Endoultrasonography (EUS) examination of the esophagus in the diagnosis of esophageal duplication: a case report and a review of a literature.

Esophageal duplication cysts are a rare medical entity. In most cases they are located at the level of the distal esophagus. Although our case is not unique, we want to focus on it as a reflection on diagnostic methods. The aim of this article is to show through the report on a case of esophageal duplication treated by us, followed by a review of similar cases in the literature, the utility of EUS in the diagnosis of upper-diaphragmatic and not communicating esophageal duplication. We report a case of a 43 year-old woman. She came to our attention for heartburn and retrosternal sense of space. The patient underwent an endoultrasonography (EUS) examination of the esophagus. The framework put EUS diagnosis of cystic formation of the esophagus (esophageal duplication cysts likely). We demonstrate that only EUS has a correlation with the determination of the pre-operative diagnosis with a statistical significance (p <0.001). In the diagnosis of esophageal not communicating duplication cysts EUS is the most specific diagnostic exam.

Peptic ulcer bleeding: comparison of two hemostatic procedures.

OBJECTIVE: Bleeding is a serious complication of peptic ulcer. Endoscopic injection therapy is accepted as a homeostatic endoscopic treatment in acute nonvariceal of upper GI hemorrhages, particularly in bleeding peptic ulcers. The risk of rebleeding is predicted by the endoscopic appearance of ulcer features classified according to Forrest's criteria. METHODS: Two hundred twenty-three patients were selected from 1,003 emergency upper endoscopies for GI bleeding. According to Forrest's criteria, 99 well-matched patients with ulcers F1 and F2 were considered at risk of rebleeding; 54 patients (group A) received local ulcer injection of epinephrine solution 1:10,000, whereas (group B) patients were treated with local epinephrine injection and then with endoscopic Hemoclips. (1) We considered the control of bleeding, the number of rebleeding episodes, the need for emergency surgery, and mortality. RESULTS: Bleeding ulcers stopped completely in 83.3% group A patients, and in 95.6% group B patients (p = not significant). In a subset of F1b patients the rebleeding rate was 31 % for group A and 0% for group B (p < 0.05). There was no mortality as a result of the procedure. There was a trend toward reducing surgery in favor of the combined therapy (0% vs 7.4%). No differences were found in transfusion requirements or mean hospitalization days. CONCLUSIONS: We conclude that endoscopic injection of l:10,000 epinephrine solution alone and epinephrine solution plus application of Hemoclips are equivalent therapies in treating bleeding and rebleeding from peptic ulcers. There was no difference between therapies in terms of need for surgery or mortality. Possibly combination therapy is more effective in treating ulcers that are actively oozing.

Relapse of low-grade gastric MALT lymphoma after Helicobacter pylori eradication: true relapse or persistence? Long-term post-treatment follow-up of a multicenter trial in the north-east of Italy and evaluation of the diagnostic protocol's adequacy.

The effect of eradication of Helicobacter pylori on early stage gastric low-grade MALT lymphoma in 76 patients with follow-up of at least 1 year (12-63 months, mean 28) is reported. No regression was found in five cases after 12-48 months. In one case surgical resection detected the involvement of perigastric lymph nodes overlooked by endoscopic ultrasonography (EUS). Neither progression of the disease nor a high-grade component was documented by repeated gastric mappings, EUS and complete stagings in the other four cases. After histological remission five relapses of low-grade and one relapse of high-grade MALT lymphoma were found 12-48 months after eradication. Subsequent histological remission, without any additional therapy, was found in three relapsed cases. A rapid and persistent histological remission was obtained in 56 patients (73%). A late remission was observed in six cases. Monoclonal remission was found in half of the patients and was frequently delayed. Persistent monoclonality was associated with histological remission in the vast majority of patients. Our data confirm H. pylori eradication as the first choice therapy for early stage gastric low-grade MALT lymphoma and recommend extensive bioptic mapping and endoscopic sonography both in the local staging and in the regression evaluation. The rare cases of late remission encourage us to wait for at least 1 year after eradication of H. pylori. Longer follow-up studies will clarify the meaning of histological relapse/persistence and late remission. The study of non-responder cases could show us a step in lymphomagenesis.

Antigenic mimicry between Helicobacter pylori and gastric mucosa in the pathogenesis of body atrophic gastritis.

BACKGROUND & AIMS: The majority of patients with Helicobacter pylori infection have autoantibodies cross-reacting with gastric antigens. In this study, the relation between autoantibody status, histopathology of body mucosa, and antigenic profile of H. pylori was investigated. METHODS: One hundred patients were examined for H. pylori infection, body gastritis, and gastric autoantibodies. Balb/c mice were analyzed for serum autoantibodies after immunization with H. pylori from patients with and without atrophic gastritis. RESULTS: Immunoglobulin G autoantibodies were detected in 57 of the 87 infected patients (65.5%) but in none of the 13 patients without infection and gastritis. The autoreaction involved mainly the luminal surface of glandular cells and secretory canaliculi of parietal cells. The autoantibody status correlated with the presence and degree of inflammation and atrophy of the glands. H. pylori from patients with atrophic gastritis showed a higher capacity to induce autoantibodies than H. pylori from patients with a minimal superficial gastritis. Monoclonal antibodies showed differences in the bacterial expression of cross-reacting determinants. CONCLUSIONS: H. pylori-mediated autoimmunity is involved in the pathogenesis of chronic atrophic gastritis. The grade of antigenic mimicry of the infecting H. pylori strain plays a role in the progression of chronic gastritis to atrophy.

Survival after endoscopic sclerotherapy for esophageal varices in cirrhotics.

OBJECTIVES: Gastroesophageal bleeding from varices is the most life-threatening complication in liver cirrhosis with portal hypertension. Since its first application, endoscopic sclerotherapy seems to be the most widely applicable procedure to stop the bleeding and to prevent recurrences. The aim of this study was to ascertain the role of some factors as predictors of survival in different groups of cirrhotic patients. METHODS: At the time of their first hemorrhage from esophageal varices, 184 patients with portal hypertension from cirrhosis were treated by endoscopic sclerotherapy using a combined intraparavariceal procedure and Polidocanol 1% as sclerosing agent. RESULTS: The follow-up range was 1-106 months (mean, 28.2 months), and 84 patients were still alive (45.7%), 97 had died (52.7%), and three had withdrawn (1.6%) at the end of the period. The major cause of death was bleeding, and 35 patients died in the first 6 wk after sclerotherapy. Using Cox proportional hazard models, Child's grading was the most important prognostic factor of both short-term (first 6 wk) and medium/long-term survival (after the first 6 wk up to 5 years). Complete eradication of varices, too, was associated with both short- and long-term survival, whereas age, sex, etiology of cirrhosis, and the presence of esophageal stenosis as a side effect of sclerotherapy were not. The type of sclerotherapy (elective vs emergent) was associated with survival, but it was not independent from Child's grade, because only patients in Child C treated electively showed a better prognosis than those treated in emergency. CONCLUSIONS: We can conclude that patients with severe liver disease (Class C) have poor prognosis, and complete eradication represents an aim because it seems to be protective against the risk of dying.

Prevalence of aortic valve stenosis in patients affected by gastrointestinal angiodysplasia.

OBJECTIVES: Angiodysplasia is considered to be an important cause of gastrointestinal bleeding in the elderly. An association between idiopathic gastrointestinal bleeding and aortic valve stenosis has been reported in up to 25% of the patients. The association between angiodysplasia mainly of the right colon and aortic valve stenosis has been suggested, but is not proven. The aim of this study was to examine the prevalence of aortic valve stenosis in patients with gastrointestinal angiodysplasia. METHODS: We studied retrospectively 83 patients submitted to gastrointestinal endoscopy and found affected by angiodysplasia. Of them 24 (16M and 8F) had died from causes unrelated to cardiovascular diseases. The 59 patients still alive (27M and 32F) underwent a complete clinical, electrocardiographic and echocardiographic (M-mode, B-mode, pulsed and continuous-wave Doppler) evaluation. RESULTS: Fifteen patients (25%) had a normal examination, both clinical and echocardiographic. Eleven (19%) had minor cardiac abnormalities but had no murmurs. Although no murmurs were present in 15 patients (25%), some echocardiographic abnormalities such as aortic leaflet sclerosis, mitral annular calcification, their association, or trivial mitral regurgitation detectable only at PW-Doppler were found. In 18 patients (31%) both systolic murmurs and valvular abnormalities, as revealed by echocardiographic examination, were detected: 10 had a regurgitant and 8 an ejectional murmur; of these only 1 (1.6%) had a true severe calcified aortic valve stenosis at echo-Doppler examination. CONCLUSIONS: The low prevalence of aortic valve stenosis in patients with gastrointestinal angiodysplasia (1/59 or 1.6%) in this retrospective study argues against the association of gastrointestinal angiodysplasia and aortic valve stenosis.

Adult "idiopathic" extrahepatic venous thrombosis. Importance of putative "latent" myeloproliferative disorders and comparison with cases with known etiology.

The etiology of extrahepatic venous obstruction (EHVO) is unknown in 50% of cases. Recently the presence of a "latent" myeloproliferative disorder has been reported in adults with "idiopathic" EHVO. We evaluated the course of these patients to establish if any putative latent myeloproliferative disorder influenced the clinical course compared to those with a known cause. Among 132 EHVO patients, 78 (59%) had a known etiology, 7 (5%) with an overt myeloproliferative disorder. The "idiopathic" group had 54 patients; 24 (13 men, 11 women) were diagnosed after 15 years of age, (median 38 years, range 17-70) with a median follow up of 96 months (19-372). Only 2 (8%) developed an overt myeloproliferative disorder. These 24 had a similar pattern of bleeding and onset of ascites as those with known cause. In EHVO failure to diagnose a latent myeloproliferative disorder does not influence the course of variceal bleeding, and thus has little prognostic significance.

The effect of non-protein liquid meals on the hepatic venous pressure gradient in patients with cirrhosis.

It has been suggested that protein feeding increases portal pressure in cirrhotic patients, but that carbohydrate and fat have little effect. We examined the relationship between feeding and portal pressure, using different liquid test meals (250 or 500 ml non-protein, 250 ml protein-containing, 500 ml water), in 29 alcoholic patients with cirrhosis and portal hypertension. The mean hepatic venous pressure gradient (HVPG) increased significantly 30 min after the protein meal (10% increase; p = 0.009) and returned to basal levels at 60 min. The mean HVPG also increased significantly after the non-protein meal: after 500 ml the increase was 23% at 30 min (p = 0.046) and 17% at 60 min (p = 0.12); and after 250 ml it was 15% at 30 min (p = 0.012) and 7% at 60 min (p = 0.05). Ingestion of 500 ml water caused a small, non-significant, increase in mean HVPG. Plasma glucagon levels increased significantly at 30 and 60 min after the protein meal, but did not change significantly after the non-protein meal or water. Both protein-containing and non-protein meals significantly elevate HVPG in alcoholic patients with cirrhosis and portal hypertension.