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Publications and source records attributed to P J Mehta.
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Obesity is known to be associated with diabetes, hypertension and hyperlipidemia in the majority of the patients. There could be inaccuracy in measuring the blood pressure in obesity, therefore a cuff of sufficient size is important in blood pressure measurement. All parameters of obesity have been found to have a correlation with hypertension and it has been suggested that change in weight would cause a change in blood pressure. A weight reduction of 12 kg results in a blood pressure fall of 21/13 mm Hg. Such changes in blood pressures have been noted in untreated hypertensives. A few studies have negated the role of change in weight to have any influence on hypertension. Obesity causes a higher cardiac output and higher blood volume leading to hypertension. There may be increased intracellular sodium and reduced sodium-potassium-ATPase activity in obesity which causes increased sodium loading in hypertension. Abnormalities related to the insulin-carbohydrate metabolism and the renin-angiotensin aldosteron system have also been demonstrated in obese patients. Weight reduction also causes reduced dietary salt intake and diminished sympathetic activity. The benefits of weight reduction appear to be directly related to the amount of weight lost.
This is an analysis of 42 adult patients with 97 episodes of thrombophlebitis following 167 venepunctures. Almost all commonly used fluids had contributed to the development of thrombophlebitis. The observations showed significantly higher chances of development of thrombophlebitis with the quantity of fluids more than 2500 ml. (chi 2 = 15.50, P less than 0.001), autoclaved containers (chi 2 = 5.5, P less than 0.05) use of rubber tubing for infusion set (chi 2 = 4.7, P less than 0.05) and infusion rate more than 20 drops per minute (chi 2 = 15.25. P less than 0.001). Average time interval between beginning of IV infusion and development of thrombophlebitis was found to be 18 hours and average extent of thrombophlebitis was 7 cm. The commonest micro-organism isolated from needles was Pseudomonas aeruginosa.
An unusual case of right atrial myxoma who had a ten year symptom free interval, following the initial manifestation is presented.
Hypertension is a complex, heterogeneous disorder of which the exact etiology is unknown. The difficulty in ascribing an independent role to a single dietary constituent in blood pressure regulation may be due to interactions among nutrients which influence blood pressure. The effect of any one nutrient, particularly magnesium, on hypertension should be considered within the context of overall nutrition in each patient. Clinical, experimental and epidemiologic studies support the role of magnesium in hypertension, whereas a few studies negate this role. Magnesium ions are important in arterial smooth muscle contraction. Since magnesium is found mainly at the inner surface of the cell membranes, it could play a role in cell membrane permeability for sodium and calcium which is important in the etiopathogenesis of hypertension. Magnesium deficiency can predispose to increased contractility of the arteries and its excess can modulate smooth muscle contractility caused by bradykinin, angiotensin II, serotonin, prostaglandins and catecholamines. Magnesium therapy can prevent the development of resistant hypertension and arrhythmias in hypertensives with diuretic-induced hypomagnesemia. It might also reduce blood pressure at least up to 10/5 mm Hg provided adequate magnesium salts are given for an adequate period of time. In view of the still ill defined role of magnesium in hypertension, magnesium supplementation is advised only to those hypertensives who are receiving diuretics and develop resistant hypertension or who have frank magnesium deficiency. A diet rich in magnesium may be used for prevention of hypertension in predisposed communities because of the other advantages of such a diet in prevention.
A rare form of plasma cell dyscrasia, primary plasma cell leukemia is presented. The clinical picture resembled an acute leukaemia with a fulminant course and a rapidly fatal outcome.
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Albert Szent-Gyorgyi around 30 years ago proposed that "ions were the powerful tools of life as it developed in oceans". The purpose of this fundamental concept was to divert the attention of investigators towards the basic role of cations such as Na, K, Ca and Mg in muscle contraction. There is now sufficient evidence to support this prediction. Until recently the strongest evidence pointed to a positive relationship between raised Ca and blood pressure. More recent evidence claimed that increased dietary Ca can lower blood pressure and populations taking lowered dietary Ca, have a higher incidence of hypertension. It has been suggested that in susceptible persons, in the presence of high Na intake, Ca accumulation in the arterial cell becomes rapid due to impaired Na-Ca exchange causing an early rise in blood pressure. This is possibly due to abnormal handling of Ca by the smooth muscle cells in most forms of hypertension. Clinical experimental and epidemiologic studies showed that Ca not only mediates arterial smooth muscle contraction but excess of Ca can also cause an increase in peripheral vascular resistance leading to essential hypertension. Ca entry blockers such as verapamil and nifedipine which reduce the influx of Ca into the arterial smooth muscle cell have been successfully used in the management of these patients. The effect of Ca on blood pressure could be independent of other factors. Recent studies strongly favour a significant relationship between raised serum Ca and high blood pressure. Such a relationship has also been described between dietary Ca, 24 urinary Ca and high blood pressure. A large number of studies, particularly from the USA, contradicting the above view, suggest that the rate of Ca flux rather than the absolute quantity that enters the cell, is the deciding factor in arterial smooth muscle contraction. These investigators in the last 6 years have studied a large area of north America and suggested that Ca deficiency rather than an excess is the cause of hypertension. Persons consuming less than 300 mg Ca per day have 11-14% risk of developing hypertension compared to person taking 1200 mg per day of dietary Ca and exposed to only 3-6% risk.(ABSTRACT TRUNCATED AT 400 WORDS)
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A multichannel continuous-flow apparatus for dissolution rate measurements is described. Typical data are presented to demonstrate its utility for studies with bulk drug powders as well as with tablets and capsules without any change of setup. Procedures are given for the preparation of powder samples for dissolution studies and for a simple method of changing pH for "retard" tablets. The precision in dissolution rates obtained with this apparatus and method is 1-10% mean RSD. The advantages of the method are flexibility, reproducibility, and ability to obtain data in integral or differential form.
To study the role of diet in cardiovascular risk-factor intervention, 458 high-risk individuals were asked to eat for either a cardiovasoprotective diet (group A, n = 228) or their usual diet (group B, n = 230) in a randomized single-blind fashion. Ages varied between 25 and 63 yr, and 414 were men. Group A received significantly more calories in relation to the amount of complex carbohydrates, vegetable proteins, polyunsaturated fats, fiber, potassium, magnesium, and vitamin C and fewer calories in saturated fat and cholesterol compared with group B. Age, risk factors, nutritional factors, complications, and laboratory data were similar at entry to the study. Dietary adherence was obtained by questionnaire. After 1 yr, there was a significant (P less than 0.02) decrease in total risk factors (32.0%) in group A compared with group B, and 1-yr mean serum cholesterol was significantly lower than the initial mean cholesterol in group A. There was a significant (P less than 0.02) decrease in total complications (38.3%) in group A compared with group B in association with a significant (P less than 0.02) decrease in cardiovascular end points (38.3%), including postexercise electrocardiographic changes, fatal and nonfatal myocardial infarction, and sudden death. Overall mortality and mortality due to ischemic heart disease was less in group A (8 and 3.5%) than group B (11 and 4.8%). However, because of the few cases, differences were insignificant. It is possible that diet causes a significant reduction in blood cholesterol and modification of other risk factors leading to a decrease in complications and cardiovascular end points in patients with risk factors of coronary heart disease.
Recent studies show that diet and aspirin therapy inhibit platelet aggregation and may independently reduce complications and mortality in patients after acute myocardial infarction (AMI). To compare the effects of diet and aspirin, 140 patients, who were 4-6 wk post acute myocardial infarction, were assigned either to Group A (placebo with cardiovasoprotective diet) or Group B (aspirin [180 mg daily]) with fat-modified control diet in a single-blind controlled fashion. Of the 140 patients, 7 left the trial before it was completed. Of the remaining 133 patients, 68 in Group A and 65 in Group B were followed for one year. When the study began, the following factors were comparable for both groups: mean age, sex, risk factors, complications of myocardial infarction, electrocardiographic changes, and laboratory data. Group A received a significantly higher caloric intake (P less than 0.02) from complex carbohydrates, vegetable proteins, polyunsaturated fats, and larger amounts of dietary fibers, potassium, magnesium, and vitamin C compared with Group B, which received significantly larger amounts of saturated fats and cholesterol (P less than 0.01). The rehabilitation program, which included reduced smoking, increased exercise and drug therapy, was comparable in both groups. After one year, mean serum cholesterol (223.2 +/- 32.0 mg/dl) and triglyceride (156.2 +/- 13.5 mg/dl) levels in Group A, but not in Group B, were significantly (P less than 0.02) lower compared with mean serum cholesterol (241.2 +/- 39.5 mg/dl) and triglyceride (175.5 +/- 18.5 mg/dl) levels at the beginning of the study.(ABSTRACT TRUNCATED AT 250 WORDS)
Weight reduction by a low-energy diet and a high-polyunsaturates-, fiber- and potassium-rich diet may be independently useful to hypertensives. To study the effect of such diets, 416 hypertensives were randomized to either a low-energy cardiovasoprotective (CVP) diet (Group A; n = 106), a low-energy usual diet (Group B; n = 104), an optimal-energy CVP diet (Group C; n = 104), or an optimal-energy, usual pre-experimental diet (Group D; n = 102) plus drug therapy in a single-blind and controlled fashion. Groups A and B received significant (p less than 0.02) fewer calories per day than Groups C and D. Groups A and C also received significantly (p less than 0.02) more calories per amount of complex carbohydrates, polyunsaturates, potassium, and magnesium than did Groups B and D. Dietary compliance and drug intake was checked weekly. After 3 months, there was a significant fall in mean serum cholesterol (p less than 0.01) and mean serum triglycerides (p less than 0.05) in Group A compared with Group D. Group A and B patients had a loss of around 10kg of mean body weight, with no weight change seen in Group D. Weight loss was associated with a significant fall in systolic and diastolic pressures in both Group A (22/18mmHg) and Group B (16/13mmHg) compared with Group D at the end of the study. Group C patients also showed a significant fall in pressure (13/10mmHg) compared with Group D. Drug therapy, exercise, and salt intake were similar in all the groups.(ABSTRACT TRUNCATED AT 250 WORDS)