Effect of Oral Minoxidil on Monilethrix

Dear Editor, Monilethrix (phenotype MIM number 158000) is an autosomal dominant hair disorder that is caused by mutations affecting the genes KRTHB1 (KRT81), KRTHB3 (KRT83), or KRTHB6 (KRT86) which code for type II hair cortex keratins resulting in short, fragile, broken hair that appears beaded. The beading is the result of a periodic narrowing of the shaft with nodes separated by about 0.7 mm. Individuals with monilethrix have normal hair at birth, but within the first few months of life develop fragile, brittle hair that tends to fracture and produce varying degrees of alopecia. Light microscopic examination is diagnostic and reveals elliptical nodes of normal thickness and intermittent constrictions [Figure 1] at which the hair easily breaks. There may be spontaneous improvement with time, but the condition never resolves completely. An autosomal recessive form of monilethrix-like congenital hypotrichosis (phenotype MIM number 607903) is caused by mutation in the DSG4 gene. The clinical picture of autosomal recessive monilethrix is more severe than the dominant form, with more extensive alopecia.[1]Figure 1: Scalp dermoscopy in monilethrix: beaded appearance of elliptical nodes of normal thickness and intermittent constrictionsWe observed a 14-year-old female patient with monilethrix over a time period of 10 years who eventually developed female androgenetic alopecia (AGA) at the age of 23 that was successfully treated with 1.25 mg oral minoxidil with residual structural hair anomaly of monilethrix [Figure 2a-d].Figure 2: Treatment with oral minoxidil: (a and b) global photographic assessment (a) before, and (b) after treatment, (c and d) epiluminescence microscopy (c) before, and (d) after treatment. Note significant improvement of diversity of hair shaft diameters with residual structural anomaly of monilethrixNo specific treatment exists for the monilethrix. Spontaneous resolution following puberty or during pregnancy has occurred in some cases. Other treatment is symptomatic and supportive. And yet, there have been reports of successful treatment with topical[2,3] or oral minoxidil.[4] Monilethrix is a primary disorder of hair keratinization, whereas minoxidil affects the potassium channels present in hair follicles resulting in an increase of the duration of anagen and hair thickness. Therefore, the effect of minoxidil can be regarded as nonspecific in monilethrix and due to a beneficial effect on comorbid AGA, hair length, and thickness. In analogy, we formerly observed acquired hair fragility in a patient with pili annulati in causal relationship with the onset of AGA.[5] Both pili annulati and AGA are not associated with increased hair fragility, but the progressive reduction of hair shaft diameter due to AGA in combination with the abnormality of pili annulati may cause hair shaft fracturing within the areas of hair shaft cavities following seemingly inadequate trauma. This observation underscores the importance of recognizing the opportunity of multiple causal relationships underlying disorders of hair growth and resilience, specifically AGA as a frequent comorbid condition, with their implications for hair fragility and treatment. The advantage of oral minoxidil is that of reducing the trauma to the fragile hair of monilethrix that is associated with the topical application of minoxidil solution. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given his consent for images and other clinical information to be reported in the journal. The guardian understands that names and initials will not be published and due efforts will be made to conceal patient identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.