The purpose of this study was to determine the incidence of hemorrhage due to vascular ectasia of the upper gastrointestinal tract in patients with liver cirrhosis and to assess the prevalence in cirrhotic patients without clinically overt gastrointestinal bleeding. Out of 96 cirrhotic patients with upper gastrointestinal bleeding, vascular ectasia was diagnosed in 6 patients (6.3%) as the cause of bleeding. These 6 patients had numerous spotty or confluent erythemas consisting of ectatic and tortuous capillaries throughout the antrutn and 4 patients required blood transfusion before diagnostic endoscopy. Several sessions of endoscopic electrocoagulation resulted in eradication of almost all the abnormal vascular lesions and marked improvement of their anemia without further transfusion. The procedure was well tolerated and no resultant complications were encountered. Among 206 cirrhotic patients without clinically overt gastrointestinal bleeding 25 patients (12.1 %) were diagnosed with vascular ectasia. The hemoglobin level was significantly lower in patients with vascular ectasia than those without vascular ectasia but the other features did not differ between the two groups. Vascular ectasia is an important cause of upper gastrointestinal bleeding and anemia in patients with liver cirrhosis. Endoscopic electrocoagulation may be a safe and effective treatment for controlling blood loss from gastroduodenal vascular ectasia in this subset of patients. (Dig Endosc 1999; 11 : 241-245)

We present a rare case of Peutz-Jeghers(P-J) syndrome in a 29-year-old woman who developed adenocarcinoma of the thyroid and polyps in the gastrointestinal tract. Polyps removed from the stomach, colon and ileum showed features typical of hamartomas. Histological examination indicated that the tumor resected from the right lobe of the thyroid was a papillary adenocarcinoma. This appears to be the first precise report of a P-J syndrome associated with thyroid carcinoma. This case adds an example of predisposition of P-J syndrome to extra intestinal malignancy and indicates the importance of long-term observation of malignancy.

No abstract

Twenty Syrian golden hamsters recieved weekly injections of pancreatic cancer inducing DHPN. Their Poly (U) specific serum RNase levels were significantly elevated when compared to the control levels. Following salt fractionation, Poly (U) specific activity was present in both the 40% and 50% salt saturated fractions. Tissue assays showed that Poly (U) specific RNase was present in both pancreas and liver tissue extract, although the liver tissue RNase had a different pH maximum than that of the serum RNase.

In December 1998, a 56-year-old Japanese man was admitted to our hospital exhibiting epigastralgia. The patient had been found to have asymptomatic proteinuria at an annual medical check-up and had complained of a dry mouth for several years, but did not visit a physician. He had no history of habitual alcohol consumption and no family history of pancreatic, renal or collagen diseases. On admission, physical examination was normal except for slight tenderness in the epigastrium. Enlarged superficial lymph nodes, ascites and peripheral edema were not detected. His laboratory data showed the following abnormalities: hemoglobin, 9.9 g/dL (normal 13-17 g/dL); lipase, 464 U/L (normal 8-49 U/L); serum amylase (Amy), 942 IU/L (normal 45-145 IU/L); serum creatinine (Cr), 3.5 mg/dL (normal 0.6-1.0 mg/dL); proteinuria and microhematuria (Table 1). Abdominal computed tomography (CT) (Fig. 1a) and ultrasonography (US) demonstrated a diffusely enlarged pancreas without localized pancreatic mass or para-aortic lymphadenopathy. Neither calcification nor cysts were detected in the pancreas. Endoscopic retrograde cholangiopancreatography (ERCP) revealed a diffuse narrowing of the main pancreatic duct with an irregular wall and an extrinsic compressive stenosis of the inferior common bile duct (Fig. 1b). The epigastralgia responded to 200 mg/day of Digestive Endoscopy (2001) 13, 94-98We recently encountered a 56-year-old Japanese man with pancreatitis who had hyperglobulinemia, was autoantibodypositive and responded to steroid therapy. The patient had been found to have asymptomatic proteinuria at an annual medical check-up and had experienced a dry mouth for several years. He was diagnosed as having Sjögren's syndrome indicated by the dry mouth and positive findings from a lip biopsy and a Schirmer's test. Tubulointerstitial nephritis, causing proteinuria, was verified by percutaneous renal biopsy. Antinuclear antibody was positive at the 1 : 160 titer. Serum g-globulin and IgG values were markedly increased, whereas complement components C3 and C4 were lowered. Abdominal computed tomography and ultrasonography demonstrated a diffusely enlarged pancreas without localized pancreatic mass or para-aortic lymphadenopathy. Neither calcification nor cysts were detected in the pancreas. Endoscopic retrograde cholangiopancreatography revealed a diffuse narrowing of the main pancreatic duct with an irregular wall. Wedged biopsy specimens of the pancreas by an exploration of the abdomen showed prominent lymphocytic infiltrates including some plasmacytes, as well as decreased exocrine parenchyma and inter-and intralobular fibrosis. These findings suggested a diagnosis of autoimmune-related pancreatitis. Steroid therapy was carried out with a marked improvement of his clinical symptoms and laboratory data.