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Are
there alternative explanations for the development of alopecia areata
for which research is being conducted?
A minority of dermatologists dispute the idea of alopecia areata
being an autoimmune initiated disease. Using PCR (polymerase chain
reaction) methods, gene sequences that code for cytomegalovirus
(CMV) have been found in skin biopsies taken from people with alopecia
areata (Skinner 1995a, Skinner 1995b). In comparison, biopsies from
the general population were shown not to contain similar CMV genes.
The work is at the preliminary stage but the researchers are suggesting
that CMV may be present in hair follicles and that the immune system
is mounting a normal response against the virus to get rid of it.
In doing so it also disrupts and destroys adjacent hair follicle
tissue.
There is however much work to be done before the hypothesis could
become more widely accepted. Not least it needs to be shown that
the CMV virus is capable of initiating alopecia areata. Considering
the target antigen(s) for immune cells in alopecia areata have not
been defined, the possibility that the targets are from an external
source somehow transferred to the hair follicle is still feasible.
This would not mean that potential mechanisms of alopecia areata
development based on immune cell activity are wrong. Because the
immune cells would be responding to viral antigens, the initiating
mechanism could not be described as autoimmune in nature, but the
mechanism by which hair production is stopped may remain the same.
Initial response to viral antigens could later lead to a wider autoimmune
action.
Some reports from a separate laboratories which also tried to
identify CMV in alopecia areata affected hair follicles failed
to reveal any positive results (Tosti 1996, Garcia-Hernandez
1998,
Jackow 1998). The involvement of CMV in alopecia areata is currently
wide open to question. It has been suggested that other, as yet
undiscovered, viruses are locally infecting the hair follicle
and causing hair loss through inflammation.
Dr Theodore J. Daly, Located in Garden City, Long Island, New
York has had an article published in the Archives of Dermatology
(September 1998). This article has been publicized by several
news
networks (July 1998). DR Daly's research has focused on examining
the blood plasma levels of the vasodilator/immunomodulator CGRP
(Calcitonin Gene-Related Peptide) in people with alopecia areata.
He took serum samples from 18 people with alopecia areata and
69
control samples from people without alopecia areata. The serum
samples were analyzed using a technique called "radial immunodiffusion"
(RIA). This is a simple technique to define concentrations of biological
substances in solution. DR Daly found that in people with alopecia
areata the concentration of CGRP in the plasma was about half (53%)
that of control samples.
DR Daly suggests that this apparent lack of CGRP could have an
important influence on alopecia areata development. He believes
that without the vasodilatory properties of CGRP there may be a
reduced blood flow to hair follicles and this may result in dystrophic
hair follicles less able, or unable, to produce hair fiber. He also
suggests that lack of blood flow may also account for nail pitting,
eczema, and pigmentary abnormalities.
CGRP also has immunomodulatory properties and apparently suppresses
antigen presentation to lymphocytes and slows down their proliferation
and reactivity. This suggests that people with a deficiency of CGRP
may have a greater susceptibility to inflammatory reactions as occur
in alopecia areata.
DR Daly believes that this deficiency in CGRP shows that people
develop alopecia areata as a result of deficient thyroid production
and that the autoimmune hypothesis of alopecia areata development
needs to be modified or may be entirely wrong. He believes that
using treatments directed at replacing and/or increasing levels
of CGRP in the blood stream of people with alopecia areata may be
an effective promoter of hair regrowth.
DR Dalys treatment may have potential even if CGRP
is not fundamentally involved in alopecia areata development.
If CGRP does have immunosuppressive effects then it may be useful
regardless
of the native CGRP concentrations in people with alopecia areata.
Are
there alternative explanations for the development of alopecia areata
for which research is being conducted references
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