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This study was designed to assess whether transcendental meditation (TM) could influence various endocrine responses in 10 experienced male meditators. Nine matched subjects, uninformed of the TM procedure, acted as controls. Meditators successfully practised their technique for 40 min in the morning while controls relaxed for this period. No significant differences emerged between these 2 groups with respect to carbohydrate metabolism (plasma glucose, insulin and pancreatic glucagon concentrations), pituitary hormones (growth hormone and prolactin) or the 'stress' hormones, cortisol and total catecholamines-although meditators tended to have higher mean catecholamine levels. Plasma free fatty acids were significantly elevated in meditators 40 min after completing the period of TM. No clear evidence was thus obtained that any of the stress, or stress-related, hormones were suppressed during or after meditation in the particular setting examined. [ABSTRACT FROM PUBLISHER]

The prevalence and pathogenesis of hyperglycaemia were investigated in a consecutive series of 27 black infants admitted to hospital with gastroenteritis over a period of three months. Hyperglycaemia (plasma glucose concentration greater than 10 mmol/l) occurred in 15 (55%) of these patients. The pathogenesis was not clear but possible contributory factors included raised concentrations of the stress hormones pancreatic glucagon, growth hormone, and cortisol; hypokalaemia; and peripheral insulin resistance. Intravenous rehydration, without insulin, corrected the plasma glucose concentrations and restored the hormonal profile towards normal within 36 to 48 hours. [ABSTRACT FROM AUTHOR]

The use of calcium (Ca) supplements by postmenopausal women is growing rapidly. A commercial preparation of tricalcium phosphate (TCP) is available in the USA. Depending on the relative absorption of Ca versus phosphate, a rise in serum phosphorus (P) could stimulate parathyroid hormone (iPTH) secretion. We therefore compared Ca absorption and the metabolic responses following TCP to that of Ca carbonate (CC) on separate occasions in each of 10 women, aged 22-40 years. The subjects were fasted overnight for 12 hours while good hydration was maintained. Following a 2-hour baseline-urine collection, 1200 mg calcium (as CC or TCP) was ingested and two 2-hour postload urine collections were made. Blood was drawn at 1, 2, and 4 hours after the Ca load. Serum (S) and urine (U) Ca, P, and creatinine, and U cyclic AMP (cAMP) were determined. iPTH levels following TCP were also measured. Ca absorption was determined by the postload rise in Uca above baseline. Uca excretion increased significantly and was accompanied by significant rises in Sca after both preparations. Following TCP, S and U phosphorus increased. Urinary cAMP did not change after either preparation, and iPTH levels fell after oral TCP. We conclude that Ca taken as TCP is absorbed adequately and, thus, despite a rise in the S phosphorus level does not stimulate parathyroid activity. [ABSTRACT FROM AUTHOR]

Acute thyroiditis is an extremely rare complication of nocardiosis. We report a patient with hyperthyroidism due to suppurative thyroiditis caused by Nocardia brasiliensis. A 38-year-old Black male presented with features of thyrotoxicosis, sepsis and airway obstruction. He had no evidence of underlying thyroid disease, but was severely immunocompromised as a result of acquired immunodeficiency syndrome. He had previously been diagnosed with pulmonary nocardiosis and also had nocardial abscesses on his anterior chest wall. Investigations revealed thyrotoxicosis, with a FT4 of 43.2 pmol/l and a suppressed TSH <0.01 mIU/l. Serum anti-thyroperoxidase and anti-thyroglobulin antibodies were absent. Computed tomography scan showed a large abscess in the anterior neck involving the left lobe and isthmus, as well as inhomogeneous changes in the right lobe of the thyroid. The radioisotopic scan showed absent uptake of tracer in keeping with thyroiditis. Although the initial presentation was that of hyperthyroidism, destruction of the gland later resulted in sustained hypothyroidism, necessitating thyroid hormone supplementation. The hyperthyroidism can be explained by the release of presynthesized and stored thyroid hormone into the circulation as a result of inflammation and disruption of the thyroid follicles, and the subsequent hypothyroidism by the fact that much of the gland was destroyed by the abscess and the extensive inflammatory process. This is the first documented case of hyperthyroidism in a patient with acute suppurative thyroiditis caused by Nocardia.

Alcohol-induced chronic pancreatitis is associated with bone loss, but bone histomorphometric data describing the mechanism of cortical (Ct) and trabecular (Tb) bone loss are scarce. In this case-control study, we investigated 13 black male patients aged 41.2 +/- 8.9 years with alcohol-induced chronic pancreatitis by routine iliac crest cortical and trabecular histomorphometry and by biochemistry relevant to bone, liver function, and iron overload. Patients showed lower values for Ct thickness (P = 0.018), endocortical (Ec) wall thickness (P = 0.0002), Tb bone volume (0.019), Tb thickness (0.001), Tb wall thickness (P < 0.0001), Ec osteoid thickness (P = 0.001), Ec mineral apposition rate (P = 0.011), and Ec bone formation rate (P = 0.035). Ec eroded surface (P = 0.004) was elevated compared to controls. Tb osteoid thickness (P = 0.14) and Tb mineral apposition rate (P = 0.195) tended to be lower than in controls. Levels of 25-hydroxyvitamin D (P < 0.005), serum magnesium (P = 0.02), and ascorbic acid (P = 0.049) were lower and urine calcium/creatinine ratios higher than in controls. Alkaline phosphatase and gamma-glutamyl transpeptidase (GGT) were negatively correlated but iron markers were positively correlated with bone structural and formation variables. The histomorphometric data were found to be consistent with alcohol bone disease. Osteomalacia was not a feature. Secondary pathogenetic factors were liver disease, hypovitaminosis D and C, diabetes mellitus, and possibly chronic pancreatitis.

Objective: To present the first report of a clinical and molecular investigation of a black South African family with complete androgen insensitivity syndrome (CAIS)., Methods: Biochemical and chromosomal analyses were performed. In addition, the molecular study included microsatellite analysis and DNA sequencing., Results: The index case, an unmarried 21-year-old black phenotypic female patient with primary amenorrhea, was identified in the Division of Endocrinology at a tertiary hospital affiliated with the University of the Witwatersrand. A detailed family history identified further potentially affected members (on the basis of primary amenorrhea), who were also included in the study. A total of 13 family members, including 6 affected subjects, were involved in the molecular study. All affected persons had a 46,XY karyotype, female phenotype, and hormonal profiles commensurate with their clinical diagnosis. The androgen receptor gene in an affected patient was examined for mutations by DNA sequencing. Mutation screening was extended to other family members. The genetic basis for CAIS in this large family is the missense mutation, D732Y, in exon 5 of the androgen receptor ligand-binding domain., Conclusion: To our knowledge, this is the first case report of CAIS in South Africa in which molecular genetic techniques were used to substantiate the clinical diagnosis. The findings in this study have implications for genetic counseling in this family.

This paper aims to examine the relative contributions made by alcohol and iron overload and hypovitaminosis C to the osteoporosis associated with African hemosiderosis. To characterize this bone disorder, we examined double-tetracycline-labeled iliac crest bone biopsies and serum biochemistry in 53 black male drinkers, 38 with (Fe+) and 15 without (Fe-) iron overload, and in controls. We reasoned that abnormalities found in both patient groups were likely to be caused by alcohol abuse and those found only in the Fe+ group to be caused by iron overload and hypovitaminosis C (iron/C-). The patient groups differed only with respect to greater erosion depth (p < 0.05) and abnormal markers of iron overload in the Fe+ group. Ascorbic acid levels were lower in the Fe+ group than in controls (p < 0.001). Bone volume and trabecular thickness were significantly lower in both patient groups compared with controls and therefore likely caused by alcohol. There were no positive correlations between formation and erosion variables in either patient group, which suggests uncoupling of formation from erosion, possibly as a result of alcohol abuse. Prolonged mineralization lag time associated with thin osteoid seams was found in 32% of patients, affecting both groups. This rules out osteomalacia and suggests osteoblast dysfunction, probably caused by alcohol. The number of iron granules in the marrow correlated with erosion depth (r = 0.373, p < 0.01), trabecular number (r = -0.295, p < 0.05), and trabecular separation (r = 0.347, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of magnesium sulphate (MgSO4) infusion on blood pressure and circulating venous catecholamine levels in 8 patients with severe gestational proteinuric hypertension is described. A significant fall in blood pressure was noted after MgSO4 infusion; the maximal fall in diastolic blood pressure correlated with the greatest rise in serum magnesium levels (P less than 0.04). No significant change was observed in mean venous plasma adrenaline or noradrenaline levels after MgSO4 infusion, although the mean dopamine concentration declined significantly. It is concluded that the decrease in systemic vascular resistance after MgSO4 infusion in gestational proteinuric hypertension is mediated predominantly by mechanisms other than a change in circulating catecholamine levels.

Since the platelets of patients with familial hypercholesterolaemia (FH) are hyperaggregable, the inhibitory effect of low-dose aspirin on platelet aggregation in response to adenosine diphosphate, collagen, adrenaline and arachidonic acid was tested in 9 young adult patients with FH and compared with that in 9 normal subjects. After a single oral dose (150 mg) of aspirin the degree of inhibition of platelet aggregation was the same in the two groups, as was the recovery time (in days) for full restoration of platelet aggregation . In a second experiment in which 162 mg aspirin was administered daily for 28 days, inhibition of platelet aggregation was sustainable in both the patient and the control groups. These results suggest that despite the recognized hyperaggregability of platelets from patients with FH, daily low-dose aspirin ingestion effectively inhibits their in vitro aggregation and may therefore prove beneficial as supplemental therapy to reduce the rate of myocardial infarction in this high-risk group.

Diabetes mellitus was induced in Lewis rats by streptozotocin, and these animals and control rats fed ad lib were studied after 7 weeks. At the time of sacrifice, nondecalcified histological sections of bone were prepared and subsequently quantitated by micromorphometric techniques. In addition, tibial alkaline phosphatase and mineral ash content were determined. The bones obtained from the diabetic animals are characterized by significant decrements in the quantities of osteoid and osteoclasts and by failure to acquire a tetracycline label. These histological features are attended by reduced quantities of urinary hydroxyproline and tibial alkaline phosphatase. As compared with control animals fed ad lib, diabetic rats are hyperphosphatemic and markedly hypercalciuric. Circulating alkaline phosphatase is also elevated and associated with a parallel increase in intestinal content of this enzyme. Although serum corticosterone levels are increased, diabetes is associated with decrements in both circulating immunoreactive parathyroid hormone and 1,25(OH)2D. We conclude that prolonged streptozotocin-induced diabetes mellitus in the rat results in reduced bone turnover. The relative roles that functional caloric deprivation, low circulating levels of 1,25(OH)2D, hypercalciuria, hypercortisolemia, and decreased blood parathyroid hormone levels play in the genesis of these skeletal abnormalities remain to be determined.

Alcohol may provoke reactive hypoglycaemia when drunk with a sucrose mixer ('gin and tonic') but does not do so when taken in the form of a starch-based beverage like sorghum beer. We examined the hypoglycaemic potential of bottled beer (Lion Lager; South African Breweries), which differs from sorghum beer in that it contains less carbohydrate (polysaccharides and simple sugars) and has a higher alcohol content. After an overnight fast 5 Black men each drank 2 litres of Lion Lager over an hour. Over the ensuing 5 hours their plasma insulin, glucose and alcohol concentrations were compared with the responses previously documented before and after consuming the same volume of sorghum beer or a 100 g control carbohydrate solution. Bottled beer elicited a prompt but short-lived rise in plasma insulin (mean +/- SEM, 37 +/- 7 mU/l at 1 hour), which was significantly greater than that produced by sorghum beer but less sustained than after drinking the control carbohydrate solution. After drinking bottled beer plasma glucose levels fell to a mean nadir of 3,6 mmol/l at 2 hours (compared with 5,4 mmol/l for sorghum beer), thereafter slowly returning to the basal value, while a substantial rise in the blood alcohol concentration occurred. We conclude that the development of alcohol-induced reactive hypoglycaemia is largely determined by the nature of the carbohydrate ingested together with alcohol.

The HLA A and B specificities in 72 Whites with type 1 or juvenile-onset diabetes mellitus (JOD), 53 Blacks with type 1 diabetes or JOD and 52 Blacks with type II or maturity-onset diabetes (MOD) were determined and compared with those in 278 Whites and 311 Blacks who were not diabetic. In Whites with JOD, frequencies of HLA A1 and B8 antigens were significantly increased, whereas those of the A3 and B17 antigens were reduced. Blacks with JOD had an increased frequency of HLA B8. By contrast, in Blacks with MOD the antigen frequencies were not significantly altered. The D-locus antigens Dw3 (DRw3) and Dw4 (DRw4), which bear the strongest associations with JOD in Whites, need to be examined in Black South African diabetics.

Cerebral deposits of choriocarcinoma tend to be multiple and usually result in a rapidly fatal course. Two patients presented with Jacksonian epilepsy due to metastatic choriocarcinoma in the brain. In the first patient, the diagnosis of metastatic choriocarcinoma was unsuspected, since curetted uterine material was normal, the haemagglutination inhibition test for pregnancy was negative and a chest radiograph was unremarkable. A diagnosis of choriocarcinoma was made by brain biopsy 2 days before death. The second patient had been previously treated with systemic chemotherapy (methotrexate and actinomycin D) for uterine and pulmonary choriocarcinoma associated with hyperthyroidism. Human chorionic gonadotrophin could not be detected in the urine when the patient presented with Jacksonian epilepsy. A brain scan showed multiple areas of increased uptake consistent with metastatic choriocarcinoma. She was treated with both systemic chemotherapy and intrathecal methotrexate and cranial irradiation. A complete remission was obtained. Intrathecal methotrexate and cranial irradiation appear to offer a hopeful new approach to the problem of metastatic cerebral choriocarcinoma.

This study comprised 100 white patients with primary hyperparathyroidism treated between 1975 and 1984. Of these, 75 attended Johannesburg Hospital and 25 were managed by private practitioners. The mean age was 56.4 +/- 1.4 years at the time of diagnosis. There were almost twice as many women as men. In patients attending Johannesburg Hospital there was a progressive increase in the detection rate after 1979, which corresponded with the introduction of automated multichannel serum analysis. The commonest major complications were renal stones (54%), renal insufficiency (27%), a history of skeletal fractures (12%), radiographic evidence of osteopenia (38%) and peptic ulcers (20%). Bone disease was particularly common in postmenopausal women (64%). Other notable features were the frequency of weakness and fatigue (40%) and hypertension (45%). Coincidental thyroid abnormalities were frequent (18%). Ninety-three patients were treated surgically; 76 (81.7%) had a single adenoma. Our findings are compared with those of other large series. This study indicates the need for a greater awareness of this condition and earlier diagnosis to forestall the development of its harmful complications, and for the collection of additional information from a prospective study.

Plasma insulin responses to a 4-hour glucose tolerance (100 g) were studied in urbanized Black people. Persons of normal weight without diabetes (12) and obese persons without diabetes (18) were compared with obese diabetics (19). Fasting serum ketone levels were measured, and the plasma potassium, triglyceride and growth hormone responses during the glucose tolerance test were determined. Obese subjects without diabetes had a twofold greater total plasma insulin response (area under curve) than their counterparts of normal weight, but there was a progressive fall in total plasma insulin response from subjects with mild diabetes (with fasting normoglycaemia) to those with severe diabetes (with fasting hyperglycaemia). The early plasma insulin responses of the group with mild diabetes were significantly impaired, and the peak response was only reached at 120 minutes. The subjects with severe diabetes had a flat insulin response curve. Fasting serum ketone levels were highest in the group with severe diabetes. The growth hormone responses were similar in all the groups. Plasma potassium and tryglyceride levels fell less during the glucose tolerance test in the group with severe diabetes than in the other three groups. These data indicate that insulin secretion is reduced in obese Blacks with chemical evidence of diabetes and this reduction becomes severe in the symptomatic diabetic.

Rats were semistarved over a 7-week period, resulting in a loss of 28.2 +/- 1.6% (SEM) of their initial body weights, while ad libitum fed controls gained 15.1 +/- 1.8% (SEM). Bone loss occurred and skeletal turnover was markedly reduced in the semistarved rats, as evidenced by a paucity of osteoid and osteoclasts, failure of the bone to assume a tetracycline label, and reduced urinary hydroxyproline excretion. Despite these changes, there were no alterations of serum or bone alkaline phosphatase activity with semistarvation, and analysis of tibial mineral content revealed reductions only in magnesium and sodium. The malnourished animals, however, were hypercalciuric and hypophosphatemic. Semistarvation had no effect on circulating levels of immunoreactive parathyroid hormone or 25-hydroxyvitamin D, but did result in reduced serum levels of corticosterone, insulin, and 1,25-dihydroxyvitamin D. Therefore, it appears that the effects of semistarvation on the rat skeleton are osteoporotic rather than osteomalacic, and that the defect is the consequence of reduced bone turnover. The contribution which the abnormalities of bone-regulating hormones play in the genesis of this skeletal lesion remains to be determined.

Hypokalemic paralysis and/or arrhythmia must be treated cautiously and replacement therapy given slowly. The differential diagnosis should include familial periodic paralysis, an autosomal dominant disorder, which may present as hypokalemia, normokalemia, or hyperkalemia.