Influenza Vaccination as a Novel Trigger of Wells Syndrome in a Child

Wells syndrome is a rare disorder of unknown etiology. Precipitants include insect bites, infections, medications, malignancies, and vaccinations. Possible mechanisms include hypersensitivity reactions to antigens. There are four reports in the literature of Wells syndrome precipitated by vaccinations (hepatitis B vaccine, tetanus vaccine, tetanus‐diptheria vaccine and triple antigen vaccine). We present a further case of Wells syndrome in a 22‐month‐old child after influenza vaccine as a novel trigger not previously reported.     

Impact of next generation sequencing on diagnostics in a genetic skin disease clinic

Individuals with inherited skin diseases often pose one of the most difficult diagnostic challenges in dermatology. The hunt for the underlying molecular pathology may involve candidate gene screening or linkage analysis, which is usually determined by the initial history, the physical findings and laboratory tests. Recent technical advances in DNA sequencing, however, are shifting the diagnostic paradigm. Notably, next‐generation sequencing allows a more comprehensive approach to diagnosing inherited diseases, with potential savings of both time and money. In the setting of a paediatric dermatology genetics clinic in Kuwait, we therefore performed whole‐exome sequencing on seven individuals without a priori detailed knowledge of the patients’ disorders: from these sequencing data, we diagnosed X‐linked hypohidrotic ectodermal dysplasia (two cases), acrodermatitis enteropathica, recessive erythropoietic protoporphyria (two siblings) and localized recessive dystrophic epidermolysis bullosa (two siblings). All these groups of disorders are clinically and genetically heterogeneous, but the sequencing data proved inherently useful in improving patient care and avoiding unnecessary investigations. Our observations highlight the value of whole‐exome sequencing, in combination with robust bioinformatics analysis, in determining the precise molecular pathology and clinical diagnosis in patients with genetic skin disorders, notably at an early stage in the clinical evaluation of these often complex disorders and thereby support a new paradigm for future diagnostics.     

Terbinafine in the treatment of dermatophyte toenail onychomycosis: a meta‐analysis of efficacy for continuous and intermittent regimens

Objective To compare mycological and complete cures of terbinafine continuous and intermittent regimens in the treatment of toenail onychomycosis. Methods The PubMed database was searched using the terms “terbinafine”, “onychomycosis”, “continuous” and “pulse(d)” or “intermittent”. The inclusion criteria were head‐to‐head comparison of terbinafine pulse and continuous regimens for dermatophyte toenail infections. Risk ratios were calculated for intention‐to‐treat and evaluable patient analyses, when possible. Pooled estimates for total and subgroup analyses were calculated using a random effect model, Mantel‐Haenszel method and their probabilities were calculated with z‐statistics. Results Nine studies from eight publications were included. Two continuous regimens and four intermittent regimens were investigated. A pooled risk ratio of 0.87 was obtained for intention‐to‐treat (95% CI: 0.79–0.96, P = 0.004, n = 6) and evaluable patient (95% CI: 0.80–0.96, P = 0.003, n = 8) analyses of mycological cure, favouring continuous terbinafine. For complete cure, pooled risk ratios of 0.97 (95% CI: 0.77–1.23, P = 0.82, n = 7) for intention‐to‐treat and 0.93 (95% CI: 0.76–1.13, P = 0.44, n = 9) for evaluable patient analyses showed equality of the two regimens. The pulse regimen that demonstrated consistently comparable results to the continuous terbinafine regimen was two pulses of terbinafine 250 mg/day for 4 weeks on/4 weeks off. Conclusions Meta‐analysis of published studies of toenail onychomycosis showed that a continuous terbinafine regimen is generally significantly superior to a pulsed terbinafine regimen for mycological cure. In contrast, some pulse terbinafine regimens were as effective as continuous terbinafine regimens for complete cure.     

Genetic architecture of acne vulgaris

Acne vulgaris is a ubiquitary skin disease characterized by chronic inflammation of the pilosebaceous unit resulting from bacterial colonization of hair follicles by Propionibacterium acnes, androgen‐induced increased sebum production, altered keratinization and inflammation. Here, we review our current understanding of the genetic architecture of this intriguing disease. We analysed genomewide association studies (GWAS) and candidate genes studies for acne vulgaris. Moreover, we included GWAS studies for the associated disease polycystic ovary syndrome (PCOS). Overall, the available data revealed sixteen genetic loci flagged by single nucleotide polymorphisms (SNPs), none of which has been confirmed yet by independent studies. Moreover, a GWAS for PCOS identified 21 susceptible loci. The genetic architecture is complex which has been revealed by GWAS. Further and larger studies in different populations are required to confirm or disprove results from candidate gene studies as well to identify signals that may overlap between different populations. Finally, studies on rare genetic variants in acne and associated diseases like PCOS may deepen our understanding of its pathogenesis.