Metabolic Studies in Paralytic

Further evidence of the extensive effects of infection with the poliomyelitis virus upon many bodily systems is presented in this paper, the second of a series (1) describing metabolic and physiological features of the natural course of paralytic acute anterior poliomyelitis during its acute, convalescent and chronic phases. The most marked alteration in metabolism noted during the immobilization of healthy subjects in body casts (2) was greatly increased excretion of calcium, progressing to urinary calcium outputs more than double those of the control phase and to large negative calcium balances. This striking result suggested that it would be pertinent to investigate the extent of mineral loss occurring in patients with a seriously immobilizing disease such as paralytic acute anterior poliomyelitis. Several indications of alteration in calcium and phosphorus metabolism in poliomyelitis have been reported, such as hypercalcemia, hypercalciuria, urinary tract lithiasis, bone rarefaction and retardation of bone growth. Orr (3) found hypercalcemia four months after onset in a nine-yearold boy with extensive paralysis and, later, in 10 of 11 other children with paralytic poliomyelitis. Wilkins (4) noted "hypercalcemia in some of the paralytic cases at Children's Hospital" in Baltimore. Hypercalciuria in poliomyelitis has been mentioned several times but quantitatively only once, by Wilkins (5) who found as much as 1 gram per day in the urine of a patient, presumably a child, with poliomyelitis. The frequence of urinary tract calculi formation in poliomyelitis is well known, particularly in severely paralyzed patients