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MMW Fortschr Med. 2002 Sep 19;144(38):42-5.
[Dyspnea, alopecia areata, protrusio bulbi. Which systemic disease is responsible?]

[Article in German]

Gutz S, Gillissen A.

Robert-Koch-Klinik, Stadtisches Klinikum St. Georg, Leipzig. sylvia.guetanktgeorg.de

Sarcoidosis is a systemic disease of unknown etiology and highly variable clinical presentation that manifests most frequently in the hilus lymph nodes, skin and eyes. The present case is a 63-year-old woman who was admitted for investigation of progressive apnea. Numerous typical, but also rare, organic symptoms were assignable to a chronic form of sarcoidosis: epileptiform attacks and depression, as also cutaneous changes affecting the scalp, and long wrongly diagnosed granulomatous "tumour" in the left orbit. The correct diagnosis was established on the basis of bronchoscopy and a chest CT that revealed inflammatory fibrotic changes in the lungs, and the histological work-up of tissue biopsies obtained from the various cutaneous lesions.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12395702&dopt=Abstract

J Interferon Cytokine Res. 2002 Sep;22(9):935-45.
Alopecia of IFN-gamma knockout mouse as a model for disturbance of the hair cycle: a unique arrest of the hair cycle at the anagen phase accompanied by mitosis.

Hirota R, Tajima S, Yoneda Y, Tamayama T, Watanabe M, Ueda K, Kubota T, Yoshida R.

Department of Physiology, Osaka Medical College, Takatsuki 569-8686, Japan.

Interferon-gamma(-/-) (IFN-gamma(-/-)) and IFN-gamma(+/+) C57BL/6 mice (3 weeks of age) completed the production of morphogenesis-derived hair. Around 6 weeks of age, however, most of the IFN-gamma(-/-) but none of the IFN-gamma(+/+) mice began to lose hairs in the dorsal and occipital areas in the absence of inflammatory reactions, and the alopecia was sustained for at least several 10-week periods of observation. A single subcutaneous injection of IFN-gamma to IFN-gamma(-/-) mice at 3, but not 4, 5, or 8 weeks of age could protect all the mice from alopecia, revealing that the lack of IFN-gamma around 3 weeks of age is directly responsible for the alopecia. Histologic features showed that the hair follicles of the IFN-gamma(+/+) mice passed through the anagen (4-5 weeks of age) and catagen/telogen ( approximately 6 weeks of age) phases, whereas those of IFN-gamma(-/-) mice (5 weeks of age or older) stayed in the anagen phase. TUNEL and bromodeoxyuridine experiments suggested that an arrest with unlimited DNA synthesis of the hair cycle in the anagen phase by the lack of IFN-gamma-dependent apoptosis in the midfollicle region and diffuse shedding of previously formed hair induced alopecia in IFN-gamma(-/-) mice.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12396715&dopt=Abstract

FASEB J. 2002 Dec;16(14):1967-9. Epub 2002 Oct 18.
Androgen-inducible TGF-beta1 from balding dermal papilla cells inhibits epithelial cell growth: a clue to understand paradoxical effects of androgen on human hair growth.

Inui S, Fukuzato Y, Nakajima T, Yoshikawa K, Itami S.

Department of Dermatology, Course of Molecular Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.

We attempted establishing an in vitro coculture system by using human dermal papilla cells (DPCs) from androgenetic alopecia (AGA) and keratinocytes (KCs) to explore the role of androgens in hair growth regulation. Androgen showed no significant effect on the growth of KCs when they were cocultured with DPCs from AGA. Because the expressions of mRNA of androgen receptor (AR) decreased during subcultivation of DPCs in vitro, we transiently transfected the AR expression vector into the DPCs and cocultured them with KCs. In this modified coculture, androgen significantly suppressed the growth of KCs by approximately 50%, indicating that overexpression of AR can restore the responsiveness of the DPCs to androgen in vivo. We found that androgen stimulated the expression of TGF-beta1 mRNA in the cocultured DPCs. ELISA assays demonstrated that androgen treatment increased the secretion of both total and active TGF-beta1 in the conditioned medium. Moreover, the neutralizing anti-TGF-beta1 antibody reversed the androgen-elicited growth inhibition of KCs in a dose-dependent manner. These findings suggest that androgen-inducible TGF-beta1 derived from DPCs of AGA is involved in epithelial cell growth suppression in our coculture system, providing the clue to understand the paradoxical effects of androgens for human hair growth.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12397096&dopt=Abstract

Being such a complex biological process, hair growth biology is still a work in progress. Noetheless, several therapeutic methods, including drugs, surgery, and suppelements have been in use to help those who attempt to restore their hair. None of these approaches are perfect due to the diversity in the causes underlying hair loss. Also, most of chemical drugs and hair transplantation surgeries are accompanied by undesirable side effects.

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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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