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A 63-year-old woman who presented with chest and back pain underwent an upper gastrointestinal endoscopy which revealed elevated legion in the antrum mucosa. Histologic examinations of gastric biopsies were showing monoclonal proliferation plasma cells containing Russell bodies. Differential diagnosis from B-cell lymphoma and plasmacytoma is difficult, because of monoclonality. Molecular analyses of immunoglobulin heavy chain (IgH) gene demonstrated that gene rearrangement was negative. Thus, diagnosis of Russell body gastritis was made. The Giemsa stains were also showing infection of Helicobacter pylori (H.pylori). After eradication therapy for H.pylori, follow-up upper gastrointestinal endoscopy was performed. She then recovered.

A 17-year-old girl who had right lower abdominal pain with multiple swelling of lymph nodes in the ileocecal region and she was admitted to a neighboring hospital. Since there was no improvement of condition with antibiotic resistance, we were consulted. Lymph node biopsy under laparoscopy demonstrated nonspecific findings. She then developed erythema nodosum, suggesting the presence of autoimmune etiology. Treatment with systemic corticosteroid resulted in symptomatic improvement. Mesenteric lymphadenitis like this case is rare.

Perforated duodenal ulcer was clinically evaluated with respect to Helicobacter pylori infection and rate of recurrence in 38 ulcer patients perforated and 154 patients with non-perforated duodenal ulcer who visited our hospital in past 5 years and 6 months. The frequency of occurrence of H. pylori-positivity was 42.1% in patients with perforated duodenal ulcer, significantly lower than that of 92.9% in patients with non-perforated lesions. This result suggests that H. pylori is hardly involved in the development of perforated duodenal ulcer. The rate of recurrence was significantly lower for perforated duodenal ulcer than for non-perforated ulcer. In particular, perforated duodenal ulcer did not recur in the group on maintenance therapy with H2-recepter antagonists. Maintenance therapy using inhibitors of gastric acid secretion seems effective for the prevention of recurrence of perforated duodenal ulcer.

The prevalence and risk factors of hypertriglyceridemia during the administration of interferon (IFN) were examined in 78 patients with chronic hepatitis C who were treated with 6 MU of IFN-beta once or 3 MU of IFN-beta twice a day for 6 weeks. Hypertriglyceridemia (serum triglyceride (TG) above 150 mg/dl) was found before the start of IFN treatment in 9% of the patients. During the administration of IFN, elevation of serum TG above 150 mg/dl was found in 82% of patients. In addition, serum TG level exceeded 500 mg/dl at least once during the administration of IFN in 13% of patients. On stepwise multiple regression analysis, three risk factors, high serum TG value before the administration of IFN, high ALT value before the administration of IFN, and divided administration of IFN-beta twice daily were found to be associated with hypertriglyceridemia during IFN administration.

Six patients with hepatocellular carcinoma were subjected to percutaneous microwave coagulation therapy (PMCT) by ultrasonic guiding. The size of the main tumor in the present cases was limited to not more than 2 cm. From 18 to 48 days after PMCT, each patient was subjected to surgery and pathological examination. By macroscopic observation, the PMCT area including both non-tumor and tumor regions looked yellowish white, and the boundary was clearly recognized. In the histological examination, the coagulation area surrounded by fibrous capsule was found, and deletion of nuclei and changes in stainability were observed in the marginal region. These changes indicated obvious coagulation necrosis, but the changes became less intense toward the center in the area, and in some portions, the tissue was indistinguishable from viable cells by light microscopy. In 2 cases out of the 6, part of the tumor remained outside the coagulation area. Since only the area determined by the microwave electrode is coagulated to cause necrosis on PMCT, sufficient safety margin should be required.

Up to now, the diagnosis of H. pylori infection has been made by the breath test using 13C-urea. In this study, 13C-urea breath samples were tested in 34 patients (peptic ulcer scar 17, chronic gastritis 17 cases) with an automated breath 13C analyzer (ABCA. Europa Scientific, Crewe, UK) and compared with the results of endoscopical diagnosis for H. pylori infection. Endoscopic and 13C-urea breath test (13C-UBT) were performed before eradicative medication. We described a modified protocol for the growth grade of H. pylori colonies in microbiology (H. pylori score), and for the delta 13C area under curve (AUC; permil*hr) obtained from each sample of expired breath. There was a significant correlation between delta 13C-AUC and the delta 13C level of each sample, but the correlation coefficient obtained at 10min (R2 = 0.582) was lower than that obtained at the other four time points (20min; 0.891, 30min; 0.949, 40min; 0.946, 50min; 0.946, 60min; 0.820). The delta 13C-AUC well correlated with H. pylori score (p < 0.01), none of 26 H. pylori positive patients detected by culture was 13C-UBT negative (delta 13C-AUC < 8.2 permil*hr in mean + 2SD of H. pylori negative group). In conclusion, 13C-UBT using ABCA has high sensitivity and specificity, and it provides a non-invasive method for the detection of H. pylori urease activity.

We compared the usefulness of proton pump inhibitors (PPIs) every other day, with H2-blocker, in terms of inhibitory effect on gastric acid secretion. The dosages were as follows; cimetidine (CIM), 800mg and 400mg every day; omeprazole (OPZ) 20mg, and lansoprazole (LPZ), 30mg every other day. We continuously measured intragastric pH and calculated the time that pH was maintained at pH4 or more (pH4 holding time). The pH4 holding time as a part of total measurement time was significantly longer in the PPI every other day groups than in the H2-blocker groups, but there were no significant differences between the groups during the night. In PPI every other day groups, pH4 holding time of daytime period was suggested to be longer than on H2-blocker groups. In conclusion, their efficacy was greater than in the CIM group, and they appear to have a broad range of applications to the treatment of peptic ulcer.

To evaluate prognostic significance of echogenic lesion within small hepatocellular carcinoma (SHCC, less than or equal to 2 cm in diameter), clinical and pathological findings of 32 cases with SHCC containing echogenic lesion (echogenic SHCC) were compared with those of 55 cases with non-echogenic SHCC. Compared with the non-echogenic SHCC group, the frequency of clinical stage I was significantly higher, and there were significantly more cases with solitary tumor relative to cases with multiple tumors in the echogenic SHCC group. Histologically, the incidence of the HCC composed of well-differentiated tumor cells corresponding to Edmondson's grade I was significantly higher in the echogenic SHCC group than in the non-echogenic SHCC group. Although HCCs tended to become progressively less differentiated with increasing tumor sizes in the both groups, the process of cellular change appeared to proceed more slowly in the echogenic SHCC group. Survival rate after tumor detection was 73% at three years, 56% at five years and 48% at seven years and nine years in the echogenic SHCC group, while it was 46% at three years, 42% at five years and 0% at seven years in the non-echogenic SHCC group. The present results showed that the presence of echogenic lesion within SHCC could be useful prognostic indicator.

A multi-center double-blind controlled trial of ursodeoxycholic acid (UDCA) for treatment of primary biliary cirrhosis (PBC) was carried out. Twenty two and 23 patients were treated with 600 mg/day UDCA and placebo, respectively, for 24 weeks. In UDCA-treated patients, fall of serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma-glutamyltranspeptidase activities started within 4 weeks after start of the trial and continued throughout the trial period. The serum IgM level fell in 7 UDCA-treated patients examined but not in 10 placebo-treated patients examined. Serum bilirubin concentration showed no significant change at the end of the study in either of UDCA- and placebo-treated group of patients. There was no significant difference between these two groups with respect to the frequency of improvement of pruritus. In UDCA-treated patients, serum bile acid composition changed markedly, though its concentration showed no significant change. The percentage of total bile acid which ursodeoxycholic acid took up increased, whereas those which cholic acid, chenodeoxycholic acid and deoxycholic acid took up were decreased.

Previous studies have demonstrated that plasma tissue plasminogen activator (t-PA) level was elevated in patients with liver disease. In this study, t-PA antigen levels were investigated in patients with acute hepatitis (AH; N = 12), chronic hepatitis (CH; N = 8), compensated liver cirrhosis (CLC; N = 40), decompensated liver cirrhosis (DLC; N = 23) and hepatocellular carcinoma (HCC; N = 35). The increased t-PA levels (higher than 14 ng/ml) were found in 33% (4/12) of AH on the early hospital days, 25% (2/8) of CH, 45% (18/40) of CLC and 91% (21/23) of DLC, and 60% (21/35) of Hcc cases. In patient with LC, the correlations between t-PA levels and serum total bilirubin (T.Bill) and hepatic synthetic functions were investigated. The results were that the t-PA levels correlated positively with T. Bil and negatively with liver synthetic functions such as albumin, protein C and choline-esterase, indicating that t-PA increased almost in proportion to the deterioration of hepatic function. Serial determination of t-PA in patients with HCC treated by transcatheter arterial embolization (TAE) revealed that TAE failed to normalize the t-PA levels. In one case of HCC complicated with disseminated intravascular coagulation (DIC), t-PA showed a marked increase at acute phase of DIC and subsequent decrease after the successful treatment for DIC by gabexate mesilate (FOY) infusion. These results suggest that increased t-PA in liver disease is due mainly to deterioration of hepatic function, and that secondary fibrinolytic state, such as DIC, is also a contributing factor.

In order to predict prognosis and clinical course of BPC, theory quantification was applied and the discriminated rate was calculated concerning the cases of PBC national survey in Japan. We examined the prediction of three and five year's survival about all cases, the prediction of appearance of symptoms about asymptomatic PBC and that of jaundice about asymptomatic PBC and symptomatic PBC alone with pruritus. The useful items for the prediction of prognosis were serum bilirubin, albumin and the presence of esophageal varices at first medical examination. Fairly good discriminated rate was obtained on the prediction of three and five year's survival. However poor results were obtained concerning the prediction of appearance of symptoms. In conclusion we can predict the prognosis of PBC based on clinical features.

In the isolated perfused rat liver, the effects of calmodulin (CaM) antagonists, chlorpromazine (CPZ), trifluoperazine (TFP), W-7 and W-5, on secretion of bile and bile acid were compared. Without addition of taurocholic acid to the perfusate, TFP (200 microM or higher), CPZ (200 microM) and W-7 (400 microM) decreased the bile flow transiently. In contrast, W-5 did not decrease the bile flow. Taking into consideration the binding of TFP and CPZ to bovine serum albumin in the perfusate, they diminished the bile flow by inhibiting CaM function. This was also supported by the difference between the effects of W-7 and W-5. These findings suggested that CaM was involved in the secretion of bile. Under the constant infusion of taurocholic acid into the perfusate, CaM antagonists decreased the secretion of bile acid. However this might be due to the inhibition of bile acid uptake, because these agents inhibited the uptake into isolated rat hepatocytes. The concentrations required for inhibition of the uptake were near to those which decreased the viability, suggesting that the inhibition was due to their non-specific cytotoxic effect. Future studies must be carried out to determine whether CaM is involved in the secretion of bile acid.

Of 34 solitary small hepatocellular carcinomas (HCC) 2 cm in diameter or less, 13 with hyperechoic lesions were observed serially by sonography, and 11 of these were examined histologically. Serial examination showed that hypoechoic areas appeared at the periphery of or within, the hyperechoic tumor, and that these areas expanded more with tumor growth than the hyperechoic areas as if compressing or displacing the existing hyperechoic areas. Histologically, the hyperechoic lesions were composed mostly of well-differentiated cancer cells containing fat droplets, whereas the hypoechoic lesions were composed of cancer cells without fat droplets. In the two tumors that were formed almost completely of cancer cells showing fatty metamorphosis, cancer cells without fat droplets proliferated mainly in the periphery of the tumor. These findings suggest that, in hyperechoic HCC, cancer cells with fat droplets appear in the early stage of HCC, and probably change into concer cells without fat droplets by the time that a certain tumor size is reached, with gradual displacement by the latter type of cell during tumor growth.

The effect of glucagon on human exocrine pancreatic secretion was evaluated in ten patients by analysis of pure pancreatic juice. Pancreatic juice was obtained by endoscopic cannulation of the pancreatic duct at 2-min intervals during constant intravenous infusion of secretin (1 U per kg of body weight per hr) plus caerulein (0.04 micrograms per kg of body weight per hr). Since steady secretion was established 20 minutes after the start of juice collection, a further five 2-min fractions were collected as controls, then constant intravenous infusion of glucagon (15 micrograms per kg of body weight per hr) was commenced. Pancreatic juice was collected for a further 20 minutes. The control fractions and post-glucagon fractions were compared in each patient using Student's test. Glucagon depressed secretin-caerulein-stimulated pancreatic secretions. More uniform reductions were observed in the concentration and output of protein and enzymes. Individual variations were observed in the secretory volume and bicarbonate concentration and output. Amylase and lipase were depressed in a parallel fashion in seven patients and in the remaining three, amylase was more depressed than lipase. The post-glucagon reduction in pancreatic secretion was not proportional to the rise in plasma glucagon and blood glucose.

Prolyl hydroxylase was purified from human placentae, specific antiserum against it was prepared, and a new radioimmunoassay system employing 125I-labelled enzyme preparation was established. The molecular weight of the placental enzyme was shown to be 320,000 by gel filtration. SDS-polyacrylamide gel electrophoresis showed two bands of unequal intensity having molecular weights of 60,000 and 130,000. Their amino acid compositions were identical to each other, suggesting the polypeptide with a molecular weight of 130,000 might be a dimer of the polypeptide with a molecular weight of 60,000. The new radioimmunoassay established had a sensitivity of the order of 10 ng/ml, indicating it was more sensitive than previous radioimmunoassay employing 3H-labelling method. Clinical studies on patients with liver diseases disclosed that the concentrations of serum immunoreactive prolyl hydroxylase were elevated both in cases of hepatocellular damage and in cases of cholestasis. In cases of hepatocellular damage the enzyme behaved like cytoplasmic enzymes such as glutamic oxaloacetic transaminase, glutamic pyruvic transaminase and lactic dehydrogenase, but in cases of cholestasis it resembled biliary enzymes such as alkaline phosphatase and gamma-glutamyl transpeptidase. This result might be associated with the peculiar location of the enzyme within the cell, in the membrane of rough endoplasmic reticulum.

Twenty-six patients with fulminant hepatic failure were treated with daily infusions of antithrombin III concentrate until recovery of consciousness or death. Seven patients were alive (group A), 7 survived 17 to 47 days after treatment (group B), and 12 died within 9 days (group C). Decreased plasma antithrombin III levels increased on the day after treatment, irrespective of the pretreatment levels in all patients. Continuous or temporary normalization was seen in all patients in groups A and B, but in only 5 in group C patients whose bleeding was extensive (p less than 0.05). An abrupt drop in peripheral platelet counts occurred when plasma antithrombin III levels were below normal. General bleeding accompanied this drop. These results suggest that maintained normal plasma antithrombin III levels are beneficial for prolonged survival time in fulminant hepatic failure, probably through controlling intravascular coagulation, and that antithrombin III infusion may be useful for such treatment.

The records of 57 patients with acute viral hepatitis (28 given hormones and 29 placebo) in a double blind controlled trial of one week of glucagon and insulin therapy were analyzed. In the placebo group, SGPT values dropped after treatment with improved prothrombin time and serum levels of total bilirubin and albumin. In the hormone group, they changed similarly, except serum albumin levels which were reversed during treatment (P less than 0.05). There was a bottom line of serum albumin levels which preceded a peak of serum alpha-fetoprotein levels within one week in the placebo group, but was around the peak in the hormone group. There were 12 patients in the hormone group in whom serum alpha-fetoprotein levels rose with treatment and decreased after its discontinuation, and 5 in the placebo group (P less than 0.05). Such a change in serum alpha-fetoprotein levels was accompanied by decreased serum albumin levels in 6 of 10 patients given hormones and none of the 5 given placebo (P less than 0.05). These results indicate reciprocal changes in serum albumin and alpha-fetoprotein levels appearing during the recovery course of acute viral hepatitis, and suggest that this therapy may stimulate its development. Stimulation of liver regeneration by this therapy merits consideration.

A cooperative study was conducted to determine the efficacy of one week of treatment with infusion of 1 mg glucagon and 10 units insulin twice daily in severe acute hepatitis. Ninty-eight patients with either prothrombin time less than 60% or thrombotest or hepaplastin test less than 50% of normal were randomly assigned to hormone or placebo treatment. SGOT and SGPT values dropped after treatment with a gradual decrease or increase in total serum bilirubin or cholesterol levels similarly in both groups receiving hormone or placebo. Deranged prothrombin time improved more rapidly in the hormone group than in the placebo group. Glucagon and insulin infusion may stimulate recovery of the liver from injury.