The government warned Friday that those chic baby slings that hip moms and dads are sporting these days can be dangerous, even deadly for their little ones.

At Virginia Tech, where tailgating and raucous apartment complex parties are time-honored rituals, university officials are turning increasingly to parents to curb the problem of  underage drinking.

Objective  To examine the association between nonsteroidal anti-inflammatory drug (NSAID) use and cutaneous squamous cell carcinoma (SCC).

Design  Retrospective case-control study.

Setting  Kaiser Permanente Northern California (KPNC), a large population based-health maintenance organization.

Patients  Random sample of 415 KPNC members diagnosed as having a pathologically verified SCC in 2004 and 415 age-, sex-, and race-matched controls with no history of skin cancer.

Main Exposure Measure  Self-reported NSAID use in the 10 years prior to baseline. Use of NSAIDs was categorized based on type (any NSAIDs, aspirin, ibuprofen, and nonaspirin NSAIDs). Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using conditional logistic regression to estimate the association of SCC with regular use, dose, and duration of exposure to the different NSAID types. Information on pharmacy-dispensed NSAIDs was also examined to assess its association with SCC risk. Models were adjusted for all ascertained SCC risk factors (fully adjusted model) and only those variables associated with both SCC risk and NSAID use (parsimonious model).

Results  Fully adjusted analyses showed no statistically significant reduction in SCC risk with self-reported regular use of any NSAID (OR, 1.32; 95% CI, 0.92-1.89), aspirin (OR, 1.38; 95% CI, 0.96-1.97), ibuprofen (OR, 0.74; 95% CI, 0.46-1.19), or nonaspirin NSAIDs (OR, 0.84; 95% CI, 0.56-1.26). Analyses examining duration, dose, and variables combining duration and dose of NSAID exposure did not appreciably change results. An analysis using the parsimonious model showed similar results. The data on pharmacy-dispensed NSAIDs also showed no association with SCC risk.

Conclusion  Neither self-reported nor pharmacy-dispensed NSAID exposure was associated with cutaneous SCC risk.

Published online February 15, 2010 (doi:10.1001/archdermatol.2009.374).

Background  Voriconazole is a triazole antifungal agent approved by the US Food and Drug Administration for serious fungal infections, including with Aspergillus, Fusarium, Pseudallescheria, and Scedosporium species. In initial clinical trials, approximately 2% of patients developed cutaneous reactions, including photosensitivity, cheilitis, and xerosis. Subsequent reports have implicated voriconazole as a cause of severe photosensitivity and accelerated photoaging, pseudoporphyria cutanea tarda, and aggressive squamous cell carcinoma.

Observation  We report 5 melanoma in situ lesions in the setting of extreme photosensitivity associated with long-term voriconazole therapy.

Conclusions  We recommend surveillance for skin cancer formation in all patients who require long-term voriconazole treatment, particularly those who manifest signs or symptoms of photosensitivity or chronic photodamage. Further study of the mechanism underlying voriconazole photosensitivity and oncogenesis is warranted.

Published online January 18, 2010 (doi:10.1001 /archdermatol.2009.362).

Objectives  To investigate the extent antibodies to adalimumab are formed in patients with plaque psoriasis and whether these antibodies have clinical consequences. Also, to examine the relationship between antibodies to adalimumab and adalimumab trough titers.

Design  Prospective observational cohort study.

Setting  Two Dutch dermatology departments in university hospitals.

Patients  All consecutive patients starting a regimen of adalimumab for chronic plaque psoriasis. Patients were screened and fulfilled the Dutch reimbursement criteria for adalimumab to treat psoriasis.

Intervention  Adalimumab treatment (per label).

Main Outcome Measures  The titer of antibodies to adalimumab, the adalimumab trough concentration, and the Psoriasis Area and Severity Index at weeks 12 and 24.

Results  Antibodies to adalimumab were detected in 13 of 29 patients (45%) during 24 weeks of treatment. Differences in response rates among patients with low, high, and no titers of antibodies to adalimumab were significant at weeks 12 and 24 (P = .04 and P < .001, respectively). The median adalimumab trough concentrations varied significantly among patients with low, high, and no titers of antibodies to adalimumab (1.30 [range, 0.01-5.50], 0.0 [range, 0.0-0.0], and 9.6 [range, 0.0-22.6] mg/L, respectively; P < .001). At week 24, the median adalimumab trough concentrations also differed significantly among good responders, moderate responders, and nonresponders (9.7 [range, 0.0-22.6], 8.9 [range, 3.2-12.6], and 0.0 [range, 0.0-13.3] mg/L, respectively; P = .01).

Conclusion  Antibodies to adalimumab are associated with lower serum adalimumab trough concentrations and with nonresponse or loss of response to adalimumab in patients with plaque psoriasis.

Objective  To assess the safety and efficacy of ablative fractional resurfacing (AFR) for nonacne atrophic scarring.

Design  In this before-and-after trial, each scar received 3 AFR treatments and 6 months of follow-up.

Setting  Private academic practice.

Patients  Fifteen women with Fitzpatrick skin types I to IV, aged 21 to 66 years, presented with 22 nonacne atrophic scars between June 1 and November 30, 2007. Three patients (3 scars) were excluded from the study after receiving 1 AFR treatment and not returning for follow-up visits. The remaining 12 patients (19 scars) completed all 3 treatments and 6 months of follow-up.

Interventions  Each scar received 3 AFR treatments at 1- to 4-month intervals.

Main Outcome Measures  Erythema, edema, petechiae, scarring, crusting, and dyschromia were graded after treatment and through 6 months of follow-up. Skin texture, pigmentation, atrophy, and overall appearance were evaluated after treatment and through 6 months of follow-up by the patient and a nonblinded investigator. A 3-dimensional optical profiling system generated high-resolution topographic representations of atrophic scars for objective measurement of changes in scar volume and depth.

Results  Adverse effects of treatment were mild to moderate, and no scarring or delayed-onset hypopigmentation was observed. At the 6-month follow-up visit, patient and investigator scores demonstrated improvements in skin texture for all scars (patient range, 1-4 [mean, 2.79]; investigator range, 2-4 [mean, 2.95]), pigmentation for all scars (patient range, 1-4 [mean, 2.32]; investigator range, 1-4 [mean, 2.21]), atrophy for all scars (patient range, 1-4 [mean, 2.26]; investigator range, 2-4 [mean, 2.95]), and overall scar appearance for all scars (patient range, 2-4 [mean, 2.89]; investigator range, 2-4 [mean, 3.05]). Image analysis revealed a 38.0% mean reduction of volume and 35.6% mean reduction of maximum scar depth.

Conclusion  The AFR treatments represent a safe, effective treatment modality for improving atrophic scarring due to surgery or trauma.

Objectives  To evaluate the effectiveness of a teaching method that uses 3-dimensional (3D) silicone-based prosthetic mimics of common serious lesions and eruptions and to compare learning outcomes with those achieved through the conventional method of lectures with 2-dimensional (2D) images.

Design  Prospective and comparative.

Setting  University of Massachusetts Medical School.

Participants  Ninety second-year medical students.

Intervention  A 1-hour teaching intervention using a lecture with 2D images (2D group) or using 3D prosthetic mimics of lesions and eruptions (3D group).

Main Outcome Measures  Mean scores in the domains of morphology, lesion and rash recognition, lesion and rash management, and overall performance assessed at baseline, immediately after, and 3 months after each group's respective teaching intervention.

Results  Immediately after the teaching intervention, the 3D group had significantly higher mean percentage scores than did the 2D group for overall performance (71 vs 65, P = .03), lesion recognition (65 vs 56, P = .02), and rash management (80 vs 67, P = .01). Three months later, the 3D group still had significantly higher mean percentage scores than did the 2D group for lesion recognition (47 vs 40, P = .03). The 3D group better recognized lesions at 3 months compared with at baseline, whereas the 2D group was no better at recognizing lesions at 3 months compared with at baseline.

Conclusions  Despite limited curricular time, the novel teaching method using 3D prosthetic mimics of lesions and eruptions improves immediate and long-term learning outcomes, in particular, lesion recognition. It is also a preferred teaching format among second-year medical students.

Objectives  To describe clinical and immunohistochemical findings in patients with cutaneous Langerhans cell histiocytosis (LCH) beginning in the first 3 months of life and to define predictors of disease evolution.

Design  Observational retrospective survey from July 15, 1989, to April 30, 2007.

Setting  Referral center in pediatric dermatology.

Patients  Thirty-one patients with a diagnosis of cutaneous LCH in the first 3 months of life and no previous visceral LCH.

Main Outcome Measures  Cutaneous lesion characteristics, regulatory T-lymphocyte density, and E-cadherin expression were assessed. Data were compared between the patient groups with self-regressive vs non–self-regressive forms of cutaneous LCH. Pathologic analysis was performed blinded to patient group.

Results  Self-regressive cutaneous LCH was found in 21 patients and non–self-regressive cutaneous LCH in 10 patients. Monolesional forms, necrotic lesions, hypopigmented macules at presentation, and distal topography of limb lesions were seen only in patients with self-regressive cutaneous LCH. Regulatory T-lymphocyte density correlated with interleukin 10 expression in lesions (r = 0.77, P = .003) but was not predictive of disease evolution. E-cadherin expression by Langerhans cells was found in 7 patients with disease limited to the skin whether self-regressive or not. One patient with secondary disseminated disease showed loss of E-cadherin expression in Langerhans cells.

Conclusions  Some morphologic traits of skin lesions can orient the diagnosis to a self-regressive form of cutaneous LCH. Regulatory T-lymphocyte density does not seem to be predictive of disease evolution. E-cadherin expression seems to be an indicator of limited skin disease but not of disease regression. Additional immunohistochemical study is required to confirm these data.

Background  Botulinum toxin type A (BTX) is used prophylactically to reduce the frequency of migraine headaches, with inconsistent responses reported in the literature. The purpose of our study was to determine whether BTX injections at doses used for upper-face cosmetic purposes, which differ from doses typically used by headache specialists, could prevent imploding and ocular but not exploding migraines.

Observations  Study participants were recruited among patients who had received or were planning to receive BTX injections for upper-face cosmetic purposes but also reported having migraines. Among the 18 patients who completed the study, most with imploding and ocular migraines experienced a significant reduction in their headache frequency, whereas those with exploding migraines generally did not.

Conclusions  Our study supports the hypothesis that patients with imploding and ocular migraines are more responsive to BTX than those with exploding migraines. Injections of BTX at doses appropriate for cosmetic purposes may be sufficient to prevent migraine attacks.

Background  Specific cutaneous lesions of Waldenström macroglobulinemia are rare and include neoplastic cell infiltrates, IgM bullous disease, and so-called IgM-storage papules, which characterize cutaneous macroglobulinosis (CM).

Observations  We report 2 patients with CM. In patient 1, CM started as small papules, as reported in most of the previously published case studies of CM. In patient 2, lesion evolution was remarkable by its severity, with large ulcerated nodules, and the disease progressed rapidly. As mentioned for half the previously described patients, peripheral neuropathy was suspected in patient 2 and demonstrated in patient 1, with production of antibodies to myelin-associated glycoprotein.

Conclusions  To the best of our knowledge, rituximab treatment of Waldenström macroglobulinemia associated with CM has not been described previously. Rituximab caused complete remission of the lesions in patient 1, whereas disease rapidly progressed in patient 2, and the patient died. These observations suggest that evolution of the cutaneous IgM-storage lesions reflects that of the underlying Waldenström macroglobulinemia, and CM is not a prognostic marker.

Background  Patients with cystic fibrosis classically present with evidence of pulmonary disease, exocrine pancreatic insufficiency, and high sweat chloride concentrations. Dermatitis as an initial manifestation of the disease is uncommon and has been attributed to multiple nutritional deficiencies.

Observation  We describe the case of a 3-month-old female infant with cystic fibrosis presenting with dermatitis in the setting of protein-energy malnutrition. A review of the laboratory study results in this case and others showed that a deficiency in zinc, essential fatty acids, and protein likely contributes to the development of the rash seen in cystic fibrosis.

Conclusions  Given the frequent delay in diagnosis, as well as the increased morbidity and mortality associated with protein-energy malnutrition in these patients, it is important to consider cystic fibrosis as a possible diagnosis in any infant presenting with a rash and other signs of malnutrition. The relative contribution of specific nutritional deficiencies and the degree to which they influence and interact with each other in producing the dermatitis remain unclear, although they may all affect a common underlying metabolic pathway.

Background  Primary cutaneous B-cell lymphoma manifested by anetoderma has been reported in 7 cases. In all, the secondary anetoderma developed in lesions of marginal-zone lymphoma or posttransplant lymphoproliferative disorder resembling marginal-zone lymphoma. The mechanisms underlying the destruction of elastic tissue in anetoderma are unclear. However, there is growing evidence linking primary anetoderma with a wide range of immunologic abnormalities, the most common being the presence of antiphospholipid antibodies.

Observations  We analyzed data from 5 patients (3 male, 2 female) with clinical and histopathological features of anetodermic primary cutaneous B-cell lymphoma. Three had marginal-zone lymphoma and 2 had follicle-center cell lymphoma. In all, secondary anetoderma developed in self-regressing nodules/plaques of the lymphoma. Two patients also had lesions clinically and histopathologically compatible with primary anetoderma. Associated immunologic diseases were systemic lupus erythematosus–like disease and rheumatoid arthritis (1 patient each; not in patients with primary anetoderma). Antiphospholipid antibodies were found in 4 patients.

Conclusions  Anetodermic primary cutaneous B-cell lymphoma is a rare and unique clinicopathological manifestation not only of marginal-zone lymphoma, as previously described, but also of follicle-center cell lymphoma. This type of secondary anetoderma, like primary anetoderma, might be associated with immunologic disorders, particularly antiphospholipid antibodies.