Delaying the clamping of the umbilical cord for 3 minutes after delivery decreased anemia for as long as 8-12 months in a population at high risk for the disorder, according to a report published online Jan. 17 in JAMA Pediatrics.

If early (within 1 minute of birth) cord clamping is avoided after delivery, fetoplacental blood moves into the newborn, augmenting his or her blood volume by 30%-40%. This is known to increase iron stores and prevent iron deficiency for at least 6 months, but until now there has been little evidence of how long this beneficial effect persists, said Ashish KC, MD, PhD, of International Maternal and Child Health, Uppsala (Sweden) University and the United Nations Children’s Fund, Lalitpur, Nepal, and associates.

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Delaying the clamping of the umbilical cord for 3 minutes after delivery decreased anemia for as long as 8-12 months in a population at high risk for the disorder, according to a report published online Jan. 17 in JAMA Pediatrics.

If early (within 1 minute of birth) cord clamping is avoided after delivery, fetoplacental blood moves into the newborn, augmenting his or her blood volume by 30%-40%. This is known to increase iron stores and prevent iron deficiency for at least 6 months, but until now there has been little evidence of how long this beneficial effect persists, said Ashish KC, MD, PhD, of International Maternal and Child Health, Uppsala (Sweden) University and the United Nations Children’s Fund, Lalitpur, Nepal, and associates.

arztsamui/Thinkstock

Delaying the clamping of the umbilical cord for 3 minutes after delivery decreased anemia for as long as 8-12 months in a population at high risk for the disorder, according to a report published online Jan. 17 in JAMA Pediatrics.

If early (within 1 minute of birth) cord clamping is avoided after delivery, fetoplacental blood moves into the newborn, augmenting his or her blood volume by 30%-40%. This is known to increase iron stores and prevent iron deficiency for at least 6 months, but until now there has been little evidence of how long this beneficial effect persists, said Ashish KC, MD, PhD, of International Maternal and Child Health, Uppsala (Sweden) University and the United Nations Children’s Fund, Lalitpur, Nepal, and associates.

arztsamui/Thinkstock

Asthma was ruled out in 33% of adults in the general Canadian population who had been diagnosed by a physician during the preceding 5 years, according to a report published online Jan. 17 in JAMA.

In a prospective multicenter cohort study involving 613 asthma patients, 203 had no evidence of current asthma when they underwent serial assessments of respiratory symptoms, lung function, and bronchial provocation testing while not taking asthma medications. More than 90% of these 203 participants safely refrained from using the medications for an additional 1-year follow-up period, said Shawn D. Aaron, MD, of Ottawa (Ont.) Hospital Research Institute, and his associates in the Canadian Respiratory Research Network.

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Asthma was ruled out in 33% of adults in the general Canadian population who had been diagnosed by a physician during the preceding 5 years, according to a report published online Jan. 17 in JAMA.

In a prospective multicenter cohort study involving 613 asthma patients, 203 had no evidence of current asthma when they underwent serial assessments of respiratory symptoms, lung function, and bronchial provocation testing while not taking asthma medications. More than 90% of these 203 participants safely refrained from using the medications for an additional 1-year follow-up period, said Shawn D. Aaron, MD, of Ottawa (Ont.) Hospital Research Institute, and his associates in the Canadian Respiratory Research Network.

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[email protected]

Asthma was ruled out in 33% of adults in the general Canadian population who had been diagnosed by a physician during the preceding 5 years, according to a report published online Jan. 17 in JAMA.

In a prospective multicenter cohort study involving 613 asthma patients, 203 had no evidence of current asthma when they underwent serial assessments of respiratory symptoms, lung function, and bronchial provocation testing while not taking asthma medications. More than 90% of these 203 participants safely refrained from using the medications for an additional 1-year follow-up period, said Shawn D. Aaron, MD, of Ottawa (Ont.) Hospital Research Institute, and his associates in the Canadian Respiratory Research Network.

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An assay designed to distinguish between bacterial and viral infections of the lower respiratory tract appears effective and shows promise for helping hospital physicians reduce overprescribing of antibiotics to children, a study showed.

“It is often not possible to differentiate between bacterial and nonbacterial disease on the basis of clinical judgment alone, [so] antibiotics are prescribed almost twice as often as required in children with acute respiratory tract infections in the USA,” wrote Chantal B. van Houten of the University Medical Centre Utrecht (the Netherlands) and associates in a study published in the Lancet Infectious Diseases.

The assay in question is called ImmunoXpert, which uses three biomarkers – tumor necrosis factor–related apoptosis-inducing ligand (TRAIL), interferon-gamma–induced protein-10 (IP-10), and C-reactive protein (CRP) – to determine if a lower respiratory tract infection has a viral or bacterial origin. A total of 777 subjects, aged 2-60 months, were recruited from four hospitals in the Netherlands and two hospitals in Israel between October 16, 2013, and March 1, 2015 (Lancet Inf Dis. 2016 Dec. doi: 10.1016/S1473-3099(16)30519-9).

The patients all had fevers with unidentified sources when they presented, and had a follow-up assessment carried out 28 days after baseline. Blood samples and nasal swabs were collected within 24 hours of presentation for assay analysis. Additionally, every subject was diagnosed as “bacterial” or “viral” by a three-member panel of pediatricians, whose diagnoses were based on the data available from the follow-up assessment and from clinical and laboratory data. The panel diagnosis for each subject was used as the reference standard.

Of the 777 subjects initially recruited, 200 were excluded from the final analysis for various reasons. Of the 577 who remained, the panel diagnosed 435 as having a viral infection and 71 as having a bacterial infection; 71 were deemed “inconclusive.” The panel was unanimous in 354 of these cases, and a majority of the panel (two of the three experts) agreed in 443 of these cases. In unanimous cases, the sensitivity of distinguishing between viral and bacterial cases correctly was 87.8%, with a specificity of 93.0%. The panel’s positive and negative predictive value were 62.1% and 98.3%, respectively.

The assay’s sensitivity rate in distinguishing between viral and bacterial infections was very close: 86.7%, with a specificity of 91.1%, which the authors noted was “promising diagnostic accuracy.” The positive predictive value of the assay was 60.5%, while the negative predictive value was found to be 97.8%.

Regarding the 71 cases that were deemed “inconclusive,” Dr. van Houten and coauthors acknowledged that “such inconclusive cases are inherent to studies without a gold standard, and this was taken into account when calculating the sample size.” Additionally, they noted that follow-up studies should take into consideration the costs of utilizing assay testing like ImmunoXpert, in order to better assess the financial implications that adopting the technology would have on a health care facility.

Nevertheless, the investigators concluded, “our findings [support] the need for implementation research to examine the added clinical utility of ImmunoXpert to diagnose bacterial infection in clinical care for children with lower respiratory tract infection and fever without source presenting at the hospital.”

Funding for this study was provided by MeMed Diagnostics. Dr. van Houten and coauthors did not report any relevant financial disclosures.

[email protected]

An assay designed to distinguish between bacterial and viral infections of the lower respiratory tract appears effective and shows promise for helping hospital physicians reduce overprescribing of antibiotics to children, a study showed.

“It is often not possible to differentiate between bacterial and nonbacterial disease on the basis of clinical judgment alone, [so] antibiotics are prescribed almost twice as often as required in children with acute respiratory tract infections in the USA,” wrote Chantal B. van Houten of the University Medical Centre Utrecht (the Netherlands) and associates in a study published in the Lancet Infectious Diseases.

The assay in question is called ImmunoXpert, which uses three biomarkers – tumor necrosis factor–related apoptosis-inducing ligand (TRAIL), interferon-gamma–induced protein-10 (IP-10), and C-reactive protein (CRP) – to determine if a lower respiratory tract infection has a viral or bacterial origin. A total of 777 subjects, aged 2-60 months, were recruited from four hospitals in the Netherlands and two hospitals in Israel between October 16, 2013, and March 1, 2015 (Lancet Inf Dis. 2016 Dec. doi: 10.1016/S1473-3099(16)30519-9).

The patients all had fevers with unidentified sources when they presented, and had a follow-up assessment carried out 28 days after baseline. Blood samples and nasal swabs were collected within 24 hours of presentation for assay analysis. Additionally, every subject was diagnosed as “bacterial” or “viral” by a three-member panel of pediatricians, whose diagnoses were based on the data available from the follow-up assessment and from clinical and laboratory data. The panel diagnosis for each subject was used as the reference standard.

Of the 777 subjects initially recruited, 200 were excluded from the final analysis for various reasons. Of the 577 who remained, the panel diagnosed 435 as having a viral infection and 71 as having a bacterial infection; 71 were deemed “inconclusive.” The panel was unanimous in 354 of these cases, and a majority of the panel (two of the three experts) agreed in 443 of these cases. In unanimous cases, the sensitivity of distinguishing between viral and bacterial cases correctly was 87.8%, with a specificity of 93.0%. The panel’s positive and negative predictive value were 62.1% and 98.3%, respectively.

The assay’s sensitivity rate in distinguishing between viral and bacterial infections was very close: 86.7%, with a specificity of 91.1%, which the authors noted was “promising diagnostic accuracy.” The positive predictive value of the assay was 60.5%, while the negative predictive value was found to be 97.8%.

Regarding the 71 cases that were deemed “inconclusive,” Dr. van Houten and coauthors acknowledged that “such inconclusive cases are inherent to studies without a gold standard, and this was taken into account when calculating the sample size.” Additionally, they noted that follow-up studies should take into consideration the costs of utilizing assay testing like ImmunoXpert, in order to better assess the financial implications that adopting the technology would have on a health care facility.

Nevertheless, the investigators concluded, “our findings [support] the need for implementation research to examine the added clinical utility of ImmunoXpert to diagnose bacterial infection in clinical care for children with lower respiratory tract infection and fever without source presenting at the hospital.”

Funding for this study was provided by MeMed Diagnostics. Dr. van Houten and coauthors did not report any relevant financial disclosures.

[email protected]

An assay designed to distinguish between bacterial and viral infections of the lower respiratory tract appears effective and shows promise for helping hospital physicians reduce overprescribing of antibiotics to children, a study showed.

“It is often not possible to differentiate between bacterial and nonbacterial disease on the basis of clinical judgment alone, [so] antibiotics are prescribed almost twice as often as required in children with acute respiratory tract infections in the USA,” wrote Chantal B. van Houten of the University Medical Centre Utrecht (the Netherlands) and associates in a study published in the Lancet Infectious Diseases.

The assay in question is called ImmunoXpert, which uses three biomarkers – tumor necrosis factor–related apoptosis-inducing ligand (TRAIL), interferon-gamma–induced protein-10 (IP-10), and C-reactive protein (CRP) – to determine if a lower respiratory tract infection has a viral or bacterial origin. A total of 777 subjects, aged 2-60 months, were recruited from four hospitals in the Netherlands and two hospitals in Israel between October 16, 2013, and March 1, 2015 (Lancet Inf Dis. 2016 Dec. doi: 10.1016/S1473-3099(16)30519-9).

The patients all had fevers with unidentified sources when they presented, and had a follow-up assessment carried out 28 days after baseline. Blood samples and nasal swabs were collected within 24 hours of presentation for assay analysis. Additionally, every subject was diagnosed as “bacterial” or “viral” by a three-member panel of pediatricians, whose diagnoses were based on the data available from the follow-up assessment and from clinical and laboratory data. The panel diagnosis for each subject was used as the reference standard.

Of the 777 subjects initially recruited, 200 were excluded from the final analysis for various reasons. Of the 577 who remained, the panel diagnosed 435 as having a viral infection and 71 as having a bacterial infection; 71 were deemed “inconclusive.” The panel was unanimous in 354 of these cases, and a majority of the panel (two of the three experts) agreed in 443 of these cases. In unanimous cases, the sensitivity of distinguishing between viral and bacterial cases correctly was 87.8%, with a specificity of 93.0%. The panel’s positive and negative predictive value were 62.1% and 98.3%, respectively.

The assay’s sensitivity rate in distinguishing between viral and bacterial infections was very close: 86.7%, with a specificity of 91.1%, which the authors noted was “promising diagnostic accuracy.” The positive predictive value of the assay was 60.5%, while the negative predictive value was found to be 97.8%.

Regarding the 71 cases that were deemed “inconclusive,” Dr. van Houten and coauthors acknowledged that “such inconclusive cases are inherent to studies without a gold standard, and this was taken into account when calculating the sample size.” Additionally, they noted that follow-up studies should take into consideration the costs of utilizing assay testing like ImmunoXpert, in order to better assess the financial implications that adopting the technology would have on a health care facility.

Nevertheless, the investigators concluded, “our findings [support] the need for implementation research to examine the added clinical utility of ImmunoXpert to diagnose bacterial infection in clinical care for children with lower respiratory tract infection and fever without source presenting at the hospital.”

Funding for this study was provided by MeMed Diagnostics. Dr. van Houten and coauthors did not report any relevant financial disclosures.

[email protected]

CHICAGO – Applying the key principles for limiting radiation exposure for vascular surgeons and staff – not to mention patients – during endovascular procedures involves a thorough understanding of dose metrics as well as risk factors for high-dose interventions, according to recent findings reported at a symposium on vascular surgery sponsored by Northwestern University.

Melissa Kirkwood, MD, of the University of Texas Southwestern Medical Center in Dallas, reported on her institution’s experience with limiting radiation exposure in typically high-dose cases. “What we found was that even though we had a substantial amount of dose in these cases – they included a significant proportion of 5- to 10-Gy and greater than 10-Gy cases – there were still no skin injuries detected in these patients,” she said, referencing retrospective and prospective analyses (J Vasc Surg. 2014;60:742-8; J Vasc Surg. 2015;61:902-6).

CHICAGO – Applying the key principles for limiting radiation exposure for vascular surgeons and staff – not to mention patients – during endovascular procedures involves a thorough understanding of dose metrics as well as risk factors for high-dose interventions, according to recent findings reported at a symposium on vascular surgery sponsored by Northwestern University.

Melissa Kirkwood, MD, of the University of Texas Southwestern Medical Center in Dallas, reported on her institution’s experience with limiting radiation exposure in typically high-dose cases. “What we found was that even though we had a substantial amount of dose in these cases – they included a significant proportion of 5- to 10-Gy and greater than 10-Gy cases – there were still no skin injuries detected in these patients,” she said, referencing retrospective and prospective analyses (J Vasc Surg. 2014;60:742-8; J Vasc Surg. 2015;61:902-6).

CHICAGO – Applying the key principles for limiting radiation exposure for vascular surgeons and staff – not to mention patients – during endovascular procedures involves a thorough understanding of dose metrics as well as risk factors for high-dose interventions, according to recent findings reported at a symposium on vascular surgery sponsored by Northwestern University.

Melissa Kirkwood, MD, of the University of Texas Southwestern Medical Center in Dallas, reported on her institution’s experience with limiting radiation exposure in typically high-dose cases. “What we found was that even though we had a substantial amount of dose in these cases – they included a significant proportion of 5- to 10-Gy and greater than 10-Gy cases – there were still no skin injuries detected in these patients,” she said, referencing retrospective and prospective analyses (J Vasc Surg. 2014;60:742-8; J Vasc Surg. 2015;61:902-6).

About two-thirds of patient advocacy organizations report receiving funds from for-profit firms, including pharmaceutical, device and biotechnology manufacturers, according to new survey results.

The study, published online Jan. 17 in JAMA Internal Medicine, sought responses from a randomly chosen sample of 439 executives at patient advocacy organizations (PAOs), of whom 66% (n = 289) responded. The median annual revenue for the groups surveyed was nearly $300,000, and 67% (n = 165) reported receiving at least some industry funding. Of those, 12% reported that more than half their annual funding comes from industry sources.

A total of 22 PAO leaders surveyed (8%) reported that they perceived pressure to conform their organizational interests to those of corporate donors (JAMA Intern Med. 2017 Jan 17. doi: 10.1001/jamainternmed.2016.8443).

The vast majority of respondents (82%) said they found conflicts of interest to be relevant to PAOs, and most reported having a written policy on conflicts. More than half said they viewed their own organizations’ conflict of interest policies as sound.

The findings warrant a broad re-examination of PAO conflict-of-interest policies and disclosures, and a detailed examination of the specific ways in which PAOs are influenced or pressured, wrote Susannah L. Rose, PhD, of the Cleveland Clinic, and her colleagues.

PAOs do not routinely and publicly disclose all their sources of funding on websites, tax returns, or annual reports, and there are media investigations into some groups “regarding their ties to industry and the integrity of their activities,” the investigators wrote.

Dr. Rose and her colleagues recommended that PAOs disclose detailed information about industry funding on their websites and on Open Payments, a government website. The researchers acknowledged that their study relied on self-reported data, and though it was designed to obscure the identity of respondents and their organizations, the possibility of response bias exists.

Harvard University’s Edmond J. Safra Center for Ethics funded the study. One coauthor, Steven Joffe, MD, MPH, disclosed past funding from Genzyme Sanofi. No other conflicts were reported.

About two-thirds of patient advocacy organizations report receiving funds from for-profit firms, including pharmaceutical, device and biotechnology manufacturers, according to new survey results.

The study, published online Jan. 17 in JAMA Internal Medicine, sought responses from a randomly chosen sample of 439 executives at patient advocacy organizations (PAOs), of whom 66% (n = 289) responded. The median annual revenue for the groups surveyed was nearly $300,000, and 67% (n = 165) reported receiving at least some industry funding. Of those, 12% reported that more than half their annual funding comes from industry sources.

A total of 22 PAO leaders surveyed (8%) reported that they perceived pressure to conform their organizational interests to those of corporate donors (JAMA Intern Med. 2017 Jan 17. doi: 10.1001/jamainternmed.2016.8443).

The vast majority of respondents (82%) said they found conflicts of interest to be relevant to PAOs, and most reported having a written policy on conflicts. More than half said they viewed their own organizations’ conflict of interest policies as sound.

The findings warrant a broad re-examination of PAO conflict-of-interest policies and disclosures, and a detailed examination of the specific ways in which PAOs are influenced or pressured, wrote Susannah L. Rose, PhD, of the Cleveland Clinic, and her colleagues.

PAOs do not routinely and publicly disclose all their sources of funding on websites, tax returns, or annual reports, and there are media investigations into some groups “regarding their ties to industry and the integrity of their activities,” the investigators wrote.

Dr. Rose and her colleagues recommended that PAOs disclose detailed information about industry funding on their websites and on Open Payments, a government website. The researchers acknowledged that their study relied on self-reported data, and though it was designed to obscure the identity of respondents and their organizations, the possibility of response bias exists.

Harvard University’s Edmond J. Safra Center for Ethics funded the study. One coauthor, Steven Joffe, MD, MPH, disclosed past funding from Genzyme Sanofi. No other conflicts were reported.

About two-thirds of patient advocacy organizations report receiving funds from for-profit firms, including pharmaceutical, device and biotechnology manufacturers, according to new survey results.

The study, published online Jan. 17 in JAMA Internal Medicine, sought responses from a randomly chosen sample of 439 executives at patient advocacy organizations (PAOs), of whom 66% (n = 289) responded. The median annual revenue for the groups surveyed was nearly $300,000, and 67% (n = 165) reported receiving at least some industry funding. Of those, 12% reported that more than half their annual funding comes from industry sources.

A total of 22 PAO leaders surveyed (8%) reported that they perceived pressure to conform their organizational interests to those of corporate donors (JAMA Intern Med. 2017 Jan 17. doi: 10.1001/jamainternmed.2016.8443).

The vast majority of respondents (82%) said they found conflicts of interest to be relevant to PAOs, and most reported having a written policy on conflicts. More than half said they viewed their own organizations’ conflict of interest policies as sound.

The findings warrant a broad re-examination of PAO conflict-of-interest policies and disclosures, and a detailed examination of the specific ways in which PAOs are influenced or pressured, wrote Susannah L. Rose, PhD, of the Cleveland Clinic, and her colleagues.

PAOs do not routinely and publicly disclose all their sources of funding on websites, tax returns, or annual reports, and there are media investigations into some groups “regarding their ties to industry and the integrity of their activities,” the investigators wrote.

Dr. Rose and her colleagues recommended that PAOs disclose detailed information about industry funding on their websites and on Open Payments, a government website. The researchers acknowledged that their study relied on self-reported data, and though it was designed to obscure the identity of respondents and their organizations, the possibility of response bias exists.

Harvard University’s Edmond J. Safra Center for Ethics funded the study. One coauthor, Steven Joffe, MD, MPH, disclosed past funding from Genzyme Sanofi. No other conflicts were reported.

Among critically ill patients admitted to the ICU with a suspected infection, defining sepsis by an increase of 2 or more points in the Sequential Organ Failure Assessment score yielded greater prognostic accuracy for in-hospital mortality, compared with the quick SOFA and the systemic inflammatory response syndrome criteria, results from a large analysis showed.

“Accurate diagnostic criteria and consensus definitions have an important role in adult intensive care medicine, providing tools for research, benchmarking, performance monitoring, and accreditation,” researchers from The Australian and New Zealand Intensive Care Society Centre for Outcomes and Resource Evaluation reported in the Jan. 17, 2017 edition of JAMA. “Seymour and colleagues published data concerning the validity of a 2 or more–point change in the Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score as a means of identifying sepsis among patients who are critically ill with suspected infection, assuming a SOFA of 0 for patients not known to have preexisting organ dysfunction (JAMA. 2016; 315[8]:762-74). In addition, the concept of the quick SOFA (qSOFA) score was introduced as a possible predictive tool among encounters with suspected infection outside the intensive care unit (ICU). These data were drawn from North American cohorts and a single German cohort and have not been validated externally.”

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Among critically ill patients admitted to the ICU with a suspected infection, defining sepsis by an increase of 2 or more points in the Sequential Organ Failure Assessment score yielded greater prognostic accuracy for in-hospital mortality, compared with the quick SOFA and the systemic inflammatory response syndrome criteria, results from a large analysis showed.

“Accurate diagnostic criteria and consensus definitions have an important role in adult intensive care medicine, providing tools for research, benchmarking, performance monitoring, and accreditation,” researchers from The Australian and New Zealand Intensive Care Society Centre for Outcomes and Resource Evaluation reported in the Jan. 17, 2017 edition of JAMA. “Seymour and colleagues published data concerning the validity of a 2 or more–point change in the Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score as a means of identifying sepsis among patients who are critically ill with suspected infection, assuming a SOFA of 0 for patients not known to have preexisting organ dysfunction (JAMA. 2016; 315[8]:762-74). In addition, the concept of the quick SOFA (qSOFA) score was introduced as a possible predictive tool among encounters with suspected infection outside the intensive care unit (ICU). These data were drawn from North American cohorts and a single German cohort and have not been validated externally.”

invisioner/thinkstockphotos

[email protected]

Among critically ill patients admitted to the ICU with a suspected infection, defining sepsis by an increase of 2 or more points in the Sequential Organ Failure Assessment score yielded greater prognostic accuracy for in-hospital mortality, compared with the quick SOFA and the systemic inflammatory response syndrome criteria, results from a large analysis showed.

“Accurate diagnostic criteria and consensus definitions have an important role in adult intensive care medicine, providing tools for research, benchmarking, performance monitoring, and accreditation,” researchers from The Australian and New Zealand Intensive Care Society Centre for Outcomes and Resource Evaluation reported in the Jan. 17, 2017 edition of JAMA. “Seymour and colleagues published data concerning the validity of a 2 or more–point change in the Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score as a means of identifying sepsis among patients who are critically ill with suspected infection, assuming a SOFA of 0 for patients not known to have preexisting organ dysfunction (JAMA. 2016; 315[8]:762-74). In addition, the concept of the quick SOFA (qSOFA) score was introduced as a possible predictive tool among encounters with suspected infection outside the intensive care unit (ICU). These data were drawn from North American cohorts and a single German cohort and have not been validated externally.”

invisioner/thinkstockphotos

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To the Editor:

A 39-year-old man with a history of hypertension and vitiligo presented with a rapid-onset, generalized, pruritic rash covering the body of 4 weeks’ duration. He reported that the rash progressively worsened after developing mild sunburn. The patient stated that the rash was extremely pruritic with a burning sensation and was tender to touch. He was treated with betamethasone valerate cream 0.1% by an outside physician and an over-the-counter anti-itch lotion with no notable improvement. His only medication was telmisartan-hydrochlorothiazide (HCTZ) for hypertension. He denied any drug allergies.

Physical examination revealed multiple discrete and coalescent planar erythematous papules and plaques involving only the depigmented vitiliginous skin of the forehead, eyelids, and nape of the neck (Figure 1A), and confluent on the lateral aspect of the bilateral forearms (Figure 1B), dorsal aspect of the right hand, and bilateral dorsi of the feet. Wickham striae were noted on the lips (Figure 1C). A clinical diagnosis of lichen planus (LP) was made. The patient initially was prescribed halobetasol propionate ointment 0.05% twice daily. He reported notable relief of pruritus with reduction of overall symptoms and new lesion formation.

A 4-mm punch biopsy was performed on the left forearm. Histopathology revealed LP. Microscopic examination of the hematoxylin and eosin–stained specimen revealed a bandlike lymphohistiocytic infiltrate that extended across the papillary dermis, focally obscuring the dermoepidermal junction where there were vacuolar changes and colloid bodies. The epidermis showed sawtooth rete ridges, wedge-shaped foci of hypergranulosis, and compact hyperkeratosis (Figure 2).

On further questioning during follow-up, the patient revealed that his hypertensive medication was changed from HCTZ, which he had been taking for the last 8 years, to the combination antihypertensive medication telmisartan-HCTZ before the onset of the skin eruption. Due to the temporal relationship between the new medication and onset of the eruption, the clinical impression was highly suspicious for drug-induced eruptive LP with Köbner phenomenon caused by the recent sunburn. Systemic workup for underlying causes of LP was negative. Laboratory tests revealed normal complete blood cell counts. The hepatitis panel included hepatitis A antibodies; hepatitis B surface, e antigen, and core antibodies; hepatitis B surface antigen and e antibodies; hepatitis C antibodies; and antinuclear antibodies, which were all negative.

The patient continued to develop new pruritic papules clinically consistent with LP. He was instructed to return to his primary care physician to change the telmisartan-HCTZ to a different class of antihypertensive medication. His medication was changed to atenolol. The patient also was instructed to continue the halobetasol propionate ointment 0.05% twice daily to the affected areas.

The patient returned for a follow-up visit 1 month later and reported notable improvement in pruritus and near-complete resolution of the LP after discontinuation of telmisartan-HCTZ. He also noted some degree of perifollicular repigmentation of the vitiliginous skin that had been unresponsive to prior therapy (Figure 3).

Lichen planus is a pruritic and inflammatory papulosquamous skin condition that presents as scaly, flat-topped, violaceous, polygonal-shaped papules commonly involving the flexor surface of the arms and legs, oral mucosa, scalp, nails, and genitalia. Clinically, LP can present in various forms including actinic, annular, atrophic, erosive, follicular, hypertrophic, linear, pigmented, and vesicular/bullous types. Koebnerization is common, especially in the linear form of LP. There are no specific laboratory findings or serologic markers seen in LP.

The exact cause of LP remains unknown. Clinical observations and anecdotal evidence have directed the cell-mediated immune response to insulting agents such as medications or contact allergy to metals triggering an abnormal cellular immune response. Various viral agents have been reported including hepatitis C virus, human herpesvirus, herpes simplex virus, and varicella-zoster virus.^1-5 Other factors such as seasonal change and the environment may contribute to the development of LP and an increase in the incidence of LP eruption has been observed from January to July throughout the United States.⁶ Lichen planus also has been associated with other altered immune-related disease such as ulcerative colitis, alopecia areata, vitiligo, dermatomyositis, morphea, lichen sclerosis, and myasthenia gravis.⁷ Increased levels of emotional stress, particularly related to family members, often is related to the onset or aggravation of symptoms.^8,9

Many drug-related LP-like and lichenoid eruptions have been reported with antihypertensive drugs, antimalarial drugs, diuretics, antidepressants, nonsteroidal anti-inflammatory drugs, antimicrobial drugs, and metals. In particular, medications such as captopril, enalapril, labetalol, propranolol, chlorothiazide, HCTZ, methyldopa, chloroquine, hydroxychloroquine, quinacrine, gold salts, penicillamine, and quinidine commonly are reported to induce lichenoid drug eruption.¹⁰

Several inflammatory papulosquamous skin conditions should be considered in the differential diagnosis before confirming the diagnosis of LP. It is important to rule out lupus erythematosus, especially if the oral mucosa and scalp are involved. In addition, erosive paraneoplastic pemphigus involving primarily the oral mucosa can resemble oral LP. Nail diseases such as psoriasis, onychomycosis, and alopecia areata should be considered as the differential diagnosis of nail disease. Genital involvement also can be seen in psoriasis and lichen sclerosus.

Treatment of LP is mainly symptomatic because of the benign nature of the disease and the high spontaneous remission rate with varying amount of time. If drugs, dental/metal implants, or underlying viral infections are the identifiable triggering factors of LP, the offending agents should be discontinued or removed. Additionally, topical or systemic treatments can be given depending on the severity of the disease, focusing mainly on symptomatic relief as well as the balance of risks and benefits associated with treatment.

Treatment options include topical and intralesional corticosteroids. Systemic medications such as oral corticosteroids and/or acitretin commonly are used in acute, severe, and disseminated cases, though treatment duration varies depending on the clinical response. Other systemic agents used to treat LP include griseofulvin, metronidazole, sulfasalazine, cyclosporine, and mycophenolate mofetil.

Phototherapy is considered an alternative therapy, especially for recalcitrant LP. UVA1 and narrowband UVB (wavelength, 311 nm) have been reported to effectively treat long-standing and therapy-resistant LP.¹¹ In addition, a small study used the excimer laser (wavelength, 308 nm), which is well tolerated by patients, to treat focal recalcitrant oral lesions with excellent results.¹² Photochemotherapy has been used with notable improvement, but the potential of carcinogenicity, especially in patients with Fitzpatrick skin types I and II, has limited its use.¹³

Our patient developed an unusual extensive LP eruption involving only vitiliginous skin shortly after initiation of the combined antihypertensive medication telmisartan-HCTZ, an angiotensin receptor blocker with a thiazide diuretic. Telmisartan and other angiotensin receptor blockers have not been reported to trigger LP; HCTZ is listed as one of the common drugs causing photosensitivity and LP.^14,15 Although it is possible that our patient exhibited a delayed lichenoid drug eruption from the HCTZ, it is noteworthy that he did not experience a single episode of LP during his 8-year history of taking HCTZ. Instead, he developed the LP eruption shortly after the addition of telmisartan to his HCTZ antihypertensive regimen. The temporal relationship led us to direct the patient to the prescribing physician to discontinue telmisartan-HCTZ. After changing his antihypertensive medication to atenolol, the patient presented with improvement within the first month and near-complete resolution 2 months after the discontinuation of telmisartan-HCTZ.

Our patient’s LP lesions only manifested on the skin affected by vitiligo, sparing the normal-pigmented skin. Studies have demonstrated an increased ratio of CD8⁺ T cells to CD4⁺ T cells as well as increased intercellular adhesion molecule 1 at the dermal level.^10,16 Both vitiligo and LP share some common histopathologic features including highly populated CD8⁺ T cells and intercellular adhesion molecule 1. In our case, LP was triggered on the vitiliginous skin by telmisartan. Vitiligo in combination with trauma induced by sunburn may represent the trigger that altered the cellular immune response and created the telmisartan-induced LP. As a result, the LP eruption was confined to the vitiliginous skin lesions.

Perifollicular repigmentation was observed in our patient after the LP lesions resolved; the patient’s vitiligo was unresponsive to prior treatment. The inflammatory process occurring in LP may exert and interfere in the underlying autoimmune cytotoxic effect toward the melanocytes and the melanin synthesis. It may be of interest to find out if the inflammatory response of LP has a positive influence on the effect of melanogenesis pathways or on the underlying autoimmune-related inflammatory process in vitiligo. Further studies are needed to investigate the role of immunotherapy targeting specific inflammatory pathways and the impact on the repigmentation in vitiligo.

Acknowledgment—Special thanks to Paul Chu, MD (Port Chester, New York).

To the Editor:

A 39-year-old man with a history of hypertension and vitiligo presented with a rapid-onset, generalized, pruritic rash covering the body of 4 weeks’ duration. He reported that the rash progressively worsened after developing mild sunburn. The patient stated that the rash was extremely pruritic with a burning sensation and was tender to touch. He was treated with betamethasone valerate cream 0.1% by an outside physician and an over-the-counter anti-itch lotion with no notable improvement. His only medication was telmisartan-hydrochlorothiazide (HCTZ) for hypertension. He denied any drug allergies.

Physical examination revealed multiple discrete and coalescent planar erythematous papules and plaques involving only the depigmented vitiliginous skin of the forehead, eyelids, and nape of the neck (Figure 1A), and confluent on the lateral aspect of the bilateral forearms (Figure 1B), dorsal aspect of the right hand, and bilateral dorsi of the feet. Wickham striae were noted on the lips (Figure 1C). A clinical diagnosis of lichen planus (LP) was made. The patient initially was prescribed halobetasol propionate ointment 0.05% twice daily. He reported notable relief of pruritus with reduction of overall symptoms and new lesion formation.

A 4-mm punch biopsy was performed on the left forearm. Histopathology revealed LP. Microscopic examination of the hematoxylin and eosin–stained specimen revealed a bandlike lymphohistiocytic infiltrate that extended across the papillary dermis, focally obscuring the dermoepidermal junction where there were vacuolar changes and colloid bodies. The epidermis showed sawtooth rete ridges, wedge-shaped foci of hypergranulosis, and compact hyperkeratosis (Figure 2).

On further questioning during follow-up, the patient revealed that his hypertensive medication was changed from HCTZ, which he had been taking for the last 8 years, to the combination antihypertensive medication telmisartan-HCTZ before the onset of the skin eruption. Due to the temporal relationship between the new medication and onset of the eruption, the clinical impression was highly suspicious for drug-induced eruptive LP with Köbner phenomenon caused by the recent sunburn. Systemic workup for underlying causes of LP was negative. Laboratory tests revealed normal complete blood cell counts. The hepatitis panel included hepatitis A antibodies; hepatitis B surface, e antigen, and core antibodies; hepatitis B surface antigen and e antibodies; hepatitis C antibodies; and antinuclear antibodies, which were all negative.

The patient continued to develop new pruritic papules clinically consistent with LP. He was instructed to return to his primary care physician to change the telmisartan-HCTZ to a different class of antihypertensive medication. His medication was changed to atenolol. The patient also was instructed to continue the halobetasol propionate ointment 0.05% twice daily to the affected areas.

The patient returned for a follow-up visit 1 month later and reported notable improvement in pruritus and near-complete resolution of the LP after discontinuation of telmisartan-HCTZ. He also noted some degree of perifollicular repigmentation of the vitiliginous skin that had been unresponsive to prior therapy (Figure 3).

Lichen planus is a pruritic and inflammatory papulosquamous skin condition that presents as scaly, flat-topped, violaceous, polygonal-shaped papules commonly involving the flexor surface of the arms and legs, oral mucosa, scalp, nails, and genitalia. Clinically, LP can present in various forms including actinic, annular, atrophic, erosive, follicular, hypertrophic, linear, pigmented, and vesicular/bullous types. Koebnerization is common, especially in the linear form of LP. There are no specific laboratory findings or serologic markers seen in LP.

The exact cause of LP remains unknown. Clinical observations and anecdotal evidence have directed the cell-mediated immune response to insulting agents such as medications or contact allergy to metals triggering an abnormal cellular immune response. Various viral agents have been reported including hepatitis C virus, human herpesvirus, herpes simplex virus, and varicella-zoster virus.^1-5 Other factors such as seasonal change and the environment may contribute to the development of LP and an increase in the incidence of LP eruption has been observed from January to July throughout the United States.⁶ Lichen planus also has been associated with other altered immune-related disease such as ulcerative colitis, alopecia areata, vitiligo, dermatomyositis, morphea, lichen sclerosis, and myasthenia gravis.⁷ Increased levels of emotional stress, particularly related to family members, often is related to the onset or aggravation of symptoms.^8,9

Many drug-related LP-like and lichenoid eruptions have been reported with antihypertensive drugs, antimalarial drugs, diuretics, antidepressants, nonsteroidal anti-inflammatory drugs, antimicrobial drugs, and metals. In particular, medications such as captopril, enalapril, labetalol, propranolol, chlorothiazide, HCTZ, methyldopa, chloroquine, hydroxychloroquine, quinacrine, gold salts, penicillamine, and quinidine commonly are reported to induce lichenoid drug eruption.¹⁰

Several inflammatory papulosquamous skin conditions should be considered in the differential diagnosis before confirming the diagnosis of LP. It is important to rule out lupus erythematosus, especially if the oral mucosa and scalp are involved. In addition, erosive paraneoplastic pemphigus involving primarily the oral mucosa can resemble oral LP. Nail diseases such as psoriasis, onychomycosis, and alopecia areata should be considered as the differential diagnosis of nail disease. Genital involvement also can be seen in psoriasis and lichen sclerosus.

Treatment of LP is mainly symptomatic because of the benign nature of the disease and the high spontaneous remission rate with varying amount of time. If drugs, dental/metal implants, or underlying viral infections are the identifiable triggering factors of LP, the offending agents should be discontinued or removed. Additionally, topical or systemic treatments can be given depending on the severity of the disease, focusing mainly on symptomatic relief as well as the balance of risks and benefits associated with treatment.

Treatment options include topical and intralesional corticosteroids. Systemic medications such as oral corticosteroids and/or acitretin commonly are used in acute, severe, and disseminated cases, though treatment duration varies depending on the clinical response. Other systemic agents used to treat LP include griseofulvin, metronidazole, sulfasalazine, cyclosporine, and mycophenolate mofetil.

Phototherapy is considered an alternative therapy, especially for recalcitrant LP. UVA1 and narrowband UVB (wavelength, 311 nm) have been reported to effectively treat long-standing and therapy-resistant LP.¹¹ In addition, a small study used the excimer laser (wavelength, 308 nm), which is well tolerated by patients, to treat focal recalcitrant oral lesions with excellent results.¹² Photochemotherapy has been used with notable improvement, but the potential of carcinogenicity, especially in patients with Fitzpatrick skin types I and II, has limited its use.¹³

Our patient developed an unusual extensive LP eruption involving only vitiliginous skin shortly after initiation of the combined antihypertensive medication telmisartan-HCTZ, an angiotensin receptor blocker with a thiazide diuretic. Telmisartan and other angiotensin receptor blockers have not been reported to trigger LP; HCTZ is listed as one of the common drugs causing photosensitivity and LP.^14,15 Although it is possible that our patient exhibited a delayed lichenoid drug eruption from the HCTZ, it is noteworthy that he did not experience a single episode of LP during his 8-year history of taking HCTZ. Instead, he developed the LP eruption shortly after the addition of telmisartan to his HCTZ antihypertensive regimen. The temporal relationship led us to direct the patient to the prescribing physician to discontinue telmisartan-HCTZ. After changing his antihypertensive medication to atenolol, the patient presented with improvement within the first month and near-complete resolution 2 months after the discontinuation of telmisartan-HCTZ.

Our patient’s LP lesions only manifested on the skin affected by vitiligo, sparing the normal-pigmented skin. Studies have demonstrated an increased ratio of CD8⁺ T cells to CD4⁺ T cells as well as increased intercellular adhesion molecule 1 at the dermal level.^10,16 Both vitiligo and LP share some common histopathologic features including highly populated CD8⁺ T cells and intercellular adhesion molecule 1. In our case, LP was triggered on the vitiliginous skin by telmisartan. Vitiligo in combination with trauma induced by sunburn may represent the trigger that altered the cellular immune response and created the telmisartan-induced LP. As a result, the LP eruption was confined to the vitiliginous skin lesions.

Perifollicular repigmentation was observed in our patient after the LP lesions resolved; the patient’s vitiligo was unresponsive to prior treatment. The inflammatory process occurring in LP may exert and interfere in the underlying autoimmune cytotoxic effect toward the melanocytes and the melanin synthesis. It may be of interest to find out if the inflammatory response of LP has a positive influence on the effect of melanogenesis pathways or on the underlying autoimmune-related inflammatory process in vitiligo. Further studies are needed to investigate the role of immunotherapy targeting specific inflammatory pathways and the impact on the repigmentation in vitiligo.

Acknowledgment—Special thanks to Paul Chu, MD (Port Chester, New York).

To the Editor:

A 39-year-old man with a history of hypertension and vitiligo presented with a rapid-onset, generalized, pruritic rash covering the body of 4 weeks’ duration. He reported that the rash progressively worsened after developing mild sunburn. The patient stated that the rash was extremely pruritic with a burning sensation and was tender to touch. He was treated with betamethasone valerate cream 0.1% by an outside physician and an over-the-counter anti-itch lotion with no notable improvement. His only medication was telmisartan-hydrochlorothiazide (HCTZ) for hypertension. He denied any drug allergies.

Physical examination revealed multiple discrete and coalescent planar erythematous papules and plaques involving only the depigmented vitiliginous skin of the forehead, eyelids, and nape of the neck (Figure 1A), and confluent on the lateral aspect of the bilateral forearms (Figure 1B), dorsal aspect of the right hand, and bilateral dorsi of the feet. Wickham striae were noted on the lips (Figure 1C). A clinical diagnosis of lichen planus (LP) was made. The patient initially was prescribed halobetasol propionate ointment 0.05% twice daily. He reported notable relief of pruritus with reduction of overall symptoms and new lesion formation.

A 4-mm punch biopsy was performed on the left forearm. Histopathology revealed LP. Microscopic examination of the hematoxylin and eosin–stained specimen revealed a bandlike lymphohistiocytic infiltrate that extended across the papillary dermis, focally obscuring the dermoepidermal junction where there were vacuolar changes and colloid bodies. The epidermis showed sawtooth rete ridges, wedge-shaped foci of hypergranulosis, and compact hyperkeratosis (Figure 2).

On further questioning during follow-up, the patient revealed that his hypertensive medication was changed from HCTZ, which he had been taking for the last 8 years, to the combination antihypertensive medication telmisartan-HCTZ before the onset of the skin eruption. Due to the temporal relationship between the new medication and onset of the eruption, the clinical impression was highly suspicious for drug-induced eruptive LP with Köbner phenomenon caused by the recent sunburn. Systemic workup for underlying causes of LP was negative. Laboratory tests revealed normal complete blood cell counts. The hepatitis panel included hepatitis A antibodies; hepatitis B surface, e antigen, and core antibodies; hepatitis B surface antigen and e antibodies; hepatitis C antibodies; and antinuclear antibodies, which were all negative.

The patient continued to develop new pruritic papules clinically consistent with LP. He was instructed to return to his primary care physician to change the telmisartan-HCTZ to a different class of antihypertensive medication. His medication was changed to atenolol. The patient also was instructed to continue the halobetasol propionate ointment 0.05% twice daily to the affected areas.

The patient returned for a follow-up visit 1 month later and reported notable improvement in pruritus and near-complete resolution of the LP after discontinuation of telmisartan-HCTZ. He also noted some degree of perifollicular repigmentation of the vitiliginous skin that had been unresponsive to prior therapy (Figure 3).

Lichen planus is a pruritic and inflammatory papulosquamous skin condition that presents as scaly, flat-topped, violaceous, polygonal-shaped papules commonly involving the flexor surface of the arms and legs, oral mucosa, scalp, nails, and genitalia. Clinically, LP can present in various forms including actinic, annular, atrophic, erosive, follicular, hypertrophic, linear, pigmented, and vesicular/bullous types. Koebnerization is common, especially in the linear form of LP. There are no specific laboratory findings or serologic markers seen in LP.

The exact cause of LP remains unknown. Clinical observations and anecdotal evidence have directed the cell-mediated immune response to insulting agents such as medications or contact allergy to metals triggering an abnormal cellular immune response. Various viral agents have been reported including hepatitis C virus, human herpesvirus, herpes simplex virus, and varicella-zoster virus.^1-5 Other factors such as seasonal change and the environment may contribute to the development of LP and an increase in the incidence of LP eruption has been observed from January to July throughout the United States.⁶ Lichen planus also has been associated with other altered immune-related disease such as ulcerative colitis, alopecia areata, vitiligo, dermatomyositis, morphea, lichen sclerosis, and myasthenia gravis.⁷ Increased levels of emotional stress, particularly related to family members, often is related to the onset or aggravation of symptoms.^8,9

Many drug-related LP-like and lichenoid eruptions have been reported with antihypertensive drugs, antimalarial drugs, diuretics, antidepressants, nonsteroidal anti-inflammatory drugs, antimicrobial drugs, and metals. In particular, medications such as captopril, enalapril, labetalol, propranolol, chlorothiazide, HCTZ, methyldopa, chloroquine, hydroxychloroquine, quinacrine, gold salts, penicillamine, and quinidine commonly are reported to induce lichenoid drug eruption.¹⁰

Several inflammatory papulosquamous skin conditions should be considered in the differential diagnosis before confirming the diagnosis of LP. It is important to rule out lupus erythematosus, especially if the oral mucosa and scalp are involved. In addition, erosive paraneoplastic pemphigus involving primarily the oral mucosa can resemble oral LP. Nail diseases such as psoriasis, onychomycosis, and alopecia areata should be considered as the differential diagnosis of nail disease. Genital involvement also can be seen in psoriasis and lichen sclerosus.

Treatment of LP is mainly symptomatic because of the benign nature of the disease and the high spontaneous remission rate with varying amount of time. If drugs, dental/metal implants, or underlying viral infections are the identifiable triggering factors of LP, the offending agents should be discontinued or removed. Additionally, topical or systemic treatments can be given depending on the severity of the disease, focusing mainly on symptomatic relief as well as the balance of risks and benefits associated with treatment.

Treatment options include topical and intralesional corticosteroids. Systemic medications such as oral corticosteroids and/or acitretin commonly are used in acute, severe, and disseminated cases, though treatment duration varies depending on the clinical response. Other systemic agents used to treat LP include griseofulvin, metronidazole, sulfasalazine, cyclosporine, and mycophenolate mofetil.

Phototherapy is considered an alternative therapy, especially for recalcitrant LP. UVA1 and narrowband UVB (wavelength, 311 nm) have been reported to effectively treat long-standing and therapy-resistant LP.¹¹ In addition, a small study used the excimer laser (wavelength, 308 nm), which is well tolerated by patients, to treat focal recalcitrant oral lesions with excellent results.¹² Photochemotherapy has been used with notable improvement, but the potential of carcinogenicity, especially in patients with Fitzpatrick skin types I and II, has limited its use.¹³

Our patient developed an unusual extensive LP eruption involving only vitiliginous skin shortly after initiation of the combined antihypertensive medication telmisartan-HCTZ, an angiotensin receptor blocker with a thiazide diuretic. Telmisartan and other angiotensin receptor blockers have not been reported to trigger LP; HCTZ is listed as one of the common drugs causing photosensitivity and LP.^14,15 Although it is possible that our patient exhibited a delayed lichenoid drug eruption from the HCTZ, it is noteworthy that he did not experience a single episode of LP during his 8-year history of taking HCTZ. Instead, he developed the LP eruption shortly after the addition of telmisartan to his HCTZ antihypertensive regimen. The temporal relationship led us to direct the patient to the prescribing physician to discontinue telmisartan-HCTZ. After changing his antihypertensive medication to atenolol, the patient presented with improvement within the first month and near-complete resolution 2 months after the discontinuation of telmisartan-HCTZ.

Our patient’s LP lesions only manifested on the skin affected by vitiligo, sparing the normal-pigmented skin. Studies have demonstrated an increased ratio of CD8⁺ T cells to CD4⁺ T cells as well as increased intercellular adhesion molecule 1 at the dermal level.^10,16 Both vitiligo and LP share some common histopathologic features including highly populated CD8⁺ T cells and intercellular adhesion molecule 1. In our case, LP was triggered on the vitiliginous skin by telmisartan. Vitiligo in combination with trauma induced by sunburn may represent the trigger that altered the cellular immune response and created the telmisartan-induced LP. As a result, the LP eruption was confined to the vitiliginous skin lesions.

Perifollicular repigmentation was observed in our patient after the LP lesions resolved; the patient’s vitiligo was unresponsive to prior treatment. The inflammatory process occurring in LP may exert and interfere in the underlying autoimmune cytotoxic effect toward the melanocytes and the melanin synthesis. It may be of interest to find out if the inflammatory response of LP has a positive influence on the effect of melanogenesis pathways or on the underlying autoimmune-related inflammatory process in vitiligo. Further studies are needed to investigate the role of immunotherapy targeting specific inflammatory pathways and the impact on the repigmentation in vitiligo.

Acknowledgment—Special thanks to Paul Chu, MD (Port Chester, New York).

The Diagnosis: Allergic Contact Dermatitis

An allergic contact dermatitis (ACD) to acrylates was suspected and 4 patches were applied to the forearm (the North American Standard Series of the North American Contact Dermatitis Group). The patches were 2-hydroxyethyl methacrylate (2-HEMA) 2.0% permissible exposure limit (peL), ethyl acrylate 0.1% peL, tosylamide formaldehyde resin 10.0% peL, and methyl methacrylate 2.0% peL. A reading at 72 hours was performed and showed a positive reaction to hydroxyethyl methacrylate, ethyl acrylate, and methyl methacrylate, and a negative patch test to tosylamide formaldehyde resin (nail polish)(Figure). The patient was diagnosed with an allergic contact hypersensitivity to the aforementioned acrylates and instructed to avoid artificial nails and acrylate glues. She also was started on oral biotin supplements. On 6-month follow-up the patient had regrowth of all 10 fingernails without brittleness or splitting. She was able to use nail polishes but avoided all acrylic artificial nails and acrylate-containing personal care products.

Acrylate Allergy and Artificial Nails

Acrylates are plastic materials formed by polymerization of acrylic or methacrylic acid monomers and have been cited as a major cause of occupational and nonoccupational contact dermatitis. Contact dermatitis to acrylates in artificial nails was first reported in the 1950s.^1,2 Products containing 100% methyl methacrylate monomers in acrylic nails were banned by the US Food and Drug Administration in the early 1970s after receiving a number of complaints.³ However, no regulation prohibits the use of methyl methacrylate monomer in cosmetic products, and various methacrylate and acrylate monomers remain widely used.⁴ With a growing popularity in artificial nails, it is expected the number of sensitized persons will increase.

Acrylate allergy from sculptured nails concern self-curing resins made from a polymer powder and a liquid monomer solution. Advantages of new UV-cured products include the lack of unpleasant smell and simplified modeling. They also do not require an irritant, such as methacrylic acid, as a bonding agent. Instead, 2-HEMA and 2-hydroxypropyl methacrylate are added. These photobonded nails colloquially are called gel nails (acid free) as opposed to acrylic nails (using methacrylic acid as a primer). It is important to note that the esters of acrylic acid but not the acid itself sensitize patients, and sensitization is not caused by the uncured gel or the monomer solution but by the remaining monomers in the cured plastic nail and the dust filings that are produced during the finishing process.

Clinical Presentation

Symptoms of an ACD to nail acrylates include pruritus and fingertip dermatitis along with nail plate dystrophy. There may be pruritus at the nail base, with subsequent dryness, thickening, and onycholysis. The brittle nails may become split, discolored, and develop paronychia. Inadvertent contact with glue monomers or other acrylate-containing substances may cause eczematous lesions at distant sites. Avoidance of the allergen often results in complete restoration of the normal nail and fingertip within months.

Sensitization

Acrylates and methacrylates are ubiquitous materials used for both industrial and commercial applications. Due to their widespread industrial use, contact allergies to acrylates including 2-HEMA, 2-hydroxypropyl methacrylate, and triethyleneglycol diacrylate (TREGDA) are common. Cross-reaction of these compounds has been observed and is postulated to be due to reaction of the (meth)acrylate carboxyethyl group with the receptors of antigen-presenting cells.⁵ As a result, an individual with an acrylate allergy sensitized to one allergen often is allergic to its similar compounds and cross-reactors and must avoid the assortment of compounds containing these ingredients, which is important for individuals with occupational sensitization to a particular acrylate who is subsequently susceptible to other acrylate-containing compounds triggering allergic reactions when reexposure occurs in different settings.

Allergens and Occupational Exposure

Acrylates in cosmetic nail products are a source of ACD for not only the customer but also the manicurist.⁶ The most frequently cited sources of ACD in beauticians are acrylate chemicals.⁷ However, acrylate compounds are an occupational hazard for a number of other specialists, including dentists and dental technicians, histology technicians, and individuals in the printing industry.^8,9 Other individuals may be sensitized to acrylates through their inclusion in adhesives, dental bonding agents, hearing aids, electrocardiogram electrodes, artificial bone cement, and a myriad of other medical and nonmedical applications.^4,10-12 For workers who cannot avoid occupational exposure to these allergens, polyvinyl alcohol and multilayer laminate gloves are recommended, as natural rubber latex gloves do not always provide adequate protection from many of these agents.¹⁰

Testing for Suspected Acrylate Allergy

Cross-reactivity among acrylates is widely considered in the literature but remains enigmatic and is an important consideration with regard to routine patch test screening.¹³ In the case of an acrylate allergy to nail products, using 2-HEMA and ethylene glycol dimethacrylate is effective in detecting sensitization by photobonded nails and in patients sensitized by powder liquid products.¹⁴ One study showed a patch test panel including 2-HEMA, ethylene glycol dimethacrylate, and TREGDA was effective in identifying the majority of individuals with an allergy to acrylates in nail products and nail technicians.¹⁵ Another study has shown the most commonly positive testing allergens to be HEMA, ethyl acrylate, and methyl methacrylate.¹⁶ If one is patch testing only one chemical, it appears 2-HEMA is preferred.¹⁷ However, broader panels of screening allergens are necessary to achieve an accurate diagnosis. Furthermore, different panels of test allergens have been shown to vary in their ability to detect an acrylate allergy in different occupational exposures.¹² 

The time to patch test read also is important. A standard read at 72 hours is warranted; however, one study showed if only one read at day 3 was done without a subsequent day 7 read, then 25% of TREGDA and 50% of 2-HEMA allergies would have been missed in patients with occupational acrylate allergy.¹⁵ Other studies have reported late-appearing and long-lasting test reactions when testing for an acrylate allergy.^18,19 Clinicians should be cognizant that an acrylate allergy may be present even if initial screening is negative but the history and clinical picture are suggestive.

The Diagnosis: Allergic Contact Dermatitis

An allergic contact dermatitis (ACD) to acrylates was suspected and 4 patches were applied to the forearm (the North American Standard Series of the North American Contact Dermatitis Group). The patches were 2-hydroxyethyl methacrylate (2-HEMA) 2.0% permissible exposure limit (peL), ethyl acrylate 0.1% peL, tosylamide formaldehyde resin 10.0% peL, and methyl methacrylate 2.0% peL. A reading at 72 hours was performed and showed a positive reaction to hydroxyethyl methacrylate, ethyl acrylate, and methyl methacrylate, and a negative patch test to tosylamide formaldehyde resin (nail polish)(Figure). The patient was diagnosed with an allergic contact hypersensitivity to the aforementioned acrylates and instructed to avoid artificial nails and acrylate glues. She also was started on oral biotin supplements. On 6-month follow-up the patient had regrowth of all 10 fingernails without brittleness or splitting. She was able to use nail polishes but avoided all acrylic artificial nails and acrylate-containing personal care products.

Acrylate Allergy and Artificial Nails

Acrylates are plastic materials formed by polymerization of acrylic or methacrylic acid monomers and have been cited as a major cause of occupational and nonoccupational contact dermatitis. Contact dermatitis to acrylates in artificial nails was first reported in the 1950s.^1,2 Products containing 100% methyl methacrylate monomers in acrylic nails were banned by the US Food and Drug Administration in the early 1970s after receiving a number of complaints.³ However, no regulation prohibits the use of methyl methacrylate monomer in cosmetic products, and various methacrylate and acrylate monomers remain widely used.⁴ With a growing popularity in artificial nails, it is expected the number of sensitized persons will increase.

Acrylate allergy from sculptured nails concern self-curing resins made from a polymer powder and a liquid monomer solution. Advantages of new UV-cured products include the lack of unpleasant smell and simplified modeling. They also do not require an irritant, such as methacrylic acid, as a bonding agent. Instead, 2-HEMA and 2-hydroxypropyl methacrylate are added. These photobonded nails colloquially are called gel nails (acid free) as opposed to acrylic nails (using methacrylic acid as a primer). It is important to note that the esters of acrylic acid but not the acid itself sensitize patients, and sensitization is not caused by the uncured gel or the monomer solution but by the remaining monomers in the cured plastic nail and the dust filings that are produced during the finishing process.

Clinical Presentation

Symptoms of an ACD to nail acrylates include pruritus and fingertip dermatitis along with nail plate dystrophy. There may be pruritus at the nail base, with subsequent dryness, thickening, and onycholysis. The brittle nails may become split, discolored, and develop paronychia. Inadvertent contact with glue monomers or other acrylate-containing substances may cause eczematous lesions at distant sites. Avoidance of the allergen often results in complete restoration of the normal nail and fingertip within months.

Sensitization

Acrylates and methacrylates are ubiquitous materials used for both industrial and commercial applications. Due to their widespread industrial use, contact allergies to acrylates including 2-HEMA, 2-hydroxypropyl methacrylate, and triethyleneglycol diacrylate (TREGDA) are common. Cross-reaction of these compounds has been observed and is postulated to be due to reaction of the (meth)acrylate carboxyethyl group with the receptors of antigen-presenting cells.⁵ As a result, an individual with an acrylate allergy sensitized to one allergen often is allergic to its similar compounds and cross-reactors and must avoid the assortment of compounds containing these ingredients, which is important for individuals with occupational sensitization to a particular acrylate who is subsequently susceptible to other acrylate-containing compounds triggering allergic reactions when reexposure occurs in different settings.

Allergens and Occupational Exposure

Acrylates in cosmetic nail products are a source of ACD for not only the customer but also the manicurist.⁶ The most frequently cited sources of ACD in beauticians are acrylate chemicals.⁷ However, acrylate compounds are an occupational hazard for a number of other specialists, including dentists and dental technicians, histology technicians, and individuals in the printing industry.^8,9 Other individuals may be sensitized to acrylates through their inclusion in adhesives, dental bonding agents, hearing aids, electrocardiogram electrodes, artificial bone cement, and a myriad of other medical and nonmedical applications.^4,10-12 For workers who cannot avoid occupational exposure to these allergens, polyvinyl alcohol and multilayer laminate gloves are recommended, as natural rubber latex gloves do not always provide adequate protection from many of these agents.¹⁰

Testing for Suspected Acrylate Allergy

Cross-reactivity among acrylates is widely considered in the literature but remains enigmatic and is an important consideration with regard to routine patch test screening.¹³ In the case of an acrylate allergy to nail products, using 2-HEMA and ethylene glycol dimethacrylate is effective in detecting sensitization by photobonded nails and in patients sensitized by powder liquid products.¹⁴ One study showed a patch test panel including 2-HEMA, ethylene glycol dimethacrylate, and TREGDA was effective in identifying the majority of individuals with an allergy to acrylates in nail products and nail technicians.¹⁵ Another study has shown the most commonly positive testing allergens to be HEMA, ethyl acrylate, and methyl methacrylate.¹⁶ If one is patch testing only one chemical, it appears 2-HEMA is preferred.¹⁷ However, broader panels of screening allergens are necessary to achieve an accurate diagnosis. Furthermore, different panels of test allergens have been shown to vary in their ability to detect an acrylate allergy in different occupational exposures.¹² 

The time to patch test read also is important. A standard read at 72 hours is warranted; however, one study showed if only one read at day 3 was done without a subsequent day 7 read, then 25% of TREGDA and 50% of 2-HEMA allergies would have been missed in patients with occupational acrylate allergy.¹⁵ Other studies have reported late-appearing and long-lasting test reactions when testing for an acrylate allergy.^18,19 Clinicians should be cognizant that an acrylate allergy may be present even if initial screening is negative but the history and clinical picture are suggestive.

The Diagnosis: Allergic Contact Dermatitis

An allergic contact dermatitis (ACD) to acrylates was suspected and 4 patches were applied to the forearm (the North American Standard Series of the North American Contact Dermatitis Group). The patches were 2-hydroxyethyl methacrylate (2-HEMA) 2.0% permissible exposure limit (peL), ethyl acrylate 0.1% peL, tosylamide formaldehyde resin 10.0% peL, and methyl methacrylate 2.0% peL. A reading at 72 hours was performed and showed a positive reaction to hydroxyethyl methacrylate, ethyl acrylate, and methyl methacrylate, and a negative patch test to tosylamide formaldehyde resin (nail polish)(Figure). The patient was diagnosed with an allergic contact hypersensitivity to the aforementioned acrylates and instructed to avoid artificial nails and acrylate glues. She also was started on oral biotin supplements. On 6-month follow-up the patient had regrowth of all 10 fingernails without brittleness or splitting. She was able to use nail polishes but avoided all acrylic artificial nails and acrylate-containing personal care products.

Acrylate Allergy and Artificial Nails

Acrylates are plastic materials formed by polymerization of acrylic or methacrylic acid monomers and have been cited as a major cause of occupational and nonoccupational contact dermatitis. Contact dermatitis to acrylates in artificial nails was first reported in the 1950s.^1,2 Products containing 100% methyl methacrylate monomers in acrylic nails were banned by the US Food and Drug Administration in the early 1970s after receiving a number of complaints.³ However, no regulation prohibits the use of methyl methacrylate monomer in cosmetic products, and various methacrylate and acrylate monomers remain widely used.⁴ With a growing popularity in artificial nails, it is expected the number of sensitized persons will increase.

Acrylate allergy from sculptured nails concern self-curing resins made from a polymer powder and a liquid monomer solution. Advantages of new UV-cured products include the lack of unpleasant smell and simplified modeling. They also do not require an irritant, such as methacrylic acid, as a bonding agent. Instead, 2-HEMA and 2-hydroxypropyl methacrylate are added. These photobonded nails colloquially are called gel nails (acid free) as opposed to acrylic nails (using methacrylic acid as a primer). It is important to note that the esters of acrylic acid but not the acid itself sensitize patients, and sensitization is not caused by the uncured gel or the monomer solution but by the remaining monomers in the cured plastic nail and the dust filings that are produced during the finishing process.

Clinical Presentation

Symptoms of an ACD to nail acrylates include pruritus and fingertip dermatitis along with nail plate dystrophy. There may be pruritus at the nail base, with subsequent dryness, thickening, and onycholysis. The brittle nails may become split, discolored, and develop paronychia. Inadvertent contact with glue monomers or other acrylate-containing substances may cause eczematous lesions at distant sites. Avoidance of the allergen often results in complete restoration of the normal nail and fingertip within months.

Sensitization

Acrylates and methacrylates are ubiquitous materials used for both industrial and commercial applications. Due to their widespread industrial use, contact allergies to acrylates including 2-HEMA, 2-hydroxypropyl methacrylate, and triethyleneglycol diacrylate (TREGDA) are common. Cross-reaction of these compounds has been observed and is postulated to be due to reaction of the (meth)acrylate carboxyethyl group with the receptors of antigen-presenting cells.⁵ As a result, an individual with an acrylate allergy sensitized to one allergen often is allergic to its similar compounds and cross-reactors and must avoid the assortment of compounds containing these ingredients, which is important for individuals with occupational sensitization to a particular acrylate who is subsequently susceptible to other acrylate-containing compounds triggering allergic reactions when reexposure occurs in different settings.

Allergens and Occupational Exposure

Acrylates in cosmetic nail products are a source of ACD for not only the customer but also the manicurist.⁶ The most frequently cited sources of ACD in beauticians are acrylate chemicals.⁷ However, acrylate compounds are an occupational hazard for a number of other specialists, including dentists and dental technicians, histology technicians, and individuals in the printing industry.^8,9 Other individuals may be sensitized to acrylates through their inclusion in adhesives, dental bonding agents, hearing aids, electrocardiogram electrodes, artificial bone cement, and a myriad of other medical and nonmedical applications.^4,10-12 For workers who cannot avoid occupational exposure to these allergens, polyvinyl alcohol and multilayer laminate gloves are recommended, as natural rubber latex gloves do not always provide adequate protection from many of these agents.¹⁰

Testing for Suspected Acrylate Allergy

Cross-reactivity among acrylates is widely considered in the literature but remains enigmatic and is an important consideration with regard to routine patch test screening.¹³ In the case of an acrylate allergy to nail products, using 2-HEMA and ethylene glycol dimethacrylate is effective in detecting sensitization by photobonded nails and in patients sensitized by powder liquid products.¹⁴ One study showed a patch test panel including 2-HEMA, ethylene glycol dimethacrylate, and TREGDA was effective in identifying the majority of individuals with an allergy to acrylates in nail products and nail technicians.¹⁵ Another study has shown the most commonly positive testing allergens to be HEMA, ethyl acrylate, and methyl methacrylate.¹⁶ If one is patch testing only one chemical, it appears 2-HEMA is preferred.¹⁷ However, broader panels of screening allergens are necessary to achieve an accurate diagnosis. Furthermore, different panels of test allergens have been shown to vary in their ability to detect an acrylate allergy in different occupational exposures.¹² 

The time to patch test read also is important. A standard read at 72 hours is warranted; however, one study showed if only one read at day 3 was done without a subsequent day 7 read, then 25% of TREGDA and 50% of 2-HEMA allergies would have been missed in patients with occupational acrylate allergy.¹⁵ Other studies have reported late-appearing and long-lasting test reactions when testing for an acrylate allergy.^18,19 Clinicians should be cognizant that an acrylate allergy may be present even if initial screening is negative but the history and clinical picture are suggestive.

Asymptomatic first-degree relatives of multiple sclerosis patients at high risk for developing the disease were significantly more likely to show subclinical signs of MS than were family members at lower risk, in the Genes and Environment in Multiple Sclerosis prospective cohort study. The findings were published online on Jan. 17 in JAMA Neurology.

The Genes and Environment in Multiple Sclerosis (GEMS) project is the first prospective study of populations at risk for MS and is the first detailed cross-sectional examination of higher-risk and lower-risk family members to date, according to investigators led by Zongqi Xia, MD, PhD, of Brigham and Women’s Hospital, Boston. Although the totality of evidence put together through neuroimaging and numerous clinical tests in the study indicate that individuals with the highest risk for MS have higher risk for the disease than do those with the lowest risk, simple vibration threshold testing gave the best results, Dr. Xia and his colleagues reported.

copyright Zerbor/Thinkstock

Asymptomatic first-degree relatives of multiple sclerosis patients at high risk for developing the disease were significantly more likely to show subclinical signs of MS than were family members at lower risk, in the Genes and Environment in Multiple Sclerosis prospective cohort study. The findings were published online on Jan. 17 in JAMA Neurology.

The Genes and Environment in Multiple Sclerosis (GEMS) project is the first prospective study of populations at risk for MS and is the first detailed cross-sectional examination of higher-risk and lower-risk family members to date, according to investigators led by Zongqi Xia, MD, PhD, of Brigham and Women’s Hospital, Boston. Although the totality of evidence put together through neuroimaging and numerous clinical tests in the study indicate that individuals with the highest risk for MS have higher risk for the disease than do those with the lowest risk, simple vibration threshold testing gave the best results, Dr. Xia and his colleagues reported.

copyright Zerbor/Thinkstock

Asymptomatic first-degree relatives of multiple sclerosis patients at high risk for developing the disease were significantly more likely to show subclinical signs of MS than were family members at lower risk, in the Genes and Environment in Multiple Sclerosis prospective cohort study. The findings were published online on Jan. 17 in JAMA Neurology.

The Genes and Environment in Multiple Sclerosis (GEMS) project is the first prospective study of populations at risk for MS and is the first detailed cross-sectional examination of higher-risk and lower-risk family members to date, according to investigators led by Zongqi Xia, MD, PhD, of Brigham and Women’s Hospital, Boston. Although the totality of evidence put together through neuroimaging and numerous clinical tests in the study indicate that individuals with the highest risk for MS have higher risk for the disease than do those with the lowest risk, simple vibration threshold testing gave the best results, Dr. Xia and his colleagues reported.

copyright Zerbor/Thinkstock

Want to know what your colleagues are talking about? Here are the top discussion threads in ACS Communities (all from the General Surgery community):
 

1. A lap appy ain’t always easy ...

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Want to know what your colleagues are talking about? Here are the top discussion threads in ACS Communities (all from the General Surgery community):
 

1. A lap appy ain’t always easy ...

To join communities, log in to ACS Communities at http://acscommunities.facs.org/home, go to “Browse All Communities” near the top of any page, and click the blue “Join” button next to the community you’d like to join. If you have any questions, please send them to [email protected].

Want to know what your colleagues are talking about? Here are the top discussion threads in ACS Communities (all from the General Surgery community):
 

1. A lap appy ain’t always easy ...

To join communities, log in to ACS Communities at http://acscommunities.facs.org/home, go to “Browse All Communities” near the top of any page, and click the blue “Join” button next to the community you’d like to join. If you have any questions, please send them to [email protected].