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Br J Dermatol 2002 Oct;147(4):789-92
Loose anagen syndrome as a severity factor for trichotillomania.
Loose anagen syndrome (LAS) is a condition of childhood where anagen hairs are easily and painlessly extracted. The condition is due to poor adhesion between the cuticle of the hair shaft and the inner root sheath. A 4-year-old girl presented with patches of hair loss and a clinical diagnosis of trichotillomania was made. A hair pull test extracted multiple hairs easily and painlessly. Light microscopic examination was consistent with LAS. A biopsy was performed, which showed features of trichotillomania. However, on request the child did not display sufficient dexterity to pull out her own hair. It was subsequently determined that her hair loss was likely to be due to a third person plucking out her hair. It appears that in this case the LAS was not the cause of her hair loss, but rather acted as a severity factor for trichotillomania by proxy in that the lack of pain on plucking the hairs removed the principle deterrent.
Ther Umsch 2002 May;59(5):217-22
Diffuse hair loss in women
The complaint "Doctor, I am losing my hair" represents a particular challenge to the physician, and involves making a specific diagnosis, selecting an appropriate therapy, and expressing empathy for the patient's anxiety. Diffuse hair loss in women was formerly classified as an entity of its own. Since the identification of female pattern hair loss, most cases have been recognized to be due to androgenetic alopecia, often during phases of life characterized by fluctuations of sexual hormone levels or in connection with intake or cessation of hormonal therapy. The most difficult differential diagnosis includes androgenetic alopecia, chronic telogen effluvium, and psychogenic pseudo efflvuium. Androgenetic alopecia is due to androgen-induced, non-synchronized, progressive shortening of the hair growth cycle and gradually leads to thinning of the central scalp area. Idiopathic chronic telogen effluvium typically occurs in women, starting abruptly without a recognizable initiating factor, and involves the entire scalp area with increased shedding of telogen hair. It is believed to be due to synchronization phenomena of the cyclic hair growth. Psychogenic pseudo effluvium affects fashion-oriented, self-conscious women suffering of a discrepancy between the actual state of their hair and idealized expectations. Later the problem of age-related hair thinning oft becomes a surrogate for the more generalized problem of senescence. Rational therapy of androgenetic alopecia aims at blocking the androgen effect on hair follicles with estrogens and antiandrogens or at pharmacologically reversing vellus hair transformation with topical minoxidil. In contrast, women with idiopathic chronic telogen effluvium should be reassured that their problem is rather a state of exaggerated "hair shedding" than of actual "hair loss".
Ther Umsch 2002 May;59(5):211-6
Androgenetic alopecia in the man
Androgenetic alopecia (AGA) occurs in approximately 40% of men at the age of 40 and 50% at 50, respectively. Especially for young men progressive hair loss can be distressing. Therefore, understanding of these patients' concerns is important for appropriate management. Current understanding of the pathophysiology of AGA mainly focuses on androgen metabolism as it affects hair growth. As a result, pharmacologic treatment has made considerable progress through the introduction of selective 5 alpha-reductase inhibition with finasteride. In placebo-controlled clinical trials in men with AGA, treatment with oral finasteride proved to be effective. Minoxidil is the only pharmacological substance for topical application with proven efficacy. So far, other treatment modalities have no proven efficacy in clinical trials, so that their use cannot be recommended. Options for advanced AGA not amenable to pharmacologic treatment are autologous hair transplantation and hair replacement, both of which have recently also made progress in terms of cosmetic appeal.
Am J Pathol. 2003 Mar;162(3):803-14.
Stress inhibits hair growth in mice by induction of premature catagen development and deleterious perifollicular inflammatory events via neuropeptide substance P-dependent pathways.
It has been much disputed whether or not stress can cause hair loss (telogen effluvium) in a clinically relevant manner. Despite the paramount psychosocial importance of hair in human society, this central, yet enigmatic and controversial problem of clinically applied stress research has not been systematically studied in appropriate animal models. We now show that psychoemotional stress indeed alters actual hair follicle (HF) cycling in vivo, ie, prematurely terminates the normal duration of active hair growth (anagen) in mice. Further, inflammatory events deleterious to the HF are present in the HF environment of stressed mice (perifollicular macrophage cluster, excessive mast cell activation). This provides the first solid pathophysiological mechanism for how stress may actually cause telogen effluvium, ie, by hair cycle manipulation and neuroimmunological events that combine to terminate anagen. Furthermore, we show that most of these hair growth-inhibitory effects of stress can be reproduced by the proteotypic stress-related neuropeptide substance P in nonstressed mice, and can be counteracted effectively by co-administration of a specific substance P receptor antagonist in stressed mice. This offers the first convincing rationale how stress-induced hair loss in men may be pharmacologically managed effectively.
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