Hypercalcaemia in active pulmonary tuberculosis

This study was done on 86 patients with active pulmonary tuberculosis. Hypercalcaemia was found in 26 patients. The majority of cases [75.2%] has mild rise in the calcium. Hypercalcaemia was detected on presentation in 18 patients and developed in 8 others two weeks after starting antituberculous chemotherapy. Moreover, hypercalcaemia was more frequent in patients older than 50 years [P< 0.05], but this did not correlate with the extent of the disease shown on radiological pictures. Serum calcium was reverted to normal spontaneously two to four months following the start of antituberculosis treatment. The prevalence of hypercalcaemia inspite of absence of vitamin D supplements support the view that vitamin D intake does not play a major role in inducing hypercalcaemia in patients with active pulmonary tuberculosis. We suggest that this may be the result of the tuberculous process as it cleared with continuation of chemotherapy

Echocardiographic detection of cardiac involvement in chronic renal failure

Echocardiography was performed for 57 male uraemic patients with no apparent coronary artery disease, pericardial effusion, valvular heart disease or heart failure. 38 patients were on maintenance haemodialysis of varying duration [from 4 to 50 months], their ages ranged from 21 to 60 years. The remaining 19 patients have been on medical treatment. Their ages ranged from 20 to 60 years. 20 healthy subjects age and sex matched were studied as controls. Six patients [15.8%] of the study group had completely normal echocardiogram. Five patients [13.15%] on regular haemodialysis had pericardial effusion, whereas two patients [10.53%] of medical treatment group had pericardial effusion. 84% of haemodialysis patients had abnormal left ventricular function with one or more abnormal echocardiographic parameters. The significant abnormalities were symmetric septal hypertrophy [40 patients], reduction of myocardial contractility [26 patients], enlargement of left ventricular cavity [18 patients] and thickening of left ventricular posterior wall [12 patients]. Similar findings were present in 11 of the 18 undialyzed uraemic patients. Five of the 38 patients on regular hemodialysis [13.2%] showed the typical picture of congestive cardiomyopathy. Their clinical data were not different from other patients in this study. Moreover, calcified mitral valve was observed in three patients [7.9%] and dilated aorta in two patients [5.3%] of dialyzed group. Also, it was observed that patients who had been on dialysis for a longer period had less cardiac abnormalities, suggesting that chronic dialysis might reverse these changes. In conclusion, the cardiac involvement in chronic renal failure [CRF] is suggested to be due to a specific uraemic cardiomyopathy. As hemodilysis gradually reverse the haemodynamic changes to normal. Moreover, echocardiography was more sensitive than chest X-ray and ECG in detecting clinically unsuspected cardiac abnormalities and provides useful information in the overall evaluation of cardiac function in uraemic patients

High density lipoprotein subfractions and apolipoprotein-A1[Apo-A1] In chronic hemodialysis patients

Cholesterol content in high density lipoprotein [HDL] subfractions and the serum concentration of opoprotein A-1 [Apo-A1] have been studied in 32 patients at the end stage of chronic renal failure [CRF] undergoing haemodialysis. High density lipoprotein-cholesterol [HDL-C] subfractions were significantly decreased in the patient's group compared to the control group. However, serum concentrations of Apo-A1 were not significantly different. The raised Apo-A1/HDL2 cholesterol ratio in the patients group suggests the existence of qualitative changes in HDL subfractions in patients with CRF receiving haemodialysis. The abnormalities in the relative composition of HDL subfractions could play an important role as a cardiovascular risk factor in patients with CRF undergoing haemodialysis

Clinical and electrophysiological studies in diabetic peripheral Neuropathy

This work was done to study the clinical sensory findings and to investigate the influence of hyperglycaemia on nerve sensory conduction. A group of 120 maturity-onset diabetic patients [86 females and 34 males] and 30 normal control subjects were studied. The patients were classified into two groups according to whether they had diabetic neuropathy [32 patients] or not had [88 patients]. The modalities of light touch and vibration sense were the most frequently diminished, two-point discrimination was less frequently affected and proprioception was rarely affected. Sensory nerve conduction velocity of median, ulnar and sural nerves, using the antidromic technique, was significantly [P < 0.001] slowed in the diabetic patients compared to controls. Levels of fasting plasma glucose as well as levels of glycosylated haemoglobin, and index of long-term glycaemia, were correlated with slowing of sensory conduction velocity of the tested nerves. These associations could not be explained by patient age or duration of diabetes. These findings suggest that the degree of hyperglycemia of maturity-onest diabetes contributes to the sensory nerve abnormalities in this disease. We can conclude that sensory nerve conduction parameters are the objective criteria for peripheral nerve involvement. It tends to be impaired in diabetics even those without clinical evidence of neuropathy. Moreover, the sensory nerve conduction parameters are probably the most sensitive index of peripheral neuropathy in diabetic patients. The present study also concluded that altered nerve metabolism associated with hyperglycaemia may contribute to the distal sensory polyneuropathy of diabetes. This support the hypothesis for the existence of endoneurial oedema and hydration of peripheral nerves secondary to overactivity of aldolase reductase pathway. These structural changes are recently quantitatively defined by magnetic resonance proton image. This increased level of peripheral nerve water represents a new finding in the development of diabetic neuropathy. Treatment with an aldolase reductase inhibior is a prospect which might halt, if not reverse, the development of diabetic neuropathy