Tetsuro Hamamoto

Nonoxidative metabolism of ethanol in the pancreas; implication in alcoholic pancreatic damage

Alcohol dehydrogenase activity and fatty acid ethyl ester synthase activity were measured in various organs of male Wistar strain rats. The mean (+/- SE) values of alcohol dehydrogenase activity in liver, testis, pancreas and brain were 223 +/- 34, 35 +/- 13, 27 +/- 17 and 24 +/- 15 nmol/hr/mg protein, respectively, but not detectable in heart and skeletal muscle. Fatty acid ethyl ester synthase activity in pancreas, liver, testis and heart were 1348 +/- 263, 23 +/- 14, 17 +/- 3 and 2 +/- 1 nmol/hr/mg protein, respectively, but not detectable in brain and skeletal muscle. Alcohol dehydrogenase activity, fatty acid ethyl ester synthase activity, fatty acid ethyl ester content and amylase activity were measured in pancreas of rat after 7 weeks of ethanol feeding. Compared with control rats, ethanol-fed rats had normal fatty acid ethyl ester synthase activity and alcohol dehydrogenase activity. However, fatty acid ethyl ester content increased five-fold and amylase activity decreased up to 20% of the control group. Fatty acid ethyl ester content was inversely correlated with amylase activity. These results suggest that fatty acid ethyl ester may be responsible for the development of pancreatic damage by ethanol.

Marked Elevation of Serum CA19-9 and Stomach Carcinoma

Accessible online at: http://BioMedNet.com/karger Carbohydrate antigen 19-9 (CA19-9) is a tumor-associated antigen defined by a murine monoclonal antibody, NS 19-9, which was established from the colon cancer cell line SW1116 in 1979 by Koprowski et al. [1]. We concentrated on the fact that signet ring cell carcinoma of the pancreas in two cases manifested very high levels of carcinoembryonic antigen (CEA) despite the absence of hepatic metastasis [2]. We reported that a marked elevation of plasma CEA may contribute histologically to signet ring cell and/ or poorly differentiated adenocarcinoma of the stomach [3]. In a survey of plasma CEA in 300 cases of stomach carcinoma, we occasionally found a markedly elevated level of

Bleeding Risk Related to Upper Gastrointestinal Endoscopic Biopsy in Patients Receiving Antithrombotic Therapy: A Multicenter Prospective Observational Study

Background Although antithrombotic agents are widely used for cardiac and cerebrovascular disease prevention, they increase the risk of gastrointestinal (GI) bleeding. Objective To examine GI bleeding risk in association with an esophagogastroduodenoscopy (EGD) biopsy performed in patients without cessation of antithrombotic therapy. Methods This study was prospectively conducted at 14 centers. EGD biopsies were performed in patients receiving antithrombotic agents without cessation, as well as age- and sex-matched controls not receiving antithrombotic therapy. Patients treated with warfarin before the biopsy had a prothrombin time-international normalized ratio level <3.0. The proportion of GI bleeding events was compared between the groups. Results The patient group (n = 277) underwent a total of 560 biopsies while continuing antithrombotic therapy, of whom 24 were receiving multiple antiplatelet drugs, and 9 were receiving both antiplatelet and anticoagulant agents. The control patients (n = 263) underwent 557 biopsies. The upper-GI bleeding rate within 30 days after the EGD biopsy did not increase in patients without cessation of antithrombotic treatment, regardless of receiving single or multiple antithrombotic agents. Conclusions We found no significant increase in upper-GI bleeding risk following an EGD biopsy in patients taking antithrombotic agents, suggesting its safety without the need for antithrombotic treatment interruption.