What’s new in hair — November 2016 | Dr. Yuval Ramot

Tofacitinib for the treatment of severe alopecia areata and variants: A study of 90 patients

J Am Acad Dermatol. 2016 Nov 2. doi.org/10.1016/j.jaad.2016.09.007. [Epub ahead of print]

In the September review of “What’s new in hair”, we have reported on two studies summarizing the effects of tofacitinib and ruxolitinib on alopecia areata (AA) (published in JCI Insight). This month, Liu et al. from Yale University report their experience with tofacitinib in the largest cohort of AA patients to date treated with JAK inhibitors. They treated 90 patients with severe AA with 10-20 mg daily of tofacitinib, with some of them receiving an adjuvant treatment with prednisone. Seventy seven percent of the patients showed a clinical response, and as was shown before, the patch type of AA responded better than the alopecia totalis and universalis types. Notably, this study reports on patients that were followed for long periods, up to 18 months, and no serious adverse events were noted. This is an important study, which expands the available data on the use of JAK inhibitors for AA, and further emphasizes the importance of conducting a well-controlled study on the use of JAK inhibitors for AA.

 

Tofacitinib for the treatment of alopecia areata and variants in adolescents

J Am Acad Dermatol. 2016 Nov 2. doi.org/10.1016/j.jaad.2016.09.006. [Epub ahead of print]

While the use of JAK inhibitors for alopecia areata (AA) has been described in a large number of patients, its use in the adolescent population has not been published so far. This is particularly important, since this group of patients is especially prone to the social and emotional effects of this disorder. Cragilow et al. describe their experience with the use of tofacitinib in 13 adolescent AA patients, between the ages of 12-17 years. They report that nine patients had significant hair regrowth, and the median SALT score percent change was 93%. Side effects were mild in nature. Although the sample size in this study is small, it shows that tofacitinib can be used effectively to treat AA in adolescents, and again demonstrates the importance of performing further studies with this group of medications.

 

Therapeutic role of human hepatocyte growth factor (HGF) in treating hair loss

PeerJ. 2016 Nov 1;4:e2624. eCollection 2016

The hepatocyte growth factor (HGF) is a paracrine hormone that plays an important part in epithelial-mesenchymal transition, and has also been demonstrated to be secreted by dermal papilla cells. In this study, Qi et al. assessed the potential effects of HGF on hair growth in vivo using a mouse model. They constructed a plasmid that contains the hHGF gene and transfected it into human fibroblasts. These fibroblasts were then injected into mice, and resulted in faster hair regeneration, improved follicle development, and significantly increased HGF receptor and β-catenin expression. The authors suggest that this nonviral vector of hHGF could potentially serve in the future as gene therapy for hair loss disorders.

 

Mutations in three genes encoding proteins involved in hair shaft formation cause uncombable hair syndrome

Am J Hum Genet, 2016 Nov 2. http://dx.doi.org/10.1016/j.ajhg.2016.10.004

Uncombable hair syndrome (UHS) is a hair condition characterized by dry, frizzy, and often fair hair, which is resistant to combing. Some of the cases are inherited, and autosomal dominant and recessive patterns of inheritance have been reported. In this paper, Basmanav et al. evaluated 11 patients with UHS, and using whole-exome sequencing revealed homozygous or compound heterozygous mutations in one of three genes: PADI3 (peptidylarginine deiminase 3), TGM3 (transglutaminase 3), and TCHH (trichohyalin). PADI3 and TGM3 are responsible for posttranslational modifications of trichohyalin, an important structural protein in the hair shaft. Using in vitro and knock out mouse model, the authors of this report could show that the mutations detected in these genes resulted in significant defects in the structural organization and activity of the affected proteins. This finding provides better understanding of the protein interactions that take part in hair formation, an insight that may be harnessed by the cosmetic and pharmaceutic industries.

 

Expression analysis of the stem cell marker Pw1/Peg3reveals a CD34 negative progenitor population in the hair follicle

Stem Cells. 2016 Nov 15. doi: 10.1002/stem.2540. [Epub ahead of print]

Characterization of the stem cells markers of the hair follicle is important for both research and clinical purposes. The parentally imprinted gene Pw1/Peg3 was demonstrated previously to be expressed by stem cells in different tissues. In this manuscript, Besson et al. used a Pw1/Peg3 reporter mouse to examine the expression of this marker during the bulge formation and to compare its expression with other known stem cells markers. They show that Pw1/Peg3 starts to be expressed during the formation of the placode, and is continuously expressed during postnatal life. Pw1/Peg3 is expressed by both CD34+ and CD34- cells, and both types of cells can generate new hair follicles, reconstitute their niche, and maintain the capacity for self-renewal. Nevertheless, there are differences in cell-cycle behavior between these two cell populations. This study gives more details on the stem cell markers of the hair follicle, and provides evidence that Pw1/Peg3 can serve as a marker for the full population of stem cells.

 

Frontal fibrosing alopecia: reflections and hypotheses on aetiology and pathogenesis

Exp Dermatol. 2016 Nov;25(11):847-852. doi: 10.1111/exd.13071.

The interest in frontal fibrosing alopecia (FFA) has increased substantially in the last decade, due to the general feeling among dermatologists that its incidence is increasing. Being a scarring condition, with very limited therapeutic options, better understanding of its pathogenesis is crucial. In this viewpoint, Tziotzios et al. provide an overview of the evidence on the possible etiologies and pathogenesis for this devastating disorder. They highlight the possible role of genetics in this disorder, which is based on familial cases of FFA, and other factor, such as hormones and trauma (based on women predominance and surgery as a precipitating event, respectively). They conclude the viewpoint in an especially interesting section, aimed to formulate the experimental strategies that should be used to address the different suggested hypotheses. This viewpoint can serve as an excellent starting point for researchers interested in this emerging disorder.

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