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Abstract Background Alopecia areata (AA) can have a significant impact on wellbeing. Consequently, individuals with AA often seek treatments or products to promote hair regrowth or camouflage their hair loss that incur a financial cost to the individual. Objectives The current study aimed to examine the direct financial burden of AA to understand the wider impact of the condition and the factors which influence spending on products and services. Methods A total of 829 United Kingdom based participants completed an online survey. Demographic and condition‐specific data were collected, alongside spending on AA‐related products and services. Participants were asked about their use of products and services, the associated costs, how they financed these costs, and their household income to determine what percentage of income they spent on products and services. Results Participants predominantly identified as female (85.9%), white (92.7%) with a mean age of 42.7 years and a median AA duration of 10.94 years. Female gender, Asian ethnicity, lower income, and worse AA symptoms predicted higher spend from income. Wigs were the most common product used and incurred the greatest cost (median £700). The highest cost for men was private dermatology services (median = £550). On average people spent 3% of their disposable income (prior to housing costs) on AA‐related products and services. Conclusions This study outlines the risk factors associated with higher financial burden from managing AA which require consideration by health providers, commissioners, and policy makers when designing services to support the wellbeing of people living with AA.

Frontal fibrosing alopecia (FFA) features lichenoid cutaneous inflammation and scarring hair loss. Here, Tziotzios et al. identify four genetic loci associated with FFA by GWAS followed by Bayesian fine-mapping, co-localisation and HLA imputation which highlights HLA-B*07:02 as a risk factor.

Hypotrichosis simplex (HS) with and without woolly hair (WH) comprises a group of rare, monogenic disorders of hair loss. Patients present with a diffuse loss of scalp and/or body hair, which usually begins in early childhood and progresses into adulthood. Some of the patients also show hair that is tightly curled. Approximately 10 genes for autosomal recessive and autosomal dominant forms of HS have been identified in the last decade, among them five genes for the dominant form. We collected blood and buccal samples from 17 individuals of a large British family with HS and WH. After having sequenced all known dominant genes for HS in this family without the identification of any disease causing mutation, we performed a genome-wide scan, using the HumanLinkage-24 BeadChip, followed by a classical linkage analysis; and whole exome-sequencing (WES). Evidence for linkage was found for a region on chromosome 4q35.1-q35.2 with a maximum LOD score of 3.61. WES led to the identification of a mutation in the gene SORBS2, encoding sorbin and SH3 domain containing 2. Unfortunately, we could not find an additional mutation in any other patient/family with HS; and in cell culture, we could not observe any difference between cloned wildtype and mutant SORBS2 using western blotting and immunofluorescence analyses. Therefore, at present, SORBS2 cannot be considered a definite disease gene for this phenotype. However, the locus on chromosome 4q is a robust and novel finding for hypotrichosis with woolly hair. Further fine mapping and sequencing efforts are therefore warranted in order to confirm SORBS2 as a plausible HS disease gene.