Urinary excretion of aldosterone was measured (since 1963) by the modified method. of Neher & ¥'Vettstein, in 10 patients with myasthenia gravis including 2 cases of fulminant form, 4 cases of generalized form and 4 cases of ocular form.
The normal range of aldosterone values was 2.2 to 11.2 μg/day (average : 5.5±2.2 μg/day) in 8 healthy adults, and the total recovery was 55.0 to 59.3% (average : 57.7%) with the addition of 30 μg of d-aldosterone free in 900 c.c. of boiled urine, and the average value of paper blank was 0.025±0.002.
A slight to moderate increase of urinary excretion of aldosterone was observed during the period “with” extremity weakness in 6 patients of fulminant form or generalized form, and then the value decreased to normal limits during the period “without” extremity weakness in 4 cases of 6 patients, whose muscle weakness was diminished by anticholinesterase therapy. In 4 cases of ocular form, however, aldosterone excretion was constantly within normal range.
The increase of sodium to potassium ratio in urine was also observed during the period “without” muscle weakness. No significant difference between both periods in the urinary excretion of 17-ketosteroids, 17-hydroxycorticosteroids and catecholamines was observed.
Transient hyperaldosteronuria, occuring during the period “with” extremity weakness in myasthenia gravis, might be explained by the following findings; 1) the abnormality in neuromuscular transmission with changes of intracellular electrolytes, wihch was considered to be one of the etiologic factors of myasthenia, 2) the occurence of clinically obvious muscle weakness with slight changes of mineralocortiocid activity, 3) the effectiveness of aldosterone antagonists and KCL tablets in this disease, notwithstanding normal electrolytes in serum, 4) the decrease of intracellular potassium caused by aldosterone, if potas-sium depletion was to occur in muscle tissue, 5) the inhibitory effect of aldosterone on acetylcholine in vitro.
The significance of the relation of the demonstrated hyperaldosteronuria, which may be secondary, in myasthenia gravis (of fulminant or generalized form), to the basic disorder in this desease is not yet apparent.