The term Alopecia Areata is used to describe hair loss occurring in patches anywhere on the body however this condition almost always occurs on the scalp. Alopecia Totalis refers to total loss of the hair on the scalp and Alopecia Universalis, the most extreme form of Alopecia results in complete loss of all hair on the body. This booklet contains general information about alopecia areata (al-oh-PEE-shah ar-ee-AH-tah). It describes what alopecia is, its causes, and treatment options. While heredity is a possible determinant for the basis of alopecia areata , there are facts supporting the role of anomalous immune system. This irregularity culminates into a condition called autoimmunity.
The frequency of allele 2 increased from 24.1% in the control population to 25.9% in patchy alopecia areata, 36.1% in alopecia totalis, and 47.2% in alopecia universalis (p = 0.005). This severity association is similar to that found in other epithelial-related diseases, including inflammatory bowel disease, lichen sclerosus, and systemic lupus erythematosus. We have studied 10 patients with untreated acute alopecia areata, and three normal patients without hair loss. Morphologic changes, studied by conventional light and electron microscopy, in the cytoplasm of affected melanocytes often predated nuclear hyperchromatism. Because FK506 has been described as suppressing T cell mediated autoimmune diseases, we addressed the question whether topical treatment of C3H/HeJ mice with FK506 has a beneficial effect on alopecia areata (AA). For this purpose six C3H/HeJ mice with AA were treated topically with 0.1% FK506 ointment, four mice received the vehicle only.
Alopecia areata occurs more often in Down’s syndrome than would be expected by chance, sixty cases being found among 1000 patients with this syndrome compared with one case among 1000 subnormal controls. Because alopecia areata is associated with some organ-specific autoimmune disease and thyroid antibodies are often found in Down’s syndrome sera from affected patients were examined for the presence of fluorescent autoantibodies. Therefore, contact allergy is proposed as a therapeutic concept for alopecia areata. Furthermore, they demonstrate for the first time that apoptotic mechanisms involving granzyme B and Fas-Fas ligand pathways may play a major role in the persistence of chronic alopecia areata.
By combining protein microarray technology with the use of large cDNA expression libraries, we profiled the autoantibody repertoire of sera from alopecia areata patients against a human protein array consisting of 37,200 redundant, recombinant human proteins. The data sets obtained from incubations with patient sera were compared with control sera from clinically healthy persons and to background incubations with anti-human IgG antibodies. Scientists hope the registry will be useful in locating the gene or genes associated with alopecia areata. It will also link patients with other researchers studying the cause or treatment of this disease. It is possible that TNF-alpha may not be involved in the pathogenesis of alopecia areata, as in vitro studies have suggested.
It is not yet known what causes alopecia areata. It is believed to be an autoimmune disease triggered by a person�s autoimmune system, which decides to attack its own hair follicles. In many cases when a parent first approaches their doctor about alopecia areata, the doctor will refer the patient along to dermatologists. The very delay between seeing the doctor and dermatologist can be extremely stressful as the problem will usually be getting worse. The causal relation between alopecia areata and Helicobacter pylori is discussed in this study. We have prospectively studied 31 patients with alopecia areata and 24 healthy volunteers of similar gender, for the presence of H.
Although the results of some studies have proven negative, the influence of psychological factors in the development, evolution and therapeutic management of alopecia areata is, in general, well documented. Life events and intrapsychically generated stress can play an important role in triggering of some episodes. Alopecia areata (AA) is a T cell mediated disease directed against hair follicles that results in bald patches. It can range in severity from patchy (AA), to total scalp hair loss (alopecia totalis; AT) or body hair loss (alopecia universalis; AU). The “active” edges of patches of alopecia areata and normal areas from the same scalp (i.e., bearing normal terminal hair) from seven patients with alopecia areata were investigated immunohistologically. Similar areas from a further eight patients were examined using light and electronmicroscopy.
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