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Dermatology 2002;205(4):374-7
Hair pain (trichodynia): frequency and relationship to hair loss and patient gender.
Background: Patients complaining of hair loss frequently claim that their hair has become painful. Objective and Methods: The aim of the study was to evaluate the frequency of this phenomenon and its relationship to hair loss. Patients seeking advice for hair loss either spontaneously reported or were questioned about painful sensations of the scalp. Hair loss activity was quantified by a hair pull, daily count and wash test. Telogen percentage was obtained by a hair pluck. The scalp surface was examined by dermatoscopy. Results: Of 403 examined patients, 20% of women and 9% of men reported hair pain, irrespective of the cause and activity of hair loss. A minority presented scalp telangiectasia. This strongly correlated with hair pain. Conclusions: Hair pain (trichodynia) affects a significant proportion of patients complaining of hair loss and may increase the anxiety. The symptom neither allows discrimination of the cause nor correlates with the activity of hair loss. A higher prevalence of female patients might be connected to gender-related differences in pain perception in relation to anxiety. The role of vasoactive neuropeptides in the interaction between the central nervous system and skin reactivity is discussed. In the absence of any correlation with quantitative parameters of hair loss or specific morphologic changes of the scalp, management remains empiric and tailored to the individual.
Pediatr Dermatol 2002 Nov-Dec;19(6):482-5
Alopecia areata in children: a clinical profile.
Alopecia areata (AA) is prevalent among children in Kuwait. In this prospective survey we studied 215 children with AA to determine their clinical and epidemiologic features. Ninety-seven percent of the children were of Arab ancestry. Girls outnumbered boys by a 2.5:1 ratio. The peak age of onset was seen between 2 and 6 years of age with a mean age of onset at 5.7 +/- 2.8 years. A majority of the patients (80.5%) had mild disease and extensive disease (more than 50% hair loss) was seen in 13% of the children. A positive family history of AA was obtained in 51.6% of cases and nail changes were seen in 26.5% of the children. The age of onset, a positive family history of AA, and associated atopic disorders were observed to have no influence on the extent and severity of the disease. The results were compared with those reported elsewhere for this age group.
J Am Acad Dermatol 2002 Nov;47(5):795
Female pattern hair loss.
In this issue of the Journal (pages 733-9), Shum et al1 describe 4 female patients with increased androgens whose central scalp hair loss responded to finasteride. This is an important observation and one that highlights why the term androgenetic or androgenic alopecia, as used to describe the hereditary pattern balding of men, should be replaced with the term female pattern hair loss when applied to women.2 It is clear that only a small but distinct subset of women with central scalp pattern hair loss, such as the patients presented in the report by Shum et al, has signs of hyperandrogenism such as acne, hirsutism, and irregular periods with or without elevation of serum androgens. Therefore these women may have hair loss resulting from a different mechanism and may respond differently to treatments targeted at androgen blockade than women with a similar type of hair loss but without evidence of hyperandrogenism. Certainly these women with hyperandrogenemia may develop, in contradistinction to those without hyperandrogenemia, a Hamilton pattern of hair loss (male pattern baldness). Many of these women may, on more careful evaluation, have polycystic ovarian syndrome.
It is not surprising that a 5-reductase inhibitor such as finasteride, which has documented efficacy in men with androgenetic alopecia3,4 and has been shown to advantageously affect hirsutism,5,6 may cause hair growth in women with female pattern hair loss and hyperandrogenism. The fact that finasteride has not previously been shown to induce hair growth in postmenopausal women with “androgenetic alopecia”7 speaks for (1) adoption of different terminology for this type of hair loss in women and (2) separate evaluation of the different subgroups of women with female pattern hair loss as recently described,2 that is, early onset with and without hyperandrogenemia and late onset/postmenopausal with and without hyperandrogenemia. We should not be too quick to rule out efficacy of a potential therapeutic agent in all women with female pattern hair loss without first testing it in all the various subsets of women.
Clearly, finasteride may be an effective treatment for women with early-onset female pattern hair loss and hyperandrogenemia, but definitive results would require a large, well-controlled trial. Such a trial would likely necessitate inclusion of a “placebo” run-in phase with an oral contraceptive, both to protect these women of child-bearing potential from getting pregnant while taking a drug known to cause genital abnormalities in male fetuses and to rule out any effect from the oral contraceptive alone on female pattern hair loss (a study that needs to be conducted in any case). Anecdotal reports, such as that presented by Shum et al,1 should ignite interest in evaluating finasteride and other 5-reductase inhibitors, either type II or combination type I/II, in women with female pattern hair loss, a group of patients whose current treatment options are extremely limited.
Arch Dermatol 2002 Jul;138(7):916-22
Mediation of alopecia areata by cooperation between CD4+ and CD8+ T lymphocytes: transfer to human scalp explants on Prkdc(scid) mice.
OBJECTIVE: To determine the role of CD4+ and CD8+ T lymphocytes in the pathogenesis of alopecia areata. DESIGN: Relapse of alopecia areata was induced in autologous human scalp grafts on Prkdc(scid) mice by injection of activated T lymphocytes derived from lesional skin. CD4+ and CD8+ T cells were separated by magnetic beads before injection. SETTING: University-based dermatology practice. PARTICIPANTS: Eleven patients with either alopecia totalis or severe alopecia areata. MAIN OUTCOME MEASURES: Hair regrowth, hair loss, and immunohistochemical findings of scalp explants. INTERVENTION: Transfer of scalp T cells to autologous lesional scalp explants on Prkdc(scid) mice. RESULTS: Injection of unseparated T cells and mixed CD4+ plus CD8+ T cells resulted in significant hair loss (P<.01) in 5 of 5 experiments. However, injection of purified CD4+ or CD8+ T cells alone did not result in reproducible hair loss. CD4+ and CD8+ T cells induced follicular expression of intercellular adhesion molecule 1 (CD54), HLA-DR, and HLA-A, HLA-B, and HLA-C after injection into scalp grafts. CONCLUSIONS: CD4+ and CD8+ T cells have a role in the pathogenesis of alopecia areata. It is hypothesized that CD8+ T cells act as the effector cells, with CD4+ T cell help. It is now necessary to look for HLA-A, HLA-B, and HLA-C associations with alopecia areata. Therapeutic manipulations that interfere with CD8+ activity should be examined.
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