Fast-growing gastric inflammatory pseudotumor: a rare manifestation of peptic ulcer disease.
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Biomedical subjects
Publications and source records attributed to H Mörk.
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ETIOLOGY: The hereditary non-polyposis colorectal carcinoma (HNPCC) is the most common monogenic colon cancer syndrome. It is characterized by autosomal dominant inherited cancers of the colon, rectum, and the endometrium. Less frequently, cancer of the upper gastrointestinal tract, the hepatobiliary system and the urogenital tract may occur. Typical characteristics are an early onset, usually before the age of 50, manifestation of colorectal cancer proximal of the splenic flexure, and often poorly differentiated carcinomas. GENETICS: Recently, germline mutations in several DNA mismatch repair genes have been identified as the molecular basis of HNPCC, resulting in deficient DNA repair and genetic instability, indicated by microsatellite instability in tumor specimens. DIAGNOSIS: New insights into pathogenesis, clinical features, and diagnosis of HNPCC have improved the identification of HNPCC patients and persons at risk. Diagnosis of HNPCC is primarily based on family history and is complemented by molecular findings. After detection of the underlying germline mutation in families with HNPCC, screening procedures can be restricted to mutation carriers. TREATMENT: Recommendations for therapy and prevention are in part controversial and are under investigation in several studies.
Chronic liver diseases often lead to cirrhosis of that organ. As this progresses, hepatic function decreases, and the risk of life-threatening complications increases. Common complications are variceal bleeding, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, hepatorenal syndrome and hepatocellular carcinoma. The only therapeutic option that offers a chance of a cure is transplantation which, however, owing to strict selection criteria and the limited number of donor organs, can be applied only in a minority of patients. For most of the cases, the therapeutic strategy comprises treatment of the underlying disease, prevention and symptomatic treatment of typical complications.
Tolerance of interferon-a therapy for hepatitis C is often poor and medication is expensive. Compliance with diagnostic procedures and, even more important, with medical treatment is obviously critical to minimize the rate of dropouts and to maximize cost efficiency. Moreover, a good concordance with scheduled follow-ups is important for early recognition and treatment of interferon-associated side effects. Therefore, we investigated psychiatric symptoms, interpersonal problems, different modes of acquisition, and sociodemographic factors in HCV-infected patients as possible predictor variables of good versus poor compliance. In a longitudinal study, 74 patients with chronic hepatitis C (CHC) who fulfilled the criteria for treatment with interferon (IFN)-alpha-2b with or without ribavirin were investigated prospectively to identify those at risk for poor compliance during IFN medication. To assess predictive factors, we used both IIP-C (Inventory of Interpersonal Problems) and SCL-90-R (Symptom Check List 90 Items Revised) as psychometric instruments. Sociodemographic and somatic variables as well as compliance during IFN therapy were also evaluated. Poor compliance before or during medication was demonstrated by 23% (N = 17) of HCV patients. Sociodemographic factors and mode of acquisition, particularly former intravenous drug (IVD) abuse were not significantly linked with compliance. Logistic regression analysis demonstrated that the subgroup of patients with compliance problems was best identified by both pretherapeutic psychiatric symptoms and interpersonal problems. Predictive value was best and significant for anger-hostility (P = 0.009), intrusive (P = 0.014), depression (P = 0.015), and phobic anxiety (P = 0.049). Adopting this statistical prediction model, sensitivity was 47.1%, but specificity reached 98.3%. In total, 86.5% of cases were classified correctly. In situations of unclear indication for IFN therapy, psychological variables assessment of before the beginning of treatment may represent an additional decision-making factor.
Gastro-esophageal reflux disease--one of the most common diagnoses in gastroenterology--is characterized by its symptoms or mucosal lesions caused by the non-physiological exposure of the esophagus to gastric juice. For its acute treatment, proton pump inhibitors are distinctly superior to histamine 2 receptor antagonists, and are the treatment of choice. Since relapse is common, long-term treatment is often necessary. Although PPI are the most effective substances over the long-term too, cisapride and/or histamine receptor antagonists may suffice to prevent relapse. In severe and complicated cases, however, the long-term use of proton pump inhibitors is mandatory. While, in such cases, laparoscopic antireflux surgery offers an alternative, neither long-term data nor controlled studies comparing this approach with long-term medical treatment have been carried out. A major complication of reflux disease is Barrett's metaplasia with its associated risk for adenocarcinoma development. Barrett's epithelium can be eradicated by endoscopic thermal ablation combined with acid suppression. However, as endoscopic therapy bears risks and data on long-term efficacy are still lacking, the significance of thermal ablation has further to be evaluated in specialized centers.
Noonan's syndrome is a rare congenital disorder that may be associated with abnormalities in the lymphatic drainage. In this case of a 21-year-old man CT after bipedal lymphangiography confirmed the diagnosis of intestinal lymphangiectasy causing protein-losing enteropathy in Noonan's syndrome by showing contrast-enhanced abnormal lymphatic vessels in the mesentery and the intestinal wall. Because of the benefit of diet in case of intestinal involvement, we recommend a thorough documentation of the lymphatic drainage with lymphangiography followed by CT, if clinical signs of lymphatic dysplasia, such as pleural effusions, lymphedema, or hypoproteinemia are present.
Four selenocysteine-containing proteins (gastrointestinal glutathione peroxidase, plasma glutathione peroxidase, selenoprotein P, and thioredoxin reductase-alpha) are expressed in the colonic mucosa. Because of their antioxidant functions, a protective role in colon carcinogenesis is discussed. The aim of this study was to elucidate an involvement of gastrointestinal selenoproteins during the adenoma-carcinoma sequence. Matched pairs of biopsies of colorectal adenomas and adjacent normal mucosa from 11 patients were analyzed for mRNA expression, protein expression, or enzyme activity of selenoproteins by Northern blot, Western blot, or enzymatic tests. All adenomas revealed a marked reduction of selenoprotein P and a variable increase of gastrointestinal glutathione peroxidase mRNA compared with adjacent tissue. Thioredoxin reductase-alpha and plasma glutathione peroxidase mRNA expression were not altered in adenomas. The Northern blot results were confirmed by Western blot analysis or enzyme activity measurement, respectively. We conclude that gastrointestinal glutathione peroxidase and selenoprotein P play a complementary role in the antioxidative cell defense along the adenoma-carcinoma sequence. It remains to be shown whether upregulation of gastrointestinal glutathione peroxidase in adenomas represents a compensatory mechanism to reduce susceptibility for oxidative damage resulting from the loss of selenoprotein P.
Reactivation of chronic hepatitis B in patients receiving cytotoxic treatment for non-Hodgkin's lymphoma is well documented. We report a case of a patient with chronic hepatitis B who was treated by chemotherapy because of non-Hodgkin's lymphoma. After the second cycle of chemotherapy she developed a severe flare-up of hepatitis B. Liver biopsy revealed highly active hepatitis and confluent necroses. Within 3 weeks, the patient recovered spontaneously. Prophylactic treatment with lamivudine (Epivir,Glaxo-Wellcome, 150 mg b.i.d.) led to a decrease of HBV-DNA below the detection limit. Further chemotherapy was administered and autologous stem cell transplantation was successfully performed without another reactivation of hepatitis B. Antiviral treatment was stopped 16 weeks after stem cell retransfusion. So far, no further flare-up of hepatitis B has occurred and the patient's lymphoma has not relapsed. Thus, the case described here indicates a possible role of lamivudine in preventing hepatitis B flare-up during antineoplastic chemotherapy. We suggest that lamivudine be considered for prophylaxis against fulminant hepatitis in patients with chronic HBV infection undergoing high-dose antineoplastic therapy.
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BACKGROUND: Barrett's oesophagus is a premalignant condition. Recent reports have suggested that laser coagulation or photodynamic therapy combined with acid suppression may induce reconstitution of squamous mucosa. However, a high percentage of residual glands remain in cases treated with both techniques. Argon plasma coagulation (APC) appears to be an attractive alternative to other thermoablative techniques. The aim of this study was to investigate the reconstitution of squamous epithelium in Barrett's oesophagus after APC. METHODS: Fifteen patients with histologically proven Barrett's oesophagus were included in a prospective study. After base-line documentation by videotaping and biopsies, Barrett's epithelium was treated by repeated APC at intervals of 4-6 weeks until complete squamous restoration was achieved. All patients were kept under high-dose proton pump inhibitor therapy. RESULTS: In 13 patients complete reconstitution of squamous epithelium was achieved. Buried glands after squamous restoration were detected transiently in only one case after the first session. As side effects seven patients had mild retrosternal discomfort. One patient reported severe retrosternal pain for 1 week. He then refused further APC sessions. Another patient was excluded because of noncompliance. During the follow-up period (6-13 months) recurrence of Barrett's epithelium was observed in one patient. CONCLUSIONS: APC is a suitable technique for achieving squamous restoration in Barrett's oesophagus. The rare occurrence of remaining buried glands may result from the homogeneous coagulation achieved by the ionized argon gas beam.
There is experimental and epidemiological evidence for an association between low selenium levels and gastrointestinal cancer incidence, prevalence, and mortality. To identify targets for selenium supplementation in the human digestive tract, we examined mRNA expression of various selenocysteine-containing proteins in normal mucosa biopsy specimens. Tissue samples from the esophagus and from different sites of the stomach, small bowel, and colon were obtained during endoscopies of the upper and lower gastrointestinal tract. Northern blot analyses revealed a lack of cytosolic glutathione peroxidase mRNA but a differential mRNA expression pattern of gastrointestinal and plasma glutathione peroxidase, selenoprotein P, and thioredoxin reductase. Glutathione peroxidase and thioredoxin reductase activities were detected in the mucosa of all biopsies, but the differential pattern did not reflect the differential mRNA steady-state levels. In addition to gastrointestinal glutathione peroxidase, which was found to play a role in colon cancer resistance, we identified further gastrointestinal selenoproteins, which may be involved in gastrointestinal cell defense and cell differentiation.
Iron deficiency anemia is a common symptom of chronic occult gastrointestinal bleeding. There are numerous potential sources of gastrointestinal hemorrhage, most of which can be detected with the aid of endoscopy of the upper and lower digestive tract. Diagnostic procedures for the small bowel are less sensitive and usually more invasive. On the basis of the relevance of information they provide, the various diagnostic procedures and their indication in the diagnosis of iron deficiency anemia are critically reviewed, and a systematic diagnostic strategy developed.
BASIS: Selenium is an essential trace element, which is incorporated as selenocysteine (secys) into specific proteins in a regulated fashion. In the presence of a hairpin loop structure within the 3' untranslated region of the mRNA the opal stop codon UGA is coding for selenocysteine. Selenoprotein functions are dependent on secys incorporation. Members of the family of deiodinases as well as the family of glutathione peroxidases, selenoprotein P and thioredoxin reductase are selenoproteins. DISCUSSION: Bone, the intestine and the thyroid rely on antioxidant systems against potential cell and DNA damage through endogenous and environmental peroxides and reactive oxygen species (ROS) potentially promoting inflammation and tumorigenesis. Optimized cell defense through antioxidant selenoproteins requires optimal selenium supplementation of the organism. We have analyzed the expression of selenoproteins in these tissues, thus providing molecular tools to further elucidate optimal selenium supply on a cellular level. CONCLUSION: Clinical intervention studies that focus on the development of disease must confirm the relevance of optimized selenium supply for the pathogenesis, prevention and therapy of metabolic bone disease as well as chronic (autoimmune) inflammation and tumorigenesis in the thyroid and intestine.
Primary biliary cirrhosis (PBC) is frequently associated with other autoimmune disorders. Although antibodies against gastric parietal cells are found in nearly all PBC patients, autoimmune gastritis is only very rarely associated. We describe a woman with PBC in whom chronic autoimmune gastritis complicated by a large pedunculated gastric carcinoid tumor was found. Additionally, the patient had autoimmune thyroiditis. This was interpreted as the rare association of PBC with Schmidt's syndrome type III. The carcinoid tumor was removed endoscopically. We conclude from the case that an endoscopic screening for autoimmune gastritis should at least be performed in patients with PBC and autoimmune thyroiditis, keeping in mind the possible occurrence of a polyendocrinopathy and the potentially serious complication of a gastric carcinoid tumor.
BACKGROUND: Pancreatic antibodies occur in about one third of patients with Crohn's disease. AIMS: To evaluate the relevance of pancreatic antibodies as a genetic marker in patients with Crohn's disease and their first degree family members and spouses. To characterise further pancreatic antibodies by assessment of IgG subclasses. METHODS: Six hundred and fifty serum samples were tested for pancreatic antibodies by immunofluorescence on sections of human pancreas. Incidence of pancreatic antibodies and their subtypes were studied on 212 serum samples from patients with Crohn's disease. In the familial study, 72 patients with Crohn's disease and 196 first degree family members and 26 patients with ulcerative colitis and 90 first degree family members were included. Ten healthy families served as controls. RESULTS: Pancreatic antibodies were found in 58 (27%) of the patients with Crohn's disease and in none of the controls. Thirty patients had pancreatic antibodies of subtype I characterised by a drop-like fluorescence in the pancreatic acini, 28 patients had subtype II with a fine speckled staining in the acinar cells. Pancreatic antibodies of subtype I were both IgG1 and IgG2 antibodies by contrast with subtype II which were mainly of IgG1 subclass. Only five of 196 first degree relatives of patients with Crohn's disease had pancreatic antibodies. Four of these people had anamnestic data compatible with inflammatory bowel disease. Further investigations showed Crohn's disease in two of these people. In families with more than one member positive for pancreatic antibodies, pancreatic antibodies were of the same subtype in all cases. CONCLUSIONS: Pancreatic antibodies are a specific marker for Crohn's disease. Two subgroups of pancreatic antibodies can be distinguished by their pattern and immunoglobulin subclasses. Pancreatic antibodies rarely occur in family members of patients with Crohn's disease. These family members may also have Crohn's disease.
Drug-induced cholestasis can rarely persist for a considerable time period even after withdrawal of the drug. We report the case of a 55-year-old man with progressive jaundice after oral therapy with 17-alpha-methyltestosterone. Under empiric therapy with ursodeoxycholic acid the condition resolved completely. According to this observation, we suggest a therapeutic trial with ursodeoxycholic acid in cases of prolonged androgen-induced cholestasis.