The Effect of Hypercalcemia on the Creatin Output in Myasthenia Gravis.

Abstract

The discovery by Fiske and Subbarow 1 of muscle phosphocreatine as a labile compound with a definite relation to the functional condition of the muscle, again awakened the interest in those diseases of the (neuro) muscular system, which are characterized by creatinuria, viz., progressive muscular dystrophy and myasthenia gravis. The occurrence of acute attacks of muscular incompetence in myasthenia gravis versus the more steadily yet slowly progressive course of the muscular dystrophy made us choose the former disease for our experiments. The question whether the escape of the creatine from the muscle is due to an error of metabolism of the sarcoplasm or to an abnormal permeability of the sarcolemma presents itself. Through the parathyroid hormone preparation by Collip it has become possible to influence the blood calcium level sufficiently for the carrying out of cell-membrane permeability experiments in human subjects.

We report briefly an experiment designed to demonstrate the effect of hypercalcemia on the creatin output in myasthenia gravis. The patient was 45 years, with myasthenia gravis of one year's duration, the diagnosis having been made in the neurological division. This patient is also the chief subject of the observations reported in the following paper. During the experiment the patient was on a creatine- and creatinine-free diet. The usual Folin methods were used for the urine determinations, and Clark's and Collips' method 2 for the plasma calcium.

We report briefly an experiment designed to demonstrate the effect of hypercalcemia on the creatin output in myasthenia gravis. The patient was 45 years, with myasthenia gravis of one year's duration, the diagnosis having been made in the neurological division.