No abstract

Apoptotic cell death in confluent Caco-2 cells was induced by acute and low concentrations of ethanol. These results suggest that clinically achievable doses of ethanol impair intestinal barrier function by induction of apoptosis in intestinal epithelial cells. This impairment of the barrier function would allow endotoxin to enter the circulation and evoke hepatic inflammation.

Ethanol-induced apoptosis was potentiated by physiological concentrations of estradiol, especially at the higher level which is found only in females. Our data suggest that enhanced ethanol-induced intestinal epithelial cell apoptosis in the presence of estradiol could cause greater intestinal permeability, which allows endotoxin to enter the circulation and eventually results in more severe ALD in females.

Although it has been demonstrated that acromegalic patients have an increased risk of neoplasms, especially colon neoplasms, gastric cancer with acromegaly is very rare--only five cases have been reported to date in Japan. We report here a rare case of gastric cancer with acromegaly in a 58-year-old woman, whose acromegalic change began at age 44. This patient showed typical clinical features of acromegaly, with increased concentrations of blood growth hormone (GH) and insulin-like growth factor I (IGF-I); she had four types of neoplasms; gastric cancer, colon tubular adenoma with moderate atypia, pancreatic mucinous cystadenoma, and subcutaneous lipoma. The gastric cancer was macroscopically 0-IIc type, 3.0 x 2.5 cm in size, and histologically diagnosed as a poorly differentiated adenocarcinoma with limited invasion of the mucosal layer. The previously documented stimulatory effects of GH and/or IGF-I on tumorigenesis and cell proliferation may have been responsible for the development of the multiple neoplasms in our patient.