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J Thorac Cardiovasc Surg 1995;109:183-184
© 1995 Mosby, Inc.
BRIEF COMMUNICATIONS |
Tokyo, Japan
Myasthenia gravis (MG) complicated by sarcoidosis is rare. Whether this complication represents the association between the two diseases or a simple coincidence is unclear. We encountered a patient in whom MG seemed to have induced sarcoidosis.
A 32-year-old woman visited our department because of blepharoptosis in February 1990. The blepharoptosis was improved by the tension test. X-ray examination and computed tomographic scanning of the chest showed no abnormalities. Results of the serum acetylcholine receptor antibody test were positive. Electromyography showed the typical waning phenomenon after continuous peripheral nerve stimulation. On the basis of these findings, a diagnosis of MG was made. She was followed up without administration of anticholinesterase drugs.
In November 1992, she noticed fatigability of the skeletal muscles, difficulty in speech and swallowing, and frequent choking Because of the exacerbation of MG, pyridostigmine bromide (60 mg) was administered daily. In July 1993, she was admitted to our department because of an abnormal shadow on chest X-ray films. Physical examinations revealed no palpable lymph nodes in the neck, axilla, or inguen. Examination of the eyes showed no uveitis.
Examination of peripheral blood samples showed no abnormalities in the leukocyte, erythrocyte, or platelet counts but an increase in the CD4 /CD8 ratio among lymphocyte subsets Urinary findings were within normal limits. The asparate aminotransferase, alanine aminotransferase, alkaline phosphatase, and 
-guanosine triphosphate levels were within normal limits, but the thymol turbidity test level was 14.6 U, and the zinc turbidity test level was 24.2 U. The total protein concentration was 8.8 gm/dl with 51.0% 
2 -globulin and 29.8% -globulin. The serum level of angiotensin-converting enzyme was 23.4 U/ml, and the lysozyme level was 14.3 µg/ml. The erythrocyte sedimentation rate was 56 mm/hr. The serum levels of triiodothyronine, thyroxine, and thrombin-stimulating hormone were within normal limits. Tests for thyroglobulin and mitochondria antibodies were negative. Rheumatoid factor and antinuclear antibody tests were negative, as was the positive protein derivative reaction.
Chest X-ray examination showed bilateral hilar lymphadenopathy. Chest computed tomographic scanning also showed marked bilateral hilar lymphadenopathy but no enlargement of the thymus or thymoma. Gallium 67 scintigraphy revealed accumulation-positive images on the bilateral hilar areas. A diagnosis of sarcoidosis complicated by MG (Osserman IIA) was made.
An operation was performed on October 19, 1993. After a T-shaped skin incision and longitudinal sternotomy had been done, the mediastinum was reached and extended thymectomy and biopsy of the hilar lymph nodes were performed. Histopathologic examination of the hilar lymph nodes demonstrated noncaseous granuloma, supporting the diagnosis of sarcoidosis.
Four months after the operation, she showed improvement in symptoms of MG with decreased blepharoptosis and diplopia and no fatigability of the skeletal muscles without administration of pyridostigmine bromide. Sarcoidosis has been observed after the operation without treatment, but no substantial changes have occurred in serum levels of angiotensin-converting enzyme or lysozyme.
MG is an autoimmune disease induced by the appearance of antiacetylcholine antibody T cell abnormality is observed in the peripheral blood,
1 and germinal center formation is frequently observed in the thymus tissue. MG is closely associated with thymus abnormalities. On the other hand, sarcoidosis is a systemic disease characterized by formation of epithelioid cell granulomatous lesions not accompanied by necrosis, and its pathogenesis is unclear. However, recent information has suggested the following mechanism of the establishment of epithelioid cell granulomatous lesions, although the details are still unknown 2 : (1) T cells are activated after nonspecific stimulation or stimulation as an immune response to unknown cause, and activated T cells accumulate in the lesion; (2) accumulated T cells produce lymphokine; (3) lymphokine promotes the differentiation of monocytes/macrophages to epithelioid cells, resulting in the formation of epithelioid granuloma. Because the thymus plays an important role in the differentiation and growth of T cells, it is speculated that MG as "an unknown cause" activates the T cell line, inducing the formation of sarcoidosis lesions.
Some case reports of MG complicated by sarcoidosis have been reported Sarcoidosis developed during the remission of MG in some cases 3 but during the exacerbation period in others, 4 showing no consistent tendency. Regression of MG and sarcoidosis after thymectomy was also reported. 4 In our patient, MG became less severe after thymectomy, but sarcoidosis did not.
Footnotes
From the First Department of Surgery,a First Department of Pathology,b Tokyo University School of Medicine, Tokyo, Japan. 
J THORAC CARDIOVASC SURG 1995;109:183-4.
References
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