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Biomedical subjects

D W Westring

Publications and source records attributed to D W Westring.

18 recordsLinked to original sources
PubMed1991

Eastern Cooperative Oncology Group study 1879: mitotane and adriamycin in patients with advanced adrenocortical carcinoma.

From November 1979 to July 1986, 52 patients (27 women and 25 men; median age 52 years) with advanced adrenocortical carcinoma entered a prospective, nonrandomized study evaluating moderate-dose mitotane and doxorubicin hydrochloride (Adriamycin). Thirty-two tumors (62%) were well differentiated and evidence of hormone production was present in 24 patients (46%). Patients with well-differentiated or functional tumors received mitotane, 6 gm daily; patients for whom mitotane failed or those with poorly differentiated, non-hormone-producing tumors received Adriamycin, 60 mg/m2 every 3 weeks. Initially, 36 patients were treated with mitotane and 16 patients with Adriamycin. Eight patients (22%) responded to mitotane and three (19%) responded to Adriamycin. No response was noted in the 15 patients for whom mitotane failed and who then received Adriamycin. Severe toxicity occurred in 36% of patients who received mitotane and in 26% who received Adriamycin. Overall median survival after onset of treatment was 14 months. We conclude that mitotane or Adriamycin used initially can induce tumor regression in about 22% and 19% of selected patients, respectively. However, Adriamycin is ineffective as second-line chemotherapy for patients with well-differentiated or functioning tumors for whom mitotane is ineffective.

Adrenal Cortex Neoplasms↗
PubMed1982

A case of leukemic reticuloendotheliosis responding to oxymetholone.

A 63-year-old man presented with fever, easy bruisability, splenomegaly and pancytopenia. Bone marrow aspiration was unsuccessful, and marrow biopsy revealed crowding by sheets of mononuclear cells; a diagnosis of leukemic reticuloendotheliosis (LRE) was made and the patient underwent splenectomy. There was no hematologic improvement, and the patient continued to have a significant requirement for erythrocytes and platelet transfusions. Within two months of beginning oxymetholone therapy (50 mg orally three times a day) the patient's platelet count had normalized, followed by improved erythrocyte and leukocyte counts. When the drug was discontinued, the peripheral blood counts deteriorated drastically; he again demonstrated hematologic improvement when oxymetholone therapy was reinstated. We feel that by demonstrating a hematologic response to oxymetholone, relapse when it was withdrawn, and another remission upon readministration, that we have provided stronger evidence than previously reported for the efficacy of this drug in LRE.

Adult↗
PubMed1980

A clinical and pathological study of adrenocortical carcinoma: therapeutic implications.

Twenty-one patients with adrenocortical carcinoma (ACC) diagnosed at three hospitals over a ten-year period were reviewed for clinical and pathologic features that might have therapeutic implications. Depending upon the extent of cellular pleomorphism, ACC could be defined as anaplastic or differentiated. Anaplastic ACC occurred more often in male patients, produced more frequent cutaneous metastases (P = 0.01), and was associated with a lack of clinical or laboratory evidence of hormone production (P = 0.01). In contrast, differentiated ACC usually occurred in women and produced clinical or laboratory evidence of hormonal excess. Median survival time of patients with anaplastic ACC was only five months, while median survival time of those with differentiated ACC was 40 months (P = 0.005). Patients with differentiated ACC survived for long periods, even with metastatic disease. Three of 5 such patients had objective responses to o,p'-DDD (Mitotane) therapy. The histopathology of ACC is an important prognostic factor and should be considered in the design of future therapeutic trials.

17-Ketosteroids↗
PubMed1975

"Cold" lesions on bone imaging.

Photon-deficient foci or "cold" lesions were demonstrated on 99mTc-polyphosphate bone imaging in eight individuals with various malignancies and one in sickle cell crisis. The bone radiographs of five of these persons failed to show corresponding bony changes at the time of the imaging. Most of the "cold" lesions observed on bone imaging were located in the denser and tubular bones. A postulate has been advanced regarding the factors that might influence the different gamma-imaging manifestations of radiographically demonstrable lytic lesions. The cases presented herein further emphasize the importance of recognizing the existence of "cold" areas in the images of bones and the need to place these in proper perspective when interpreting scans.

Adult↗
PubMed1970

Acetylsalicylic acid--induced hemolysis and its mechanism.

Acetylsalicylic acid (ASA) is known to cause severe hemolytic anemia in some glucose-6-phosphate-dehydrogenase-deficient (G-6-PD-deficient) individuals. To study its mechanism, erythrocytes from an ASA-sensitive patient were transfused into a normal compatible recipient. The administration of 2,5-dihydroxybenzoic (gentisic) acid, a known ASA metabolite with redox properties, to the recipient resulted in a marked decrease in the survival of the patient's erythrocytes. Similar studies with red cells from individuals with A- and Mediterranean variants of G-6-PD revealed no alteration in the erythrocytes' survival. Further studies disclosed that both salicylate and gentisate competitively inhibited the G-6-PD from the ASA-sensitive patient resulting in a marked change in the K(m) for NADP. These drugs also inhibited the A- and Mediterranean variants of G-6-PD. The magnitude of inhibition, however, was comparatively small and not different from that observed with a normal enzyme. The above studies suggested that enzyme inhibition by salicylate and gentisate may play an important role in ASA-induced hemolysis. Such an inhibition would further curtail NADPH regeneration, rendering the cells more vulnerable to oxidants. In this connection, gentisate seems to play a major role in ASA-induced hemolysis for it is both a G-6-PD inhibitor and an "oxidant."

Adolescent↗