Alopecia areata is probably an autoimmune disease

Alopecia areata hair loss information for men and women
Alopecia Areata 
Alopecia Areata Biology
Alopecia Areata Treatments

  Evidence of an Autoimmune Etiology for Alopecia Areata
 
Alopecia areata is a hair loss disorder affecting all hair bearing regions of the body, particularly the scalp. Until 1958, it was known that dystrophic hair follicles in alopecia areata were due to a leokocytic infiltrate composed mainly of activated T-cell lymphocytes with a preponderance of CD4 cells and Langerhan’s cells. In that year a paper authored by Van Scott mooted the possibility that alopecia areata was an autoimmune disease. Acceptance was initially slow and until recently the evidence for an autoimmune basis for alopecia areata was largely circumstantial. But now, because of strong direct and indirect evidence, it is widely accepted that alopecia areata is an immune mediated disease.

However, the understanding of the etiology of alopecia areata, as its other aspects, is far from complete. This imperfect understanding poses problem in effective alopecia areata treatment, which presently is less than satisfactory.

As yet, what causes alopecia areata is not known, since the particular antigen responsible for the disorder has not been identified. Studies indicate that there seems to be a destructive response mainly from lymphocytes and macrophages to certain antigens in the hair follicle. It is now known what the immune abnormalities are with which alopecia areata is associated. They are non-specific as well as specific. Some of the non-specific abnormalities are:

  • Increased manifestation of class I and II antigens and Langerhan’s cell in the hair bulb.
  • The presence of peri and intra follicular mononuclear infiltrate.
  • Deposit of immune reactants around the hair follicle.
  • All effective therapies have in common between them an immunosuppressive effect on immune cells in skin.

The specific abnormalities include abnormal antibody responses specifically directed to a component of the anagen hair follicle.

Despite these findings, however, nothing can be said, with certainty, about the etiology of alopecia areata.

Research showed that many autoimmune diseases are associated with HLA hapolotypes. Studies were therefore also made to find similar association with alopecia areata. While these studies did not show any conclusive evidence to indicate association with class I hapolotypes, there was strong evidence to show that the disorder had some sort of association with some class II hapolotypes. Later studies also seemed to confirm the findings of these earlier studies. The expression of some of this class II hapolotypes seems to separate alopecia areata of different types.

These studies also showed that alopecia areata may have a linkage with the expression of some alleles of the IL-1 acceptor genes, a familiar occurrence with other inflammatory autoimmune diseases.

But these extensive studies on HLA linkages provided firm evidence supporting alopecia areata linkages in only two cases. They were atopy and Downs syndrome. It has been observed that atopy patients contract alopecia areata early in life. Alopecia areata in such patients takes a more severe form. The prognosis is also severer and their response to the treatment is not very satisfactory.

Downs syndrome is a disorder associated with functional deficiencies in T-cell mediated immune response and decreases in serum IgG levels. Patients with Downs’s syndrome appear to have an increased incidence of alopecia areata. It has been seen that, on average, 5% of patients with Down syndrome have alopecia areata, whereas it is only around 0.1% in concurrent control mentally retarded patients.

Observations seem to indicate a correlation between the severity and extent of the alopecia areata lesions and the severity of the mentally retarded cases. The incidence of clinically evident cases of thyroid abnormalities such as Hashimoto’s chronic lymphocyte thyroiditis, thyrotoxicosis, exopthalmic goiter, and myxedema does not differ significantly in alopecia areata patients from the patients in historical controls. However, because the reports are conflicting, it is difficult to arrive at the conclusion that there is an association between alopecia areata and thyroid disease.

There are increasing reports of an increase of incidence of diabetes mellitus, particularly the type I insulin-dependent diabetes in relatives of patients with alopecia areata. However, the alopecia patients themselves were not affected. Such findings point to a genetic connection between alopecia areata and insulin-dependent diabetes. These findings further suggest that, probably, the incidence of alopecia areata acts against the development of diabetes mellitus.

Several studies conducted earlier, have shown that the incidence of vitiligo increases in patients with alopecia areata. Recent studies however do not show any significant correlation between alopeca areata and vitiligo or the family history of vitiligo patients. The conclusion that can be derived from such contradictory findings is that, there could be rare cases of co-localisation of vitiligo and alopecia areata. Recent evidence suggests that vitiligo may result from an inherent biochemical defect of the entire epidermal melanin unit in the skin.

Alopecia areata is a systemic disease because, apart from affecting the hair follicles, it also often affects the nails and the eyes. Therefore the disease is probably extrinsic to hair follicles. The prognosis of this disease seems to be worse when there are nail abnormalities present. It is reported that eye abnormalities could be detected in the case of 80% of the patients affected by alopecia areata. These patients had otherwise no other ocular symptoms as compared to 30% of patients in normal concurrent controls, which had such symptoms.

In conclusion, it must be mentioned that the majority of alopecia areata patients are, by and large in good health. It has been estimated that only 3% to 5% of patients of alopecia areata have any other autoimmune or endocrine diseases. Therefore the association of alopecia areata with other autoimmune diseases is more an exception rather than the rule.

Conclusion

While alopecia areata is now much better understood, its pathogenesis is still not known. Treatment, therefore, continues to be directed towards limiting the effects of the symptoms rather than treating its root causes. More research, using the latest cellular and molecular biology techniques, needs to be done to find out more about the autoimmune response in alopecia areata. The key to more effective and targeted therapeutic method lies in identification of the specific antigen associated with the disorder.



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