myasthenia gravis and alopecia areata
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Myasthenia gravis and alopecia areata

Myasthenia gravis is a chronic progressive disease caused by a deficiency of acetylcholine [a neurotransmitter] at the neuromuscular junctions. It is characterized by chronic fatigue and muscular weakness, especially in the face and neck region. Patients affected with myasthenia gravis often have autoimmune skin disorders and they are seen to be affected by alopecia areata too. Hence, a study to understand the relationship between myasthenia gravis and alopecia areata was conducted on 159 Japanese myasthenia gravis patients comprising of 75 men and 84 women. These patients were diagnosed with myasthenia gravis following clinical, physiological and immunological tests and assessed for the condition based on the recommendations put forth by the myasthenia gravis foundation of America.

Patients were evaluated for thymoma and thymectomy was performed on some patients. All were tested for serum levels of anti-acetylcholine receptor antibodies. Thymoma is an epithelial neoplasm or tumor of the thymus gland. It can be benign [in an encapsulated form] or rarely invasive. Thymomas are mostly slow growing tumors and about 15% of patients with Myasthenia gravis are seen to be affected by them. The surgical removal of the thymus gland is done by a procedure known as thymectomy. The thymus gland has a major role to play in the body’s immune system and is large during childhood but regresses during the onset of adulthood. Since the immune system is already established by the time an individual progresses towards adulthood, the removal of the thymus does not significantly affect the immune system of the patient. By way of thymectomy, the Myasthenia gravis patient’s weakness is greatly reduced and so is the medication required to treat the disease.

Using Polymerase Chain Reaction [PCR] and Restriction Fragment Length Polymorphism [RFLP] methods, alleles of human leukocyte antigen (HLA) DQB-1 and DRB-1 genes were analyzed. All the experimental results were statistically analysed.

The results of the whole study are as follows:-

1. Amongst the 159 patients, 6 had a family history for alopecia areata of which 3 had alopecia totalis and all of them developed alopecia areata after myasthenia gravis was clinically diagnosed.

2. 129 of the patients tested positive for serum anti-acetylcholine receptor antibodies and the levels were higher when myasthenia gravis was associated with Alopecia areata.

3. Alopecia areata in some patients was due to lymphocyte infiltration in the peribulbular region of the hair shaft which was ascertained by histological studies. The number of cells was higher in patients who had developed alopecia areata after myasthenia gravis as compared to those who had only myasthenia gravis.

4. In this study 89 patients underwent thymectomy out of which 44 had confirmed thymoma. When alopecia areata was also diagnosed, an advanced stage of thymoma was very common in these patients and only 1 patient out of the 6 had no thymoma. 2 of the 5 had recurring thymoma. The one who did not have thymoma and 2 others with thymoma were treated with topical corticosteroids and they showed marked improvement in their hair loss condition. The remaining 3 were given oral corticosteroids as art of immunosuppressive therapy but they failed to respond to their alopecia totalis condition.

5. Amongst the 6 patients with both myasthenia gravis and alopecia areata, 3 had alopecia totalis, 1 had giant cell myocarditis [inflammation of the muscular tissue of the heart] and myositis [inflammation of muscle tissue] and the rest 2 had pure red cell aplasia.

6. The patient who had myocarditis and was on oral corticosteroids expired due to his inflammatory condition of the heart. The other 2 patients are alive even after 4-12 years after alopecia areata onset.

7. HLA class II gene alleles are seen to be associated with patients with myasthenia gravis and both myasthenia gravis and alopecia areata. So the relative frequencies of the alleles DRB1 and DQB1 were studied in 6 patients with myasthenia gravis and alopecia areata and 82 patients with only alopecia areata. The DQB1-0301 allele was reported to be associated with alopecia areata in Caucasians while DQB1-0402 was associated with Japanese who have myasthenia gravis with thymoma. None of the patients under study had any of these two.

DRB1-0901 and DQB1-0303 were observed to be frequent in patients with alopecia areata and these two haplotypes are seen frequently in the Japanese population. There is no concrete evidence about the percentage prevalence of myasthenia gravis and alopecia areata in Caucasian and Japanese populations, but the report suggests that the percentage may be higher in Japanese due to these haplotypes.

Many patients develop alopecia areata independent of myasthenia gravis. Myasthenia gravis is an auto-antibody mediated disease while alopecia areata is mediated by CD8+ T cells, that infiltrate into the hair follicles, supported by CD4+ cells. However in this study, since most of the auto-immune diseases developed after the myasthenia gravis patients underwent thymectomy and peripheral blood cells were also affected, an intensive study on the T-cell mechanism may be helpful in finding the appropriate solution to patients afflicted with both the diseases.


Myasthenia gravis and alopecia areata references

  • Suzuki S, Shimoda M, Kawamura M, Sato H, Nogawa S, Tanaka K, Suzuki N, Kuwana M. Myasthenia gravis accompanied by alopecia areata: clinical and immunogenetic aspects. Eur J Neurol. 2005 Jul;12(7):566-70. PMID: 15958099
  • Kamada N, Hatamochi A, Shinkai H. Alopecia areata associated with myasthenia gravis and thymoma: a case of alopecia with marked improvement following thymectomy and high level prednisolone administration. J Dermatol. 1997 Dec;24(12):769-72. PMID: 9492440
  • Korn-Lubetzki I, Virozov Y, Klar A. Myasthenia gravis and alopecia areata. Neurology. 1998 Feb;50(2):578. No abstract available. PMID: 9484415
  • Kubota A, Komiyama A, Hasegawa O. Myasthenia gravis and alopecia areata. Neurology. 1997 Mar;48(3):774-5. PMID: 9065564
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