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Biomedical subjects

D S Harry

Publications and source records attributed to D S Harry.

13 recordsLinked to original sources
PubMed1992

Randomized comparison of cisplatin plus epirubicin or doxorubicin for advanced epithelial ovarian carcinoma. A multicenter trial.

Stage III and IV epithelial ovarian cancer patients were prospectively randomized to receive eight courses of 60 mg/m2 of cisplatin plus either 75 mg/m2 of epirubicin (62 patients) or 60 mg/m2 of doxorubicin (54 patients). Clinical response rates for cisplatin/epirubicin of 42% [15% complete response (CR) and 27% partial response (PR)] and for cisplatin/doxorubicin of 55% (24% CR and 31% PR) were not statistically different (p = 0.14). The negative second look rate was 35% (10/29) for cisplatin/doxorubicin and 17% (5/30) for cisplatin/epirubicin (p = 0.12). The progression-free interval for cisplatin/epirubicin (13 months) was not statistically different (p = 0.09) from that for cisplatin/doxorubicin (19 months). The median survivals for cisplatin/epirubicin (756 days) and cisplatin/doxorubicin (739 days) were similar (p = 0.70). Cardiotoxicity was greater for the cisplatin/doxorubicin group (p = 0.0003). With similar survival and less cardiotoxicity, the cisplatin/epirubicin regimen had the more favorable therapeutic index.

Adolescent↗
PubMed1988

Plasma lipid and lipoprotein response to carbohydrate feeding in cirrhotic patients.

Serum lipids and lipoproteins, and glucose and insulin, were measured after an overnight fast, and during 3 days of a eucaloric diet rich in carbohydrate, in 15 patients with cirrhosis and seven normal subjects. Following the high-carbohydrate diet triglyceride rose in all groups but the increase in cirrhotics was lower than in normals. In normals and in cirrhotics with good liver function most of the triglyceride increment was carried in VLDL; in cirrhotics with poor liver function only 31% of the increment was found in VLDL, and 56% in triglyceride-rich LDL. In an earlier study on fat feeding, our cirrhotic patients with poor liver function had an impaired chylomicron and VLDL response; they also carried most of the triglyceride increment in triglyceride-rich LDL. The markedly impaired response of triglyceride-rich lipoproteins to both carbohydrate and fat feeding suggests that sick cirrhotics may have a problem with storage of dietary energy and that this contributes to loss of their adipose tissue.

Adult↗
PubMed1979

Lecithin-cholesterol acyltransferase and the lipoprotein abnormalities of parenchymal liver disease.

1. Detailed studies have been made of the plasma lipoprotein abnormalities in parenchymal liver disease to test the hypothesis that the abnormalities would correlate with plasma lecithin-cholesterol acyltransferase (LCAT) activity. 2. When LCAT was high, very-low-density-lipoproteins (VLDL) were normal in composition and had a normal pre-beta electrophoretic mobility. When LCAT was low, VLDL concentrations were greatly reduced. 3. With high LCAT low-density lipoproteins (LDL) were normal. The LDL particles found with low LCAT activity were of normal size but of abnormal composition, being triglyceride rich and cholesteryl ester poor. Regardless of LCAT activity LDL were present in normal amounts. 4. High-density lipoproteins (HDL) were normal in composition and electron-microscopic appearance when LCAT activity was high. When LCAT activity was low HDL were abnormal in composition and 'stacked discs' were seen on electron microscopy. 5. These results suggest that low LCAT activity may be the cause of at least some of the lipoprotein changes of parenchymal liver disease.

Adult↗
PubMed1978

Lecithin--cholesterol acyltransferase and the lipoprotein abnormalities of obstructive jaundice.

1. We have studied the plasma lipoprotein abnormalities in obstructive jaundice to test the hypothesis that the abnormalities would correlate with plasma lecithin--cholesterol acyltransferase activity. 2. Very-low-density lipoproteins (VLDL) were normal in composition and had a normal pre-beta electrophoretic mobility when lecithin--cholesterol acyltransferase activity was high. When it was low VLDL had abnormal composition and ran in the beta position. 3. With high lecithin--cholesterol acyltransferase activity, low-density lipoprotein (LDL) was normal and cholestatic LDL (LP-X) was not found. With low lecithin--cholesterol acyltransferase activity up to three LDL fractions were found: (i) large triglyceride-rich particles, (ii) LP-X and (iii) a triglyceride-rich cholesteryl ester-poor particle of normal dimensions. 4. High-density lipoprotein (HDL) concentrations correlated with lecithin--cholesterol acyltransferase activity and HDL were normal in composition and electron-microscopic appearance when the activity was high. When lecithin--cholesterol acyltransferase activity was low HDL was abnormal in composition and 'stacked discs' were seen on electron microscopy as well as normal spherical particles. 5. These results suggest that low lecithin-cholesterol acyltransferase activity may cause at least some of the lipoprotein changes of obstructive jaundice.

Adult↗
PubMed1977

Screening for liver disease in vinyl chloride workers.

Following the occurrence of hepatic fibrosis and angiosarcoma in polyvinyl chloride autoclave workers, a screening programme was set up for workers at risk in a large production plant. There was no significant difference in liver function tests between workers and a control group of men in the same factory, not exposed to vinyl chloride. Four exposed workers out of 422 were found to have enlarged spleens compared with none out of 202 controls. Liver biopsies from selected cases showed no significant pathological changes, although there was minimal increase in portal tract and sinusoidal fibrosis in exposed workers.

Adult↗