PubMed Health⌕ Search

Biomedical subjects

R A Minow

Publications and source records attributed to R A Minow.

10 recordsLinked to original sources
PubMed1992

Clinical significance of antibodies to bovine and human thrombin and factor V after surgical use of bovine thrombin.

Two patients exposed during surgery to bovine thrombin developed antibodies reacting with both bovine and human thrombin and Factor V. Their thrombin times were markedly prolonged with bovine thrombin and modestly prolonged with human thrombin. High titer anti-bovine Factor V created diagnostic confusion in one patient by neutralizing bovine Factor V in a prothrombin assay substrate. Although weaker, antibody activity against human Factor V led to postoperative factor V deficiency in both patients. Such cross-reacting antibodies, recognizable by their higher titer against bovine than human Factor V, should be suspected when a patient surgically exposed to bovine thrombin develops a Factor V anticoagulant after operation. Crossed immunoelectrophoresis of adsorbed bovine plasma with each patient's plasma as antibody revealed many precipitin arcs indicative of immunization of the patients to additional proteins in a commercial thrombin preparation.

Aged↗
PubMed1978

QRS voltage change with adriamycin administration.

A decrease in the electrocardiographic limb lead QRS voltage of greater than or equal to 30% was highly correlated with the development of congestive heart failure in patients treated with adriamycin (ADM). It is felt that if a decrease in limb lead QRS voltage greater than or equal to 30% were detected in a patient receiving ADM, cardiomyopathy might be avoided or ameliorated by discontinuation of the drug.

Adolescent↗
PubMed1977

Adriamycin cardiomyopathy--risk factors.

The records of 53 patients treated with Adriamycin, 17 of whom developed congestive heart failure and 36 of whom received a similar total dose of Adriamycin without developing congestive heart failure, were analyzed for factors associated with Adriamycin cardiomyopathy. The risk of cardiomyopathy was significantly greater in patients who developed a larger than or equal to 30% decrease in limb-lead QRS voltage. Concurrent cyclophosphamide and mediastinal radiotherapy lowered the cumulative Adriamycin dose necessary for the development of cardiac toxicity. Uncontrolled hypertension also appears to be a risk factor in potentiating the development of Adriamycin cardiomyopathy at lower doses. Congestive heart failure was more likely to be fatal if it developed shortly after the last dose of Adriamycin. These findings can be utilized to increase the safety of Adriamycin therapy in the future.

Adolescent↗
PubMed1976

Clinico-pathologic correlation of liver damage in patients treated with 6-mercaptopurine and Adriamycin.

Eleven adults with refractory leukemia treated with a combination of 6-mercaptopurine and Adriamycin developed hepatic dysfunction manifested by elevations of serum total bilirubin, alkaline phosphatase, and glutamic oxaloacetic transaminase. Liver tissue obtained at necropsy showed intrahepatic cholestasis (eight cases), hepatocellular necrosis (ten cases), leukemic infiltration (two cases), and fatty change (nine cases). Neither this frequency nor severity of hepatocellular destruction has hitherto been associated with 6-mercaptopurine at the dose levels used in this study, nor has Adriamycin previously been found to be hepatotoxic. It is postulated that Adriamycin potentiated the hepatotoxicity of 6-mercaptopurine in these patients.

Adult↗
PubMed1975

Combination 6-mercaptopurine-adriamycin in refractory adult acute leukemia.

Remission induction therapy with 6MP and adriamycin in combination was administered to 19 adult leukemic patients refractory to previous therapy. Eight patients also received vincristine and prednisone. Thirteen patients had acute myelogenous leukemia, 3 undifferentiated leukemia, and 3 blastic transformation of chronic myelogenous leukemia. Four patients achieved remission but in only 2 were the remissions complete. Eleven patients failed to respond. Ten of the 19 patients developed unexpected severe liver toxicity manifested by a clinical picture of cholestasis (in the majority) or ascending cholangitis (in 2 patients). In the postmortem examination of 8 patients there was cholestasis and mild to severe hepatocellular damage in all.

Acute Disease↗
PubMedDate not supplied

Phase I-II evaluation of cyclocytidine.

A phase I-II study of cyclocytidine was conducted in 102 patients, 96 of whom had metastatic solid tumors and six of whom had acute leukemia. The drug was administered in 5- or 10-day courses of single daily iv or sc injections of 100-675 mg/m2 day. Two complete and six partial responses were observed in 64 solid tumor patients evaluable for response, 52 of whom had malignant melanoma or adenocarcinoma of gastrointestinal origin. The median duration of the responses was 6 months. An additional seven patients achieved stabilization of their disease for greater than or equal to 2 months. No responses occurred in six patients with acute leukemia. Side effects included nausea and vomiting, postural hypotension, and parotid pain, occurring in approximatley one third of patients receiving greater than 200 mg/m2/day. No myelosuppression was observed in six patients receiving 5-day courses of 100-200 mg/m2/day. Myelosuppressive toxicity became increasingly severe with doses greater than 200 mg/m2/day x 10, related at least in part to prior chemotherapy exposure including the nitrosoureas.

Adenocarcinoma↗