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Biomedical subjects

P Mehta

Publications and source records attributed to P Mehta.

At least 253 records · Page 14Linked to original sources
PubMed1980

Ineffectiveness of laetrile in the treatment of acute lymphoblastic leukemia.

Much controversy remains over the use of laetrile in the treatment of leukemia. Public opinion has been responsible for several state legislatures enacting bills allowing the use of laetrile for patients with leukemia and other malignancies. We recently cared for a 3 1/2-year-old child with acute lymphoblastic leukemia, who had low initial white blood cell count, limited organomegaly, and absence of T or B cell markers. A good prognosis was anticipated. Conventional therapy was interrupted for long periods of time with laetrile. Laetrile was ineffective in maintaining or inducing remission. Despite favorable prognosis, the child developed several relapses and died with widespread infiltration of leukemia in the central nervous system, bone marrow and viscera.

Amygdalin↗
PubMed1979

Platelet function studies in coronary artery disease. V. Evidence for enhanced platelet microthrombus formation activity in acute myocardial infarction.

Circulating platelet microthrombi were evaluated during the acute and convalescent phases of illness in 44 patients admitted to the hospital for chest pain. Similar studies were performed in 10 healthy volunteers and 6 patients with infection. Circulating platelet microthrombi were significantly increased during the acute phase in 22 patients with transmural myocardial infarction compared with values in the other 22 patients without myocardial infarction, the healthy volunteers and the patients with infection alone. This increase in circulating platelet microthrombi declined to normal levels by the 7th hospital day in all but two patients who had evidence of extension of myocardial infarction and died. In contrast, circulating platelet microthrombi were similar in acute and convalescent phases of patients with chest pain but without myocardial infarction and were comparable with values in healthy volunteers. This study suggests that increased circulating platelet microthrombi may be related to tissue necrosis associated with transmural myocardial infarction.

Acute Disease↗
PubMed1979

Platelet function studies in heart disease. VI. Enhanced platelet aggregate formation activity in congestive heart failure: inhibition by sodium nitroprusside.

We studied 11 patients with congestive heart failure and 10 normal volunteers for in vivo platelet aggregate formation activity. The patients with heart failure had significantly (p less than 0.01) more circulating platelet aggregates than the normal volunteers. During sodium nitroprusside infusion, the number of circulating platelet aggregates declined to normal levels and in vitro platelet aggregation responses to epinephrine and adenosine diphosphate were also suppressed significantly (p less than 0.01). This was associated with a 30% decline in systemic vascular resistance and a 28% increase in cardiac output. In other in vitro experiments, sodium nitroprusside was found to have direct, dose-related platelet aggregation inhibitory actions. This study suggests that an increase in vascular resistance in certain heart failure patients may in part be related to an increase in circulating platelet aggregates. Direct inhibition of platelet aggregation by sodium nitroprusside may be a mechanism of its beneficial effects in heart failure.

Adult↗
PubMed1978

Differences in platelet aggregation in coronary sinus and aortic blood in patients with coronary artery disease: effect of propranolol.

Platelet aggregation was studied in aortic and coronary sinus blood samples obtained from 18 patients with coronary artery disease (CAD). Using epinephrine and ADP as aggregating agents, platelet aggregation was lower in coronary venous blood than in aortic blood. In nine patients on long-term propranolol therapy, platelet aggregation was lower in both aortic and coronary venous blood compared to the nine patients not taking propranolol. Four other subjects without angiographic evidence of coronary disease exhibited no difference in platelet aggregation in aortic and coronary sinus blood. These data suggest that platelet aggregation is lower in the coronary venous blood of certain patients with coronary disease and chronic propranolol treatment may reduce aggregation in both aortic and coronary sinus blood.

Adult↗
PubMed1978

Platelet aggregation studies in coronary artery disease. Past 4. Effect of aspirin.

We evaluated platelet aggregation in vitro in blood samples drawn simultaneously from aorta and coronary sinus. Platelet aggregation was significantly lower in the coronary venous blood than in the aortic blood in patients with coronary artery disease. Lower platelet counts were also observed in coronary venous blood. No such differences were seen in subjects with normal coronary arteries. Oral administration of aspirin eliminated the differences in platelet aggregation and counts across the myocardial vascular bed. These observations suggest that platelet sequestration in the myocardial vasculature may be related to the presence of disease in the coronary arteries.

Adult↗
PubMed1978

Platelet aggregation in aortic and coronary venous blood in patients with and without coronary disease. 3. Role of tachycardia stress and propranolol.

We studied 16 patients with coronary artery disease (CAD) to evaluate platelet aggregation in blood samples withdrawn simultaneously from the aorta and coronary sinus. At rest, mean platelet aggregation in coronary venous blood was significantly lower than that in aortic blood. Platelet counts in coronary venous blood were also lower than in the aortic blood in each of the six CAD patients in whom counts were done. Platelet aggregation was lower in seven patients who were taking propranolol than in the remaining nine who were not taking propranolol. During tachycardia stress, platelet aggregation increased in all patients, but the magnitude of increase was greater in patients not taking propranolol. In four other patients without CAD, platelet aggregation and counts were also studied in the same fashion and were similar in both the aortic and coronary venous blood. These data suggest that in certain CAD patients, platelet consumption or destruction within atherosclerotic vasculature may occur. Propranolol may reduce platelet aggregation at rest and modify excessive aggregation during tachycardia stress in certain CAD patients.

Aorta↗