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We report an 84-year-old man with perforation caused by emphysematous cholecystitis who showed flare on the skin of the right dorsal lumbar region and intraperitoneal free gas. The patient was admitted for abdominal pain, abdominal swelling, and consciousness disorder 18 days after the onset. Abdominal computed tomography (CT) revealed emphysema in the gallbladder and a small amount of intraperitoneal free gas. Intraoperative findings suggested gangrenous cholecystitis. The gallbladder wall was perforated, and an abscess involving the right subphrenic region, the periphery of the liver and gallbladder, and the right paracolonic groove, was detected. The flare on the body surface may have reflected abscess formation in the right abdominal cavity. Emphysematous cholecystitis induces necrosis and perforation in many patients, and immediate strategies such as emergency surgery are important.

SummaryMale Wistar rats received intraperitoneal injections of adriamycin (4mg/kg body weight/day) and/or riboflavin-butyrate (20mg/kg body weight/day) for 6 consecutive days. Cardiac mitochondria were then prepared for our present experiment. The combined use of riboflavin-butyrate with adriamycin was evaluated for reduction of lipid peroxide formation in rat cardiac mitochondria. In order to find the mechanism of the effect of riboflavin-butyrate, the glutathione peroxidase glutathione reductase system was examined. Adriamycin reduced the glutathione reductase activity in rat cardiac mitochondria, but did not affect the glutathione peroxidase activity. The mitochondrial content of flavin adenine dinucleotide, a prosthetic group of glutathione reductase, was greatly reduced and apoprotein of glutathione reductase also de creased. The administration of riboflavin-butyrate with adriamycin in creased flavin adenine dinucleotide and glutathione reductase activity. These results suggest that exogenous administration of riboflavin-butyrate is capable of reducing lipid peroxide by both enzymatic detoxification through glutathione reductase and non-enzymatic detoxification due to direct reaction with lipid peroxide.

This study attempted to elucidate the pathological role of peripheral blood polymorphonuclear leukocytes (PMNs) in the damage to hepatic sinusoidal endothelial cells (HSECs) in hepatic injury. Wistar male rats weighing about 200 g received a single injection of 1 g/kg body weight of galactosamine (GalN) intraperitoneally for the induction of hepatitis. The level of serum glutamic pyruvate transaminase activity increased time-dependently concomitantly with serum endotoxin level and hepatic lipid peroxide content. Histological studies using light and electron microscopy showed that a large number of PMNs infiltrated the midzonal area of the liver and that HSECs in contact with the PMNs were injured 6 h after GalN injection. Superoxide anion production by PMNs isolated from the peripheral blood of rats treated with GalN was increased significantly compared with that from control rats, as estimated by the reduction of exogenously added cytochrome c in the presence of phorbol myristate acetate. A cytotoxicity study using the 51Cr release assay revealed that PMNs isolated from GalN-treated rats caused more serious injury to the HSECs than those from control rats. These results suggest that the oxygen-derived free radicals released from the activated PMNs directly injure HSECs and lead to a disturbance of sinusoidal microcirculation, causing an extended liver cell necrosis in GalN hepatitis.

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