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Biomedical subjects

D Chatzopoulos

Publications and source records attributed to D Chatzopoulos.

13 recordsLinked to original sources
PubMed2006

Rheumatic-like syndrome as a symptom of underlying gastric cancer.

Several observations imply that atypical rheumatic manifestations may be associated with occult neoplasia. A 71-year-old woman was admitted to the hospital three times in 2 years. Initially, she was admitted for investigation of an iron-deficient anemia associated with upper intestinal tract symptoms. Endoscopy revealed hiatus hernia, esophagitis, and duodenal ulcer with a Helicobacter pylori infection, but there were no signs of malignancy, and the patient received appropriate drug treatment. Two years later, she presented with arthralgias concerning the upper and lower limbs in an asymmetrical distribution, low fever, and persistence of the anemia, despite the treatment she had received and the fact that her gastrointestinal symptoms had long ceased. Immunological assays showed no specific rheumatic disorder, and the patient was discharged after showing significant improvement with the use of COX-2 selective NSAIDs. Finally, 4 months later, she was readmitted with worsening of the arthralgias, arthritis in the right radiocarpal joint, and severe anemia. Hematemesis that occurred during her hospital stay led to an emergency endoscopy and the diagnosis of gastric adenocarcinoma. Only a few cases have been reported so far concerning rheumatic manifestations as signs of an occult gastric cancer. Thus, there must be some degree of suspicion when dealing with patients with anemia and rheumatic symptoms that cannot be classified into a particular rheumatologic entity, because they might conceal a gastrointestinal malignancy not yet evident.

Adenocarcinoma↗
PubMed2006

Relationship between Helicobacter pylori infection and Alzheimer disease.

The authors investigated the association between Helicobacter pylori infection (Hp-I) and Alzheimer disease (AD) by using histology for diagnosis of Hp-I. Fifty patients with AD and 30 iron deficiency anemic control participants without AD were included. The histologic prevalence of Hp-I was 88% in patients with AD and 46.7% in controls (p < 0.001).

Adult↗
PubMed2005

Association between Helicobacter pylori infection and acute inflammatory demyelinating polyradiculoneuropathy.

The aim of this study was to investigate a possible association between Helicobacter pylori infection and acute inflammatory demyelinating polyradiculoneuropathy (AIDP). Of 17 consecutive patients with Guillain-Barre syndrome (GBS), 13 patients (six females; mean age 50 +/- 24 years) with AIDP were investigated. Clinical status was evaluated according to Hughes' score, and electrophysiological tests were performed within 2 weeks from disease onset. Helicobacter pylori infection was detected histologically and serum H. pylori-specific IgG antibodies were analysed by ELISA. Twenty asymptomatic patients (12 females; mean age 63 +/- 8 years), undergoing upper gastrointestinal endoscopy for investigation of mild iron deficiency anaemia, served as controls. Helicobacter pylori was found in 12 of 13 AIDP patients (92%), and in 10 of 20 controls (50%), (P = 0.02). Electrophysiological studies showed demyelination in all AIDP patients. High levels of anti-H. pylori IgG antibodies correlated with advanced clinical status. Five of seven AIDP patients with high levels of anti-H. pylori IgG antibodies had delayed F-wave latencies, indicating affection of proximal segments of peripheral nerves. Helicobacter pylori infection seems to be more frequent in AIDP patients. Anti-H. pylori titre might reflect advanced clinical status. Anti-H. pylori IgG antibodies are also associated with involvement of the proximal parts of peripheral nerves in AIDP.

Adolescent↗
PubMed2003

Apoptosis in hepatitis C.

The apoptotic process appears to be a host defence mechanism against viral infections and tumourigenesis. However, many viral genomes encode proteins, which repress apoptosis so as to escape from immune attack by the host. Therefore, virus-host interactions may determine viral persistence, extent and severity of liver inflammation and possibly viral hepatocarcinogenesis. Apoptosis of liver cells may play a significant role in the pathogenesis of hepatitis C. Pathomorphologic features of increased apoptosis include shrinkage and fragmentation of nuclei/cytoplasm in piecemeal necrosis areas, acidophilic bodies, and focal cell dropout in the liver lobule. The hepatitis C virus (HCV) core protein exhibits both proapoptotic or antiapoptotic actions. Modulation of apoptosis may involve binding of HCV core protein to the intracellular signal transducing portion of death receptors and displacement of signalling molecules. Apoptosis may occur in the absence of significant transaminase elevation, thereby explaining the lack of correlation between biochemical activity and liver cell histological injury. Monitoring caspase activation might provide a reliable tool to estimate the efficacy of HCV therapy, and might open challenging therapeutic strategies in HCV infection. The antiviral effect of interferon may be mediated through induction of apoptosis. Lastly, administration of the antiapoptotic ursodeoxycholic acid in HCV infection is compatible with the notion that apoptosis may represent a mechanism for viral shedding rather than for viral elimination, thereby raising the concept that inhibition of apoptosis could ameliorate hepatitis C.

Antiviral Agents↗
PubMed2001

Relationship between Helicobacter pylori infection and glaucoma.

OBJECTIVE: To determine the frequency of Helicobacter pylori (H. pylori) infection in glaucoma patients and in anemic control participants. DESIGN: Prospective, nonrandomized, comparative study. PARTICIPANTS: The authors investigated 32 patients with chronic open-angle glaucoma (COAG), 9 patients with pseudoexfoliation glaucoma (PEG), and 30 age-matched anemic control participants. METHODS: Upper gastrointestinal endoscopy was performed to evaluate macroscopic abnormalities, and gastric mucosal biopsy specimens were obtained for the presence of H. pylori infection tested by rapid urease slide test (CLO test) and by Cresyl fast violet staining, Giemsa staining, or both. The presence of gastritis was classified in accordance with the Sydney system by using hematoxylin and eosin stain. In addition, intestinal metaplasia was evaluated with Alcian blue stain. Saliva samples were also tested by CLO. Serum was analyzed for the presence of H. pylori-specific IgG antibodies by enzyme-linked immunosorbent assay. MAIN OUTCOME MEASURE: Histologic examination for the presence of H. pylori. RESULTS: In 87.5% of the COAG patients, 88.9% of the PEG patients, and 46.7% of the anemic control participants, H. pylori infection was histologically confirmed (odds ratio, 8.00; chi-square, 11.81; P = 0.0006 and 9.14; chi-square, 5.01; P = 0.02, respectively). H. pylori was detected by urease test: (1) in the gastric mucosa in 71.9% of the COAG patients, in 77.8% of the PEG patients, and in 46.7% of the anemic control participants (P = 0.03 and P > 0.05, respectively); and (2) in the saliva in 37.5% of the COAG patients, in 55.6% of the PEG patients, and in 30% of the anemic control participants (P > 0.05). Sixty-eight percent of glaucoma patients and 30% of anemic control participants were seropositive for H. pylori (P = 0.002). When compared with anemic control participants, glaucoma patients exhibited less often endoscopic normal appearance of gastric mucosa (P = 0.01), and more often antral gastritis (P = 0.0004) or peptic ulcer disease (P = 0.01). Histologic grade 3 gastritis was observed only in the glaucoma patients (P = 0.03). CONCLUSIONS: H. pylori infection seems more frequent in glaucoma patients. If confirmed, this may indicate either a common factor that causes susceptibilities to both glaucoma and H. pylori infection or that H. pylori may be a causal factor for developing glaucoma.

Adult↗
PubMedDate not supplied

A concept on the role of Helicobacter pylori infection in autoimmune pancreatitis.

Autoimmune pancreatitis, an inflammatory process of the pancreas due to an autoimmune mechanism establishing etiology of chronic pancreatitis, is characterized by the presence of autoantibodies, hypergammaglobulinemia, pancreatic enlargement, pancreatic duct strictures, and pathologic features of fibrotic changes with intense, mainly lymphocytic infiltrations, which may contribute to tissue destruction probably by apoptosis. In almost 60% of the cases, this type of pancreatitis coexists with other autoimmune diseases such as Sjogren's syndrome, sclerosing extrahepatic cholangitis, primary biliary cirrhosis, autoimmune hepatitis, or other extrapancreatic disorders, and recently with gastric peptic ulceration. The diversity of extrapancreatic lesions with similar histopathologic findings suggests general involvement of the digestive system in this disease, although the presence of such involvement has not been fully elucidated. Similarly, Helicobacter pylori (H. pylori) infection, a well known cause of gastric ulcer, has been associated, via molecular mimicry of host structures by its constituents with the same autoimmune conditions, also characterized by fibrotic changes and/or lymphoplasmacytic inflammations, accompanied by aberrations of T cell apoptosis that contribute to hepatobiliary- or extrahepatic-tissue destruction. Considering that H. pylori is involved in the pathogenesis and pathophysiology of these autoimmune disorders, we propose that this organism might trigger autoimmune pancreatitis through induction of autoimmunity and apoptosis.

Apoptosis↗
PubMedDate not supplied

Reactive oxygen metabolites and upper gastrointestinal diseases.

Reactive oxygen metabolites play an important role in the pathogenesis of gastroduodenal mucosal inflammation (mucosal ischemic injury and other models of mucosal damage induced by nonsteroidal anti-inflammatory drugs, ethanol, or H. pylori), peptic ulcer disease, and gastric cancer. H. pylori achieves its pathogenetic role by triggering an intense leukocyte infiltration of the gastric mucosa, and neutrophil activation provides a major source of reactive oxygen metabolites which can cause tissue damage mainly in the absence of antioxidants. H. pylori virulence factors promote release of a variety of chemoattractants/inflammatory mediators. Circulating leukocytes are recruited to sites of inflammation by a well-regulated and coordinated process that largely occurs in postcapillary venules. Adhesion molecules are expressed on the surface of endothelial cells and leukocytes serve to ensure an orderly sequence of cell-to-cell interactions that sustain leukocyte adherence to vascular endothelium and the subsequent transendothelial migration into inflamed tissue. Transcriptional factors are involved in the expression of endothelial adhesion molecules, and regulation of activity of these factors (i.e., NF-kappa B) is a very attractive target for therapeutic interventions. Longstanding H. pylori-associated gastritis predisposes to gastric cancer development and reactive oxygen metabolites play a part in H. pylori-related gastric carcinogenesis. Various regimens of reactive oxygen metabolite scavengers appear to be new treatment strategies for upper gastrointestinal diseases.

Animals↗
PubMedDate not supplied

Efficacy of trimebutine therapy in patients with gastroesophageal reflux disease and irritable bowel syndrome.

BACKGROUND/AIMS: GERD (gastroesophageal reflux disease) occurs in 25-51% of IBS (irritable bowel syndrome) patients. Trimebutine has been effective in some IBS patients by modulating colonic motility. Furthermore, it increases gastric emptying rates, and controls esophageal motility. The aim of this study was to investigate the efficacy of trimebutine therapy in GERD patients with IBS. METHODOLOGY: Sixty-nine patients with GERD and IBS underwent upper gastrointestinal endoscopic, histologic and clinical evaluation prior to and 3 months post-treatment. H. pylori presence was determined by histology and CLOtest. Forty patients (Group A) were treated with omeprazole plus trimebutine for 3 months: in 32 H. pylori-positive patients (subgroup A1), a standard triple eradication regimen was introduced. Twenty-nine patients (Group B) were treated with omeprazole for 3 months: in 24 H. pylori-positive patients (subgroup B1), the same eradication therapy was employed. RESULTS: Specialized intestinal metaplasia of the gastroesophageal junction was observed in 20% and in 17.2% of the patients in Groups A and B, respectively. Eradication rates were similar in subgroups A1 (84%) and B1 (83%). In Group A there was a significant improvement in GERD (P = 0.003) and IBS symptoms (P < 0.0001) as well as esophagitis (P = 0.029), when compared with Group B. CONCLUSIONS: Trimebutine appears to be effective in patients with GERD and IBS.

Adult↗