Philip H. Henneman

THE METABOLIC DEFECT RESPONSIBLE FOR URIC ACID STONE FORMATION

The composition of a urinary tract stone often may be related to increased urinary concentration of one or more of the stone constituents or to characteristic hydrogen ion concentrations in the urine (1). Thus calcium phosphate and calcium oxalate are the major constituents of stones in patients with hypercalciuria, cystine stones are limited to patients with increased urinary cystine due to cystinuria (2), and calcium magnesium ammonium phosphate stones are generally found in patients with constantly alkaline urine due to ureasplitting infections. Boyce and King (3) have suggested that formation of an organic matrix may be the primary abnormality in stone formers and that the mineral content of the stone may reflect merely the chemical composition of the urine at the time the matrix was formed. This paper concerns studies of certain chemical factors in patients known to form uric acid stones.

EFFECTS OF HUMAN GROWTH HORMONE ON LEVELS OF BLOOD AND URINARY CARBOHYDRATE AND FAT METABOLITES IN MAN

In an accompanying paper (1) human growth hormo.ne (HGH) was reported to have stimulated the rate of linear growth, produced retention of nitrogen, phosphorus, magnesium, calcium, sodium and potassium, and perhaps increased the rate of fat mobilization in ten human subjects. This paper describes the response of blood and urinary levels of fat and carbohydrate intermediary metabolites in seven of these and in one infant with hyperinsulinism.1 Some effects of HGHon carbohydrate and fat metabolism have already been published. Raben and Hollenberg (2) observed a prompt and significant rise in plasma free fatty acids (FFA). Beck, McGarry, Dyrenfurth and Venning (3) reported alterations in glucose tolerance in four of six patients and Ikkos, Luft and Gemzell (4) in two of two patients. Ikkos and associates also observed elevations in ketone bodies in three of four patients. The data to be reported in general confirm these observations and include the simultaneous measurements of blood and urinary glucose, lactate, pyruvate, citrate, a-ketoglutarate, free fatty acids and ketones during short and longterm HGHtherapy.

The cardiac output in paget's disease before and after treatment with cortisone

Abstract 1.1. Observations on the cardiac output have been made in six patients with extensive Pagets disease before and during treatment with large doses of cortisone. 2.2. In all cases, cardiac output was elevated before treatment. High doses of cortisone for a sufficient duration, more than three days and less than nine days, produced a pronounced fall to normal levels. Serum alkaline phosphatase levels changed in the same direction as the cardiac output. 3.3. Cortisone had no consistent effect on oxygen consumption, large vessel hematocrit, total blood volume, pulse pressure or mean arterial pressure. Cortisone therapy resulted in a pronounced drop in pulse rate in three of the six patients studied. 4.4. The mechanism through which cortisone exerts its effect on cardiac output in Pagets disease was not elucidated by these studies.