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Biomedical subjects

Paulette Mehta

Publications and source records attributed to Paulette Mehta.

22 records · Page 2Linked to original sources
PubMed2002

Thalidomide in chronic graft-versus-host disease after stem cell transplantation: effects on quality of life.

Thalidomide is being increasingly used after stem cell transplantation as immunosuppression for patients with chronic graft-versus-host disease, as well as for antiangiogenesis effects in patients with multiple myeloma, brain tumors, leukemia, or other malignancies. The goal of this study was to determine if thalidomide improved the quality of life by virtue of its associated sleep-promoting, anxiety-reducing, antiwasting, and antidiarrheal effects. We therefore studied 28 patients with resistant chronic graft-versus-host disease who were treated with thalidomide (13 patients) or other immunosuppressive drugs (15) and compared them with healthy control subjects (16). All patients completed quality-of-life questionnaires prospectively before beginning regimens of thalidomide or other immunosuppressive drugs and completed similar questionnaires at 3- and 6-month intervals thereafter. The Transplant Symptom Frequency score was similar for healthy control subjects and both groups of patients with chronic graft-versus-host disease, regardless of whether they had received thalidomide or not. Quality of sleep was equally poor in patients who received or did not receive thalidomide. The most common complaint of patients with chronic graft-versus-host disease was fatigue, followed in frequency by overeating. The control group had similar concerns. This pilot study suggests that patients with chronic graft-versus-host disease have a quality of life similar to that of their health care workers, regardless of whether they are treated with thalidomide or other immunosuppressive drug, and that fatigue and overeating are the most common complaints.

Case-Control Studies↗
PubMed2002

Aspirin in the prophylaxis of coronary artery disease.

Aspirin has been used for more than 100 years, but its mechanisms of action have only been understood in the past 20 years. Aspirin interferes with arachidonic acid metabolism in platelets and endothelial cells and thereby reduces thromboxane A2 and prostacyclin. It also has other mechanisms of action, including anti-inflammatory roles, protection from oxidative stress, enhancement of fibrinolysis, and suppression of plasma coagulation and platelet-dependent inhibition of thrombin generation. It has been used for primary and secondary prevention of myocardial ischemia, and for primary and secondary prevention of cerebrovascular ischemia. We review the 5 pivotal studies relating to primary prevention for cardiovascular risk and the many studies relating to secondary prevention of myocardial ischemia. We also review the utility of aspirin in primary prevention of myocardial infarction and stroke. We conclude that aspirin is one of the most potent drugs ever discovered and that its effects extend well beyond those of cycloxoxygenase enzyme inhibition. Aspirin treatment does not preclude control of underlying and comorbid conditions such as diabetes mellitus, hypertension, and dyslipidemia. For most patients, a daily dose of 325 mg is optimal. Patients must understand the potential for gastrointestinal upset and hemorrhagic complications. The utility of aspirin is greater in coronary artery disease prevention than in cerebrovascular prevention.

Aspirin↗
PubMedDate not supplied

Differential toxicity of anthracyclines on cultured endothelial cells.

Anthracyclines are known for their endothelial toxicity. Newer derivatives may have fewer toxic effects on endothelium. The authors therefore evaluated the effects of doxorubicin, doxorubicin analogs (daunorubicin, idarubicin), and pegylated liposomal doxorubicin (doxil) in human coronary artery endothelial cells (HCAECs). Endothelial viability did not change significantly with doxil, but was decreased with doxorubicin, daunorubicin, or idamycin. Similarly caspase-3 activity was significantly elevated in HCAECs treated with doxorubicin, daunorubicin, and idamycin. In contrast, doxil did not cause significant increase in caspase activity. The authors also characterized the levels of antiapoptotic and prosurvival proteins using Western blot analysis. There was no significant difference in the expression levels of Bcl-2, Bax, and phospho-Akt in endothelial cells treated with anthracycline derivatives. However, the expression levels of Mcl-l protein were unaltered in endothelial cells treated with doxil but were significantly decreased when treated with other anthracycline analogs. Doxil minimally affected the expression levels of p53, whereas other anthracyclines induced p53 protein levels to a significant level, resulting in endothelial cell apoptosis. The authors conclude that the liposomal anthracycline protects endothelial cells from injury by preventing caspase-3 activation and maintaining the expression of antiapoptotic molecule Mcl-1.

Anthracyclines↗