Ralph M. Trüeb

Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in men

Androgenetic alopecia is the most common hair loss disorder, affecting both men and women. Initial signs of androgenetic alopecia usually develop during teenage years leading to progressive hair loss with a pattern distribution. Moreover, its frequency increases with age and affects up to 80 % Caucasian men and 42 % of women.

Oxidative stress in ageing of hair

Experimental evidence supports the hypothesis that oxidative stress plays a major role in the ageing process. Reactive oxygen species are generated by a multitude of endogenous and environmental challenges. Reactive oxygen species or free radicals are highly reactive molecules that can directly damage cellular structural membranes, lipids, proteins, and DNA. The body possesses endogenous defence mechanisms, such as antioxidative enzymes and non-enzymatic antioxidative molecules, protecting it from free radicals by reducing and neutralizing them. With age, the production of free radicals increases, while the endogenous defence mechanisms decrease. This imbalance leads to the progressive damage of cellular structures, presumably resulting in the ageing phenotype. Ageing of hair manifests as decrease of melanocyte function or graying, and decrease in hair production or alopecia. There is circumstantial evidence that oxidative stress may be a pivotal mechanism contributing to hair graying and hair loss. New insights into the role and prevention of oxidative stress could open new strategies for intervention and reversal of the hair graying process and age-dependent alopecia.

Association between smoking and hair loss: another opportunity for health education against smoking?

Besides being the single most preventable cause of significant morbidity and an important cause of death in the general population, tobacco smoking has been associated with adverse effects on the skin. Smoke-induced premature skin ageing has attracted the attention of the medical community, while only recently an observational study has indicated a significant relationship between smoking and baldness. The mechanisms by which smoking causes hair loss are multifactorial and are probably related to effects of cigarette smoke on the microvasculature of the dermal hair papilla, smoke genotoxicants causing damage to DNA of the hair follicle, smoke-induced imbalance in the follicular protease/antiprotease systems controlling tissue remodeling during the hair growth cycle, pro-oxidant effects of smoking leading to the release of pro-inflammatory cytokines resulting in follicular micro-inflammation and fibrosis and finally increased hydroxylation of oestradiol as well as inhibition of the enzyme aromatase creating a relative hypo-oestrogenic state. In view of the psychological impact of androgenetic alopecia on affected men and women, increasing public awareness of the association between smoking and hair loss offers an opportunity for health education against smoking that may be more effective than the link between smoking and facial wrinkles or grey hair, since the latter can be effectively counteracted by current aesthetic dermatologic procedures, while treatment options for androgenetic alopecia are limited.

Finasteride Treatment of Patterned Hair Loss in Normoandrogenic Postmenopausal Women

Background: Finasteride, an inhibitor of type 2 5α-reductase, inhibits conversion of testosterone to dihydrotestosterone, resulting in a decrease in serum and scalp dihydrotestosterone levels believed to be pathogenic in androgenetic alopecia. Oral finasteride has been shown to be effective in the treatment of hair loss in men, while its efficacy in women has remained controversial. Methods: 5 postmenopausal women without clinical or laboratory signs of hyperandrogenism were given 2.5 or 5 mg/day oral finasteride for the treatment of pattern hair loss. Efficacy was evaluated by patient and investigator assessments, and review of photographs taken at baseline and at months 6, 12 and 18 by an expert panel. Results: Finasteride treatment improved scalp hair by all evaluation techniques. The patients’ self-assessment demonstrated that finasteride treatment decreased hair loss, increased hair growth and improved appearance of hair. These improvements were confirmed by investigator assessment and assessments of photographs. No adverse effects were noted. Conclusions: Oral finasteride in a dosage of 2.5 mg/day or more may be effective for the treatment of pattern hair loss in postmenopausal women in the absence of clinical or laboratory signs of hyperandrogenism.

Acute Generalized Exanthematous Pustulosis due to Doxycycline

Sterile epidermal neutrophilic pustulation can be observed in a variety of diseases. Though drug hypersensitivity is an uncommon cause, it is yet a known entity to be considered in the differential diagnosis of generalized pustulosis. In a 40-year-old woman, who developed a generalized pustular eruption after starting on doxycycline therapy of bronchitis, the rash was concluded to be drug induced after exclusion of other pustular dermatoses. Sensitization to doxycycline was demonstrated by in vitro lymphocyte testing and correlated with clinical drug hypersensitivity after recurrence of the pustular eruption on nonintentional rechallenge with doxycycline.

Systematic approach to hair loss in women

Diffuse hair loss is a common complaint and cause of significant emotional distress particularly in women. The best way to alleviate the anxiety is to effectively treat the hair loss. It is paramount to address the symptom systematically. In addition to its psychological impact, hair loss may be a manifestation of a more general medical problem. The diagnosis can be established with a detailed patient history focussing on chronology of events, examination of the scalp and pattern of hair loss, a pull test with examination of bulbs of shed hairs, trichoscopy, and few pertinent screening blood tests. In selected cases a scalp biopsy may be required. The most important differential diagnoses include acute and chronic telogen effluvium, female pattern hair loss, and diffuse alopecia areata. Occasionally, patients seeking advice are not necessarily losing hair. In the absence of convincing evidence of hair loss, they are suffering of psychogenic pseudoeffluvium, and thought should be given to an underlying psychological disorder. Once the diagnosis is established, treatment appropriate for that diagnosis is likely to control the hair loss. Finally, appropriate psychological support and education about the basics of the hair cycle, and why considerable patience is required for effective cosmetic recovery, are essential to help limit patient anxiety.

Is androgenetic alopecia a photoaggravated dermatosis

Progressive thinning of the scalp hair in androgenetic alopecia (AGA) results in a gradual decline in natural protection of the scalp from ultraviolet radiation (UVR). A number of pathologic conditions of the scalp are evidently related to UVR, particularly photosensitive diseases and disorders of the chronically photodamaged bald scalp. The most important chronic effects of UVR are photocarcinogenesis and solar elastosis. Besides these, erosive pustular dermatosis and ‘red scalp’ are distinct disorders peculiar to the balding scalp. While the consequences of sustained UVR on the unprotected scalp are well appreciated, the effects of UVR on hair loss have widely been ignored. However, clinical observations and theoretical considerations suggest that UVR may have negative effects: acute telogen effluvium from UVR has been described, and the production of porphyrins by Propionibacterium sp. in the pilosebaceous duct, with photoactivation of porphyrins leading to oxidative tissue injury, has been implicated in follicular microinflammation. Alternatively, keratinocytes themselves may respond to physicochemical stress from UVR, besides irritants and pollutants, by producing radical oxygen species and nitric oxide and by releasing proinflammatory cytokines, eventually leading to injury of the putative site of follicular stem cells in the superficial portion of the hair follicle. Since all of these processes involved in hair loss share the common feature that they are induced or exacerbated by exposure to sunlight, it is proposed that AGA is a photoaggravated dermatosis that requires photoprotection.

URTICARIAL VASCULITIS FOLLOWING COCAINE USE

supports the ®ndings that allergy to plain henna is extremely rare. Allergy to henna is related to the colouring material itself, a hydroxynaphthoquinone. The main allergens responsible for the reactions occurring in the `art of henna in the UAE are additives, especially PPD and a scented oil. The result of contact dermatitis to henna painting is that lesions develop along the pattern of the initial drawing (Fig. 2a,b).

Pyoderma gangrenosum. Pyoderma gangraenosum

Pyoderma gangrenosum (PG) is a non‐infectious reactive neutrophilic dermatosis which typically starts with pustules which rapidly evolve to painful ulcers of variable size and depth with undermined violaceous borders. Since its first description in 1930, the pathogenesis of PG has remained elusive even as an ever‐widening range of systemic diseases has been described in association with it. The diagnosis of PG is based on clinical and pathologic features and requires exclusion of other conditions that produce ulcerations, since misdiagnosis exposes patients to risks associated with treatment. Critical to proper management are correct diagnosis, identification and treatment of any underlying disorder, and the appropriate choice of topical and systemic therapy. PG has four distinctive clinical and histologic variants, and the specific clinical features of the lesion may provide a clue to the associated disease. The most common associated diseases are inflammatory bowel disease, rheumatological or hematological disease or malignancy. Although there is no single successful treatment for PG, certain type of PG lesions are recognized to respond more readily to accepted therapies than others. Local treatment may be sufficient for mild disease, while systemic immunosuppressive therapy is necessary for severe cases. The treatments with the best clinical evidence are oral or pulse intravenous corticosteroids, and cyclosporine. Surgical therapy is useful in selected cases in conjunction with immunosuppression. Wound stabilization is obtained only through control of the systemic and local inflammatory process. Emerging therapies include use of platelet‐derived growth factor and cell culture grafts when re‐epithelialization is slow, and the TNF‐alpha blocking agent infliximab for refractory disease. Despite advances in therapy, the long‐term outcome for patients with PG remains unpredictable, because relapses are common.

Hermansky-Pudlak syndrome type 4 in a patient from Sri Lanka with pulmonary fibrosis

Hermansky–Pudlak syndrome (HPS) is a rare autosomal recessive disorder characterized by oculocutaneous albinism and a platelet storage pool deficiency. Some patients also develop fatal pulmonary fibrosis and some have granulomatous colitis. Six human genes HPS1, ADB3A, HPS3, HPS4, HPS5, and HPS6 have been identified as cause of the six known subtypes of HPS. While there exist nearly 500 Puerto Rican and non‐Puerto Rican HPS‐1 patients, very few HPS‐4 patients have been reported, and most of these have not been described in detail. We now delineate the clinical characteristics of an HPS‐4 patient homozygous for a novel HPS‐4 mutation, P685delC. The patient, the first individual with HPS reported from Sri Lanka, had severe pulmonary fibrosis, typical of HPS‐1 disease, without granulomatous colitis. We conclude that pulmonary fibrosis occurs as part of HPS‐4 and that HPS should be considered in all ethnic groups.