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Clin Exp Dermatol 2002 Jul;27(5):396-404
Nutritional factors and hair loss.
The literature reveals what little is known about nutritional factors and hair loss. What we do know emanates from studies in protein-energy malnutrition, starvation, and eating disorders. In otherwise healthy individuals, nutritional factors appear to play a role in subjects with persistent increased hair shedding. Hard, 40 years ago, demonstrated the importance of iron supplements in nonanaemic, iron-deficient women with hair loss. Serum ferritin concentrations provide a good assessment of an individual's iron status. Rushton et al. first published data showing that serum ferritin concentrations were a factor in female hair loss and, 10 years later, Kantor et al. confirmed this association. What level of serum ferritin to employ in subjects with increased hair shedding is yet to be definitively established but 70 micro g/L, with a normal erythrocyte sedimentation rate (< 10 mm/h), is recommended. The role of the essential amino acid, l-lysine in hair loss also appears to be important. Double-blind data confirmed the findings of an open study in women with increased hair shedding, where a significant proportion responded to l-lysine and iron therapy. There is no evidence to support the popular view that low serum zinc concentrations cause hair loss. Excessive intakes of nutritional supplements may actually cause hair loss and are not recommended in the absence of a proven deficiency. While nutritional factors affect the hair directly, one should not forget that they also affect the skin. In the management of subjects with hair loss, eliminating scaling problems is important as is good hair care advice and the need to explain fully the hair cycle. Many individuals reduced their shampooing frequency due to fear of losing more hair but this increases the amount seen in subsequent shampoos fuelling their fear of going bald and adversely affecting their quality of life.
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".
Br J Dermatol. 2003 Mar;148(3):553-7.
Compound heterozygosity for mutations in the hairless gene causes atrichia with papular lesions.
BACKGROUND: Congenital atrichias represent a complex and heterogeneous group of genodermatoses, which have been shown in several consanguineous families to result from homozygous mutations in the hairless gene (HR). OBJECTIVES: To identify the molecular basis of congenital atrichia in a non-consanguineous family. METHODS: Genetic analysis was carried out in a two-generation family with two children with congenital atrichia and one healthy child. RESULTS: We established a diagnosis of atrichia with papular lesions based on clinical and histopathological data. We identified a heterozygous 11-bp deletion (189-199del) in the two affected children and their mother. In addition, the two affected children and their father were shown to carry a non sense mutation (Q478X), which has previously been described in a Pakistani family. Haplotype analysis revealed that mutation Q478X occurred independently in the two families. CONCLUSIONS: We have identified the first case of compound heterozygosity for mutations in HR as well as the first instance of a recurrent mutation in this gene. These data further expand our understanding of the molecular pathomechanisms underlying congenital atrichias.
Eur J Dermatol. 2003 Mar-Apr;13(2):150-60.
Efficacy and tolerability of finasteride 1 mg in men aged 41 to 60 years with male pattern hair loss.
A 24-month double-blind, randomized, placebo-controlled, parallel-group, multicenter study of 424 men was conducted to determine the efficacy and tolerability of finasteride 1 mg on hair growth/loss in men aged 41 to 60 years with mild-to-moderate, predominantly vertex male pattern hair loss. Efficacy was evaluated by review of global photographs of the vertex scalp taken at baseline and at Months 6, 12, 18, and 24 and by patient self-assessments and investigator clinical assessments of change from baseline in hair growth/loss collected at Months 6, 12, 18, and 24. Safety analyses included assessment of clinical and laboratory adverse experiences, including sexual adverse experiences. Analysis of global photographic assessment data showed significant improvement in hair growth for men in the finasteride group compared with those taking placebo beginning at Month 6 (p < 0.001) and maintained through Month 24 (p < 0.001). Results of the patient self-assessment and investigator assessments were consistent with those from the global photographic assessment. Finasteride 1 mg improved scalp hair growth in men aged 41 to 60 years with predominantly vertex male pattern hair loss compared with results seen with placebo. Improvement was evident by 6 months of treatment and continued through 24 months. Treatment with finasteride 1 mg was generally well tolerated.
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