This investigation was undertaken to seek quantitative information concerning the relative activity of certain enzymes in hepatic cells in various parts of the lobule. The enzymes selected for study are chiefly those with important nwtabohc roles.
The formation of ascites in patients with cirrhosis of the liver probably depends on at least three factors: (1) hypoalbuminemia, (2) portal hypertension, and (3) increased amounts of circulating antidiuretic substance. The relative importance of these factors varies with the individual patients. Although the formation and disappearance of ascites do not correlate perfectly with levels of serum albumin in all patients, in the majority of cases the two findings are coincident and apparently related (1, 2). The use of concentrated human serum albumin in these patients for its osmotic effect would be expected to cause a diuresis. The extent to which this diuresis is produced would depend in large part upon the relative importance of the various factors of ascites production, being most marked in those patients in whom hypoalbuminemia is most specifically at fault.The observations of Janeway (3) and Thorn (4) and their co-workers in patients with liver disease demonstrated that the albumin level of the serum could be raised to normal by repeated injections of albumin. Certain of their patients showed a loss of edema and ascites but the oncotic effects were disappointing in their experience.
The diminished excretion of creatinine in progressive muscular dystrophy is a more striking and specific phenomenon than the excess excretion of creatine, marked though this is. While creatinuria is invariably encountered in all cases of long-standing dystrophy, the extent to which the excretion of creatinine is decreased provides a more reliable indication of the severity of the disease since an excess output of creatine may occur physiologically in normal human subjects and in many pathological conditions not known to be associated with muscle disease.
In progressive muscular dystrophy the residual muscle mass, as inferred from the excretion of creatinine, provides a useful index of the state of the disease at any given time.
Although there is excessive creatinuria in progressive muscular dystrophy, there is no evidence that a deprivation of methyl stores occurs through a loss of urinary creatine. The loss of methyl groups contained in the excess creatine is, under ordinary conditions of diet, almost exactly compensated for by a drop in the excretion of methyl groups in the urinary creatinine.
Testosterone propionate, administered over variable periods of time, resulted in the retention of creatine both in normal male children and in male children with progressive muscular dystrophy, as shown in the normal subjects by a diminution in creatine output, and in both by an excess creatinuria for variable periods of time following withdrawal of the hormone. An increase in the excretion of creatine in progressive muscular dystrophy occurred following the administration of methyl testosterone. Neither testosterone propionate nor methyl testosterone appeared to effect any consistent change in the output or urinary creatinine.
No effects on the excretion of creatine and creatinine were observed following the prolonged administration of concentrate of gonadotropic and thyrotropic principles of the hypophysis, or from the administration of desoxycorticosterone acetate to patients with progressive muscular dystrophy.
Except in one case, in which marked improvement was observed following the administration of testosterone propionate, no effects on the clinical course of the patients with progressive muscular dystrophy were observed as a result of treatment by any of the various hormones employed in this study.
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