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Spontaneous or propranolol-induced hypoglycemia can occur in uremic humans. We studied glucose kinetics (using [3-3H]glucose) in five uremic humans 24 h after hemodialysis and in seven normal controls. The effect of glucagon infusion at rates of 3, 6, 12, and 18 ng X kg-1 X min-1 at 60-min intervals was compared with either saline or beta-adrenergic blockade (propranolol infusion). In uremics, plasma glucose increased by 20-25% and by 40-50% at the 3 and 6 ng X kg-1 X min-1 glucagon doses, respectively, with no further increases at higher infusion rates. Glucose production increased transiently and in tandem with glucose uptake at each glucagon increment (P less than 0.0001). During beta-adrenergic blockade, the effect of glucagon in stimulating glucose production was blunted by 14-24% at the 6-18 ng X kg-1 X min-1 doses (P less than 0.05). During saline infusion, plasma insulin concentrations increased progressively to peak levels fourfold above basal at the 18 ng X kg-1 X min-1 dose. This increase in plasma insulin was virtually abolished by concomitant beta-adrenergic blockade (P = 0.0002). In contrast to uremic subjects, normal controls exhibited lesser degrees of hyperglycemia and hyperinsulinemia at all glucagon infusion rates. Propranolol infusion had no effect on the increments in glucose production and uptake nor on the plasma insulin response. These results suggest that in uremic humans propranolol independently reduces the hepatic response to glucagon and the insulin secretory response to hyperglycemia and/or hyperglucagonemia. These observations provide a possible mechanism for the adrenergic regulation of glucose homeostasis in uremia.

Nine patients, six men and three women, 40 to 73 years of age, were included in the study. All of the patients had severe heart failure refractory to aggressive therapy including digitalis, diuretics, and vasodilators. Eight patients underwent one treatment of peritoneal dialysis while the remaining patient received two dialyses. The urine output was measured by an indwelling catheter; glomerular filtration rate (GFR) was determined by creatinine and inulin clearance, and renal blood flow (RBF) was determined by sodium paraamino hippurate (PAH) clearance. Following one peritoneal dialysis, the mean fluid loss/patient was 3,995 ml (range 3,200 to 5,100 ml). Dialysis was generally well tolerated. One patient, who had underlying hepatic cirrhosis and underwent two dialyses, developed hepatic failure and died 10 days after the second dialysis. At postmortem, peritonitis was discovered. All of the patients showed a marked subjective and objective clinical improvement. The mean plasma urea decreased from 154 to 71 mg/dl (P less than 0.005), and mean plasma creatinine decreased from 1.83 to 1.13 mg/dl (P less than 0.005). Blood pH was 7.30 before dialysis and increased to 7.37 (P less than 0.0125) after treatment. Mean urine output predialysis was 955 ml and increased to 1,472 ml post dialysis (P less than 0.0005). Creatinine clearance increased from 35 to 73 ml/min (P less than 0.0005). The mean inulin clearance increased from 33 ml/min predialysis to 69 ml/min post dialysis (P less than 0.0005), and mean PAH clearance increased from 96.7 to 362.5 ml/min (P less than 0.0005). Acute peritoneal dialysis is a safe and effective means for removing large quantities of excess fluid from patients with intractable heart failure.

Iodine-induced hyperthyroidism can develop even in the presence of an otherwise normal gland. One of the less common sources of iodine is tablets of seaweed, sold over the counter without prescription. We report the case of a 72 year old female who developed clinical and laboratory evidence of hyperthyroidism while ingesting sea-kelp (Vitalia) tablets. Six months after stopping the tablets, the symptoms and laboratory evidence of hyperthyroidism had disappeared. No evidence of pre-existing thyroid disease was found.

Transilial bone biopsy confirmed heparin-induced osteopenia in a 23-year-old postpartum patient. Histomorphometric measurements during the reversible stage of bone disease that followed discontinuation of the heparin sodium therapy revealed signs of recovery; these were superimposed on a loose trabecular structure typical of osteoporosis. The histomorphometric evidence of recovery correlated well with signs of clinical improvement. In the majority of patients, heparin therapy during pregnancy is innocuous; however, discontinuation of treatment is recommended at the earliest signs of osteoporosis.

Patients with primary testicular failure have increased basal TSH levels and an exaggerated TSH response to TRH in the presence of normal circulating levels of thyroid hormones. In order to evaluate it this TSH profile is an oestrogen-related phenomenon, sixteen patients with primary testicular failure were challenged with 200 micrograms TRH prior to and after the administration of clomiphene citrate. The latter was given in a dose of 100 mg/day for 4 weeks to ten patients; 200 mg/day for 4 weeks to three patients and 100 mg/day for 2 months to the final three patients. The patients demonstrated increased mean basal TSH levels with an exaggerated TSH response to TRH. Following the administration of clomiphene citrate, there were no changes in T4, T3 sephadex or total T3 levels and in basal or stimulated TSH levels. Clomiphene did produce an increase in oestradiol, testosterone, basal gonadotrophins and LH response to LHRH. Since the oestrogen antagonist, clomiphene citrate, had no effect on TSH secretion, it is unlikely that the exaggerated TSH response to TRH is mediated by oestrogens.

Astigmatism enables spatial, linear and directional discrimination. These faculties are demonstrated by astigmatic photographic experiments. Comparative anatomic deductions lead to the assumption that the eyes of early mammals were astigmatic. Thereby these animals, lacking binocularity and accommodation, could achieve visual spatial information. This assumption is supported by the fact that features of astigmatic refraction, specially straight linearity, have been adopted by various intra-ocular structures, and by the neuronal structuralisation of receptive fields in the visual cortex of mammals.

A 55 year old woman in thyrotoxic crisis developed atrial fibrillation, atrioventricular block, and sinoatrial block in rapid succession. All of these abnormalities resolved completely after antithyroid treatment. This course of events illustrates the profound effect of thyroid hormones on cardiac function. In view of the potential aggravation of atrioventricular conduction disturbance by beta adrenergic blocking agents, thyrotoxic patients should be carefully screened for electrocardiographic evidence of conduction disturbance before the administration of such drugs.

A 30-year-old man who had 12 repeated hospital admissions within a period of 7 years for localized pain and swelling of the extremities is described. Excision biopsy of several subcutaneous lesions revealed histologic changes typical of polyarteritis nodosa (PN). Systemic disease was excluded because of a normal testicular biopsy, negative abdominal angiogram, and the lack of evidence for renal or other visceral involvement. Response to steroid therapy was excellent. Cutaneous PN is a distinct subset of polyarteritis with a chronic course and excellent prognosis. The present case underlines the need for a greater awareness, and for considering early biopsy of suspected lesions in patients with multiple episodes of apparent superficial thrombophlebitis.

Prolonged hypoglycaemia (serum glucose levels of 50 mg/dl and less, for more than 12 h in spite of treatment with periodic injections of hypertonic glucose) secondary to treatment with glibenclamide was found in 13 hospitalized patients. The mean daily dose of glibenclamide was 6.7 mg. In nine patients, the hypoglycaemia developed within 7 days of treatment. In two patients the tendency to hypoglycaemia lasted for more than 60 h in spite of continuous infusion of 5% or 10% glucose. Old age seems to be a crucial predisposing factor as none of the patients was under the age of 68 years. Contributing factors were renal failure and congestive heart disease. We feel that glibenclamide should be used with care in the elderly and in patients with renal or cardiac failure.

We examined the role of the plasma glucose concentration per se in the secretion of counterregulatory hormones during exercise. Ten men (average age, 24 yr; maximal aerobic capacity, 31.8 mL/kg.min) were studied during two 50-min bicycle exercise periods at either normal glucose [87 +/- 1 (+/- SE) mg/dL (4.8 +/- 0.1 mmol/L)] or low glucose [59 +/- 1 mg/dL (3.3 +/- 0.1 mmol/L)]. The plasma glucose targets were achieved by exogenous insulin and variable glucose infusions. These results were compared to studies in which saline was infused. Exercise at normal glucose was associated with significant increments in plasma epinephrine (maximum 3- to 5-fold above baseline) and norepinephrine (2-fold), comparable to those that occurred during saline administration. Plasma GH increased only at the most intense exercise level, while plasma cortisol and glucagon did not increase significantly. In low glucose-exercise studies, the increase in plasma epinephrine during exercise was significantly greater than that at normal glucose (P less than 0.01), although proportional to basal preexercise levels (r = 0.73; P less than 0.001). Plasma glucagon increased almost 100%, and plasma cortisol and GH increased by 150% and 400%, respectively. Compared to the effect of the same degree of hypoglycemia in the absence of exercise, only plasma epinephrine (P = 0.002) and norepinephrine (P less than 0.001) displayed effects independent of hypoglycemia during exercise. When low glucose was reversed to normal at the midpoint of exercise, plasma epinephrine and glucagon returned to the levels obtained for the same duration of exercise at normal glucose, while norepinephrine, GH, and cortisol were only partially responsive to the rise in plasma glucose. These data suggest that 1) moderate exercise is a stimulus for a sympathoadrenal and GH response, but not a peripheral glucagon response; 2) during exercise and hypoglycemia, plasma epinephrine and norepinephrine are enhanced, while the glucagon response is entirely glucose dependent; and 3) the epinephrine response to hypoglycemia can be dissociated from that to exercise, suggesting differing control mechanisms. We conclude that the activation of counterregulatory hormones during exercise is regulated by glucose-independent mechanisms, although these responses may be augmented by concurrent hypoglycemia.

PRL, TSH and gonadotrophin responses to the dopaminergic antagonist, metoclopramide, were studied in mildly hyperprolactinaemic patients with normal sella radiology and CT scan. Eleven female patients with basal PRL levels ranging from 23 to 124 ng/ml were challenged with intravenous metoclopramide (10 mg) and on subsequent occasions with TRH (200 micrograms) and LHRH (100 micrograms). On the basis of the PRL secretory pattern following metoclopramide and TRH stimulation, the patients were divided into two groups. Group I comprised six subjects who were PRL non-responsive to TRH and metoclopramide. Group II (five subjects) demonstrated PRL responses to TRH and metoclopramide indistinguishable from female controls. Mean +/- SD basal PRL levels were 68.5 +/- 29.9 ng/ml in Group I and not different in Group II (40.6 +/- 12.0 ng/ml). Basal LH levels were increased in Group II, whereas FSH was increased in Group I. Basal TSH levels were lower in Group I than the controls. Following metoclopramide, Group I patients had an increase in TSH from a basal of 2.4 +/- 0.7 microU/ml to a peak of 5.9 +/- 2.7 microU/ml (P less than 0.005) which occurred at 30 min. TSH values were increased above basal at all time intervals following metoclopramide. In contrast, TSH levels did not change in Group II patients or the controls after metoclopramide administration. Both patient groups had TSH responses to TRH similar to the controls. Following LHRH, the LH increase was greater in Group II and the FSH in Group I. In neither group nor the controls did gonadotrophin levels change after metoclopramide. In Group II females, PRL responsiveness to metoclopramide was associated with TSH non-responsiveness. In Group I females, PRL levels failed to rise, whereas TSH increased. The PRL and TSH profile in Group I females is typical of a prolactinoma. It is concluded that PRL as well as TSH determinations following metoclopramide are useful indices in the assessment of hyperprolactinaemia and may be of value in differentiating the functional state from that of a pituitary tumour.