Tetany in kala azar patients treated with paromomycin.

Paromomycin, an aminoglycoside, is known to cause several side effects like nephrotoxicity and ototoxicity like other aminoglycosides but tetany has not been reported. Three cases of tetany were detected in the patients of kala-azar treated with paromomycin. They were promptly treated with intravenous 10 per cent calcium gluconate and tetany was relieved immediately and treatment with paromomycin continued with oral calcium supplement. After completion of 21 days treatment with paromomycin patients' splenic aspirates were free of parasites. Paromomycin may cause temporary tubular damage leading to calcium wasting in urine and hypocalcaemia resulting in tetany. Prompt detection of symptoms and intravenous calcium gluconate treatment promptly reverse the situation.

A kala-azar control programme for remote tribal communities.

Indigenous people have been trained to provide a culturally appropriate kala-azar control programme for the tribal population of Sahibganj, Bihar, India. Cultural resistance to modern medicine has been overcome and the influence of village witch-doctors has been countered.

PIP: In the district of Sahibganj, Bihar, India, there were 23,670 new cases of kala-azar between 1985 and 1990. The Social Development Centre, Dumka, drafted an emergency plan as a solution. 30 village health workers attended a 3-day training course regarding how to administer sodium stibogluconate intramuscularly, spray DDT, conduct door-to-door surveys, and refer affected persons to health centers. Kala-azar awareness programs in the villages imparted information on the treatment and control of the disease explaining that the disease could not be controlled by witch-doctors. DDT was sprayed during January/February and May/June on the inner walls of houses and covered cowsheds in order to eradicate sandfly prevalence. Persons who had had fever for more than 3 weeks underwent examinations for total and differential counts of white blood cells, haemoglobin concentration, aldehyde test, and thick and thin blood smears for the detection of malaria parasites. Treatment consisted of sodium stibogluconate given intramuscularly at 20 mg per kg body weight daily for 20 days in new cases and for 40 days in relapsed patients, with a maximum of 850 mg. Clinical cure was achieved if patients became afebrile and their spleens returned to normal size. If no relapse occurred in 6 months, the patients were regarded as definitively cured. Of the 1640 treated patients, 1592 were cured, and of the 48 patients who relapsed and were treated again with a 40-day course of sodium stibogluconate, 8 relapsed a second time. 44 patients became unresponsive to sodium stibogluconate and were sent to hospitals for treatment. The spraying performed by the village health workers reduced the incidence of kala-azar and malaria in 3 villages, while increased numbers of cases were recorded in 1 village. Remote tribal areas need educative, preventive, and curative programs backed up by mobile hospitals carrying diagnostic and spraying equipment.

The Ayurvedic medicines Haritaki, Amala and Bahira reduce cholesterol-induced atherosclerosis in rabbits.

Four groups of 25 rabbits each, were studied to determine the effect of Haritaki (Terminalia chebula), Amla (Emblica officinalis) and Bahira (Terminalia belerica) on cholesterol-induced hypercholesteolaemia and atherosclerosis. The control group was fed with cholesterol alone; the Haritaki group received Haritaki and cholesterol; the Bahira group received Bahira and cholesterol; and the Amla group received Amla and cholesterol for 16 weeks. Cholesterolaemia was significantly less (P less than 0.001) in the Haritaki group (166 mg/dl), the Bahira group (240 mg/dl) and the Amla group (205 mg/dl) than in the control group (630 mg/dl). The Haritaki group had significantly less cholesterolaemia (P less than 0.001) as compared to the Bahira and Amla groups. Aortic sudanophilia was significantly less (P less than 0.001) in the Haritaki group (6%), the Bahira group (16%), and the Amla group (12%) than in the control group (38%). The cholesterol contents of the liver and aorta, respectively, were significantly less in the Haritaki group (46 mg/100 g, 28 mg/100 g), the Bahira group (78 mg/100 g, 72 mg/100 g) and the Amla group (46 mg/100 g, 42 mg/100 g), than in the control group (604 mg/100 g, 116 mg/100 g). Among the drug-fed groups, the Haritaki group had significantly lower degrees of sudanophilia and cholesterol content of aorta and liver (P less than 0.001) as compared to the Bahira and Amla groups. Although all three drugs reduced serum cholesterol, aortic sudanophilia and cholesterol contents of liver and aorta, their effects were in ascending order of magnitude. The drugs did not influence serum triglyceride levels, euglobulin clot lysis time or platelet adhesiveness.(ABSTRACT TRUNCATED AT 250 WORDS)

Emblica officinalis reduces serum, aortic and hepatic cholesterol in rabbits.

Emblica officinalis reduced serum cholesterol (p less than 0.001), aortic cholesterol (p less than 0.001) and hepatic cholesterol (p less than 0.001) significantly in rabbits. Emblica officinalis did not influence euglobulin clot lysis time, platelet adhesiveness or serum triglyceride levels.

Influence of linseed oil on cholesterol-induced atherosclerosis in rabbits.

Four groups of rabbits were studied to determine the effect of linseed oil on cholesterol-induced atherosclerosis. Group C received cholesterol alone; group CL received cholesterol and linseed oil, group L were given linseed oil alone, while group N were fed the normal stock diet for 18 weeks. Cholesterolemia was marked in groups C and CL but not in groups L or N. Cholesterolemia was significantly greater (P less than 0.001) in group CL (462 mg/dl) than in group C (318.6 mg/dl). Thus, the addition of linseed oil to cholesterol led to greater hypercholesterolemia than with the cholesterol diet alone. There was no significant change in the serum triglyceride level in either group. Atherosclerotic lesions (mostly fatty streaks but some fibrous plaques) were present only in groups C and CL and were absent in groups L and N. The percentage of atherosclerotic intimal involvement was significantly greater in group CL than C (P less than 0.001). The severity of atherosclerosis correlated with serum cholesterol levels (r = 0.79, P less than 0.001), but not with serum triglyceride levels.