Abstract
Described here is a 21-year-old man, who had several episodes of generalized muscle weakness, blepharoptosis and a diffuse goiter. The results of thyroid function tests and histological findings of specimen obtained by thyroid biopsy was compatible with mild Graves' disease. Blepharoptosis was moderately improved immediately after edrophonium injection, thus established the diagnosis of occular type of myasthenia gravis. In addition, the patient had markedly diminished serum potassium level, in association with markedly elevated plasma renin activity (PRA). Plasma aldosterone concentration (PAC) and urinary aldosterone excretion (UAE) were also moderately increased. The insensitivity to pressor effect of infused synthetic angiotensin II and hyperplasia of the juxtaglomerular apparatus of the kidney in histological examination substantiated the diagnosis of Bartter's syndrome complicated with Graves' disease and myasthenia gravis.
In order to investigate the effect of indomethacin, an inhibitor of prostaglandin biosynthesis, on the biochemical abnormalities of Bartter's syndrome, indomethacin (75mg/day) was given with spironolactone and potassium treatment. However, the biochemical abnormalities were not corrected and, moreover, muscle weakness and further decrease in potassium level were observed during the treatment with indomethacin alone. The findings suggest that the abnormalities observed in this patient could not be explained by the overproduction of renal prostaglandin.
The present case with Bartter's syndrome was characterized by complicating of Graves' disease and myasthenia gravis, both of which have been regarded as autoimmune diseases. Immunological studies, including subpopulation of lymphocyte determined by surface immunoglobulin bearing cells, rosette formation and blastoid formation, revealed the suppression of B lymphocyte population in the present case. Although these immunological abnormalities were corrected after administration of azathioprine, an immunosuppressive agent, serum potassium level was not ameliorated. The result suggest that immunological mechanism is not related to the etiology of Bartter's syndrome in the present case.
