[The relationship between tuberculosis, vitamin D, potassium and AIDS. A message for South Africa?]. / Die verwantskap tussen tuberkulose, vitamien D, kalsium en VIGS. 'n Boodskap vir Suid-Afrika?

The converging epidemics of tuberculosis and acquired immunodeficiency syndrome (AIDS) in the RSA and their expected catastrophic interaction afford an ideal opportunity for well-planned and essential research by clinicians, molecular biologists, epidemiologists and other health workers. The enigmatic relationship between tuberculosis, vitamin D and calcium is a field of study which should be considered urgently. An optimal vitamin D status not only assures sound calcium-phosphorus homeostasis, but is also essential for maximal immune competency. Hypovitaminosis D probably predisposes towards vulnerability to tuberculosis due to deficient monocyte-macrophage function. In contrast, hypervitaminosis D can correct this deficiency, but would do so at the cost of both B- and T-lymphocyte efficiency. One example of such a state is the endogenous over-production of activated vitamin D by gamma-interferon-activated monocytes, tissue macrophages and granulomatous tissue in tuberculosis. This would not only cause the coincidental hypercalcaemia, but may also complicate the effective co-ordination of monocyte-lymphocyte interaction and consequently compromise an appropriate immune response. It can reasonably be expected that the raised plasma interferon levels in the AIDS patient may trigger similar vitamin D-related pathophysiological processes. It is proposed that the ideal situation for enhanced vulnerability to tuberculosis in the AIDS patient will have been created if the known destructive effects of the human immunodeficiency virus on CD4-positive lymphocytes act synergistically with the vitamin D-mediated complications listed above.

Skin conditions in epileptics.

The prevalence of skin and mucous membrane conditions occurring in 173 epileptics between the ages of 6 and 19 years was compared with that of an age-matched group of 211 non-epileptics. The most frequently used anticonvulants, singly or in combination, were carbamazepine in 54.9%, phenytoin in 47.8%, barbiturates in 36.6% and ethosuximide in 11.2% of epileptics. The most frequent combination was phenytoin and carbamazepine in 14% of the males and 18.4% of the females. An increased prevalence of acne was found in epileptic females; 80.3% compared to 30.2% in non-epileptic females. Hirsutism was found in 43.9% of the female epileptics compared to 7.5% of the non-epileptic females. Of interest was the finding of punctate and linear scars on the dorsum of the hands of 27.7% epileptics compared to 3.8% non-epileptics. Both ephilides and naevocellular naevi occurred in 12.7% of the epileptics compared to 29.4% and 52.1% respectively of the non-epileptics. Leukonychia was also found more frequently in epileptics than in non-epileptics; 52% and 28.9% respectively.

Ethanol ingestion and the development of post-exercise ketosis in non-alcoholic human subjects.

Alcoholic ketosis occurs in alcoholics, who have been shown also to be more predisposed than normal to post-exercise ketosis (Chalmers, Sulaiman & Johnson, 1977). We therefore studied post-exercise ketosis in ten normal people who drank 1.6 mol ethanol at 18.00-21.00 h, and then did a 12 km walk at 07.00 h the next morning. (The timing of the alcohol ingestion was prompted by the finding that alcoholic ketosis usually develops after the blood ethanol concentrations have fallen to zero.) Ten subjects who had not drunk alcohol for 60 h, acted as controls. All subjects were observed till 16.00 h. The blood 3-hydroxybutyrate level rose from 0.034 +/- 0.006 to 0.336 +/- 0.073 mmol/l (P less than 0.001) during the 9 h observation period in the controls, and from 0.038 +/- 0.009 to 0.352 +/- 0.127 mmol/l (P less than 0.001) in the test subjects. The differences between the two groups are not significant. Plasma free fatty acid concentrations, and insulin/glucagon ratios of the two exercise groups did not differ significantly from each other, or from those of a sedentary group (n = 16). Acute ethanol ingestion (1.6 mol/person) therefore does not predispose normal, non-alcoholic subjects to ketosis, even when ketogenesis is further stimulated by exercise.

Beta-adrenergic blockade restores glucose's antiketogenic activity after exercise in carbohydrate-depleted athletes.

1. The development of post-exercise ketosis is not abolished by the ingestion of glucose immediately after exercise, despite inducing high insulin/glucagon ratios in the peripheral (and therefore by implication in the portal) blood. 2. To investigate the possibility of autonomic control of the liver influencing its sensitivity to the major counter-regulatory hormones, we administered 50 g glucose, either on its own, or together with 0.5 mg prazosine, 40 mg propranolol, or 15 mg propantheline, to forty-seven 48 h carbohydrate-starved athletes who had just run 25 km. 3. The blood 3-hydroxybutyrate concentration rose from 0.30 +/- 0.05 (mean +/- S.E. of mean) to 0.52 +/- 0.08 mmol/l with exercise, and then to 1.32 +/- 0.40 mmol/l at 6 h after exercise in subjects who had ingested only glucose after exercise. 4. The effects of prazosine and propantheline on the blood ketone body concentration at 2 h after exercise was not statistically significant. Propranolol, on the other hand, significantly lowered the blood 3-hydroxybutyrate concentration (compared with controls) to 0.09 +/- 0.03 mmol/l at 3 h (P less than 0.01), and 0.35 +/- 0.08 mmol/l at 6 h (P less than 0.01) after exercise. 5. The plasma insulin, glucagon, glucose and free fatty acid concentrations were unaffected by propranolol, indicating that the antiketogenesis was the result of a direct effect on ketone body metabolism. 6. Since beta-adrenergic blockade has not previously been shown to have antiketogenic activity, except in somatostatin-induced hyperketonaemia, it is concluded that its effectiveness in post-exercise ketosis can probably be ascribed to a functional hepatic insulin and glucagon deficiency.

Post-exercise ketosis in post-prandial exercise: effect of glucose and alanine ingestion in humans.

This study examined ketosis in response to 90 min of running before and after the ingestion of 50 g glucose or 50 g L-alanine in thirty-three athletes. Everyone ran 20 km at 07.30 h and then rested, while fasting, till 16.00 h. There were four test groups: 'glucose-before', 'glucose-after', 'alanine-before' and 'alanine-after' according to whether glucose or alanine was ingested at 07.00 h, or 09.00 h. Controls did not ingest either test substance. The control 3-hydroxybutyrate concentration rose from 0.23 +/- 0.03 mmol/l (S.E. of mean) at 07.00 h to 0.74 +/- 0.27 mmol/l at 12.00 h, and 0.94 +/- 0.33 mmol/l at 16.00 h. Glucose ingestion before or after exercise did not influence post-exercise ketosis significantly, despite high insulin: glucagon ratios, low free fatty acid concentrations and hyperglycaemia. Alanine significantly lowered the 3-hydroxybutyrate levels, especially after exercise (to 0.14 +/- 0.07 mmol/l at 12.00 h; P less than 0.05) despite reversed insulin: glucagon ratios. This suggests that hepatic responsiveness to portal hyperglycaemia and the main hormones of metabolism is altered immediately after exercise, presumably to promote muscle glycogen synthesis in preference to liver glycogen synthesis.