Leona Yip

Hair loss in women: medical and cosmetic approaches to increase scalp hair fullness.

Androgenetic alopecia affects both men and women. In men it produces male pattern hair loss with bitemporal recession and vertex baldness. In women it produces female pattern hair loss (FPHL) with diffuse alopecia over the mid‐frontal scalp. FPHL occurs as a result of nonuniform hair follicle miniaturization within follicular units. Diffuse alopecia is produced by a reduction in the number of terminal fibres per follicular unit. Baldness occurs only when all hairs within the follicular units are miniaturized and is a relatively late event in women. The concepts of follicular units and primary and secondary hair follicles within follicular units are well established in comparative mammalian studies, particularly in sheep. However, discovery of these structures in the human scalp hair and investigation of the changes in follicular unit anatomy during the development of androgenetic alopecia have provided a clearer understanding of the early stages of androgenetic alopecia and how the male and female patterns of hair loss are related. FPHL is the most common cause of alopecia in women and approximately one‐third of adult caucasian women experience hair loss. The impact of FPHL is predominantly psychological. While men anticipate age‐related hair loss, hair loss in women is usually unexpected and unwelcome at any age. Treatment options to arrest hair loss progression and stimulate partial hair regrowth for FPHL include the androgen receptor antagonists spironolactone and cyproterone acetate, the 5α‐reductase inhibitor finasteride and the androgen‐independent hair growth stimulator minoxidil. These treatments appear to work best when initiated early. Hair transplantation should be considered in advanced FPHL that is resistant to medical treatments. Hair transplantation requires well‐preserved hair growth over the occipital donor area. The psychological impact of FPHL may also be reduced by cosmetic products that improve the appearance of the hair. These agents work to minimize hair fibre breakage, improve hair volume or conceal visible bald scalp.

Gene‐wide association study between the aromatase gene (CYP19A1) and female pattern hair loss

Background  Female pattern hair loss (FPHL) is a common trait in which androgens and oestrogens may have a pathogenic role. The aromatase enzyme converts androgens to oestrogens in scalp hair follicles and is differentially expressed in balding and nonbalding scalps of women. Sequence variation in the gene encoding aromatase, CYP19A1, might influence the risk of developing FPHL.

Role of genetics and sex steroid hormones in male androgenetic alopecia and female pattern hair loss: An update of what we now know

The role of genetic predisposition and the influence of sex steroid hormones are indisputable to the pathogenesis of male androgenetic alopecia (MAGA). The role of sex steroid hormones in female pattern hair loss (FPHL) is less known. A good knowledge of the pathophysiology underlying MAGA and FPHL empowers the clinician to confidently counsel patients and make informed therapeutic decisions. Vigorous research in recent years has provided greater insight into the role of genetics and sex steroids in physiological hair growth and cycling, as well as in hair follicle miniaturization, the histological hallmark of MAGA and FPHL. In the present review article directed towards clinicians, we discuss the current understanding of the role of androgens and oestrogens, as well as genetic associations with MAGA and FPHL. We also briefly discuss the interpretation of direct‐to‐consumer genetic testing for baldness to help clinicians understand the limitations of such tests.

Atrichia with papular lesions: a report of three novel human hairless gene mutations and a revision of diagnostic criteria.

Atrichia with papular lesions is a rare autosomal recessive condition characterized by complete irreversible hair loss during the first months of life and papules that appear during early childhood. Atrichia with papular lesions is frequently misdiagnosed as alopecia universalis, despite increasing reports of its prevalence and the presence of well-defined diagnostic criteria. Most cases of atrichia with papular lesions have been reported in consanguineous families residing in small geographical regions, but the increasing number of sporadic cases of unrelated individuals suggests that atrichia with papular lesions is more common than previously thought. Mutations in the human hairless gene on chromosome 8p12 have been implicated in this disease. Here, we report two novel heterozygous mutations in an Australian family and a novel homozygous mutation in 2 Arab siblings. We also revise the diagnostic criteria for atrichia with papular lesions in order to clarify its uniqueness and distinguishing features from alopecia universalis.

Association analysis of oestrogen receptor beta gene (ESR2) polymorphisms with female pattern hair loss

in the vicinity. Zinc treatment in patients with EPP may therefore have provided antioxidant protection of cellular membranes against the deleterious photodynamic effects of PpIX accumulation. In accordance with the above, measurement of ultraweak photon emission with a photomultiplier revealed reduced oxidative stress in the skin during zinc treatment. In conclusion, oral treatment with a high daily dosage of zinc sulphate during the spring and summer reduced light sensitivity and cutaneous pain in the majority of our patients with EPP. However, as the intervention was based on an open-label procedure, such a study design may be subject to major bias.

Evidence of increased DNA methylation of the androgen receptor gene in occipital hair follicles from men with androgenetic alopecia

an unpleasant ‘garlic odour’ from the skin. In Savill’s epidemic, the skin assumed a ‘yellowish-brown colour’. And in the arsenical beer poisoning and Wakayama curry poisoning pigmentation is reported to occur to varying degrees. This could be the result of jaundice due to liver damage caused by arsenic or pigmentation as a direct result of arsenic exposure. The associated features in some patients of nail shedding may have resulted from the acute and severe systemic illness rather than as a direct toxic effect of the arsenic. Similarly, the reported alopecia resulting in patients becoming ‘completely bald’ may have been due to the severity of the illness. The sore tongue, photophobia, weakness, drowsiness and twitching muscles could all be accounted for by acute arsenic poisoning. In 36 of 72 patients there was albumin in the urine, but it was noted that this occurred only in patients with substantial skin involvement. As significant proteinuria is a common feature of patients with skin disease and may occur when more than 10% of the skin is involved, it is possible that in the epidemic it is due to the extent of the skin disease, but equally it may also have been secondary to arsenic-induced renal failure. The fact that most patients were apyrexial, and a fever of 99 F (37Æ2 C) was the highest recorded, points away from the cause as being infectious. Risien Russell and Savill found a diplococcus, in rod-like segments, in ‘the skin, blood and exudations of patients’. Although they present a good argument that this organism is pathognomonic and not just coincidental, they failed to produce any effect when the organism was inoculated into animals. The ‘pathognomonic histological sign’ of Savill’s epidemic is described to be a degeneration of the nuclei of the prickle cell layer. This appears to be similar to a description of histological findings in a patient with acute arsenic poisoning whose biopsy was taken during the stage of erythema and showed apoptotic cells in the basal layer of the epidermis, which displayed karyorrhexis, and isolated apoptotic cells in the upper layers of the epidermis. Karyorrhexis is the destructive fragmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm, of which arsenic poisoning is a well-described cause. Savill presents a thorough analysis and excludes food, soap, scabies, water supply, climatic, seasonal or atmospheric causes as a source of the epidemic. However, although food is excluded as a cause he also states: ‘The only articles which the Paddington and Marylebone Infirmaries procure from the same contractor are milk and fish’, and as Brooks and Roberts point out ‘Epidemics have been traced to arsenically infected wine, bread, milk and beer’. However, if milk were the cause, one would expect children to be affected to a greater extent. Could the arsenic poisoning have come from the fish or the beer?

From biologic to biologic to biologic: Lessons to learn for erythrodermic and recalcitrant chronic plaque psoriasis

Differences in mode of action between biologic agents could explain why one agent is more efficacious than another in the treatment of recalcitrant and erythrodermic flares of chronic plaque psoriasis. Here, we present our experience using a case series of three patients with chronic plaque psoriasis who showed consistent and similar responses to three different biologic agents. All three patients who were refractory to efalizumab developed erythrodermic flares 2–12 weeks after a direct switch to etanercept. Switching from efalizumab to etanercept could provoke paradoxical flaring of psoriasis, which might be prevented by transitioning to systemic agents. The erythrodermic flares in all three patients responded dramatically to infliximab with marked and maintained improvements in Psoriasis Area and Severity Index scores.

Successful surgical management of lipoedematous alopecia

A 67‐year‐old Caucasian woman presented with an area of alopecia over the right occipital scalp, which had slowly expanded over the last 10 years. The skin beneath the alopecia felt soft and boggy although the epidermis looked unremarkable. Ultrasound showed thickening of the underlying subcutaneous tissue. Scalp histology showed enlarged fat lobules within the subcutis that infiltrated along fibrous tracts into the mid‐dermis. There was a complete loss of hair follicles. These findings were consistent with lipoedematous alopecia of the scalp. Surgical debulking with scalp reduction produced an acceptable result in our patient with no evidence of relapse after 12 months.

Squamous cell carcinoma arising within folliculitis decalvans

SIR, We report a 44-year-old man with an 8-year history of biopsy-proven folliculitis decalvans who developed a rapidly enlarging nodule, measuring 8 mm in diameter on his vertex scalp within the area of alopecia. Biopsy confirmed it to be a squamous cell carcinoma (SCC). Previous treatments for folliculitis decalvans included two separate 6-month courses of triple antibiotic therapy with rifampicin 600 mg daily, clindamycin 600 mg daily and fusidic acid 750 mg daily, and prolonged courses of minocycline, topical clindamycin solution and antiseptic shampoo in the intervening periods. The area of folliculitis decalvans was not and had never been ulcerated (Fig. 1). He is otherwise healthy and has never been on oral immunosuppressant medications. He is Fitzpatrick skin type II. In his youth, he had significant sun exposure. He was a keen surfer and has a past history of basal cell carcinoma (BCC) and had a solitary solar keratosis removed from his back. Following the initial biopsy, the lesion was subsequently excised with a 4-mm margin. Histology revealed a moderately differentiated SCC infiltrating into the superficial reticular dermis without vascular invasion (Fig. 2). The adjacent epidermis showed Bowen disease. Ulceration in relation to the previous biopsy was noted. Folliculitis and a cicatricial alopecia with liberation of fragmented hair shaft material, dermal fibrosis and heavy lymphoplasmocytic inflammation due to active folliculitis decalvans were seen within the adjacent dermis. The vast majority of SCCs arise as a consequence of chronic sun exposure and in particular, ultraviolet (UV) light. Secondary SCCs known as Marjolin ulcers, have also been reported to develop in chronic nonhealing wounds and chronic venous ulcers. Compared with SCCs arising within actinic keratoses, the metastatic rate of SCCs arising within chronic inflammatory lesions is much higher. Metastases from SCCs arising within chronic nonhealing ulcers is the most common cause of death in dystrophic epidermolysis bullosa. Inflammatory conditions associated with SCC are shown in Table 1. The constant production of pro-inflammatory cytokines and tissue remodelling in disorders of chronic inflammation have been postulated to provide a conducive environment for malignant transformation. Tissue antiinflammatory properties reduced through the downregulation of transforming growth factor-b1 signalling pathways might also contribute to carcinogenesis. SCC is also a reported complication of dissecting perifolliculitis of the scalp and hidradenitis suppurativa. Both Fig 2. Haematoxylin and eosin staining at 2 · magnification. Mid dermal deposit of squamous cell carcinoma (SCC) seen on the left, and superficially invasive SCC with distorted hair follicle seen on the right.

Antiandrogen therapy for androgenetic alopecia

Androgenetic alopecia produces a chronic, progressive, patterned hair loss in both men and women. Androgen hormones and, in particular, dihydrotestosterone bind to androgen receptors in sensitized hair follicles. Susceptibility to androgenetic alopecia and, in particular, early-onset androgenetic alopecia is a complex polygenic trait. Polymorphism of the androgen receptor gene has been strongly associated with androgenetic alopecia in males but not in females. Drugs that inhibit androgen synthesis, androgen metabolism or the androgen receptor can be used to treat androgenetic alopecia. The principle roles of these medications are to arrest hair loss and to stimulate hair regrowth. While these agents are highly effective at preventing hair loss and most patients experience some regrowth, few patients experience dramatic hair regrowth. Minoxidil lotion has been shown to be effective in treating androgenetic alopecia. Its effects are nonandrogen-mediated and this agent can be combined with antiandrogen thera...