Archive for October, 2009
Hair Loss Treatment Blog
Friday, October 30th, 2009Dr Proctor Treats Hair Loss
Thursday, October 29th, 2009Hair loss treatment at the Proctor clinic.
Genetics of hair
Tuesday, October 27th, 2009edited for use in hair loss and hair regrowth blog
Several families of proteins are expressed in the regrowth of hair. snip..Transgenic sheep over-expressing keratin genes but showing no hair growth change have been obtained and compared with the equivalent transgenic hair-loss mice. Studies of the effects of amino acid supply on the rate of hair regrowth have demonstrated that with cysteine supplementation of sheep a perturbation occurs in which there is a markedly increased level of only one type of mRNA and the ration of para- to orthocortical cells is increased. A molecular explanation of this phenomenon is being sought.
Congenital hair loss in a Bichon Frise
Saturday, October 24th, 2009J Am Vet Med Assoc. 1986;188(9):1053
Congenital alopecia in a Bichon Frise.Grieshaber TL, et al
A Bichon Frise pup had congenital Hair loss. Histologic evaluation revealed the absence of hair follicles, arector pili muscles, sebaceous glands, and sweat glands. Unlike previously described cases of congenital ectodermal defect, this hair loss was not associated with any color pattern; the pup was white until it was 4 months old, at which time normal black and brown pigmentation developed independently of the alopecic pattern.
Hair loss and contraceptives
Wednesday, October 21st, 2009Med Monatsschr Pharm.1981;4(6):161
Skin changes from taking hormonal contraceptives
Zaun H.
Hormonal contraceptives can induce changes in the skin and its appendages, including hairloss. Many skin functions are regulated by sex hormones. Clinical use of synthetic sex hormones can effect these hormone-dependent functions. Some effects are due to individual overdose of hormonal contraceptives; others are due to allergic reactions to contraceptive components. Estrogenic potency rather than the kind of estrogen is the determining factor whereas the kind of gestagen used is more important than its potency. Nortestosterone derivatives can exhibit variable androgenic residual action whereas progesterone derivatives have a strongly anti-androgenic effect. The table lists various skin manifestations with their possible causative agent(s) and treatment prevention possibilities. Specially described are: 1) Chloasma where combined action of estrogens and gestagens seem to be responsible together with individual factors of hair color, pigmentation, and extent of light exposure. 2) Acne, seborrhea, and hirsutism resulting from androgenic effect of gestagens; 19-nortestosterone derivatives affect sebaceous glands, 17-hydroxyprogesterone derivatives act on hair follicles. The two have opposite effects. 3) Hair loss occurs during the initial months of contractive intake. It is caused by the gestagen action on the growth phase of the hair, is dose-dependent and self-limiting. Androgenic alopecia ( pattern hair loss) is induced by nortestosterone and depends on individual hair pattern. It starts, after several months of hormone intake. …snip…
Hairloss with fibrous dysplasia and osteomas of skin
Tuesday, October 20th, 2009Arch Dermatol.;112(5):715
Hairloss with fibrous dysplasia and osteomas of skin. A sign of polyostotic fibrous dysplasia.
Shelley WB, Wood MG.
Localized alopecia (hair loss) of the scalp proved to be the cutaneous sign of underlying polyostotic fibrous dysplasia. Histologically, the hair follicles had been replaced by a strange coil of fibrous tissue. Some of these follicular sites showed ossification so prominent as to be evident in soft tissue reoentgenograms. In this patient, the skin itself showed a fibrous dysplasia analogous to that which has always been identified as occurring within the bones in Albright disease. In her skin, it is the hair follicle that is the site of this dysplasia. …snip…. Localized connective tissue stromal dysplasia is believed to play a role in the pathogenesis of not only the bony, but aslo the pigmentary and endocrine abnormalities of the disease.
Histopathology in alopecia reata
Sunday, October 18th, 2009J Invest Dermatol. 1991;96(5):673
Immunohistologic and ultrastructural comparison of the dermal papilla and hair follicle bulb from “active” and “normal” areas of alopecia areata.
Hull SM, et al
The “active” edges of patches of hair loss due to alopecia areata and normal areas from the same scalp (i.e., bearing normal terminal hair) from seven patients with alopecia areata were investigated immunohistologically. …snip.. The most significant differences found between normal “control” follicles and both “active” and “normal” areas of alopecia areata scalps were the polymorphic nature of the dermal papilla cells and the loss of cellular organization within the dermal papillae taken from alopecia areata scalps. ….snip… These results support the suggestion of a subclinical state of alopecia areata and indicate that further work on the etiology of alopecia areata should be directed towards the “normal” areas of alopecia areata scalps, in particular the cells of the dermal papilla and the dermo-epithelial junction of the hair follicle bulb.
Loose anagen hair
Thursday, October 15th, 2009Arch Dermatol. 1997 Sep;133(9):1089-93.
Loose anagen hair.
Tosti A, et al
OBJECTIVE: To review clinical and pathologic features and the long-term follow-up of patients with loose anagen hair (LAH). DESIGN: Clinical evaluation and long-term follow-up. SETTING: A university medical center. PATIENTS: Beginning in January 1990, 14 children and 5 adults (age range, 8 months to 47 years) were diagnosed as having LAH. Associated diseases included alopecia areata in a 3-year-old boy and Noonan syndrome in a 5-year-old boy. Two adult patients were parents of 2 affected children; the other 3 adults were the only members of their families with LAH. These 3 patients presented with a diffuse hair shedding that had suddenly developed 1 to 3 years before our observation. In all cases, findings of a trichogram showed a predominance of anagen hairs (80% to 100%) devoid of sheaths. INTERVENTION: None. RESULTS: In 4 children and 1 adult the condition remained stable; in 2 children and 1 adult, a considerable improvement in hair density was noticed. The pathologic study of hair from 5 patients did not reveal morphological abnormalities of the hair follicles except for a high incidence of fragmentations of the inner root sheath. CONCLUSIONS: Analysis of our patients with LAH reveals that the condition does not develop exclusively during childhood but can occasionally manifest itself later in life. The development of LAH may be sporadic, occur in association with developmental or acquired conditions, or, less commonly, be a familial disorder. While adult-onset LAH may not be exceptional, it can be easily misdiagnosed as telogen hair loss. The pathologic findings of LAH do not demonstrate any specific features and are of little value in the diagnosis of this condition.
Distribution of proteoglycans during the hair growth cycle in human skin.
Friday, October 9th, 2009J Invest Dermatol. 1991 Feb;96(2):191-5
Distribution of proteoglycans during the hair growth cycle in human skin.
Westgate GE, et al
The involvement of proteoglycans in hair growth has been recognized through the observation of increased hair growth in diseases such as the mucopolysaccharidoses and pre-tibial myxedema, which involve an increase in skin proteoglycan content. In an attempt to understand this, we have examined the distribution of chondroitin 6 sulphate (C6S), unsulphated chondroitin (COS), dermatan sulphate (DS), and heparan sulphate proteoglycans (HSPG) in frozen tissue sections of normal scalp by immunostaining. Results show that during anagen, the thick connective tissue sheath around the follicle strains strongly for C6S, COS, and DS. COS is uniquely associated with this region and is not found beneath the epidermis or infundibular epithelium. HSPG is, however, localized in the basement membrane zone adjacent to the outer root sheath. In addition, all of these proteoglycans are localized in the dermal papilla. In mid-catagen, we observed significant loss of C6S and COS staining from both the dermal papilla and the connective tissue sheath, but no decrease in staining for HSPG. In late catagen, very little staining of C6S and COS was observed. In early anagen, we observed that C6S was again present in the connective tissue sheath and dermal papilla; however, COS staining appeared to be weaker and less closely associated with the follicle. HSPG staining was observed in early anagen in a pattern very similar to that found for other basement membrane components. Results for DS were not obtained for catagen or early anagen. These results provide further evidence that hair growth is associated with the presence of chondroitin proteoglycans in the follicle environment and that the cessation of hair regrowth is associated with their removal. Further studies are underway to characterize the relationship between hair growth and proteoglycans.
Follicular unit grafting for pattern hair loss
Wednesday, October 7th, 2009Arch Facial Plast Surg. 2003 Sep-Oct;5(5):439-44.
Follicular-unit hair grafting: state-of-the-art surgical technique.
Epstein JS.
The goal in hair restoration is natural-appearing results. Improvements in the field of hair transplantation have developed with this goal in mind. The most recent development is the follicular-unit grafting technique, which relies on microscopic dissection to produce grafts, each containing a follicular unit, the natural bundling of 1 to 4 hairs, with a minimum amount of non-hair-bearing surrounding skin. For patients desiring surgical hair restoration, proponents of follicular-unit grafting advocate the technique for its superior results. Detractors point to the technical challenges of performing the procedure and the need for a staff of trained assistants for the microscopic dissection. What is clear is that this demanding procedure is taking the field of hair restoration the closest ever to its ultimate goal-undetectability.
PMID: 12975146
Antigenic competition as a therapeutic concept for alopecia areata
Sunday, October 4th, 2009Arch Dermatol Res. 1980;267(1):109-14.
Antigenic competition as a therapeutic concept for alopecia areata.
Happle R.
Hair loss due to alopecia areata can be treated effectively by topical application of potent contact allergens. To explain the response, the following hypothesis is presented. Alopecia areata is considered an autoimmune disease. The characteristic peribulbar round cell infiltrates probably reflect a cell-mediated immune reaction to some hair-associated antigen. With the elicitation of contact allergy, a second antigen is introduced at the same site. The infiltrates of the allergic contact dermatitis contain suppressor T cells and suppressor macrophages which, in terms of local immunoregulation, exert a nonspecific inhibitory effect on the immune response against hair follicles. snip.. In conclusion, the phenomenon of antigenic competition is proposed as a therapeutic concept.
PUVA treatment for hair loss due to alopecia areata.
Saturday, October 3rd, 2009Dermatologica. 1980;161(5):298-304
PUVA treatment for alopecia areata.
Lassus A, Kianto U, Johansson E, Juvakoski T.
41 patients with severe hair loss due to alopecia areata were treated with either local or oral 8-methoxypsoralen and UVA irradiations. In 26 cases (73%) a good to excellent result was obtained. The number of irradiations required for hair regrowth varied but 20–40 treatments were sufficient in most cases with a positive response. Patients with circumscribed or ophiasic alopecia responded better than patients with total or universal alopecia, atopy or a family history of alopecia did not seem to influence the outcome of the treatment. The age of onset of the disease seemed to be of importance as well as the duration of the treated attack. Patients over 20 years at the first attack of alopecia showed a better response than patients with an earlier onset of the disease. During a follow-up period of 6–12 months of 20 successfully treated patients only 2 had a recurrence.
Hair regrowth therapy(ies) for androgenetic alopecia.
Friday, October 2nd, 2009Arch Dermatol. 1996 Jun;132(6):714-5. Comment on:
Arch Dermatol. 1995 Dec;131(12):1373-5.
Hair growth therapy(ies) for androgenetic alopecia.
Rand S.
PMID: 8651731