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J Dermatol 2002 Oct;29(10):653-6
Idiopathic CD4+ T lymphocytopenia associated with disseminated flat warts and alopecia areata.
Idiopathic CD4+ T lymphocytopenia is a very rare condition characterized by persistent depletion of circulating CD4+ T lymphocytes, without evidence of HIV or HTLV infection, or other identifiable causes of immunodeficiency. The syndrome can present with dermatological diseases, including viral, fungal and bacterial infections, as well as Kaposi's sarcoma, epithelial cell malignancies, lymphoma and inflammatory dermatoses. We report the case of a 47-year-old woman with idiopathic CD4+ T lymphocytopenia who presented with a 10-year history of disseminated and refractory flat warts from which human papillomavirus type 3 DNA was identified. The patient also had alopecia areata.
Med Hypotheses 2002 Apr;58(4):261-3
Hormone-induced aberrations in electromagnetic adhesion signaling as a developmental factor of androgenetic alopecia.
In androgenetic alopecia, overactivation of the androgen hormone cascade in genetically predisposed persons leads to miniaturization of the dermal papilla of the hair follicle and to reduction in the number of papilla cells in the scalp, but the mechanisms explaining this miniaturization have remained unclear. According to our hypothesis, the increase of dihydrotestosterone (DHT) production in the overactive androgen state inhibits cell mitosis in the dermal papilla and contributes to the induction of programmed cell death (apoptosis). Normally, DNA molecules have a negative charge, which doubles in every cell mitosis. In the catagen and telogen phases, the sulphur-rich hair moves upwards, dehydrates and develops an increasing positive charge. In a normal hair-growth cycle, the epithelial column shortens and the secondary germ is formed and it invaginates the dermal papilla by electromagnetic attraction. In the mitotic inhibition state induced by DHT, the negative charge decreases, leading to a weakening of the electromagnetic adhesion forces and weaker electrical attraction between the undifferentiated germ cells and the dermal papilla. Insulin resistance has an additional pathogenic role in the excessive miniaturization of the hair follicle. The vasoactive substances associated with endothelial dysfunction in insulin resistance induce microcirculatory disturbance, perifollicular vasoconstriction and stimulation of smooth muscle cell proliferation in the vascular wall. This leads to microvascular insufficiency and local tissue hypoxia and progressive miniaturization of hair follicles.
J Am Acad Dermatol 2001 Sep;45(3 Suppl):S81-6
Possible mechanisms of miniaturization during androgenetic alopecia or pattern hair loss.
In androgenetic alopecia, or pattern hair loss, follicles undergo miniaturization, shrinking from terminal to vellus-like hairs. Traditionally, this process is thought to progress gradually over a number of follicular cycles. However, it is unlikely that miniaturization can be explained only by a series of progressively shorter anagen cycles. Simple calculations show that this process would take too long for significant miniaturization to occur secondary to shorter anagen cycles alone, especially in view of the latent lag period seen in pattern hair loss that occurs between the loss of a telogen hair and the appearance of an anagen hair. Evidence is presented to support a new concept that miniaturization is an abrupt, large-step process that also can be reversed in 1 hair cycle, as has been shown clinically, with confirmatory histologic evidence, in patients with pattern hair loss responding to finasteride treatment. It is hypothesized that the miniaturization seen with pattern hair loss may be the direct result of reduction in the cell number and, hence, size of the dermal papilla.
Australas J Dermatol. 2003 Feb;44(1):62-6.
Androgenetic alopecia in a postmenopausal woman as a result of ovarian hyperthecosis.
A 65-year-old woman presented with an 8-year history of progressive frontotemporal alopecia and hirsutism. She had elevated serum levels of testosterone, androstenedione and estradiol. Ultrasound and computed tomography imaging suggested a right ovarian mass, while bilateral ovarian venous sampling demonstrated increased testosterone levels originating from both ovarian veins. Histology obtained following bilateral oophorectomy demonstrated bilateral ovarian hyperthecosis. Six months after surgery, the patient remains well with no progression of the alopecia. Ovarian hyperthecosis is a rare cause of androgenetic alopecia in postmenopausal women. The role of hyperthecosis and its relationship to androgenetic alopecia is reviewed.
Hair growth is a sophisticated biological process, which is still not thoroughly understood.
A multitude of therapeutic measures, including drugs, surgery, and suppelements have been made available, and used. However, due to the diversity of the problems underlying hair loss, there is no single solution for all hair loss cases. Most of chemical drugs and hair transplantation surgeries are not free from varying degrees of undesirable side effects on health.
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DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones)
or estrogens (female hormones) in the cells.
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