Gastric MALT-Lymphoma: more than Helicobacter Pylori.

In this case report, we describe two cases of gastric mucosaassociated lymphoid tissue (MALT) lymphoma. The first patient, who presented with complaints of indigestion, nausea and epigastralgy, had a solid ulcer on endoscopy. Biopsies showed, next to MALT, presence of Helicobacter Pylori. The second patient was admitted with hematemesis. The multiple ulcerations in his stomach were thought to be cocaine-induced. Only after multiple biopsies the diagnosis of MALT was made. No presence of Helicobacter Pylori could be detected. The first patient was successfully treated with Helicobacter Pylori eradication therapy. Localized radiotherapy resulted in complete remission in our second patient. Hence, in absence of Helicobacter Pylori, more aggressive treatment modalities are needed.

Fast and sharp decrease in calprotectin predicts remission by infliximab in anti-TNF naïve patients with ulcerative colitis.

AIM: To evaluate the effect of infliximab induction therapy on calprotectin levels in patients with ulcerative colitis (UC). PATIENTS AND METHODS: In this prospective study 53 patients with active UC from 17 centers were treated with infliximab therapy (5 mg/kg) at baseline, week 2, and week 6. Faecal calprotectin was measured every week. Sigmoidoscopies were performed at baseline, week 6 and week 10. RESULTS: Median calprotectin levels decreased from 1260 (IQR 278.5- 3418) at baseline to 72.5 (IQR 18.5 - 463) at week 10 (p<0.001). After 10 weeks, infliximab therapy induced endoscopic remission and a decrease in calprotectin to<50 mg/kg or at least a 80% decrease from baseline level in 58% of patients. A significant and steep decrease of calprotectin levels was seen at week 2 for patients with an endoscopic remission at week 10 as compared to patients who did not show a remission. (p<0.001). At week 10 an excellent correlation was found between endoscopic remission and clinical Mayo score reflected by an AUC of ROC analyses of 0.94 (0.87-1) and with calprotectin measurements (AUC 0.91 (0.81-1)) : all patients with calprotectin levels <50 mg/kg, and a normal clinical Mayo score (=0) were in endoscopic remission. CONCLUSIONS: Infliximab induces a fast and significant decrease of faecal calprotectin levels in anti-TNF naïve patients with ulcerative colitis predictive for remission of disease.

Failure of a motilin receptor agonist (ABT-229) to relieve the symptoms of functional dyspepsia in patients with and without delayed gastric emptying: a randomized double-blind placebo-controlled trial.

INTRODUCTION: Motilin-receptor agonists are prokinetics; whether they relieve the symptoms of functional dyspepsia is unknown. We aimed to test the efficacy of the motilin agonist ABT-229 in functional dyspepsia patients with and without delayed gastric emptying. METHODS: Patients were randomized with postprandial symptoms and documented functional dyspepsia by endoscopy (n=589 in intention-to-treat analysis). Patients were assigned to either the delayed or normal gastric emptying strata, based on a validated 13C octanoic acid breath test. Patients were then further randomized within each strata, to receive one of four doses of ABT-229 (1.25, 2. 5, 5 or 10 mg b.d. before breakfast and dinner) or placebo for 4 weeks, following a 2-week baseline. The primary outcome was the assessment of change in symptom severity over the 2 weeks from baseline to final visit, based on a self-report questionnaire measuring severity on visual analogue scales. RESULTS: Baseline characteristics across the treatment arms were very similar. No significant differences in the upper abdominal discomfort severity score (maximum 800 mm) were observed for any active treatment arm vs. placebo (mean change from baseline -139, -141, -145, -160 and -134 mm for placebo, 1.25, 2.5, 5, and 10 mg, respectively, at 4 weeks by intention-to-treat). More patients on placebo reported a good or excellent global response than patients on 1.25 or 5 mg of active therapy (both P < 0.05). The results were very similar in those with and without delayed gastric emptying. Helicobacter pylori status did not predict response. Excluding patients with any baseline heartburn (total remaining n=240), ABT-229 10 mg was inferior to placebo in relief of upper abdominal discomfort. CONCLUSIONS: ABT-229 was of no value for relief of symptoms in functional dyspepsia, compared with placebo.

Nimesulide-induced acute hepatitis: evidence from six cases.

BACKGROUND/AIMS: A number of nonsteroidal anti-inflammatory drugs have been reported to provoke hepatic injury. Nimesulide is a new agent of the sulfonanilide class, and is a more selective inhibitor of cyclooxygenase type 2 than of type 1. Well-documented cases of acute hepatitis have not yet been reported with this drug. We report on six patients who developed acute liver damage after initiation of nimesulide. METHODS: Between April 1996 and January 1997, six patients with apparent nimesulide-induced liver injury were admitted. Clinical, laboratory, serologic, radiological, and histologic data of all six cases were extensively analyzed. The causal relationship between nimesulide and liver injury was assessed, using a scoring system elaborated by the French and International consensus meeting group. RESULTS: Four women developed a centrilobular (three) or panlobular (one) bridging necrosis, whereas two men showed a bland intrahepatic cholestasis. Jaundice was the presenting symptom in five of the six cases. One patient with hepatocellular necrosis and one with cholestasis had hallmarks of hypersensitivity with an increased blood and tissue eosinophilia. The causal relationship could be designated as "highly probable" in one, "probable" in four, and "possible" in one patient. One patient died from a pancreatic tumor 5 months after the diagnosis of toxic liver injury. In all other patients, liver tests returned to completely normal values within a late follow-up period of 6 to 17 months. CONCLUSIONS: Nimesulide-induced liver injury can present with hepatocellular necrosis or with pure cholestasis. From clinical and histologic data, it appears that both immunologic and metabolic idiosyncratic reactions can be invoked as the pathogenic mechanisms of nimesulide-induced liver disease.

Clinical aspects of incomplete septal cirrhosis in comparison with macronodular cirrhosis.

BACKGROUND/AIMS: Incomplete septal cirrhosis (ISC) is a form of macronodular cirrhosis characterized by slender, incomplete septa that demarcate inconspicuous nodules. Its clinical features have not been investigated in a large series. The aims of this study were to review the clinical symptoms and evolution of ISC in 42 patients. METHODS: Forty-two patients with at least one liver biopsy strongly suggestive of ISC were selected for the study covering a period between 1968 and 1987. Data for these patients were compared with the evolution of 49 patients with classical macronodular cirrhosis after chronic active hepatitis type B or C. RESULTS: Possible etiological factors for ISC were alcohol abuse, arsenic treatment, and hepatitis B infection. In three cases, a genetic factor could not be excluded. Patients with ISC had significantly lower serum concentrations of transaminases and bilirubin at diagnosis. Compared with macronodular cirrhosis, bleeding varices were more frequent (57% vs. 22%) in ISC. Ten-year survivals in the ISC and the macronodular cirrhosis groups were 54% and 57%, respectively. CONCLUSIONS: ISC represents a relatively stable burnt-out form of macronodular cirrhosis with an unusually high incidence of variceal bleeding. This could be explained by a superimposed insufficiency of the portal vascular supply.

Incomplete septal cirrhosis: histopathological aspects.

We have reviewed 60 liver specimens from 47 patients with the diagnosis of incomplete septal cirrhosis observed between 1968 and 1987. In reaching this diagnosis evaluation of the following histological features appeared to be helpful: parenchymal nodularity, thin incomplete septa, hypoplastic portal tracts, increased number of venous channels, abnormal spacing between portal tracts and veins, crowding of reticulin fibres between adjacent zones of hyperplastic parenchyma, hyperplasia of hepatocytes and dilated sinusoids. These histological features were not specific for incomplete septal cirrhosis as they were also present--although less evident and less frequent--in a series of 87 non-cirrhotic liver specimens. Reticulin stains were an essential adjunct to assess the architectural disturbance, which was often inconspicuous in needle biopsies. Histological features indicating a specific aetiology were lacking in the great majority of cases. On histological and clinical grounds, incomplete septal cirrhosis resembles idiopathic portal hypertension, nodular regenerative hyperplasia and partial nodular transformation; in these entities an obliterative portal venopathy with non-uniformity of portal blood supply to the parenchyma has been suggested as a pathogenic mechanism. In the present study phlebosclerotic lesions of the portal vein were found in only two cases. This might be explained by sampling error or, alternatively, the hypoplastic portal tracts observed might be a functional equivalent of obliterative portal venopathy resulting in a deficient portal blood supply. Non-uniformity of blood supply to the parenchyma may explain the similarities between incomplete septal cirrhosis and the diseases mentioned.