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J Assoc Physicians India 2002 Aug;50:1073-4
Alopecia universalis in a case of systemic lupus erythematosus.
We report a case of systemic lupus erythematosus (SLE) who presented with alopecia universalis. MR, a 23 years female patient was admitted with alopecia universalis and other features of SLE like peripheral arthritis, fever, nephritis, butterfly rash over the malar regions, positive ANA and anti-ds DNA antibodies. There was a gap of four years between the onset of alopecia universalis and other clinical features of SLE. The alopecia was of non-scarry variety and responded to systemic and topical steroids.
Dermatology 2002;205(2):108-10
Kenogen. A new phase of the hair cycle?
BACKGROUND: A novel phenomenon has been described by the phototrichogram: the emptiness of the follicle after teloptosis. We called this phenomenon kenogen, from the Greek kappaepsilonnuovarsigma, 'empty'. OBJECTIVE: To describe the kenogen phase in its details. METHODS: Analysis of the existing literature. RESULTS: The original observation in 2 women was confirmed in 10 balding and non-balding males studied for 14 years in whom kenogen lasted about 4 months increasing up to about 7 months and affecting 80% of all hair cycles. In 2 women with progressing androgenetic alopecia studied for 2 years, kenogen involved 22% of the hair follicles, lasting from 3 months to 1 year. In a prepubertal boy studied for 1 year, it involved 8% of hairs and lasted about 2 months. CONCLUSION: During kenogen, the hair follicle rests physiologically, but duration and frequency are greater in androgenetic alopecia, possibly accounting for baldness. In addition to the classical cycle, the hair follicle may follow an alternative route during which the telogen phase, not accompanied by a coincident new early anagen, ends with teloptosis leaving the follicle empty.
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.
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.
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