Insulin and somatostatin releasing islet cell tumor caused hypoglycemia.

We report a hypoglycemic case with normal insulin levels, which was caused by an islet cell tumor that was releasing insulin and somatostatin. A fasting test suggested the over secretion of insulin. Moreover, this hypoglycemia was enhanced by the inhibitory effect of somatostatin on the secretion of insulin counter-regulatory hormones, such as glucagon, in addition to the autonomous secretion of insulin from the tumor. In cases of hypoglycemia with apparently normal insulin levels, the measurement of somatostatin and various provocative tests are recommended. Arterial stimulation venous sampling (ASVS) was useful to detect the location of this functioning islet cell tumor.

[Three long surviving patients with gastric cancer metastasizing to the liver under interdisciplinary therapy].

In 30 patients with gastric cancer metastasizing to the liver over the past 15 years at our hospital the primary foci in the stomach could be resected in a curative manner. The authors report herein three long surviving patients in this series. [Case 1] A 49-year-old male. Distal gastrectomy was performed in November 1984. Metastasis to the liver occurred in June 1986. The right lobe of the liver was resected in November 1987 after transcatheter arterial embolization (TAE). Although hepatic arterial infusion chemotherapy was conducted, the cancer metastasized to the whole body, and the patient died in December 1991. [Case 2] A 65-year-old female. Distal gastrectomy was performed in July 1994. The left hepatic lobe and segment 5 in the right lobe were resected in June 1995. Although TAE was performed six times starting in December 1996, the patient died of hepatic failure in July 1999. [Case 3] A 73-year-old male. This patient simultaneously received distal gastrectomy and extended resection of the posterior hepatic segments in September 1997. Cancer recurred in the remaining liver in July 1998. Although microwave coagulation therapy (MCT) and TAE were performed, the patient died of hepatic failure in January 2000. In these patients who survived for a long period, the primary focus was well-differentiated adenocarcinoma under sufficient local control with metastasis limited to the nearest regional lymph nodes (group 1 lymph nodes). The patients could undergo interdisciplinary therapy, including hepatectomy, MCT, TAE, and hepatic arterial infusion chemotherapy.

Simple anti-reflux uretero-ileal anastomosis: an experimental study in dogs.

PURPOSE: To develop more simple and effective anti-reflux techniques applicable to the ileal reservoir, we examined the usefulness of a novel anti-reflux uretero-ileal anastomosis creating a flap valve mechanism. MATERIALS AND METHODS: Five dogs were used. A 4 cm. long ileal segment was isolated and its oral part (2.5 cm.) was detubularized. The detubularized ileal plate was anastomosed to the dome of the bladder. The left ureter was cut and its proximal end was spatulated and anastomosed end-to-side to the ileal plate. The end of the 1.5 cm. long afferent limb (non-detubularized part of the ileal segment) was closed and fixed down to the ileal plate to create an extramural tunnel. In this way, the reimplanted ureter was covered by the afferent limb. The dogs were evaluated between 3 and 4 months postoperatively. RESULTS: None of the 5 dogs used showed vesico-ureteral reflux or hydronephrosis. Histological examination showed an intact ureter enclosed with a normal ileal wall. CONCLUSION: Our proposed anti-reflux uretero-ileal anastomosis is simple and reliable. This technique may be suitable for applying to a urinary reservoir, especially as an alternative to the intussuscepted nipple valve.

A case of pill-induced esophagitis with mucosal dissection.

With the advance of gastrointestinal endoscopy, pill-induced esophagitis has been detected more frequently, but the association of mucosal dissection is rare. We reported a case of pill-induced esophagitis associated with mucosal dissection.A 66-year-old male with combined valvular heart disease was admitted for cardiac surgery. Cefotiam hydrochloride tablet was administered for postoperative wound infection of cardiac surgery. Next morning severe odynophagia and retrosternal pain were occurred. Upper gastrointestinal endoscopy performed 2 days after onset of the symptom showed detached mucosa at the upper thoracic esophagus and acute esophagitis at middle and lower thoracic esophagus. Histological examination of the mucosa revealed that the esophageal mucosa was detached from the lamina propria. After the treatment for esophagitis, almost normal esophageal mucosa covered the esophagus without scarring or stricture.The present case was diagnosed as cefotiam hydrochloride tablet induced esophagitis because of the onset of this disease. Mucosal dissection of the esophagus may be associated with both the esophagitis and bleeding tendencies caused by anticoagulant therapy.

Effect of an inhibitor of glucosylceramide synthesis on cultured rabbit skin fibroblasts.

1-Phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), an effective inhibitor of UDP-glucose:ceramide glucosyltransferase, caused growth inhibition of cultured rabbit skin fibroblasts in a dose-dependent manner. At 50 microM both threo and erythro isomers of PDMP completely suppressed the cell growth. Major gangliosides of the fibroblasts, GM3 and GD3, were greatly reduced in amounts in the presence of threo-PDMP and accumulation of ceramides was observed. Surface labeling with galactose oxidase and [3H]NaBH4 demonstrated that neural glycosphingolipids with four or more sugars present on the surface of control cells were not detectable when the fibroblasts were grown in medium containing threo-PDMP. Metabolic labeling of cellular glycosphingolipids with [14C]-galactose showed reduced incorporation of radioactivity into gangliosides and neutral glycosphingolipids when threo-PDMP was present in the medium. In contrast, the erythro isomer of PDMP did not affect the biosynthesis of glycosphingolipids, a result suggesting that the inhibitory effect of erythro-PDMP on cell growth was due to a mechanism other than the inhibition of glucosyltransferase.