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Biomedical subjects

A J Anand

Publications and source records attributed to A J Anand.

7 recordsLinked to original sources
PubMed1997

Radiation-induced red cell damage: role of reactive oxygen species.

BACKGROUND: Cellular blood components are irradiated to prevent graft-versus-host disease in transfusion recipients at risk for this syndrome. Because gamma radiation can result in the production of reactive oxygen species, the role of reactive oxygen species was investigated in radiation-induced red cell damage. STUDY DESIGN AND METHODS: Whole blood from normal donors was exposed to various doses of t-butyl hydroperoxide (0-1 mM) and/or to gamma-radiation (0-50 Gy). Oxidative damage was assessed by the extent of lipid peroxidation (measured by thiobarbituric acid-reactive substances [TBARS]) and hemoglobin oxidation. Fresh blood was divided into three parts-one initially irradiated and stored, another stored with portions irradiated weekly, and a third stored without irradiation. TBARS and hemoglobin oxidation were measured weekly. RESULTS: As expected, t-butyl hydroperoxide induced TBARS formation and hemoglobin oxidation in a dose-dependent fashion. The gamma-radiation not only increased hemoglobin oxidation and TBARS formation, but also enhanced the t-butyl hydroperoxide effect on red cells. Red cell storage increased TBARS generation and hemoglobin oxidation in a time-dependent fashion. When radiation was administered either initially or after weekly storage, TBARS production and hemoglobin oxidation were increased over that measured in unirradiated paired controls. CONCLUSION: Gamma radiation at clinically used doses increases lipid peroxidation and hemoglobin oxidation in human red cells. The effect of gamma-radiation is accentuated by blood storage and induces damage independent of time of storage.

Antioxidants↗
PubMed1996

Hepatocellular carcinoma in the United States. Prognostic features, treatment outcome, and survival.

BACKGROUND: The purpose of this study was to investigate prognostic factors at presentation and the survival of North American patients with hepatocellular carcinoma (HCC). METHODS: A retrospective analysis of medical records was performed for 314 patients identified through the Tumor Registry as having been evaluated for hepatocellular carcinoma at the Deaconess Hospital, Boston, Massachusetts, from 1986 through 1995. Clinical characteristics were noted, including age, sex, TNM staging, serum biochemistries, serum alpha-fetoprotein (AFP), patency of portal vasculature, cirrhosis, history of alcohol abuse, hepatitis-B or C positivity, hemochromatosis, treatment received, and ultimate survival from the date of diagnosis. RESULTS: Overall median survival was 10 months. The presence of cirrhosis, a history of alcohol abuse, low albumin, high bilirubin, abnormal AFP, and portal vein obstruction (PVO) were each associated with significantly shorter survival, as was advanced stage. Only albumin, AFP, and PVO were independent risk factors by multiple regression analysis. Patients undergoing surgery had the longest median survival (45 months), followed by those receiving chemoembolization (14 months). Those patients who were untreated or received systemic chemotherapy alone had significantly shorter survivals (2-4 months). CONCLUSIONS: Despite the difference in the underlying etiology of HCC in this population compared with Asian patients, poor prognostic indicators are similar. In this large series of patients at a single Northeastern hospital, analysis of presenting clinical characteristics was found to offer useful prognostic information.

Actuarial Analysis↗
PubMed1994

Salmonella osteomyelitis and arthritis in sickle cell disease.

Salmonellosis is one of the most frequent serious infections in sickle cell patients and remains a significant cause of morbidity and mortality in this population. Capillary occlusion secondary to intravascular sickling may devitalize and infarct the gut, permitting Salmonella invasion. Reduced function of the liver and spleen, together with interference with reticuloendothelial system function due to erythrophagocytosis, suppresses clearing of these organisms from the blood stream. Abnormal opsonizing and complement function probably also play a role. The expanded bone marrow with sluggish flow leads to an ischemic focus for salmonella localization. The majority of Salmonella infections in sickle cell patients involve bones (especially long bones) and joints and occur most frequently in early childhood. Multiple sites, often symmetrical, are usually involved. It is imperative to distinguish Salmonella osteomyelitis from bone infarctions. While clinical and hematologic data may be suggestive, radionuclide bone imaging studies, particularly combined technetium and gallium scintigraphy and technetium sulphur colloid bone marrow scans, and magnetic resonance imaging appear more sensitive and specific. Salmonella osteomyelitis is best managed medically. Chloramphenicol, ampicillin, and trimethoprim/sulfamethoxazole have been used most frequently; however, newer beta lactams and quinolones are more active. Septic arthritis carries a poorer prognosis and often requires aggressive surgical intervention.

Anemia, Sickle Cell↗
PubMed1994

Fluorouracil cardiotoxicity.

OBJECTIVE: To review the clinical manifestations, postulated mechanisms, and therapeutic implications of fluorouracil-induced cardiac toxicity. DATA SOURCE: A MEDLINE search was used to identify pertinent literature. STUDY SELECTION: Studies and case reports on fluorouracil cardiotoxicity were identified through a MEDLINE search. A manual review of bibliographies of identified articles was performed to ensure that all pertinent articles were included. DATA EXTRACTION: Data pertaining to all aspects of fluorouracil cardiac toxicity, including pathogenesis, predisposing factors, clinical manifestations, and therapeutic implications, were evaluated. DATA SYNTHESIS: Estimates from large series suggest a 1.6-2.3 percent incidence of clinically demonstrated cardiotoxicity. Predisposing factors include the presence of coronary artery disease and concurrent radiotherapy. Postulated mechanisms include direct myocardial ischemia, coronary spasm, or cardiotoxic impurities in fluorouracil formulation. Clinical manifestations include chest pain, nausea, diaphoresis with typical ischemic electrocardiographic (ECG) changes, relieved to normal after stopping the drug therapy. Nitrates and calcium-channel blockers do not protect against cardiotoxicity. CONCLUSIONS: Fluorouracil cardiotoxicity may be much more common and clinically significant than previously thought. A high index of suspicion for cardiotoxicity must be maintained when the drug is administered, especially in the presence of heart disease and concomitant radiation therapy. In the presence of chest pain, it is mandatory to stop the infusion and, if possible, to replace fluorouracil with another chemotherapeutic agent.

Chest Pain↗
PubMed1993

Newer insights into cisplatin nephrotoxicity.

OBJECTIVE: To review recent advances in the understanding of the mechanisms of cisplatin nephrotoxicity. Factors affecting this toxicity and agents that may protect against it are discussed. DATA SOURCES: A MEDLINE search was used to identify pertinent literature including reviews. A manual search of bibliographies was performed to include all articles on the subject. STUDY SELECTION: All available data relating to the mechanisms, modifying factors, and management of cisplatin nephrotoxicity were assessed. DATA EXTRACTION: As limited human data are available, all animal studies were included. Articles with hypotheses or suggestions not backed by scientific data were excluded from review. DATA SYNTHESIS: Cisplatin is one of the most effective agents available for treating a variety of solid tumors. Nephrotoxicity is the dose-limiting factor for the use of this drug. Mechanisms for renal toxicity range from definitive histologic changes found in the proximal convoluted tubules to physiologic and biochemical alterations involving a decrease in mitochondrial respiratory function, enzymatic activity in the respiratory chain and glutathione peroxidase, and effects on cellular calcium homeostasis. Important factors related to nephrotoxicity include age, renal irradiation, and concurrent alcohol intake. Agents that appear promising in attenuating the nephrotoxic effects of cisplatin include loading with NaCl solution and/or mannitol, sodium thiosulfate, WR 2721, glutathione, probenecid, and many other compounds under active investigation. CONCLUSIONS: Cisplatin is a nephrotoxic drug; however, agents that may make cisplatin therapy more safe and rewarding will be available in the near future.

Amifostine↗