(normal 5-45 ,ug/ml (5-45 mg/i)), total protein 6-3 g/dl (63 g/l) (normal 6-5-8-5 g/dl (65-85 g/l)), albumin 3X7 g/dl (37 g/l) (normal 3-2-5-0 g/dl (32-50 g/l)), globulin 2-6 g/dl (26 g/l) (normal 2-5-4-5 g/dl (25-45 g/l)), uric acid 7-0 mg/dl (1P2 mmol/l) (normal 3-0-7 5 mg/dl (0-5-1P2 mmol/l)), creatinine 1-2 mg/dl (106 ,umol/l) (normal 0-7-15

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Ovine prolactin was iodinated by the lactoperoxidase method and purified by gel filtration on Sephadex G-100. The binding ability of the labelled hormone was determined, by incubation with liver homogenate from rabbits in late pregnancy, to be 8-8% total binding/mg protein, of which 86% was specific. The fraction of 125I-labelled ovine prolactin which bound most strongly was subsequently used to study its binding to rat seminal vesicle, prostate and testicular homogenates. The total binding to the seminal vesicle homogenate taken from mature (80-day-old) rats was the highest (11-69%/mg protein), but the greatest degree of binding specificity (82-6%) was to immature (30-day-old) rat prostate. Both total and specific binding to rat testicular homogenate were consistently very low. The binding specificity was demonstrated by displacement studies: while ovine prolactin caused displacement of specific binding, human chorionic gonadotropin, rat thyrotropin and human follicle-stimulating hormone did not cause any significant displacement of bound 125I-labelled ovine prolactin. Affinity constants (Ka) and binding capacities for the seminal vesicle and prostate homogenates were determined by Scatchard analysis and the effect of age on these parameters was studied. There was no difference in Ka between the aged (220-day-old), immature and mature rat tissue homogenates; however, a significant fall in binding capacity was observed in the mature rat prostate, and a further fall in the aged rat prostate. No such change was observed in the binding capacity of the seminal vesicle, as estimated by Scatchard analysis, although total and specific binding to the mature homogenates was higher than that of the other age groups.

Pulmonary function was assessed in 11 patients with acromegaly, 8 of whom were previously treated by external pituitary irradiation. None of the patients had any overt respiratory ailment. Ventilatory function tests were normal in all patients and all had normal total lung capacity ranging from 75 to 123% (mean, 98.18 +/- 4.69%). Eight of ten patients (80%) had hypoxemia with a partial pressure of oxygen in arterial blood ranging between 58 and 90 mmHg (mean, 76.0 +/- 4.2). Calculated alveolar-arterial differences for oxygen ranged between 5.25 and 46.0 (mean, 26.0 +/- 4.7). In 4 of 5 patients in whom lung perfusion scans were performed, perfusion defects were found. There was a significant correlations (p < 0.05) between the presence of hypoxemia and the known duration of acromegaly, but not with the present growth hormone levels or previous therapy. The results indicate that pneumomegaly is not common in acromegaly. However, most patients have some degree of hypoxemia present usually as subclinical disease and it is probably due to a ventilation-perfusion derangement, which is probably a direct effect of the prolonged oversecretion of growth hormone.

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A 60-year-old woman who had been instructed to increase her water intake because of nephrolithiasis developed the syndrome of inappropriate secretion of antidiuretic hormone when treated with chlorthalidone for mild hypertension. Serum osmolality was 235 mOsm/kg with concomitant urine osmolality of 490 mOsm/kg. When serum sodium decreased to 110 mEq/liter, plasma antidiuretic hormone (ADH) was elevated at 30 pg/ml. The syndrome resolved when chlorthalidone was discontinued together with fluid intake restriction. Plasma ADH returned to normal (less than 0.5 pg/ml) after three days of treatment. The favorable outcome in this patient is attributed to early recognition of the syndrome, which might occur even with nonthiazide diuretics such as chlorthalidone.

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