Sensitization to saw palmetto and minoxidil in separate topical extemporaneous treatments for androgenetic alopecia.

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Australas J Dermatol 2002 Nov;43(4):311-2

Sensitization to saw palmetto and minoxidil in separate topical extemporaneous treatments for androgenetic alopecia.

We report a 24-year-old woman with androgenetic alopecia who became sensitized to topical minoxidil following use of an extemporaneous preparation of minoxidil 4% with retinoic acid in a propylene glycol base. She subsequently also became sensitized to saw palmetto (Serenoa repens), a topical herbal extract commonly promoted for the treatment of hair loss.

Ann Dermatol Venereol 2002 May;129(5 Pt 2):801-3

Androgenetic alopecia

Androgenetic alopecia (AGA) is the combined result of an androgen-dependent process and genetic transmission. These characteristics have mainly, if not exclusively, been demonstrated in men and perhaps improperly extended to women. When considering the androgen-dependent process, AGA must only be limited to the androgen receptor areas. In the scalp, these receptors have only been detected in the frontal and vertex areas but never in the temporal or the occipital areas. Male AGA exhibits these clinical features, whereas in women hair loss is rarely limited to this localization, even when large areas of hair loss often appear with age. It is now commonly accepted that male AGA is associated with an increase in 5 alpha reductase activity leading to an increase in local production of dihydrotestosterone. The mechanism by which the local dihydrotestosterone increase leads to hair follicle loss is not clearly demonstrated. Inhibition of cell proliferation in the dermal papilla and a vascular process based on the inhibition in local production of vascular endothelial growth factor (VEGF) have been proposed. The increase in 5 alpha reductase activity is genetic and depends on androgen receptor polymorphism, characterized by a decrease in the number of CAG sequences on the exon 1. Male AGA is associated with an insulin-resistant process and to a higher risk of polycystic ovary in the lineage. Therapeutically, this hormone-dependent process explains the well demonstrated efficacy of 5 alpha reductase inhibitors. In women, except in some rare cases, alopecia is diffuse and the mechanisms are different. Their origin is unknown, and probably ambiguous. Based on an association with Hashimoto's thyroiditis, an auto-immune origin could be suggested in some cases. Alopecia is unaffected by thyroid substitution. Pharmacological doses of oestrogens (pregnancy, contraception) have a beneficial effect on such alopecia, probably through different mechanisms: anti-androgen effect, increased VEGF, proliferative effect of dermal papilla cells. However, it is important to mention that the dermal papilla has an aromatase, particularly in the occipital area, the activity of which has not been assessed in female alopecia. In practice 5 alpha reductase inhibitors are ineffective in women. It is likely that the predominance observed in the frontal and vertex areas, occasionally in elderly women, is a result of the two combined disorders, the almost physiological androgen-dependent hair loss combined with diffuse loss. Pharmacological doses of oestrogens associated with anti-androgen progesterone-like agents are widely used with positive results, but not demonstrated by clinical trials.

Exp Gerontol 2002 Aug-Sep;37(8-9):981-90

Molecular mechanisms of androgenetic alopecia.

Androgenetic alopecia (AGA) is hereditary and androgen-dependent, progressive thinning of the scalp hair that follows a defined pattern. While the genetic involvement is pronounced but poorly understood, major advances have been achieved in understanding principal elements of the androgen metabolism involved: androgen-dependent processes are predominantly due to the binding of dihydrotestosterone (DHT) to the androgen receptor (AR). DHT-dependent cell functions depend on the availability of weak androgens, their conversion to more potent androgens via the action of 5 alpha-reductase, low enzymatic activity of androgen inactivating enzymes, and functionally active AR present in high numbers. The predisposed scalp exhibits high levels of DHT, and increased expression of the AR. Conversion of testosterone to DHT within the dermal papilla plays a central role, while androgen-regulated factors deriving from dermal papilla cells are believed to influence growth of other components of the hair follicle. Current available treatment modalities with proven efficacy are oral finasteride, a competitive inhibitor of type 2 5 alpha-reductase, and topical minoxidil, an adenosine-triphosphate-sensitive potassium channel opener which has been reported to stimulate the production of vascular endothelial growth factor in cultured dermal papilla cells. Since the clinical success rate of treatment of AGA with modulators of androgen metabolism or hair growth promoters is limited, sustained microscopic follicular inflammation with connective tissue remodeling, eventually resulting in permanent hair loss, is considered a possible cofactor in the complex etiology of AGA.

Ther Umsch 2002 May;59(5):243-50

Scarring alopecias

The irreversibility and the possible important cosmetic consequences of scarring alopecia demand special diagnostic attention in order to promptly attain a precise diagnosis and specific treatment. Scarring alopecias are either due to permanent damage to essential parts of the hair follicle or destruction of the entire hair follicle. They are classified into the categories of primary scarring alopecias, where the hair follicle is the primary target of destruction, and secondary scarring alopecias, where the follicular damage results incidentally from events around impinging on the follicular unit. The differential diagnosis of the more common primary scarring alopecias, e.g. follicular lichen planus, chronic cutaneous lupus erythematosus and folliculitis decalvans, can be difficult when based only on anamnestic and clinical findings. The scalp biopsy is essential for appropriate nosologic classification and has prognostic relevance. The primary therapeutic goal is to halt progression of the irreversible process as early as possible by means of immunomodulatory, immunosuppressive or antiinfectious agents, respectively.

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