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Contracept Fertil Sex (Paris) 1985 Dec;13(12):1265-8
Hair loss during treatment with oral contraceptives
Oral contraceptives with a dominant androgen component can cause or worsen androgen-dependent alopecia in women. This diagnosis can only be made if other causes of alopecia (which can occur at the same time as treatment with oral contraceptives) have been excluded. The patient's endocrine profile must be investigated sometimes, this being in order to detect any excess production of androgens. These types of alopecia call for the stopping of the oral contraceptive and sometimes also calls for oral anti-antigen treatment.
Dermatol Surg 2002 May;28(5):394-400; discussion 401
A method for evaluating and treating the temporal peak region in patients with male pattern baldness.
BACKGROUND: In the past, hair restoration surgeons have focused most of their attention and efforts on the reconstruction of the hairline region and the area on top of the head. However, little attention has been given to the temporal peaks and the areas immediately posterior to them. OBJECTIVE: The goals of this article are to describe the pattern baldness process at the temporal peaks and the region immediately posterior to them, and to describe a method for the evaluation and treatment of these very important and often neglected areas. METHODS: A method for evaluating and grading the temporal peak region is given. A surgical technique for treating this problem is described. This method consists of making 1.0 mm spear blade incisions at a very acute 10 degrees angle in the newly designed anterior peak and in between the hair follicles that remain in the area posterior to the peak. The grafting of the finest one-haired grafts available in between existing hair follicles is accomplished with the help of 3.5x expandable loupes. The anterior temporal peak design is coordinated with the position of the frontal hairline restoration; the more anterior the hairline, the more anterior the temporal peak and vice-versa. RESULTS: The results of evaluating the temporal peak areas and treating them appropriately have consistently restored the cosmetic harmony between the frontal hairline and the temporal peak region. It is important, however, to only utilize the finest hairs available to create an aesthetically pleasing result. CONCLUSION: When evaluating patients for hair restoration surgery, it should be a common practice to evaluate the temporal peak regions and the areas immediately posterior to them. These areas should be appropriately treated so that the frontal hair restoration coordinates with that of the temporal peak. The further anterior one comes with the hairline, the more anterior must come with the temporal peak restoration and vice-versa.
J Invest Dermatol. 2003 May;120(5):771-5.
Major locus on mouse chromosome 17 and minor locus on chromosome 9 are linked with alopecia areata in C3H/HeJ mice.
Alopecia areata is an autoimmune disease that targets actively growing (anagen) hair follicles in humans, mice, rats, dogs, horses, and cattle. C3H/HeJ mice spontaneously develop alopecia areata from 5 mo of age and older in females and later in males. Frequency of disease approached 20% in a colony by 18 mo of age. C57BL/6J mice do not develop alopecia areata. A segregating F2 population of female mice (n=1096) was generated from crossing these two strains. Alopecia areata (n=138) and clinically normal (n=214) mice were genotyped at 12 mo of age using 211 microsatellite probes. The peak logarithm of odds ratio score on mouse chromosome 17 (10.9) was around marker D17Mit134 at 16.9 cM from the centromere. The mouse histocompatibility locus, H2, the mouse equivalent of human leukocyte antigen in humans, was a likely candidate. Twelve-month-old C3H.SW-H2b/SnJ mice (C3H/HeJ congenic mice in which the H2k purported susceptibility locus was replaced with the H2b purported resistance locus) did not develop alopecia areata, supporting this locus as being important in alopecia areata. A suggestive linkage was also found on mouse Chromosome 9 (logarithm of odds ratio score 2.0) around D9Mit206, 20 cM from the centromere. The interval on mouse Chromosome 17 contains several orthologous genes potentially associated with human alopecia areata.
Dermatology. 2003;206(3):189-91.
Association between Smoking and Hair Loss: Another Opportunity for Health Education against Smoking?
Besides being the single most preventable cause of significant morbidity and an important cause of death in the general population, tobacco smoking has been associated with adverse effects on the skin. Smoke-induced premature skin ageing has attracted the attention of the medical community, while only recently an observational study has indicated a significant relationship between smoking and baldness. The mechanisms by which smoking causes hair loss are multifactorial and are probably related to effects of cigarette smoke on the microvasculature of the dermal hair papilla, smoke genotoxicants causing damage to DNA of the hair follicle, smoke-induced imbalance in the follicular protease/antiprotease systems controlling tissue remodeling during the hair growth cycle, pro-oxidant effects of smoking leading to the release of pro-inflammatory cytokines resulting in follicular micro-inflammation and fibrosis and finally increased hydroxylation of oestradiol as well as inhibition of the enzyme aromatase creating a relative hypo-oestrogenic state. In view of the psychological impact of androgenetic alopecia on affected men and women, increasing public awareness of the association between smoking and hair loss offers an opportunity for health education against smoking that may be more effective than the link between smoking and facial wrinkles or grey hair, since the latter can be effectively counteracted by current aesthetic dermatologic procedures, while treatment options for androgenetic alopecia are limited.
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