Uric acid and Stroke

This is Dr Proctor’s paper on the relationship between uric acid and stroke. many of the same processes that happen in hair loss also figure in stroke causation. Similarly, many agetns that are effective in hair loss treatment are also efrfective in experimental models of stroke.

Hair loss in a blue Doberman pinscher

Color dilution alopecia, or color mutant alopecia, is an uncommon genetic-based skin disease with delayed onset (3); it has been described in many canine breeds and is more prevalent in color dilute individuals, especially those with a fawn (a dilution of a normally red or brown coat) or blue (a dilution of the normal black and tan color) coat (3). snip… The pathogenetic mechanisms of hair loss are not clearly understood. snip.. The onset of hair loss usually begins between 4 and 18 mo of age…. The condition is progressive with a gradual onset of dry, dull, and poor hair coat (6,9). Hair shafts are brittle and broken, especially along the dorsal midline (6). After several years, hypotrichosis is evident and can progress until a complete alopecia extends from the trunk to the flanks, usually sparing the head, tail, and limbs and all nondiluted coat areas. snip…Diagnosis of CDA is based on ruling out any inflammatory causes of alopecia (demodicosis, bacterial folliculitis, and dermatophytosis) and the common noninflammatory causes of alopecia, such as hypothyroidism and hyperadrenocorticis. The primary differential diagnosis for CDA is black hair follicular dysplasia (6,9), which is virtually identical histopathologically with CDA, but tan areas are spared in CDA, whereas only black areas are affected in black hair follicular dysplasia (6)….Hair examination of dogs with CDA will typically show numerous large melanin aggregates (macromelanosomes) in the hair cortex and medulla, distortion and breakage of the hair cortex, and fractures of the hair cuticle (3), as was detected in this case. Histological analysis indicates epidermal and follicular hyperkeratosis with most of the hair follicles dilated and filled with large melanin clumps. Abnormal clumping of melanin is also observed in the epidermis, dermis, and epithelia of hair follicles and around hair bulbs (6). Free melanin deposits are present at every level of the hair follicle and shaft, often with numerous perifollicular and peribulbar melanophages and pigmentary incontinence. It has been suggested that matrix hair cells are damaged by the cytotoxic effects of melanin precursor, which initiates the hair follicle dysplasia seen in the microscopic lesions and contributes to the development of the alopecia. Presence of subcuticular and intramedullary vacuoles that deform hair structure and contain melanosomes, as seen by transmission electron microscopy, may also explain hair fragility and ease of rupture and might be responsible for liberation of the melanin clumps that are released into hair follicles. There is no specific or curative therapy for color dilution alopecia (6). The vital prognosis is good, but it is preferable to prevent affected animals from breeding. Frequent baths, given once or twice/wk, with keratomodulating/antiseborrhoeic agents (benzoyl peroxide, salicylic acid, or ethyl lactate) can control the recurrence of bacterial infections, encourage restoration of normal keratinocyte multiplication, and inhibit or reduce the formation of comedones and sebum production (6). We administered oral melatonin supplementation to encourage hair regrowth, but it did not have a beneficial
Can Vet J. 2009;50: 511

effect. ..To the authors’ knowledge, there are no reports of melatonin treatment in dogs with color mutant alopecia, but oral or topical melatonin has been used to treat various other forms of canine alopecia with variable success. The mechanism by which melatonin may result in hair regrowth is not known. Melatonin is thought to play either a direct (on hair follicles) or an indirect role (within the central nervous system to alter secretion of melanocyte-stimulating hormone or prolactin secretion, or both) in the control of moulting and hair growth in mammals (2,10), but knowledge of this process is still very incomplete. It was originally hypothesized that melatonin exerted its effect on hair growth through modulating sex hormone and adrenal steroid hormone concentrations; however, decreases in hormone concentrations were not associated with hair regrowth in neutered dogs with alopecia X (1). In a recent study, it was theorized that melatonin may cause hair regrowth in dogs with hair cycle arrest by down-regulating the expression of estrogen receptors, which seem to have a role in the regulation of the anagen and telogen phases of hair (1). There are many potential reasons for failure of the treatment of the dog in our study. First, there are reports about the possible mechanisms of action, bioavailability, dosages, and seasonal/daily timing of melatonin administration, which made it difficult to determine a correct method of administration. We chose to follow the general directions given by Paradis. Additionally, because melatonin is classified as a nutraceutical, there is lack of standardization of the product, which may result in an inconsistent drug content in the final preparation. Finally, the real mechanism for development of color mutant alopecia is unknown; therefore, treatment with melatonin simply may not be effective.

Diffuse hair loss: Its triggers and management
SHANNON HARRISON, WILMA BERGFELD, MD
Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195

exerpt (edited)

The most important aspect in the management of telogen effluvium is educating the patient about the natural history of the condition. The normal hair cycle should be explained, as well as the relationship between triggers and the timing of hair loss. For example, in telogen effluvium, shedding usually is noted 2 to 3 months after a trigger, although it can rarely begin as soon as 2 weeks after a trigger.

To help identify triggers, a health diary or calendar can be useful. The patient should be instructed to record any stresses, hospital admissions, surgical procedures, new medications, dosage changes, or other potential triggers of hair loss.

The patient should understand that, once the trigger (for hair loss) is identified and removed or treated, the shedding settles but can continue for up to 6 months.1 Regrowth can be noted 3 to 6 months after the trigger has been removed, but cosmetically significant hair regrowth can take 12 to 18 months.

In acute telogen effluvium, if the trigger can be identified and removed, the shedding is short-lived and no further treatment is required.1,4 Patients can be reassured that they are unlikely to go bald.

Clin Ther. 2009 Oct;31(10):2242-2248.

Bioequivalence of a single 10-mg dose of finasteride 5-mg

Background: Finasteride, an inhibitor of the steroid 5alpha-reductase, has been approved for the treatment of benign prostatic hyperplasia and pattern hair loss. …. Conclusions: In this single-dose study, based on the rate and extent of absorption, the test and reference formulations of finasteride met the criteria for bioequivalence in these fasting healthy adult male Han Chinese volunteers. However, a significant difference was found for T(max) between the test and reference formulations. Edited for hair regrowth blog use.

Nat Med. 1995;1:7
The feasibility of targeted selective gene therapy of the hair follicle.

Li L, Hoffman RM.

Loss of hair and hair colour is associated with ageing, and when it involves the scalp hair, it can be distressing to both sexes. Hair loss resulting from cancer chemotherapy is particularly distressing. However, safe, effective therapies directed to hair have only just started to be developed. The hair follicle is a complex skin appendage composed of epidermal and dermal tissue, with specialized keratinocytes, the hair matrix cells, forming the hair shaft. snip…. Two decades ago we introduced the technique of entrapping DNA in liposomes for use in gene therapy. In this report we describe the selective targeting of the lacZ reporter gene to the hair follicles in mice after topical application of the gene entrapped in liposomes. These results demonstrate that highly selective, safe gene therapy for the hair process is feasible.

Edited for hai rloss blogspot

J Invest Dermatol. 1987;88:564

…Class I and class II major histocompatibility antigens in alopecia areata..

Bröcker EB, et al

Edited for blog use

Fifty-eight scalp biopsies were immunohistologically investigated with monoclonal antibodies against HLA-ABC, HLA-DR, and T6 antigens. The following 3 groups were compared: control biopsies obtained from healthy volunteers or patients with unrelated scalp diseases; biopsies from untreated hair loss due to alopecia areata, …snip… In the controls and untreated AA, HLA-DR expression was confined to dendritic cells in the epidermis and the follicular infundibulum. Its expression on hair matrix epithelium was found in 15 out of 32 biopsies from untreated AA and in 4 out of 13 biopsies from treated AA. In the control series, intrabulbar T6+ dendritic cells were either absent or present in low numbers. High numbers of intrabulbar T6+ cells were present in 7 out of 32 biopsies from untreated AA and in 0 out of 13 biopsies from treated AA. The data show that abnormal expression of class I major histocompatibility (MHC) antigens on hair matrix epithelium is a constant feature in AA, whereas class II MHC antigens are less frequently expressed. Topical immunotherapy with DCP, which induced expression of HLA-DR in epidermal keratinocytes in 6 out of 13 cases, reduced the abnormal expression of both HLA-ABC and -DR antigens in the epithelium of lower hair follicles in AA.

J Dermatolog Treat. 2009:1

A case of imiquimod-induced hair loss.
Conde J, et al

Imiquimod cream 5% is an immune modifier approved for the treatment of genital warts, actinic keratoses, and basal cell carcinoma. This case report presents an isolated case of hair loss associated with telogen effluvium after 6 weeks of imiquimod treatment for an actinic keratosis on the scalp. Based on this case presentation, telogen effluvium hair losss is a potential rare side effect from imiquimod treatment.

J Am Acad Dermatol.1984;11:216

T cell subpopulations in alopecia areata-associated hair loss.
Todes-Taylor N, et al

edited

Alopecia areata is a hair loss disease of unknown cause and unsatisfactory treatment. Histologically it is characterized by a lymphocytic infiltrate that surrounds the lower half of the hair follicle. snip….The Leu 3a/Leu 2a ratio ranged from 2.6 to 19.8, the higher ratios being seen in patients with clinically active disease. The cutaneous infiltrate also is Ia-positive, indicating the activated nature of these lymphocytes.

Dr Proctor has an organic semiconductor electronic device in the Smithsonian Institution.

Hair loss and contraceptives.

Med Monatsschr Pharm. 1981 Jun;4(6):161-5.

Skin changes from taking hormonal contraceptives

Zaun H.

snip… 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 regrowth 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…..

edited or hair regrowth blog

Arch Dermatol. 196;92:332-4.

Parapsoriasis en plaques and guttate elements with secondary alopecia? (2) hair loss probably due to a mucinous degeneration of the connective tissue component of the hair follicle?
Andrade R, Petratos M.

Edited for hair loss blog