000 in 1992 to 6.8/100,000 in 2009, with a significant annual percentage change of 1.1% (P less than .001).² Thankfully, mortality rates have declined since the 1970s because of the improvements made in chemotherapy regimens.³Why are we seeing increased rates of testicular cancer?

Although several studies have investigated this issue, few have been able to determine an exact cause and effect, but several theories have been put forth as likely causes in the rising rates. Most of the established risk factors – such as cryptorchidism, age, race, and exposure to estrogen-mimicking chemicals in utero – have been well described in the literature, but what other factors are affecting our youth?

Increase in sedentary lifestyle is believed to play a role, mostly in relationship to the increase in heat exposure.⁴ As with cryptorchidism, the elevated temperatures associated with internal body temperatures and testicular exposure to it for extended time periods makes this association reasonable.

Dietary factors have shown a strong relationship to development of testicular cancer, as well. High-fat diets and large intake of dairy products were particularly implicated and correlated regionally with the highest incidences.⁵ Highest rates of testicular cancer are noted to be in Denmark and other European countries in which there is a high intake of dairy products.

Physical activity such as horseback riding, bicycle riding, and motorcycle riding had varied results when studied, but repeated low-level trauma has been associated with an increased risk of testicular cancer.⁶

Occupations that have repeated exposure to high-heat environments, such as fireman and factory workers, also showed elevated incidences. Aircraft maintenance and handling of heavy metal and pesticides also have showed a correlation. A substantial amount of evidence indicates that environmental pollutants with estrogenic or antiandrogenic activity are associated with increasing incidence of testicular cancer.⁴

Genetics have the strongest correlation as a risk factor. It has been well documented that there is an eight- to tenfold increase in risk if a brother has been diagnosed with testicular cancer and a four- to sixfold in risk for the son if a father had testicular cancer. Down syndrome also showed increased genetic risk for testicular cancer.³

Although mortality rates are declining and screening for testicular cancer is not indicated, it is important to remember the risk factors and consider it in the differential diagnosis of a symptomatic male given 26%-56% of newly diagnosed testicular cancer patients were wrongly diagnosed initially.¹ Dietary guidance also can be helpful for patients who do have increased risk factors; have them avoid high fat diets and excessive dairy intake. Make patients aware that testicular cancer is most common in younger men, and if they note any changes in their testicle, they should seek medical attention.
 

Dr. Pearce is a pediatrician in Frankfort, Ill. She said she had no relevant financial disclosures. Email her at [email protected].

References

1. Ann Intern Med. 2010;153:396-9.

2. World J Urol. 2015 May;33(5):623-31.

3. N Engl J Med. 2014;371:2005-16.

4. CMAJ. 1999 Jan 26;160(2):213-4.

5. Nat Rev Urol. 2012;9(6):339-49.

6. Int J Cancer. 2005 Sep 1;116(3):331-9.

Testicular cancer is noted to be the most common malignant cancer among men aged 15-44 years.¹ Despite its being the most common, studies show testicular cancer accounts for only 1% of cancers among men over all. Although several risk factors have been identified, there are no clear direct causes of testicular cancer, and its incidence is on the rise.

In 2004 and again in 2010, the United States Preventive Services Task Force (USPSTF) determined that routine screening in asymptomatic males for testicular cancer either by self-exam or ultrasound did not yield better health outcomes.¹ A 2015 study found that testicular cancer incidence in males over 15 years in the United States rose from 5.7/100,000 in 1992 to 6.8/100,000 in 2009, with a significant annual percentage change of 1.1% (P less than .001).² Thankfully, mortality rates have declined since the 1970s because of the improvements made in chemotherapy regimens.³Why are we seeing increased rates of testicular cancer?

Although several studies have investigated this issue, few have been able to determine an exact cause and effect, but several theories have been put forth as likely causes in the rising rates. Most of the established risk factors – such as cryptorchidism, age, race, and exposure to estrogen-mimicking chemicals in utero – have been well described in the literature, but what other factors are affecting our youth?

Increase in sedentary lifestyle is believed to play a role, mostly in relationship to the increase in heat exposure.⁴ As with cryptorchidism, the elevated temperatures associated with internal body temperatures and testicular exposure to it for extended time periods makes this association reasonable.

Dietary factors have shown a strong relationship to development of testicular cancer, as well. High-fat diets and large intake of dairy products were particularly implicated and correlated regionally with the highest incidences.⁵ Highest rates of testicular cancer are noted to be in Denmark and other European countries in which there is a high intake of dairy products.

Physical activity such as horseback riding, bicycle riding, and motorcycle riding had varied results when studied, but repeated low-level trauma has been associated with an increased risk of testicular cancer.⁶

Occupations that have repeated exposure to high-heat environments, such as fireman and factory workers, also showed elevated incidences. Aircraft maintenance and handling of heavy metal and pesticides also have showed a correlation. A substantial amount of evidence indicates that environmental pollutants with estrogenic or antiandrogenic activity are associated with increasing incidence of testicular cancer.⁴

Genetics have the strongest correlation as a risk factor. It has been well documented that there is an eight- to tenfold increase in risk if a brother has been diagnosed with testicular cancer and a four- to sixfold in risk for the son if a father had testicular cancer. Down syndrome also showed increased genetic risk for testicular cancer.³

Although mortality rates are declining and screening for testicular cancer is not indicated, it is important to remember the risk factors and consider it in the differential diagnosis of a symptomatic male given 26%-56% of newly diagnosed testicular cancer patients were wrongly diagnosed initially.¹ Dietary guidance also can be helpful for patients who do have increased risk factors; have them avoid high fat diets and excessive dairy intake. Make patients aware that testicular cancer is most common in younger men, and if they note any changes in their testicle, they should seek medical attention.
 

Dr. Pearce is a pediatrician in Frankfort, Ill. She said she had no relevant financial disclosures. Email her at [email protected].

References

1. Ann Intern Med. 2010;153:396-9.

2. World J Urol. 2015 May;33(5):623-31.

3. N Engl J Med. 2014;371:2005-16.

4. CMAJ. 1999 Jan 26;160(2):213-4.

5. Nat Rev Urol. 2012;9(6):339-49.

6. Int J Cancer. 2005 Sep 1;116(3):331-9.

The Food and Drug Administration has approved gilteritinib (Xospata) for use in adults who have relapsed or refractory acute myeloid leukemia (AML) with an FLT3 mutation, as detected by an FDA-approved test.

The FDA also expanded the approved indication for the LeukoStrat CDx FLT3 Mutation Assay to include use with gilteritinib. The LeukoStrat CDx FLT3 Mutation Assay, developed by Invivoscribe, is used to detect the FLT3 mutation in patients with AML.

Gilteritinib, developed by Astellas Pharma, has demonstrated inhibitory activity against FLT3 internal tandem duplication and FLT3 tyrosine kinase domain.

The FDA’s approval of gilteritinib was based on an interim analysis of the ADMIRAL trial, which enrolled adults with relapsed or refractory AML who had a FLT3 ITD, D835 or I836 mutation, according to the LeukoStrat CDx FLT3 Mutation Assay.

Patients received gilteritinib at 120 mg daily until they developed unacceptable toxicity or did not show a clinical benefit. Efficacy results are available for 138 patients, with a median follow-up of 4.6 months.

The complete response (CR) rate was 11.6% (16/138), the CR rate with partial hematologic recovery (CRh) was 9.4% (13/138), and the CR/CRh rate was 21% (29/138). The median duration of CR/CRh was 4.6 months.

There were 106 patients who were transfusion dependent at baseline, and 33 of these patients (31.1%) became transfusion independent during the post-baseline period.

Seventeen of the 32 patients (53.1%) who were transfusion independent at baseline remained transfusion independent.

Safety results are available for 292 patients. The median duration of exposure to gilteritinib in this group was 3 months.

The most common adverse events were myalgia/arthralgia, transaminase increase, fatigue/malaise, fever, noninfectious diarrhea, dyspnea, edema, rash, pneumonia, nausea, constipation, stomatitis, cough, headache, hypotension, dizziness, and vomiting.

A total of 8% of patients (n = 22) discontinued gilteritinib because of adverse events, the most common of which were pneumonia (2%), sepsis (2%), and dyspnea (1%).
 

[email protected]

The Food and Drug Administration has approved gilteritinib (Xospata) for use in adults who have relapsed or refractory acute myeloid leukemia (AML) with an FLT3 mutation, as detected by an FDA-approved test.

The FDA also expanded the approved indication for the LeukoStrat CDx FLT3 Mutation Assay to include use with gilteritinib. The LeukoStrat CDx FLT3 Mutation Assay, developed by Invivoscribe, is used to detect the FLT3 mutation in patients with AML.

Gilteritinib, developed by Astellas Pharma, has demonstrated inhibitory activity against FLT3 internal tandem duplication and FLT3 tyrosine kinase domain.

The FDA’s approval of gilteritinib was based on an interim analysis of the ADMIRAL trial, which enrolled adults with relapsed or refractory AML who had a FLT3 ITD, D835 or I836 mutation, according to the LeukoStrat CDx FLT3 Mutation Assay.

Patients received gilteritinib at 120 mg daily until they developed unacceptable toxicity or did not show a clinical benefit. Efficacy results are available for 138 patients, with a median follow-up of 4.6 months.

The complete response (CR) rate was 11.6% (16/138), the CR rate with partial hematologic recovery (CRh) was 9.4% (13/138), and the CR/CRh rate was 21% (29/138). The median duration of CR/CRh was 4.6 months.

There were 106 patients who were transfusion dependent at baseline, and 33 of these patients (31.1%) became transfusion independent during the post-baseline period.

Seventeen of the 32 patients (53.1%) who were transfusion independent at baseline remained transfusion independent.

Safety results are available for 292 patients. The median duration of exposure to gilteritinib in this group was 3 months.

The most common adverse events were myalgia/arthralgia, transaminase increase, fatigue/malaise, fever, noninfectious diarrhea, dyspnea, edema, rash, pneumonia, nausea, constipation, stomatitis, cough, headache, hypotension, dizziness, and vomiting.

A total of 8% of patients (n = 22) discontinued gilteritinib because of adverse events, the most common of which were pneumonia (2%), sepsis (2%), and dyspnea (1%).
 

[email protected]

The Food and Drug Administration has approved gilteritinib (Xospata) for use in adults who have relapsed or refractory acute myeloid leukemia (AML) with an FLT3 mutation, as detected by an FDA-approved test.

The FDA also expanded the approved indication for the LeukoStrat CDx FLT3 Mutation Assay to include use with gilteritinib. The LeukoStrat CDx FLT3 Mutation Assay, developed by Invivoscribe, is used to detect the FLT3 mutation in patients with AML.

Gilteritinib, developed by Astellas Pharma, has demonstrated inhibitory activity against FLT3 internal tandem duplication and FLT3 tyrosine kinase domain.

The FDA’s approval of gilteritinib was based on an interim analysis of the ADMIRAL trial, which enrolled adults with relapsed or refractory AML who had a FLT3 ITD, D835 or I836 mutation, according to the LeukoStrat CDx FLT3 Mutation Assay.

Patients received gilteritinib at 120 mg daily until they developed unacceptable toxicity or did not show a clinical benefit. Efficacy results are available for 138 patients, with a median follow-up of 4.6 months.

The complete response (CR) rate was 11.6% (16/138), the CR rate with partial hematologic recovery (CRh) was 9.4% (13/138), and the CR/CRh rate was 21% (29/138). The median duration of CR/CRh was 4.6 months.

There were 106 patients who were transfusion dependent at baseline, and 33 of these patients (31.1%) became transfusion independent during the post-baseline period.

Seventeen of the 32 patients (53.1%) who were transfusion independent at baseline remained transfusion independent.

Safety results are available for 292 patients. The median duration of exposure to gilteritinib in this group was 3 months.

The most common adverse events were myalgia/arthralgia, transaminase increase, fatigue/malaise, fever, noninfectious diarrhea, dyspnea, edema, rash, pneumonia, nausea, constipation, stomatitis, cough, headache, hypotension, dizziness, and vomiting.

A total of 8% of patients (n = 22) discontinued gilteritinib because of adverse events, the most common of which were pneumonia (2%), sepsis (2%), and dyspnea (1%).
 

[email protected]

While the majority of the presentations at this year’s San Antonio Breast Cancer Symposium, to be held Dec. 4-8, will focus on treatments, a few will focus on the treatment decisions. One such presentation will report on the findings of the phase 3 STIC CTC trial. This trial seeks to determine if circulating tumor cells (CTC) could serve as a tool to choose between first-line hormone therapy and chemotherapy for ER-positive HER2-negative metastatic breast cancer.

In the standard arm of the trial, treatment was decided by clinicians, taking into account the criteria usually used in this setting. In the CTC arm, the type of treatment was decided by CTC count: Hormone-therapy was chosen if there were fewer than 5 CTC/7.5 mL (CellSearch technique) or chemotherapy if there were 5 or more CTC/7.5 mL. The main objective was to demonstrate the noninferiority of the CTC-based strategy for progression-free survival. The secondary clinical objectives of the French trial were to compare toxicity, quality of life, and overall survival between the two arms. The cost per progression-free life-years gained will be compared in the two arms, as well.

The results and analysis of STIC CTC will be presented by Francois-Clement Bidard, MD, PhD, of Institut Curie, Paris, and the University of Versailles (France), on Thursday, Dec. 6 at 11 a.m. CST.




 

While the majority of the presentations at this year’s San Antonio Breast Cancer Symposium, to be held Dec. 4-8, will focus on treatments, a few will focus on the treatment decisions. One such presentation will report on the findings of the phase 3 STIC CTC trial. This trial seeks to determine if circulating tumor cells (CTC) could serve as a tool to choose between first-line hormone therapy and chemotherapy for ER-positive HER2-negative metastatic breast cancer.

In the standard arm of the trial, treatment was decided by clinicians, taking into account the criteria usually used in this setting. In the CTC arm, the type of treatment was decided by CTC count: Hormone-therapy was chosen if there were fewer than 5 CTC/7.5 mL (CellSearch technique) or chemotherapy if there were 5 or more CTC/7.5 mL. The main objective was to demonstrate the noninferiority of the CTC-based strategy for progression-free survival. The secondary clinical objectives of the French trial were to compare toxicity, quality of life, and overall survival between the two arms. The cost per progression-free life-years gained will be compared in the two arms, as well.

The results and analysis of STIC CTC will be presented by Francois-Clement Bidard, MD, PhD, of Institut Curie, Paris, and the University of Versailles (France), on Thursday, Dec. 6 at 11 a.m. CST.




 

While the majority of the presentations at this year’s San Antonio Breast Cancer Symposium, to be held Dec. 4-8, will focus on treatments, a few will focus on the treatment decisions. One such presentation will report on the findings of the phase 3 STIC CTC trial. This trial seeks to determine if circulating tumor cells (CTC) could serve as a tool to choose between first-line hormone therapy and chemotherapy for ER-positive HER2-negative metastatic breast cancer.

In the standard arm of the trial, treatment was decided by clinicians, taking into account the criteria usually used in this setting. In the CTC arm, the type of treatment was decided by CTC count: Hormone-therapy was chosen if there were fewer than 5 CTC/7.5 mL (CellSearch technique) or chemotherapy if there were 5 or more CTC/7.5 mL. The main objective was to demonstrate the noninferiority of the CTC-based strategy for progression-free survival. The secondary clinical objectives of the French trial were to compare toxicity, quality of life, and overall survival between the two arms. The cost per progression-free life-years gained will be compared in the two arms, as well.

The results and analysis of STIC CTC will be presented by Francois-Clement Bidard, MD, PhD, of Institut Curie, Paris, and the University of Versailles (France), on Thursday, Dec. 6 at 11 a.m. CST.




 

Three commonly used, brief cognitive tests erroneously identified dementia, resulting in more than a third of those screened being incorrectly classified, a retrospective analysis has concluded.

The likelihood of a false-positive or false-negative result declined sharply when all three tests were given, however; only about 2% of patients were misclassified in all three, David Llewellyn, PhD, and his colleagues reported in Neurology: Clinical Practice.

The Mini Mental State Examination (MMSE), Memory Impairment Screen (MIS), and animal naming (AN) were susceptible to different measurement biases, wrote Dr. Llewellyn of the University of Exeter (U.K.).

Just one variable – an informant’s perception of the patient’s memory as unimpaired – consistently predicted inaccuracy in all three tests. Most of the patients in this category carried the diagnosis of cognitively impaired but not demented (CIND), a finding that has important clinical implications.

“These participants may be in the very early stages of conversion to dementia. ... Therefore, of those with low or borderline cognitive assessment results, reassessment to detect further decline may be appropriate.”

The study comprised 824 patients included in the Aging, Demographics and Memory Study, which is a subsample of the Health and Retirement Study. They completed the tests from 2001-2004, during which time they were a mean of 82 years old. A panel of experts adjudicated diagnoses, which they then parsed into all-cause dementia, CIND, or cognitively normal. The testing included a self and informant assessment of memory decline. The investigators also looked at 22 predictors of cognition, including patient characteristics, apolipoprotein E carriage (ApoE e4), and sociodemographic factors.

The prevalence of dementia was 35.3%; of the nondemented patients, 43% met the criteria for CIND. The team found that 35.7% of cases were misclassified by at least one test, 13.4% by two, and 1.7% by all three.

The MMSE was the least accurate, with a 21% misclassification rate, reflected in an 18.6% false-positive rate for those without dementia and a 2.4% rate of false-negative for those with dementia.

The MIS had a 16% misclassification rate, with a 9.5% rate of false-positive for those with no dementia and a 6.3% rate of false-negative for those without.

The AN had a 14% misclassification rate, with a 6.8% false-positive rate for those without dementia and a 7.7% false-negative rate for those with dementia.

For the MMSE, MIS, and AN, the number of participants with false-positives that met the criteria for CIND were 74.5%, 82.1%, and 82.1%, respectively.

In the final multivariate model, seven variables predicted misclassification, including black ethnicity for the MMSE; age, visual impairment, ApoeE4 noncarrier, and depression for the MIS; and no hyperlipidemia and normal informant memory assessment for the AN. Lower years of education and heart problems predicted misclassification on both the MMSE and AN.

An absence of informant-related poor memory predicted misclassification on all three tests.

“Failing to detect dementia can delay access to treatment and support, whereas false alarms lead to unnecessary investigations, causing pressure on health care systems,” Dr. Llewellyn said in a press statement. “Identifying people with dementia in a timely fashion is important, particularly as new methods of treatment come onstream. Our findings show that we desperately need more accurate and less biased ways of detecting dementia swiftly in clinic.”

The study was supported by the Halpin Trust, the Mary Kinross Charitable Trust, the Engineering and Physical Sciences Research Council, and the U.K. National Institute for Health Research. None of the authors reported any financial conflicts relevant to the work.

[email protected]

SOURCE: Llewellyn D et al. Neuro Clin Pract. 2019;1:1-9.

Three commonly used, brief cognitive tests erroneously identified dementia, resulting in more than a third of those screened being incorrectly classified, a retrospective analysis has concluded.

The likelihood of a false-positive or false-negative result declined sharply when all three tests were given, however; only about 2% of patients were misclassified in all three, David Llewellyn, PhD, and his colleagues reported in Neurology: Clinical Practice.

The Mini Mental State Examination (MMSE), Memory Impairment Screen (MIS), and animal naming (AN) were susceptible to different measurement biases, wrote Dr. Llewellyn of the University of Exeter (U.K.).

Just one variable – an informant’s perception of the patient’s memory as unimpaired – consistently predicted inaccuracy in all three tests. Most of the patients in this category carried the diagnosis of cognitively impaired but not demented (CIND), a finding that has important clinical implications.

“These participants may be in the very early stages of conversion to dementia. ... Therefore, of those with low or borderline cognitive assessment results, reassessment to detect further decline may be appropriate.”

The study comprised 824 patients included in the Aging, Demographics and Memory Study, which is a subsample of the Health and Retirement Study. They completed the tests from 2001-2004, during which time they were a mean of 82 years old. A panel of experts adjudicated diagnoses, which they then parsed into all-cause dementia, CIND, or cognitively normal. The testing included a self and informant assessment of memory decline. The investigators also looked at 22 predictors of cognition, including patient characteristics, apolipoprotein E carriage (ApoE e4), and sociodemographic factors.

The prevalence of dementia was 35.3%; of the nondemented patients, 43% met the criteria for CIND. The team found that 35.7% of cases were misclassified by at least one test, 13.4% by two, and 1.7% by all three.

The MMSE was the least accurate, with a 21% misclassification rate, reflected in an 18.6% false-positive rate for those without dementia and a 2.4% rate of false-negative for those with dementia.

The MIS had a 16% misclassification rate, with a 9.5% rate of false-positive for those with no dementia and a 6.3% rate of false-negative for those without.

The AN had a 14% misclassification rate, with a 6.8% false-positive rate for those without dementia and a 7.7% false-negative rate for those with dementia.

For the MMSE, MIS, and AN, the number of participants with false-positives that met the criteria for CIND were 74.5%, 82.1%, and 82.1%, respectively.

In the final multivariate model, seven variables predicted misclassification, including black ethnicity for the MMSE; age, visual impairment, ApoeE4 noncarrier, and depression for the MIS; and no hyperlipidemia and normal informant memory assessment for the AN. Lower years of education and heart problems predicted misclassification on both the MMSE and AN.

An absence of informant-related poor memory predicted misclassification on all three tests.

“Failing to detect dementia can delay access to treatment and support, whereas false alarms lead to unnecessary investigations, causing pressure on health care systems,” Dr. Llewellyn said in a press statement. “Identifying people with dementia in a timely fashion is important, particularly as new methods of treatment come onstream. Our findings show that we desperately need more accurate and less biased ways of detecting dementia swiftly in clinic.”

The study was supported by the Halpin Trust, the Mary Kinross Charitable Trust, the Engineering and Physical Sciences Research Council, and the U.K. National Institute for Health Research. None of the authors reported any financial conflicts relevant to the work.

[email protected]

SOURCE: Llewellyn D et al. Neuro Clin Pract. 2019;1:1-9.

Three commonly used, brief cognitive tests erroneously identified dementia, resulting in more than a third of those screened being incorrectly classified, a retrospective analysis has concluded.

The likelihood of a false-positive or false-negative result declined sharply when all three tests were given, however; only about 2% of patients were misclassified in all three, David Llewellyn, PhD, and his colleagues reported in Neurology: Clinical Practice.

The Mini Mental State Examination (MMSE), Memory Impairment Screen (MIS), and animal naming (AN) were susceptible to different measurement biases, wrote Dr. Llewellyn of the University of Exeter (U.K.).

Just one variable – an informant’s perception of the patient’s memory as unimpaired – consistently predicted inaccuracy in all three tests. Most of the patients in this category carried the diagnosis of cognitively impaired but not demented (CIND), a finding that has important clinical implications.

“These participants may be in the very early stages of conversion to dementia. ... Therefore, of those with low or borderline cognitive assessment results, reassessment to detect further decline may be appropriate.”

The study comprised 824 patients included in the Aging, Demographics and Memory Study, which is a subsample of the Health and Retirement Study. They completed the tests from 2001-2004, during which time they were a mean of 82 years old. A panel of experts adjudicated diagnoses, which they then parsed into all-cause dementia, CIND, or cognitively normal. The testing included a self and informant assessment of memory decline. The investigators also looked at 22 predictors of cognition, including patient characteristics, apolipoprotein E carriage (ApoE e4), and sociodemographic factors.

The prevalence of dementia was 35.3%; of the nondemented patients, 43% met the criteria for CIND. The team found that 35.7% of cases were misclassified by at least one test, 13.4% by two, and 1.7% by all three.

The MMSE was the least accurate, with a 21% misclassification rate, reflected in an 18.6% false-positive rate for those without dementia and a 2.4% rate of false-negative for those with dementia.

The MIS had a 16% misclassification rate, with a 9.5% rate of false-positive for those with no dementia and a 6.3% rate of false-negative for those without.

The AN had a 14% misclassification rate, with a 6.8% false-positive rate for those without dementia and a 7.7% false-negative rate for those with dementia.

For the MMSE, MIS, and AN, the number of participants with false-positives that met the criteria for CIND were 74.5%, 82.1%, and 82.1%, respectively.

In the final multivariate model, seven variables predicted misclassification, including black ethnicity for the MMSE; age, visual impairment, ApoeE4 noncarrier, and depression for the MIS; and no hyperlipidemia and normal informant memory assessment for the AN. Lower years of education and heart problems predicted misclassification on both the MMSE and AN.

An absence of informant-related poor memory predicted misclassification on all three tests.

“Failing to detect dementia can delay access to treatment and support, whereas false alarms lead to unnecessary investigations, causing pressure on health care systems,” Dr. Llewellyn said in a press statement. “Identifying people with dementia in a timely fashion is important, particularly as new methods of treatment come onstream. Our findings show that we desperately need more accurate and less biased ways of detecting dementia swiftly in clinic.”

The study was supported by the Halpin Trust, the Mary Kinross Charitable Trust, the Engineering and Physical Sciences Research Council, and the U.K. National Institute for Health Research. None of the authors reported any financial conflicts relevant to the work.

[email protected]

SOURCE: Llewellyn D et al. Neuro Clin Pract. 2019;1:1-9.

The Food and Drug Administration has approved a biosimilar rituximab product for the treatment of non-Hodgkin lymphoma (NHL).

Celltrion’s Truxima (rituximab-abbs) is a biosimilar of Genentech’s Rituxan (rituximab) and the first biosimilar approved in the United States to treat NHL.

Truxima (formerly CT-P10) is approved to treat adults with CD20-positive, B-cell NHL, either as a single agent or in combination with chemotherapy. Truxima is approved as a single agent to treat relapsed or refractory, low grade or follicular, CD20-positive, B-cell NHL. Truxima is approved in combination with first-line chemotherapy to treat previously untreated follicular, CD20-positive, B-cell NHL.

Truxima is approved as single-agent maintenance therapy in patients with follicular, CD20-positive, B-cell NHL who achieve a complete or partial response to a rituximab product in combination with chemotherapy. Truxima also is approved as a single agent to treat nonprogressing, low-grade, CD20-positive, B-cell NHL after first-line treatment with cyclophosphamide, vincristine, and prednisone.The label for Truxima contains a boxed warning detailing the risk of fatal infusion reactions, severe skin and mouth reactions (some with fatal outcomes), hepatitis B virus reactivation that may cause serious liver problems (including liver failure and death), and progressive multifocal leukoencephalopathy.

The FDA said its approval of Truxima is “based on a review of evidence that included extensive structural and functional characterization, animal study data, human pharmacokinetic data, clinical immunogenicity data, and other clinical data that demonstrates Truxima is biosimilar to Rituxan.”

Findings from a phase 3 trial suggested that Truxima is equivalent to the reference product in patients with low-tumor-burden follicular lymphoma (Lancet Haematol. 2018 Nov;5[11]:e543-53).

[email protected]

The Food and Drug Administration has approved a biosimilar rituximab product for the treatment of non-Hodgkin lymphoma (NHL).

Celltrion’s Truxima (rituximab-abbs) is a biosimilar of Genentech’s Rituxan (rituximab) and the first biosimilar approved in the United States to treat NHL.

Truxima (formerly CT-P10) is approved to treat adults with CD20-positive, B-cell NHL, either as a single agent or in combination with chemotherapy. Truxima is approved as a single agent to treat relapsed or refractory, low grade or follicular, CD20-positive, B-cell NHL. Truxima is approved in combination with first-line chemotherapy to treat previously untreated follicular, CD20-positive, B-cell NHL.

Truxima is approved as single-agent maintenance therapy in patients with follicular, CD20-positive, B-cell NHL who achieve a complete or partial response to a rituximab product in combination with chemotherapy. Truxima also is approved as a single agent to treat nonprogressing, low-grade, CD20-positive, B-cell NHL after first-line treatment with cyclophosphamide, vincristine, and prednisone.The label for Truxima contains a boxed warning detailing the risk of fatal infusion reactions, severe skin and mouth reactions (some with fatal outcomes), hepatitis B virus reactivation that may cause serious liver problems (including liver failure and death), and progressive multifocal leukoencephalopathy.

The FDA said its approval of Truxima is “based on a review of evidence that included extensive structural and functional characterization, animal study data, human pharmacokinetic data, clinical immunogenicity data, and other clinical data that demonstrates Truxima is biosimilar to Rituxan.”

Findings from a phase 3 trial suggested that Truxima is equivalent to the reference product in patients with low-tumor-burden follicular lymphoma (Lancet Haematol. 2018 Nov;5[11]:e543-53).

[email protected]

The Food and Drug Administration has approved a biosimilar rituximab product for the treatment of non-Hodgkin lymphoma (NHL).

Celltrion’s Truxima (rituximab-abbs) is a biosimilar of Genentech’s Rituxan (rituximab) and the first biosimilar approved in the United States to treat NHL.

Truxima (formerly CT-P10) is approved to treat adults with CD20-positive, B-cell NHL, either as a single agent or in combination with chemotherapy. Truxima is approved as a single agent to treat relapsed or refractory, low grade or follicular, CD20-positive, B-cell NHL. Truxima is approved in combination with first-line chemotherapy to treat previously untreated follicular, CD20-positive, B-cell NHL.

Truxima is approved as single-agent maintenance therapy in patients with follicular, CD20-positive, B-cell NHL who achieve a complete or partial response to a rituximab product in combination with chemotherapy. Truxima also is approved as a single agent to treat nonprogressing, low-grade, CD20-positive, B-cell NHL after first-line treatment with cyclophosphamide, vincristine, and prednisone.The label for Truxima contains a boxed warning detailing the risk of fatal infusion reactions, severe skin and mouth reactions (some with fatal outcomes), hepatitis B virus reactivation that may cause serious liver problems (including liver failure and death), and progressive multifocal leukoencephalopathy.

The FDA said its approval of Truxima is “based on a review of evidence that included extensive structural and functional characterization, animal study data, human pharmacokinetic data, clinical immunogenicity data, and other clinical data that demonstrates Truxima is biosimilar to Rituxan.”

Findings from a phase 3 trial suggested that Truxima is equivalent to the reference product in patients with low-tumor-burden follicular lymphoma (Lancet Haematol. 2018 Nov;5[11]:e543-53).

[email protected]

CHICAGO – It’s clear that there’s a dose-dependent relationship between hypertension in pregnancy and poor outcomes, but, even so, treatment usually doesn’t begin until women hit 160/105 mm Hg or higher, according to Mark Santillan, MD, PhD, an assistant professor of obstetrics and gynecology – maternal fetal medicine at the University of Iowa, Iowa City.

M. Alexander Otto/MDedge News

That might soon change. The National Institutes of Health–funded CHAPS (Chronic Hypertension and Pregnancy) trial is testing whether earlier intervention improves outcomes, and it hopes to define proper treatment targets, which are uncertain at this point. Results are expected as soon as 2020.

What’s already changed is that the old treatment standby – methyldopa – has fallen out of favor for labetalol and nifedipine, which have been shown to work better. “Sometimes, we will throw on hydrochlorothiazide after we max out our beta- and calcium channel blockers,” Dr. Santillan said at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension (Cochrane Database Syst Rev. 2018 Oct 1;10:CD002252).

For severe hypertension, “most of the time we start off with IV hydralazine or IV labetalol” in the hospital. “You give a dose and check blood pressure in 10 or 20 minutes,” he said. If it hasn’t dropped, “give another dose until you reach your max dose.” When intravenous access is an issue, oral nifedipine is a good option (Obstet Gynecol. 2017 Apr;129[4]:e90-e95).

Delivery date is key; babies exposed to chronic hypertension are more likely to be stillborn. For hypertension without symptoms, delivery is at around 38 weeks. For mild preeclampsia – hypertension with only minor symptoms – it’s at 37 weeks.

In more severe cases – hypertension with pulmonary edema, renal insufficiency, and other problems – “the general gestalt is to stabilize and deliver when you can. See if you can get up to at least 34 weeks,” Dr. Santillan said. However, when women “have full-on HELLP syndrome [hemolysis, elevated liver enzymes, low platelet count], we often just deliver [immediately] because there’s not a lot of stabilization” that can be done. “We give magnesium after delivery to help decrease the risk of seizure,” he added.

Guidelines still use 140/90 mm Hg to define hypertension in pregnancy. When that level is reached, “you don’t need proteinuria anymore to diagnose preeclampsia. You need to have hypertension and something that looks like HELLP,” such as impaired liver function or neurologic symptoms, he said. Onset before 34 weeks portends more severe disease.

Daily baby aspirin 81 mg is known to help prevent preeclampsia, if only a little bit, so anyone with a history of preeclampsia or twin pregnancy, chronic hypertension, diabetes, renal disease, or autoimmune disease should automatically be put on aspirin prophylaxis. Women with two or more moderate risk factors – first pregnancy, obesity, preeclamptic family history, or aged 35 years or older – also should also get baby aspirin. Vitamin C, bed rest, and other preventative measures haven’t panned out in trials.

Investigators are looking for better predictors of preeclampsia; uterine artery blood flow is among the promising markers. However, it and other options are “expensive ventures” if you’re just going to end up in the same place, giving baby aspirin, Dr. Santillan said.

Dr. Santillan reported that he holds three patents; two on copeptin to predict preeclampsia and one on vasopressin receptor antagonists to treat it.

[email protected]

CHICAGO – It’s clear that there’s a dose-dependent relationship between hypertension in pregnancy and poor outcomes, but, even so, treatment usually doesn’t begin until women hit 160/105 mm Hg or higher, according to Mark Santillan, MD, PhD, an assistant professor of obstetrics and gynecology – maternal fetal medicine at the University of Iowa, Iowa City.

M. Alexander Otto/MDedge News

That might soon change. The National Institutes of Health–funded CHAPS (Chronic Hypertension and Pregnancy) trial is testing whether earlier intervention improves outcomes, and it hopes to define proper treatment targets, which are uncertain at this point. Results are expected as soon as 2020.

What’s already changed is that the old treatment standby – methyldopa – has fallen out of favor for labetalol and nifedipine, which have been shown to work better. “Sometimes, we will throw on hydrochlorothiazide after we max out our beta- and calcium channel blockers,” Dr. Santillan said at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension (Cochrane Database Syst Rev. 2018 Oct 1;10:CD002252).

For severe hypertension, “most of the time we start off with IV hydralazine or IV labetalol” in the hospital. “You give a dose and check blood pressure in 10 or 20 minutes,” he said. If it hasn’t dropped, “give another dose until you reach your max dose.” When intravenous access is an issue, oral nifedipine is a good option (Obstet Gynecol. 2017 Apr;129[4]:e90-e95).

Delivery date is key; babies exposed to chronic hypertension are more likely to be stillborn. For hypertension without symptoms, delivery is at around 38 weeks. For mild preeclampsia – hypertension with only minor symptoms – it’s at 37 weeks.

In more severe cases – hypertension with pulmonary edema, renal insufficiency, and other problems – “the general gestalt is to stabilize and deliver when you can. See if you can get up to at least 34 weeks,” Dr. Santillan said. However, when women “have full-on HELLP syndrome [hemolysis, elevated liver enzymes, low platelet count], we often just deliver [immediately] because there’s not a lot of stabilization” that can be done. “We give magnesium after delivery to help decrease the risk of seizure,” he added.

Guidelines still use 140/90 mm Hg to define hypertension in pregnancy. When that level is reached, “you don’t need proteinuria anymore to diagnose preeclampsia. You need to have hypertension and something that looks like HELLP,” such as impaired liver function or neurologic symptoms, he said. Onset before 34 weeks portends more severe disease.

Daily baby aspirin 81 mg is known to help prevent preeclampsia, if only a little bit, so anyone with a history of preeclampsia or twin pregnancy, chronic hypertension, diabetes, renal disease, or autoimmune disease should automatically be put on aspirin prophylaxis. Women with two or more moderate risk factors – first pregnancy, obesity, preeclamptic family history, or aged 35 years or older – also should also get baby aspirin. Vitamin C, bed rest, and other preventative measures haven’t panned out in trials.

Investigators are looking for better predictors of preeclampsia; uterine artery blood flow is among the promising markers. However, it and other options are “expensive ventures” if you’re just going to end up in the same place, giving baby aspirin, Dr. Santillan said.

Dr. Santillan reported that he holds three patents; two on copeptin to predict preeclampsia and one on vasopressin receptor antagonists to treat it.

[email protected]

CHICAGO – It’s clear that there’s a dose-dependent relationship between hypertension in pregnancy and poor outcomes, but, even so, treatment usually doesn’t begin until women hit 160/105 mm Hg or higher, according to Mark Santillan, MD, PhD, an assistant professor of obstetrics and gynecology – maternal fetal medicine at the University of Iowa, Iowa City.

M. Alexander Otto/MDedge News

That might soon change. The National Institutes of Health–funded CHAPS (Chronic Hypertension and Pregnancy) trial is testing whether earlier intervention improves outcomes, and it hopes to define proper treatment targets, which are uncertain at this point. Results are expected as soon as 2020.

What’s already changed is that the old treatment standby – methyldopa – has fallen out of favor for labetalol and nifedipine, which have been shown to work better. “Sometimes, we will throw on hydrochlorothiazide after we max out our beta- and calcium channel blockers,” Dr. Santillan said at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension (Cochrane Database Syst Rev. 2018 Oct 1;10:CD002252).

For severe hypertension, “most of the time we start off with IV hydralazine or IV labetalol” in the hospital. “You give a dose and check blood pressure in 10 or 20 minutes,” he said. If it hasn’t dropped, “give another dose until you reach your max dose.” When intravenous access is an issue, oral nifedipine is a good option (Obstet Gynecol. 2017 Apr;129[4]:e90-e95).

Delivery date is key; babies exposed to chronic hypertension are more likely to be stillborn. For hypertension without symptoms, delivery is at around 38 weeks. For mild preeclampsia – hypertension with only minor symptoms – it’s at 37 weeks.

In more severe cases – hypertension with pulmonary edema, renal insufficiency, and other problems – “the general gestalt is to stabilize and deliver when you can. See if you can get up to at least 34 weeks,” Dr. Santillan said. However, when women “have full-on HELLP syndrome [hemolysis, elevated liver enzymes, low platelet count], we often just deliver [immediately] because there’s not a lot of stabilization” that can be done. “We give magnesium after delivery to help decrease the risk of seizure,” he added.

Guidelines still use 140/90 mm Hg to define hypertension in pregnancy. When that level is reached, “you don’t need proteinuria anymore to diagnose preeclampsia. You need to have hypertension and something that looks like HELLP,” such as impaired liver function or neurologic symptoms, he said. Onset before 34 weeks portends more severe disease.

Daily baby aspirin 81 mg is known to help prevent preeclampsia, if only a little bit, so anyone with a history of preeclampsia or twin pregnancy, chronic hypertension, diabetes, renal disease, or autoimmune disease should automatically be put on aspirin prophylaxis. Women with two or more moderate risk factors – first pregnancy, obesity, preeclamptic family history, or aged 35 years or older – also should also get baby aspirin. Vitamin C, bed rest, and other preventative measures haven’t panned out in trials.

Investigators are looking for better predictors of preeclampsia; uterine artery blood flow is among the promising markers. However, it and other options are “expensive ventures” if you’re just going to end up in the same place, giving baby aspirin, Dr. Santillan said.

Dr. Santillan reported that he holds three patents; two on copeptin to predict preeclampsia and one on vasopressin receptor antagonists to treat it.

[email protected]

Legos for lunch

As any parent, teacher, or teenage babysitter knows, children try to eat everything. Six intrepid researchers from Australia and the United Kingdom decided to put their lives – or, at least, their intestines – on the line by swallowing Lego pieces to determine “typical transit times” for the commonly ingested toy. The things people do in the name of science.

Terry Rudd/MDedge News

The study participants first measured their bowel habits by the Stool Hardness and Transit (SHAT) score, and then measured the Found and Retrieved Time (FART) score once the Lego was ... expelled. The researchers found that the average FART score was 1.71 days.

At this point, all involved stopped to have a hearty laugh and a round of high-fives. Parents can rest assured that their little progeny who swallow Legos are safe. Everything is awesome.
 

Don’t wash that pacifier!

If you want to clean your child’s pacifier, you should consider passing on the sink and pop it into your own mouth instead. That’s the story from research presented at the annual scientific meeting of the American College of Allergy, Asthma, and Immunology.

DaniloAndjus/gettyimages

In a survey of 128 mothers over an 18-month period, 41% of those whose child was currently using a pacifier reported cleaning by sterilization, and 72% reported hand washing their child’s pacifier. (We will henceforth refer to these mothers as “normal people.”) Just over 10% of mothers reported cleaning through parental pacifier sucking.

Before you cringe too much, the children of these mothers had significantly lower IgE levels than the children of normal people, indicating they were at a lower risk of developing allergies or asthma.

The study authors hypothesized that exposure to adult saliva may transfer healthy microorganisms to their children, and they advocated for further study into the subject. We suggest getting the pediatricians from the Lego study involved – they’ll eat anything for science.
 

One camel latte, please

An unlikely partnership between a Saudi entrepreneur and Amish farmers might lead to a brand-new dairy market in the United States. Walid Abdul-Wahub is on a mission to put camel milk on the shelves of every grocery store in America.

© Rhombur/Thinkstock

Middle Eastern residents have been drinking camel milk for centuries, so it’s only a matter of time until some hipster coffee shop co-opts it and starts selling camel milk lattes for $9. On the plus side, camel milk has a different protein than cow milk, making it more similar to human milk than bovine milk. This could be a godsend for people with milk allergies and need alternatives to that god-awful almond milk. One camel milkshake, coming right up.
 

How healthy is your personality?

It’s a question bipedal hominins have pondered since our days scrounging for snacks in the Olduvai Gorge: Is my personality why no one wants to hunt and gather with me?

Eoneren/gettyimages

Homo sapiens researchers from the University of California, Davis, and elsewhere believe they have the answer. In fact, it is your personality that leaves you scavenging for baobab alone.

What’s a healthy personality? The Scientia sapiens split personality into five factors: agreeableness, conscientiousness, extroversion, neuroticism, and openness to experience. They then surveyed scientists and college students to construct the consensus Dream Date – er, healthy personality: low levels of neuroticism, sprinkled with lots of agreeable straightforwardness, openness to feelings, positive emotions, and warmth. It wouldn’t hurt to ease up on the Old Spice, either.
 

The taste of deprivation

At one time or another, you’ve probably seen someone who was pretty much physically attached to his or her phone and wondered about the owner’s personal priorities and where the phone fit into them.

Wonder no more.

Terry Rudd/MDedge News

In a study conducted at the University at Buffalo (N.Y.), 76 students were deprived of food for 3 hours and their smartphones for 2 hours, and then given a computer task that would earn them a serving of their favorite snack or use of their phone. To make things more interesting, the amount of work needed to earn food or phone time increased as the subjects completed their tasks.

“We knew that students would be motivated to gain access to their phones, but we were surprised that, despite modest food deprivation, smartphone reinforcement far exceeded food reinforcement,” lead investigator Sara O’Donnell said in a written statement.

Recruiting subjects for the next step in this line of research – choosing between phones and breathing – could get a little tricky. But we have to admire the creative solution that got one participant disqualified from the current study: He tried to eat his phone.

Legos for lunch

As any parent, teacher, or teenage babysitter knows, children try to eat everything. Six intrepid researchers from Australia and the United Kingdom decided to put their lives – or, at least, their intestines – on the line by swallowing Lego pieces to determine “typical transit times” for the commonly ingested toy. The things people do in the name of science.

Terry Rudd/MDedge News

The study participants first measured their bowel habits by the Stool Hardness and Transit (SHAT) score, and then measured the Found and Retrieved Time (FART) score once the Lego was ... expelled. The researchers found that the average FART score was 1.71 days.

At this point, all involved stopped to have a hearty laugh and a round of high-fives. Parents can rest assured that their little progeny who swallow Legos are safe. Everything is awesome.
 

Don’t wash that pacifier!

If you want to clean your child’s pacifier, you should consider passing on the sink and pop it into your own mouth instead. That’s the story from research presented at the annual scientific meeting of the American College of Allergy, Asthma, and Immunology.

DaniloAndjus/gettyimages

In a survey of 128 mothers over an 18-month period, 41% of those whose child was currently using a pacifier reported cleaning by sterilization, and 72% reported hand washing their child’s pacifier. (We will henceforth refer to these mothers as “normal people.”) Just over 10% of mothers reported cleaning through parental pacifier sucking.

Before you cringe too much, the children of these mothers had significantly lower IgE levels than the children of normal people, indicating they were at a lower risk of developing allergies or asthma.

The study authors hypothesized that exposure to adult saliva may transfer healthy microorganisms to their children, and they advocated for further study into the subject. We suggest getting the pediatricians from the Lego study involved – they’ll eat anything for science.
 

One camel latte, please

An unlikely partnership between a Saudi entrepreneur and Amish farmers might lead to a brand-new dairy market in the United States. Walid Abdul-Wahub is on a mission to put camel milk on the shelves of every grocery store in America.

© Rhombur/Thinkstock

Middle Eastern residents have been drinking camel milk for centuries, so it’s only a matter of time until some hipster coffee shop co-opts it and starts selling camel milk lattes for $9. On the plus side, camel milk has a different protein than cow milk, making it more similar to human milk than bovine milk. This could be a godsend for people with milk allergies and need alternatives to that god-awful almond milk. One camel milkshake, coming right up.
 

How healthy is your personality?

It’s a question bipedal hominins have pondered since our days scrounging for snacks in the Olduvai Gorge: Is my personality why no one wants to hunt and gather with me?

Eoneren/gettyimages

Homo sapiens researchers from the University of California, Davis, and elsewhere believe they have the answer. In fact, it is your personality that leaves you scavenging for baobab alone.

What’s a healthy personality? The Scientia sapiens split personality into five factors: agreeableness, conscientiousness, extroversion, neuroticism, and openness to experience. They then surveyed scientists and college students to construct the consensus Dream Date – er, healthy personality: low levels of neuroticism, sprinkled with lots of agreeable straightforwardness, openness to feelings, positive emotions, and warmth. It wouldn’t hurt to ease up on the Old Spice, either.
 

The taste of deprivation

At one time or another, you’ve probably seen someone who was pretty much physically attached to his or her phone and wondered about the owner’s personal priorities and where the phone fit into them.

Wonder no more.

Terry Rudd/MDedge News

In a study conducted at the University at Buffalo (N.Y.), 76 students were deprived of food for 3 hours and their smartphones for 2 hours, and then given a computer task that would earn them a serving of their favorite snack or use of their phone. To make things more interesting, the amount of work needed to earn food or phone time increased as the subjects completed their tasks.

“We knew that students would be motivated to gain access to their phones, but we were surprised that, despite modest food deprivation, smartphone reinforcement far exceeded food reinforcement,” lead investigator Sara O’Donnell said in a written statement.

Recruiting subjects for the next step in this line of research – choosing between phones and breathing – could get a little tricky. But we have to admire the creative solution that got one participant disqualified from the current study: He tried to eat his phone.

Legos for lunch

As any parent, teacher, or teenage babysitter knows, children try to eat everything. Six intrepid researchers from Australia and the United Kingdom decided to put their lives – or, at least, their intestines – on the line by swallowing Lego pieces to determine “typical transit times” for the commonly ingested toy. The things people do in the name of science.

Terry Rudd/MDedge News

The study participants first measured their bowel habits by the Stool Hardness and Transit (SHAT) score, and then measured the Found and Retrieved Time (FART) score once the Lego was ... expelled. The researchers found that the average FART score was 1.71 days.

At this point, all involved stopped to have a hearty laugh and a round of high-fives. Parents can rest assured that their little progeny who swallow Legos are safe. Everything is awesome.
 

Don’t wash that pacifier!

If you want to clean your child’s pacifier, you should consider passing on the sink and pop it into your own mouth instead. That’s the story from research presented at the annual scientific meeting of the American College of Allergy, Asthma, and Immunology.

DaniloAndjus/gettyimages

In a survey of 128 mothers over an 18-month period, 41% of those whose child was currently using a pacifier reported cleaning by sterilization, and 72% reported hand washing their child’s pacifier. (We will henceforth refer to these mothers as “normal people.”) Just over 10% of mothers reported cleaning through parental pacifier sucking.

Before you cringe too much, the children of these mothers had significantly lower IgE levels than the children of normal people, indicating they were at a lower risk of developing allergies or asthma.

The study authors hypothesized that exposure to adult saliva may transfer healthy microorganisms to their children, and they advocated for further study into the subject. We suggest getting the pediatricians from the Lego study involved – they’ll eat anything for science.
 

One camel latte, please

An unlikely partnership between a Saudi entrepreneur and Amish farmers might lead to a brand-new dairy market in the United States. Walid Abdul-Wahub is on a mission to put camel milk on the shelves of every grocery store in America.

© Rhombur/Thinkstock

Middle Eastern residents have been drinking camel milk for centuries, so it’s only a matter of time until some hipster coffee shop co-opts it and starts selling camel milk lattes for $9. On the plus side, camel milk has a different protein than cow milk, making it more similar to human milk than bovine milk. This could be a godsend for people with milk allergies and need alternatives to that god-awful almond milk. One camel milkshake, coming right up.
 

How healthy is your personality?

It’s a question bipedal hominins have pondered since our days scrounging for snacks in the Olduvai Gorge: Is my personality why no one wants to hunt and gather with me?

Eoneren/gettyimages

Homo sapiens researchers from the University of California, Davis, and elsewhere believe they have the answer. In fact, it is your personality that leaves you scavenging for baobab alone.

What’s a healthy personality? The Scientia sapiens split personality into five factors: agreeableness, conscientiousness, extroversion, neuroticism, and openness to experience. They then surveyed scientists and college students to construct the consensus Dream Date – er, healthy personality: low levels of neuroticism, sprinkled with lots of agreeable straightforwardness, openness to feelings, positive emotions, and warmth. It wouldn’t hurt to ease up on the Old Spice, either.
 

The taste of deprivation

At one time or another, you’ve probably seen someone who was pretty much physically attached to his or her phone and wondered about the owner’s personal priorities and where the phone fit into them.

Wonder no more.

Terry Rudd/MDedge News

In a study conducted at the University at Buffalo (N.Y.), 76 students were deprived of food for 3 hours and their smartphones for 2 hours, and then given a computer task that would earn them a serving of their favorite snack or use of their phone. To make things more interesting, the amount of work needed to earn food or phone time increased as the subjects completed their tasks.

“We knew that students would be motivated to gain access to their phones, but we were surprised that, despite modest food deprivation, smartphone reinforcement far exceeded food reinforcement,” lead investigator Sara O’Donnell said in a written statement.

Recruiting subjects for the next step in this line of research – choosing between phones and breathing – could get a little tricky. But we have to admire the creative solution that got one participant disqualified from the current study: He tried to eat his phone.

Patients with rheumatoid arthritis and a high multibiomarker disease activity (MBDA) score were more likely than were patients with low scores to add or switch to biologics or JAK inhibitors, according to a study on the uptake and influence of MBDA testing among rheumatologists and patients.

Courtesy UAB Photo

“While we cannot provide certainty that the main reason that clinicians switched therapies was the MBDA test result, we note that the median time to add or switch to a new RA treatment was 1-2 months after testing, lending plausibility to the MBDA test being influential in this decision,” wrote Jeffrey R. Curtis, MD, of the division of clinical immunology and rheumatology at the University of Alabama at Birmingham, and his coauthors. Their report is in The Journal of Rheumatology.

The researchers analyzed Medicare data from 60,596 RA patients who had taken at least one MBDA (Vectra DA) test. Patients with high MBDA scores who were not taking biologics or a JAK inhibitor were most likely to begin one of the two treatments, at 19.7%, compared with 11.8% for a moderate MBDA score and 9.0% for a low score. For patients already receiving those treatments, the proportion adding or switching was 13.5% for high, 8.3% for moderate, and 5.2% for low MBDA scores. In addition, patients with high MBDA scores who added a new medication and saw no improvement in score were prone to see treatment fail; the likelihood of failure in that scenario was 61% higher (OR = 1.61; 95% confidence index, 1.27-2.03) than in patients whose score improved to low or moderate.

The authors acknowledged that their study did not randomize clinicians nor gather data as to why the tests were ordered, which made it “difficult to assess the incremental value of the information provided by testing above and beyond clinical measurement, or to know whether the treatment changes were appropriate.” However, they also noted the MBDA score’s value as a complement to clinical assessment and an indicator of disease activity, suggesting “ongoing clinical trials and forthcoming data (e.g., MBDA to refine the patient-specific predicted risk of future radiographic damage) will be useful to further define the optimal role for the MBDA test in clinical practice to optimize longer-term outcomes.”

The study was partly supported by Myriad Genetics, which owns Crescendo Bioscience, the company that markets the MBDA test known as Vectra DA. Dr. Curtis receives support from the National Institutes of Health and the Patient-Centered Outcomes Research Institute, along with research grants and/or consulting fees from Amgen, Bristol-Myers Squibb, Corrona, Janssen, Myriad Genetics, Pfizer, and UCB. One coauthor reported receiving support from the NIH and research grants from Pfizer.

SOURCE: Curtis JR et al. J Rheumatol. 2018 Nov 15. doi: 10.3899/jrheum.180071.

Patients with rheumatoid arthritis and a high multibiomarker disease activity (MBDA) score were more likely than were patients with low scores to add or switch to biologics or JAK inhibitors, according to a study on the uptake and influence of MBDA testing among rheumatologists and patients.

Courtesy UAB Photo

“While we cannot provide certainty that the main reason that clinicians switched therapies was the MBDA test result, we note that the median time to add or switch to a new RA treatment was 1-2 months after testing, lending plausibility to the MBDA test being influential in this decision,” wrote Jeffrey R. Curtis, MD, of the division of clinical immunology and rheumatology at the University of Alabama at Birmingham, and his coauthors. Their report is in The Journal of Rheumatology.

The researchers analyzed Medicare data from 60,596 RA patients who had taken at least one MBDA (Vectra DA) test. Patients with high MBDA scores who were not taking biologics or a JAK inhibitor were most likely to begin one of the two treatments, at 19.7%, compared with 11.8% for a moderate MBDA score and 9.0% for a low score. For patients already receiving those treatments, the proportion adding or switching was 13.5% for high, 8.3% for moderate, and 5.2% for low MBDA scores. In addition, patients with high MBDA scores who added a new medication and saw no improvement in score were prone to see treatment fail; the likelihood of failure in that scenario was 61% higher (OR = 1.61; 95% confidence index, 1.27-2.03) than in patients whose score improved to low or moderate.

The authors acknowledged that their study did not randomize clinicians nor gather data as to why the tests were ordered, which made it “difficult to assess the incremental value of the information provided by testing above and beyond clinical measurement, or to know whether the treatment changes were appropriate.” However, they also noted the MBDA score’s value as a complement to clinical assessment and an indicator of disease activity, suggesting “ongoing clinical trials and forthcoming data (e.g., MBDA to refine the patient-specific predicted risk of future radiographic damage) will be useful to further define the optimal role for the MBDA test in clinical practice to optimize longer-term outcomes.”

The study was partly supported by Myriad Genetics, which owns Crescendo Bioscience, the company that markets the MBDA test known as Vectra DA. Dr. Curtis receives support from the National Institutes of Health and the Patient-Centered Outcomes Research Institute, along with research grants and/or consulting fees from Amgen, Bristol-Myers Squibb, Corrona, Janssen, Myriad Genetics, Pfizer, and UCB. One coauthor reported receiving support from the NIH and research grants from Pfizer.

SOURCE: Curtis JR et al. J Rheumatol. 2018 Nov 15. doi: 10.3899/jrheum.180071.

Patients with rheumatoid arthritis and a high multibiomarker disease activity (MBDA) score were more likely than were patients with low scores to add or switch to biologics or JAK inhibitors, according to a study on the uptake and influence of MBDA testing among rheumatologists and patients.

Courtesy UAB Photo

“While we cannot provide certainty that the main reason that clinicians switched therapies was the MBDA test result, we note that the median time to add or switch to a new RA treatment was 1-2 months after testing, lending plausibility to the MBDA test being influential in this decision,” wrote Jeffrey R. Curtis, MD, of the division of clinical immunology and rheumatology at the University of Alabama at Birmingham, and his coauthors. Their report is in The Journal of Rheumatology.

The researchers analyzed Medicare data from 60,596 RA patients who had taken at least one MBDA (Vectra DA) test. Patients with high MBDA scores who were not taking biologics or a JAK inhibitor were most likely to begin one of the two treatments, at 19.7%, compared with 11.8% for a moderate MBDA score and 9.0% for a low score. For patients already receiving those treatments, the proportion adding or switching was 13.5% for high, 8.3% for moderate, and 5.2% for low MBDA scores. In addition, patients with high MBDA scores who added a new medication and saw no improvement in score were prone to see treatment fail; the likelihood of failure in that scenario was 61% higher (OR = 1.61; 95% confidence index, 1.27-2.03) than in patients whose score improved to low or moderate.

The authors acknowledged that their study did not randomize clinicians nor gather data as to why the tests were ordered, which made it “difficult to assess the incremental value of the information provided by testing above and beyond clinical measurement, or to know whether the treatment changes were appropriate.” However, they also noted the MBDA score’s value as a complement to clinical assessment and an indicator of disease activity, suggesting “ongoing clinical trials and forthcoming data (e.g., MBDA to refine the patient-specific predicted risk of future radiographic damage) will be useful to further define the optimal role for the MBDA test in clinical practice to optimize longer-term outcomes.”

The study was partly supported by Myriad Genetics, which owns Crescendo Bioscience, the company that markets the MBDA test known as Vectra DA. Dr. Curtis receives support from the National Institutes of Health and the Patient-Centered Outcomes Research Institute, along with research grants and/or consulting fees from Amgen, Bristol-Myers Squibb, Corrona, Janssen, Myriad Genetics, Pfizer, and UCB. One coauthor reported receiving support from the NIH and research grants from Pfizer.

SOURCE: Curtis JR et al. J Rheumatol. 2018 Nov 15. doi: 10.3899/jrheum.180071.

SAN FRANCISCO – Despite the readiness of liver transplant candidates to engage in discussions about advance care planning, there are low rates of such conversations with clinicians, results from a single-center survey found.

Doug Brunk/MDedge Medical News

“Recent studies have shown that there have been low rates of these types of discussions in all areas of medicine, not just in liver transplantation per se,” Connie W. Wang, MD, said in an interview at the annual meeting of the American Association for the Study of Liver Diseases. “We were curious to see what it looked like in our practice setting.”

In an effort to evaluate current advanced care planning documentation practices in the liver transplantation setting, she and her colleagues reviewed the medical charts of 168 adults who underwent an initial liver transplant evaluation at the University of California, San Francisco, from January 2017 to June 2017. Next, to assess readiness to complete advanced care planning among liver transplant candidates, the researchers administered the Advanced Care Planning Engagement Survey to 41 adults who underwent an initial liver transplant evaluation from March 2018 to May 2018. The survey was scored on a Likert scale of 1-4, in which a score of 4 equaled “ready” or “confident,” and a score of 5 equaled “very ready” or “very confident.”

The mean age of the 168 transplant candidates was 53 years, 35% were female, and 52% were non-Hispanic white. Only 15 patients (9%) reported completing advanced care planning prior to their liver transplant evaluation and none had legal advance care planning forms scanned or end-of-life wishes documented in the medical record. Durable power of attorney for health care was discussed with 17 patients (10%). On logistic regression analysis, only white race was associated with completion of advanced care planning (OR 4.16; P = .03), but age, Child-Pugh score, and MELD-Na score were not.

The mean age of the 41 transplant candidates who completed the Advanced Care Planning Engagement Survey was 58 years, 39% were female, and 58% were non-Hispanic white. Nearly all respondents (93%) indicated that they were ready to appoint a durable power of attorney, 85% were ready to discuss end-of-life care, and 93% were ready to ask physicians questions about medical decisions. Similarly, 93% of patients felt confident to appoint a durable power of attorney, 88% felt confident to discuss end-of-life care, and 93% felt confident to ask physicians questions about medical decisions.

“It seems like from the patients’ perspective, they are very much open to having these conversations, but there hasn’t been [the right] environment or setting to have them,” said Dr. Wang, a third-year internal medicine resident at UCSF. “Or, there may be a barrier from the provider’s perspective. Clearly, there is a huge need that can be filled.” She noted that future research should focus on development of tools to facilitate discussions and documentation between transplant clinicians, patients, and their caregivers.

One of the study authors, Jennifer C. Lai, MD, reported being a consultant for Third Rock Ventures, LLC. The other researchers reported having no financial disclosures.

[email protected]

Source: Hepatol. 2018;68[S1]: Abstract 771.

SAN FRANCISCO – Despite the readiness of liver transplant candidates to engage in discussions about advance care planning, there are low rates of such conversations with clinicians, results from a single-center survey found.

Doug Brunk/MDedge Medical News

“Recent studies have shown that there have been low rates of these types of discussions in all areas of medicine, not just in liver transplantation per se,” Connie W. Wang, MD, said in an interview at the annual meeting of the American Association for the Study of Liver Diseases. “We were curious to see what it looked like in our practice setting.”

In an effort to evaluate current advanced care planning documentation practices in the liver transplantation setting, she and her colleagues reviewed the medical charts of 168 adults who underwent an initial liver transplant evaluation at the University of California, San Francisco, from January 2017 to June 2017. Next, to assess readiness to complete advanced care planning among liver transplant candidates, the researchers administered the Advanced Care Planning Engagement Survey to 41 adults who underwent an initial liver transplant evaluation from March 2018 to May 2018. The survey was scored on a Likert scale of 1-4, in which a score of 4 equaled “ready” or “confident,” and a score of 5 equaled “very ready” or “very confident.”

The mean age of the 168 transplant candidates was 53 years, 35% were female, and 52% were non-Hispanic white. Only 15 patients (9%) reported completing advanced care planning prior to their liver transplant evaluation and none had legal advance care planning forms scanned or end-of-life wishes documented in the medical record. Durable power of attorney for health care was discussed with 17 patients (10%). On logistic regression analysis, only white race was associated with completion of advanced care planning (OR 4.16; P = .03), but age, Child-Pugh score, and MELD-Na score were not.

The mean age of the 41 transplant candidates who completed the Advanced Care Planning Engagement Survey was 58 years, 39% were female, and 58% were non-Hispanic white. Nearly all respondents (93%) indicated that they were ready to appoint a durable power of attorney, 85% were ready to discuss end-of-life care, and 93% were ready to ask physicians questions about medical decisions. Similarly, 93% of patients felt confident to appoint a durable power of attorney, 88% felt confident to discuss end-of-life care, and 93% felt confident to ask physicians questions about medical decisions.

“It seems like from the patients’ perspective, they are very much open to having these conversations, but there hasn’t been [the right] environment or setting to have them,” said Dr. Wang, a third-year internal medicine resident at UCSF. “Or, there may be a barrier from the provider’s perspective. Clearly, there is a huge need that can be filled.” She noted that future research should focus on development of tools to facilitate discussions and documentation between transplant clinicians, patients, and their caregivers.

One of the study authors, Jennifer C. Lai, MD, reported being a consultant for Third Rock Ventures, LLC. The other researchers reported having no financial disclosures.

[email protected]

Source: Hepatol. 2018;68[S1]: Abstract 771.

SAN FRANCISCO – Despite the readiness of liver transplant candidates to engage in discussions about advance care planning, there are low rates of such conversations with clinicians, results from a single-center survey found.

Doug Brunk/MDedge Medical News

“Recent studies have shown that there have been low rates of these types of discussions in all areas of medicine, not just in liver transplantation per se,” Connie W. Wang, MD, said in an interview at the annual meeting of the American Association for the Study of Liver Diseases. “We were curious to see what it looked like in our practice setting.”

In an effort to evaluate current advanced care planning documentation practices in the liver transplantation setting, she and her colleagues reviewed the medical charts of 168 adults who underwent an initial liver transplant evaluation at the University of California, San Francisco, from January 2017 to June 2017. Next, to assess readiness to complete advanced care planning among liver transplant candidates, the researchers administered the Advanced Care Planning Engagement Survey to 41 adults who underwent an initial liver transplant evaluation from March 2018 to May 2018. The survey was scored on a Likert scale of 1-4, in which a score of 4 equaled “ready” or “confident,” and a score of 5 equaled “very ready” or “very confident.”

The mean age of the 168 transplant candidates was 53 years, 35% were female, and 52% were non-Hispanic white. Only 15 patients (9%) reported completing advanced care planning prior to their liver transplant evaluation and none had legal advance care planning forms scanned or end-of-life wishes documented in the medical record. Durable power of attorney for health care was discussed with 17 patients (10%). On logistic regression analysis, only white race was associated with completion of advanced care planning (OR 4.16; P = .03), but age, Child-Pugh score, and MELD-Na score were not.

The mean age of the 41 transplant candidates who completed the Advanced Care Planning Engagement Survey was 58 years, 39% were female, and 58% were non-Hispanic white. Nearly all respondents (93%) indicated that they were ready to appoint a durable power of attorney, 85% were ready to discuss end-of-life care, and 93% were ready to ask physicians questions about medical decisions. Similarly, 93% of patients felt confident to appoint a durable power of attorney, 88% felt confident to discuss end-of-life care, and 93% felt confident to ask physicians questions about medical decisions.

“It seems like from the patients’ perspective, they are very much open to having these conversations, but there hasn’t been [the right] environment or setting to have them,” said Dr. Wang, a third-year internal medicine resident at UCSF. “Or, there may be a barrier from the provider’s perspective. Clearly, there is a huge need that can be filled.” She noted that future research should focus on development of tools to facilitate discussions and documentation between transplant clinicians, patients, and their caregivers.

One of the study authors, Jennifer C. Lai, MD, reported being a consultant for Third Rock Ventures, LLC. The other researchers reported having no financial disclosures.

[email protected]

Source: Hepatol. 2018;68[S1]: Abstract 771.

A KOH (potassium hydroxide) test done at the visit was negative as well as a fungal culture of each toenail.

The patient was diagnosed with congenital malalignment of the great toenails (CMGTN) based on history and morphologic appearance.

Congenital malalignment of the great toenails is an underrecognized and underreported nail disorder characterized by lateral deviation of the nail plate, which is not parallel to the longitudinal axis of the distal phalanx.¹ The cause is unknown. Some reports suggest a genetic cause being transmitted in an autosomal dominant fashion with variable expression.² There have been reports of CMGTN in monozygotic and dizygotic twins making this theory likely.³ Other authors consider an external cause such as amniotic bands, neonatal asphyxia, vascular malformations, and uterine pressure. This condition also has been reported in patients with Rubinstein-Taybi syndrome.⁴

The nail changes can occur at birth but in some cases, such as our patient, the nails become dystrophic months to years after birth. Characteristic nail changes include shorter, discolored, hyperkeratotic nails with transverse groove or ridges. In some cases, the dystrophic nails may cause inflammation and tenderness and is the most common cause of ingrown toenails in children.

The differential diagnosis includes onychomycosis, traumatic nails, nail psoriasis, pachyonychia congenital (PC), and onychomadesis. Onychomycosis can present with white or yellow discoloration of the nail that in some cases can be associated with nail breakage, hyperkeratosis, onycholysis, and subungual debris. Either fungal culture or periodic acid shift stain of nail clippings can help confirm or exclude this diagnosis. Psoriatic nails present with nail pits, oils spots, and onycholysis. Traumatic nail changes may occur from using small shoes and trauma from running or playing soccer, and presents with subungual hemorrhage and nail dystrophy of the first or second toenail. PC is a genetic disorder caused by a mutation in certain keratin proteins of the skin (k6a, k6b, K16 and K17). These patients usually have other skin findings including palmoplantar keratoderma, white plaques on the mouth, and skin cysts (steatocystoma multiplex and vellus hair cysts). Nail changes characteristic of PC includes subungual hyperkeratosis that causes a wedge shape thickening of the nail bed (pincer nails).⁵ Onychomadesis can be seen after viral infections such as hand-foot-mouth disease or in patients taking chemotherapy drugs that affect nail growth.

CMGTN usually resolves with time, but some patients with severe deviation and paronychia may need surgical correction.⁶
 

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Email her at [email protected].

References

1. Dermatol Online J. 2014 Jan 15;20(1):21251.

2. J Dtsch Dermatol Ges. 2012 May;10(5):326-30.

3. J Am Acad Dermatol. 2007 Oct;57(4):711-5.

4. Pediatr Dermatol. 2004 Jan-Feb;21(1):44-7.

5. Curr Opin Pediatr. 2014 Aug;26(4):440-5.

6. Skin Appendage Disord. 2018 Oct;4(4):230-5.

A KOH (potassium hydroxide) test done at the visit was negative as well as a fungal culture of each toenail.

The patient was diagnosed with congenital malalignment of the great toenails (CMGTN) based on history and morphologic appearance.

Congenital malalignment of the great toenails is an underrecognized and underreported nail disorder characterized by lateral deviation of the nail plate, which is not parallel to the longitudinal axis of the distal phalanx.¹ The cause is unknown. Some reports suggest a genetic cause being transmitted in an autosomal dominant fashion with variable expression.² There have been reports of CMGTN in monozygotic and dizygotic twins making this theory likely.³ Other authors consider an external cause such as amniotic bands, neonatal asphyxia, vascular malformations, and uterine pressure. This condition also has been reported in patients with Rubinstein-Taybi syndrome.⁴

The nail changes can occur at birth but in some cases, such as our patient, the nails become dystrophic months to years after birth. Characteristic nail changes include shorter, discolored, hyperkeratotic nails with transverse groove or ridges. In some cases, the dystrophic nails may cause inflammation and tenderness and is the most common cause of ingrown toenails in children.

The differential diagnosis includes onychomycosis, traumatic nails, nail psoriasis, pachyonychia congenital (PC), and onychomadesis. Onychomycosis can present with white or yellow discoloration of the nail that in some cases can be associated with nail breakage, hyperkeratosis, onycholysis, and subungual debris. Either fungal culture or periodic acid shift stain of nail clippings can help confirm or exclude this diagnosis. Psoriatic nails present with nail pits, oils spots, and onycholysis. Traumatic nail changes may occur from using small shoes and trauma from running or playing soccer, and presents with subungual hemorrhage and nail dystrophy of the first or second toenail. PC is a genetic disorder caused by a mutation in certain keratin proteins of the skin (k6a, k6b, K16 and K17). These patients usually have other skin findings including palmoplantar keratoderma, white plaques on the mouth, and skin cysts (steatocystoma multiplex and vellus hair cysts). Nail changes characteristic of PC includes subungual hyperkeratosis that causes a wedge shape thickening of the nail bed (pincer nails).⁵ Onychomadesis can be seen after viral infections such as hand-foot-mouth disease or in patients taking chemotherapy drugs that affect nail growth.

CMGTN usually resolves with time, but some patients with severe deviation and paronychia may need surgical correction.⁶
 

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Email her at [email protected].

References

1. Dermatol Online J. 2014 Jan 15;20(1):21251.

2. J Dtsch Dermatol Ges. 2012 May;10(5):326-30.

3. J Am Acad Dermatol. 2007 Oct;57(4):711-5.

4. Pediatr Dermatol. 2004 Jan-Feb;21(1):44-7.

5. Curr Opin Pediatr. 2014 Aug;26(4):440-5.

6. Skin Appendage Disord. 2018 Oct;4(4):230-5.

A KOH (potassium hydroxide) test done at the visit was negative as well as a fungal culture of each toenail.

The patient was diagnosed with congenital malalignment of the great toenails (CMGTN) based on history and morphologic appearance.

Congenital malalignment of the great toenails is an underrecognized and underreported nail disorder characterized by lateral deviation of the nail plate, which is not parallel to the longitudinal axis of the distal phalanx.¹ The cause is unknown. Some reports suggest a genetic cause being transmitted in an autosomal dominant fashion with variable expression.² There have been reports of CMGTN in monozygotic and dizygotic twins making this theory likely.³ Other authors consider an external cause such as amniotic bands, neonatal asphyxia, vascular malformations, and uterine pressure. This condition also has been reported in patients with Rubinstein-Taybi syndrome.⁴

The nail changes can occur at birth but in some cases, such as our patient, the nails become dystrophic months to years after birth. Characteristic nail changes include shorter, discolored, hyperkeratotic nails with transverse groove or ridges. In some cases, the dystrophic nails may cause inflammation and tenderness and is the most common cause of ingrown toenails in children.

The differential diagnosis includes onychomycosis, traumatic nails, nail psoriasis, pachyonychia congenital (PC), and onychomadesis. Onychomycosis can present with white or yellow discoloration of the nail that in some cases can be associated with nail breakage, hyperkeratosis, onycholysis, and subungual debris. Either fungal culture or periodic acid shift stain of nail clippings can help confirm or exclude this diagnosis. Psoriatic nails present with nail pits, oils spots, and onycholysis. Traumatic nail changes may occur from using small shoes and trauma from running or playing soccer, and presents with subungual hemorrhage and nail dystrophy of the first or second toenail. PC is a genetic disorder caused by a mutation in certain keratin proteins of the skin (k6a, k6b, K16 and K17). These patients usually have other skin findings including palmoplantar keratoderma, white plaques on the mouth, and skin cysts (steatocystoma multiplex and vellus hair cysts). Nail changes characteristic of PC includes subungual hyperkeratosis that causes a wedge shape thickening of the nail bed (pincer nails).⁵ Onychomadesis can be seen after viral infections such as hand-foot-mouth disease or in patients taking chemotherapy drugs that affect nail growth.

CMGTN usually resolves with time, but some patients with severe deviation and paronychia may need surgical correction.⁶
 

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Email her at [email protected].

References

1. Dermatol Online J. 2014 Jan 15;20(1):21251.

2. J Dtsch Dermatol Ges. 2012 May;10(5):326-30.

3. J Am Acad Dermatol. 2007 Oct;57(4):711-5.

4. Pediatr Dermatol. 2004 Jan-Feb;21(1):44-7.

5. Curr Opin Pediatr. 2014 Aug;26(4):440-5.

6. Skin Appendage Disord. 2018 Oct;4(4):230-5.