Biomedical subjects

R Dillman

Publications and source records attributed to R Dillman.

4 recordsLinked to original sources

PubMed1998

Single-dose dexamethasone paclitaxel premedication.

Paclitaxel is one of the most active chemotherapy agents for the treatment of ovarian and other gynecologic cancers. Hypersensitivity reactions (HSR) remain one of the major clinical concerns in the use of paclitaxel. This report deals with 183 consecutive patients treated with paclitaxel chemotherapy. A total of 1010 cycles were administered. Premedication consisted of single-dose intravenous decadron, benadryl, and cimetidine administered immediately prior to chemotherapy. Four hypersensitivity reactions occurred. All patients recovered uneventfully from these reactions. Two of these patients received additional oral decadron followed by the standard premedication and were successfully retreated with multiple courses of paclitaxel therapy without reaction. Our findings confirm other reports that paclitaxel chemotherapy hypersensitivity reactions can be decreased with a single-dose intravenous decadron premedication regimen and that patients who do have paclitaxel HSRs may be safely retreated with paclitaxel.

Adult↗

PubMed1998

Length dependence of calcium- and force-transients in normal and failing human myocardium.

UNLABELLED: Two questions were analysed: (1) Is the Frank-Starling mechanism operative in failing human myocardium? (2) Are length-dependent changes in force accompanied by length-dependent changes in intracellular calcium transients in human myocardium? METHODS: (I) in electrically stimulated left-ventricular trabeculae [normal donor heart (NDH), n = 8; end stage dilated cardiomyopathy (DCM), n = 11], isometric force development was analysed as a function of muscle length (37 degrees C, oxygenated Krebs-Henseleit solution, supramaximal electrical stimulation, frequency: 1 Hz). (II) Myocardium from the same patients were loaded with the fluorescent dye FURA-2/AM for simultaneous measurements of intracellular calcium transient (ICT) and force development at different muscle lengths. Muscle length, resting force, developed force and intracellular Calcium ("ratio method") were monitored continuously. RESULTS: (I) developed force increased up to an optimum as a function of muscle length in NDH- and DCM-myocardium. The slope of this increase was flatter in DCM-myocardium (P < 0.01). (II) In NDH- and DCM-myocardium, diastolic and systolic calcium increased significantly with muscle length. With decreasing muscle lengths the ICT became broader, the diastolic decay was retarded and the peak of the ICT was flatter. At Lmax the calcium amplitude was 23% smaller in DCM than in NDH (P < 0.04). CONCLUSION: there is a clear length dependence of active force in DCM-myocardium. The length dependence of force development is associated with length-dependent modulations of the ICT. The flatter slope of the length-force curve in DCM may be partly explained by altered intracellular calcium handling in failing myocardium.

Calcium↗

PubMed1990

2' Deoxycoformycin (pentostatin) for refractory non-Hodgkin's lymphoma: a CALGB phase II study.

Seventy-six eligible patients with relapsed or refractory non-Hodgkin's lymphoma (NHL) were treated with 2'-deoxycoformycin (pentostatin) at a dose of 4 mg/m2 intravenously weekly for three weeks and then every other week for a minimum of five total treatments. All patients had measurable disease, near normal hematologic, renal, and hepatic function, and a performance status of 0 or 1. Severe hematologic toxicity was observed in 13% of patients; severe renal or neurologic toxicity was observed in less than 5% of patients. There were no treatment-related deaths. Objective therapeutic responses were seen in 16% of patients (five complete response [CR] and seven partial response [PR]). However, in three of the patients achieving CR and one patient achieving PR, dexamethasone was employed as an anti-emetic, making the response of these patients to pentostatin difficult to evaluate. There were eight responses (3 CR) in patients with diffuse histologies and four responses (2 CR) in patients with nodular or mixed histologies. Three responses were in patients with a T-cell phenotype. Three of five patients with diffuse well-differentiated lymphoma (IWF A) responded. We conclude that 2' deoxycoformycin is only minimally active at this dose and schedule against refractory or relapsed NHL. The possibility that low grade B- and T-cell malignancies are more sensitive to 2' deoxycoformycin deserves further investigation.

Aged↗

PubMed1988

Synergy between high-dose cytarabine and asparaginase in the treatment of adults with refractory and relapsed acute myelogenous leukemia--a Cancer and Leukemia Group B Study.

One hundred ninety-five adult patients with refractory or first relapse acute myelogenous leukemia (AML) were randomly assigned to receive high-dose cytarabine (HiDAC), 3 g/m2 as a three-hour intravenous (IV) infusion every 12 hours for four doses, followed by 6,000 IU/m2 asparaginase (ASNase) administered at hour 42, or HiDAC without ASNase. Treatment was repeated on day 8. The median patient age was 52 years. There was an overall superior complete remission (CR) rate for HiDAC/ASNase (40%) v HiDAC (24%), P = .02. Subset analysis according to prior response and age showed the following CR rates: 54% from HiDAC/ASNase treatment of refractory AML in patients less than 60 years, and 31% in patients greater than 60 years; CR from HiDAC in the same refractory groups were 18% (less than 60) and 0% (greater than 60); 37% from HiDAC/ASNase treatment of relapsed AML in patients less than 60 years, and 43% in patients greater than 60 years; CRs from HiDAC in the same relapsed groups were 33% (less than 60) and 21% (greater than 60). Toxicity in the two treatment arms was comparable and consisted primarily of leukopenia, thrombocytopenia, mild hepatic dysfunction, diarrhea, conjunctivitis and serositis, and hyperglycemia. There was only one case of transient cerebellar toxicity and no cutaneous toxicity. Median time to full hematologic recovery was 5 weeks. There was an overall survival benefit for patients treated with HiDAC/ASNase (19.6 weeks) compared with HiDAC (15.9 weeks), P = .046, primarily attributable to effects in refractory patients. Median time to failure for refractory patients who achieved CR was 38.5 weeks with HiDAC/ASNase, and 13.3 weeks for those treated with HiDAC. For relapsed patients in CR from HiDAC/ASNase the median time to failure was 17.7 weeks and 18.3 weeks for HiDAC. The overall 42% CR rate from HiDAC/ASNase v 12% from HiDAC in patients with refractory AML indicates that HiDAC/ASNase is not cross-resistant with standard-dose cytarabine (SDAC) and anthracyclines. We conclude that HiDAC/ASNase has substantial activity in poor-prognosis AML and that this combination warrants further trials in earlier stage disease.

Antineoplastic Combined Chemotherapy Protocols↗