References: Hair growth and hair loss
Dermatologica. 1988;177(3):170-4.
Thymopentin in the treatment of severe alopecia areata.
Tosti A, Manuzzi P, Gasponi A.
Department of Dermatology, University of Bologna, Italy.
Since alopecia areata might be due to an aberrant T-cell-mediated immunity, the purpose of our study was to compare the results obtained with Thymopentin to those of topical sensitizing therapies, such as squaric acid dibutylester or diphencyprone. Statistical analysis showed no differences between the results obtained with these two therapies. Therefore, Thymopentin can be considered to be a new therapeutic agent which, like the classic topical drugs squaric acid dibutylester or diphencyprone, has immunoreactive properties and might provide some hope to patients with severe alopecia areata.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3049174&dopt=Abstract
Arch Dermatol. 1978 Jul;114(7):1036-8.
Treatment of alopecia areata with dinitrochlorobenzene.
Daman LA, Rosenberg EW, Drake L.
Persistent refractory alopecia areata in 26 patients was treated topically with dinitrochlorobenzene (DNCB). Sixteen patients have had excellent regrowth of hair; three patients could either not be initially sensitized or an adequate allergic contact dermatitis on the scalp did not develop. Two patients discontinued therapy within two months; hair growth did not develop in five patients despite an adequate trial. Augmentation of the T-lymphocyte pool via DNCB sensitization and challenge may become effective therapy for some patients with severe alopecia areata.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=308348&dopt=Abstract
public.srce.hr
Regulation of the hair cycle takes place at the pilo-sebaceous unit with the sebaceous gland as a sex hormone-dependent part. Although minoxidil stimulates proliferation of follicular cells and activation of prostaglandin endoperoxide synthase-1, it was suggested that other mechanisms, such as an increase in the local blood flow, might mediate the drug effect on hair growth. If that is the case, it is possible that minoxidil counteracts some vasoconstrictive mediator of male-pattern alopecia. This hypothetical vasoconstrictive mediator X would have to meet some criteria: (I) vasoconstriction both in the general circulation and in the hair-growing skin; (II) local vasoconstrictive activity in the hair growing skin should be related to the circulating testosterone level; (III) only an increase in the local mediator X activity causes male-pattern alopecia, since hypertensive patients are not balder than expected. The sebaceous gland is a possible place of the mediator X secretion since it is a sex-hormone-dependent part of the pilo-sebaceous unit. ET-1 might be a suitable candidate for the mediator X, since male hormones raise ET-1 plasma levels and female hormones lower them. The speculation presented here is that ET-1, beside vasoconstriction in the general circulation, might also regulate the sebum secretion, by triggering contractions of the myoepithelial cells. This hypothetical mechanism would normally remain confined to the sebaceous gland. During puberty, sex hormones stimulate growth of sebaceous glands in both sexes. In women hypertrophied sebaceous glands under estrogen control would not increase its ET-1 content, while in men, testosterone would increase ET-1 secretion that might affect the neighboring arterioles. Induced vasoconstriction might reduce the hair growth and promote hair loss. If ET-1 plays the described role, then an ET-1 antagonist, i.e. bosentane, should also have some hair-growing properties.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10616041&dopt=Abstract
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