Unusal hair problems.

[Michel Waugh]

I want to know about Telogen effluvium and Alopecia areata . What kind of hair disease it is.

Please anybody has information regaring this please let me know.

[Michel Waugh]

I want to know about Telogen effluvium and Alopecia areata . What kind of hair disease it is.

Please anybody has information regaring this please let me know.

[Bill - Seemiller]

Michael,

 

The best thing to do is do a search on google.com for these specific medical conditions, but here's what I found.

 

Telogen Effluvium

 

From Emedicine.com

 

Background: Telogen effluvium is a form of nonscarring alopecia characterized by diffuse hair shedding, often with an acute onset. A chronic form with a more insidious onset and a longer duration also exists. Telogen effluvium is a reactive process caused by a metabolic or hormonal stress or by medications. Generally, recovery is spontaneous and occurs within 6 months.

 

 

Pathophysiology: Telogen effluvium can affect hair on all parts of the body, but, generally, only loss of scalp hair is symptomatic.

 

Understanding the pathophysiology of telogen effluvium requires knowledge of the hair growth cycle. All hair has a growth phase, termed anagen, and a resting phase, telogen. On the scalp, anagen lasts approximately 3 years, while telogen lasts roughly 3 months, although there can be wide variation in these times between individuals. During telogen, the resting hair remains in the follicle until it is pushed out by growth of a new anagen hair.

 

In most people, 5-15% of the hair on the scalp is in telogen at any given time. Telogen effluvium is triggered when a physiologic stress or hormonal change causes a large number of hairs to enter telogen at one time. Shedding does not occur until the new anagen hairs begin to grow. The emerging hairs help to force the resting hairs out of the follicle. Recent evidence suggests that the mechanism of shedding of a telogen hair is an active process that may occur independent of the emerging anagen hair. The interval between the inciting event in telogen effluvium and the onset of shedding corresponds to the length of the telogen phase, between 1 and 6 months (average 3 mo).

 

Headington has described 5 functional subtypes of telogen effluvium, based on which portion of the hair cycle is abnormally shortened or lengthened. These subtypes represent variations on the principles discussed above. It is rarely possible to distinguish these subtypes clinically.

 

 

Frequency:

 

 

Internationally: This condition is quite common, but exact prevalence is not recorded. A large percentage of adults have experienced an episode of telogen effluvium at some point in their lives.

Mortality/Morbidity: Mortality has not been reported. Morbidity is limited to mild cosmetic changes.

 

Race: No racial predilection is recognized.

 

Sex: Acute telogen effluvium can occur in either sex if the proper inciting conditions occur. Because hormonal changes in the postpartum period are a common cause of telogen effluvium, women may have a greater tendency to experience this condition. In addition, women tend to find the hair shedding more troublesome than men do; thus, more women seek medical attention for the condition. Chronic telogen effluvium has been reported mainly in women.

 

Age: Telogen effluvium can occur at any age. It is not uncommon for infants in the first months of life to experience an episode of telogen effluvium

 

Alopecia Areata

 

Also from emedicine.com

 

Background: Alopecia areata (AA) is a recurrent nonscarring type of hair loss that can affect any hair-bearing area. Clinically, AA can present with many different patterns. Although medically benign, AA can cause tremendous emotional and psychosocial stress in affected patients and their families.

 

 

Pathophysiology: The pathophysiology of alopecia areata remains unknown. The most widely accepted hypothesis is that AA is a T-cell mediated autoimmune condition that is most likely to occur in genetically predisposed individuals.

 

Autoimmunity

 

Much evidence supports the hypothesis that AA is an autoimmune condition. The process appears to be T-cell mediated, but antibodies directed to hair follicle structures also have been found in AA patients with increased frequency compared to control subjects. Using immunofluorescence, antibodies to anagen phase hair follicles were found in as many as 90% of patients with AA compared to fewer than 37% of control subjects. The autoantibody response is heterogeneous and targets multiple structures of the anagen phase hair follicle. The outer root sheath is the structure targeted most frequently, followed by the inner root sheath, the matrix, and the hair shaft. Whether these antibodies play a direct role in the pathogenesis or whether they are an epiphenomenon is not known yet.

 

Histologically, lesional biopsies of AA show a perifollicular lymphocytic infiltrate around anagen phase hair follicles. The infiltrate consists mostly of T-helper cells and, to a lesser extent, T-suppressor cells. CD4+ and CD8+ lymphocytes likely play a prominent role because the depletion of these T-cell subtypes results in complete or partial regrowth of hair in the Dundee experimental bald rat (DEBR) model of AA. The animals subsequently lose hair again once the T-cell population is replete. The fact that not all animals experience complete regrowth suggests that other mechanisms likely are involved. Total numbers of circulating T lymphocytes have been reported with both decreased and normal levels.

 

Recent studies in humans also reinforce the hypothesis of autoimmunity. Studies have shown that hair regrows when affected scalp is transplanted onto SCID (severe combined immunodeficiency) mice that are devoid of immune cells. Autologous T lymphocytes isolated from affected scalp were cultured with hair follicle homogenates and autologous antigen-presenting cells. Following initial regrowth, injection of the T lymphocytes into the grafts resulted in loss of regrown hairs. Injections of autologous T lymphocytes that were not cultured with follicle homogenates did not trigger hair loss.

 

A similar experiment on nude (congenitally athymic) mice failed to trigger hair loss in regrown patches of AA after serum from affected patients was injected intravenously into the mice. However, the same study showed that mice injected with AA serum showed an increased deposition of immunoglobulin and complement in hair follicles of both grafted and nongrafted skin compared to mice injected with control serum, which showed no deposition.

 

In addition, it has been shown that AA can be induced using transfer of grafts from AA-affected mice onto normal mice. Transfer of grafts from normal mice to AA-affected mice similarly resulted in hair loss in the grafts. In conclusion, certain factors within the hair follicles, and possibly, in the surrounding milieu, trigger an autoimmune reaction. Adding or subtracting immunologic factors profoundly modifies the outcome of hair growth.

 

Clinical evidence favoring autoimmunity suggests that AA is associated with other autoimmune conditions, the most significant of which are thyroid diseases and vitiligo (see History).

 

In conclusion, the beneficial effect of T-cell subtype depletion on hair growth, the detection of autoantibodies, the ability to transfer AA from affected animals to nonaffected animals, and the induction of remission by grafting affected areas onto immunosuppressed animals are evidence in favor of an autoimmune phenomenon.

 

Genetics

 

Many factors favor a genetic predisposition for AA. The frequency of positive family history for AA in affected patients has been estimated to be 10-20% compared to 1.7% in control subjects. The incidence is higher in patients with more severe disease (16-18%) compared to patients with localized AA (7-13%). Reports of AA occurring in twins also are of interest. No correlation has been found between the degree of involvement of AA and the type of AA seen in relatives.

 

Several genes have been studied and a large amount of research has focused on human leukocyte antigen. Two studies demonstrated that human leukocyte antigen DQ3 (DQB1*03) was found in more than 80% of patients with AA, which suggests that it can be a marker for general susceptibility to AA. The studies also found that HLA DQ7 (DQB1*0301) and human leukocyte antigen DR4 (DRB1*0401) were present significantly more in patients with alopecia totalis (AT) and alopecia universalis (AU).

 

Another gene of interest is the interleukin-1 receptor antagonist gene, which may correlate with disease severity. Finally, the high association of Down syndrome with AA suggests the involvement of a gene located on chromosome 21.

 

In summary, genetic factors are likely to play an important role in determining susceptibility and disease severity. AA is likely to be the result of polygenic defects rather than a single gene defect. The role of environmental factors in initiating or triggering the condition is yet to be determined.

 

Cytokines

 

Interleukin 1 and tumor necrosis factor were shown to be potent inhibitors of hair growth in vitro. Subsequent microscopic examination of these cultured hair follicles showed morphologic changes similar to those seen in AA.

 

Innervation and vasculature

 

Another area of interest concerns the modification of perifollicular nerves. The fact that patients with AA occasionally complain of itching or pain on affected areas raises the possibility of alterations in the peripheral nervous system. Circulating levels of the neuropeptide calcitonin gene-related peptide (CGRP) were decreased in 3 patients with AA compared to control subjects. CGRP has multiple effects on the immune system, including chemotaxis and inhibition of Langerhans cell antigen presentation and inhibition of mitogen-stimulated T-lymphocyte proliferation.

 

CGRP also increases vasodilatation and endothelial proliferation. Similar findings were reported in another study, in which decreased cutaneous levels of substance P and of CGRP but not of vasoactive intestinal polypeptide were found in scalp biopsies. The study also noted a lower basal blood flow and greater vasodilatation following intradermal CGRP injection in patients with AA compared to control subjects. More studies are needed to shed light on the significance of these findings.

 

Viral etiology

 

Other hypotheses have been proposed to explain the pathophysiology of AA, but more evidence is needed to support them. AA was believed to possibly have an infectious origin, but no microbial agent has been isolated consistently in patients. Many efforts have been made to isolate cytomegalovirus, but most studies have been negative.

 

 

Frequency:

 

 

In the US: Prevalence in the general population is 0.1-0.2%. The lifetime risk of developing AA is estimated to be 1.7%. AA is responsible for 0.7-3% of patients seen by dermatologists.

Internationally: Worldwide prevalence of AA is the same as in the US.

Mortality/Morbidity: AA is a benign condition and most patients are asymptomatic; however, it can cause emotional and psychosocial stress in affected individuals. Self-consciousness concerning personal appearance can become important. Openly addressing these issues with patients is important in helping them cope with the condition.

 

Race: All races are affected equally by AA; no increase in prevalence has been found in a particular ethnic group.

 

Sex: Data concerning the sex ratio for AA vary slightly in the literature. In one study including 736 patients, a male-to-female ratio of 1:1 was seen. In another study on a smaller number of patients, a slight female preponderance was seen.

 

Age: AA can occur at any age from birth to the late decades of life. Congenital cases have been reported. Peak incidence appears to occur from age 15-29 years. As many as 44% of people with AA have onset at younger than 20 years. Onset in patients older than 40 years is seen in fewer than 30% of patients with AA.

 

Cheers,

 

Bill

[Maria Karla]

Hi,

 

Telogen effluvium

 

A major alopecia cause Telogen effluvium (TE) is one of the most prominent alopecia causes. But it is a poorly defined condition and very little research has been done to understand this major hair disease.Telogen Effluvium is an abnormal loss of hair which is due to the alteration of the normal hair growth cycle. The alteration of the normal hair cycle can be due to various factors.

 

Alopecia Areata

 

In this major hair loss cause, the affected hair follicles are mistakenly attacked by a person's own immune system (white blood cells). It leads to the arrest of the hair growth stage. Alopecia areata in the initial stage is evident as one or more small, round, smooth bald patches on the scalp. Slowly it can progress to the total scalp and result in major hair loss. When the alopecia covers the entire scalp it is called alopecia totalis and when it leads to hair loss over the complete body then it is called alopecia universalis.