Our results suggest that out of the 13 indices evaluated, only FIB-4 index may be useful in estimating the extent of fibrosis in patients with CHB. There is a need for more comprehensive prospective studies to help determine the diagnostic value of non-invasive tests for liver fibrosis.
A central issue in the understanding of the pathogenesis of nonalcoholic fatty liver disease is the problem of the underlying mechanisms which are not fully understood. In the setting of excessive central adiposity, insulin resistance is the major underlying cause of fat accumulation in hepatocytes. Because of the difficulties with human trials, several animal models have been developed for this purpose mainly characterized as follows: genetically disturbed or murine fatty liver, methionine-choline deficient diet fed or murine steatohepatitis, and high-fat or sucrose diet fed models. Although these animal models have provided useful information, none of them accurately reflect genetic, metabolic and biochemical characteristics of the human disease.
Liver penetration is a rare but serious complication of peptic ulcer disease. Usually the diagnosis is made by operation or autopsy. Clinical and laboratory data were no specific. A 64-year-old man was admitted with upper gastrointestinal bleeding. Hepatic penetration was diagnosed as the cause of bleeding. Endoscopy showed a large gastric ulcer with a pseudotumoral mass protruding from the ulcer bed. Definitive diagnosis was established by endoscopic biopsies of the ulcer base.
Stomach endoscopic biopsies are made to determine the diagnosis of the illness, its stage, and follow-up after the treatment. It is very significant to collaborate with the clinician while evaluating endoscopic biopsies. Besides the clinical and laboratory information of the patient, the endoscopic appearance of the lesion should be known. The clinician and pathologist should use the same language and the same terminology. Although new classifications have been made to prevent the confusion of terminologies in neoplastic processes recently, most centers around the world have reported non-invasive neoplasias without giving any certain diagnosis by just commenting on it. The clinician should understand what the pathologist wants to say; pathologists should know the approach of the clinician (repetition of the biopsy, endoscopic resection, surgery). There is Helicobacter pylori (HP) in most of the stomach pathologies as the etiologic agent. No matter if the factor is HP or other etiologic agents, the tissue gives similar responses. That is why clinical-endoscopic indications should be taken into consideration, as well as histological indications, and the reports of the endoscopy should be seen. A good clinicopathologic correlation increases the accuracy of the diagnosis. Keywords: Gastritis, gastropathy, classification Gastritis is an infectious or auto-immunological inflammation. Gastropathy can be described as a pathology that displays epithelial injury and regeneration, and it is secondary to endogenous or exogenous irritants.In practice, "gastritis" may be accompanied by mucosal injury, while "gastropathy" may show, even if minimal, an inflammatory reaction. CLASSIFICATIONThere is no universal categorization of gastritis and gastropathy, but they can be categorized according to their duration of development (according to the inflammation type) and acute/chronic etiology. GASTRITISGastritis is an inflammatory condition of gastric mucosa that displays changes related to etiology and the host response. It was identified in the 1800s as a result of autopsies. There may be similar morphological images of gastritis based on different etiologies, and there may be more than one etiologic agent in a gastritis chart.Gastritis was categorized as chronic and acute in 1947 for the first time. Then, chronic gastritis was categorized into two subgroups: namely, superficial and atrophic.After Marshall and Warren demonstrated in 1983 that a bacteria called Campylobacter pylori caused gastritis, a tendency of an etiology-oriented denotation began. For this purpose, a group of gastropathologists prepared a classification in 1990 in Sydney for the first time to classify and rank gastritis. Within this period, the importance of the findings of gastritis, atrophy, and metaplasia in Correa's chart in 1992 was realized, and these findings were included in the first classification. However, due to differences between observers in the rating of especially chronic gastritis and atrophy over time, the Sydney classification was rev...
Localized colitis cystica profunda is a rare, benign disease of the lower gastro-intestinal tract, usually presenting as a rectal mass and characterized microscopically by the presence of mucus-filled cysts in the submucosa. Knowledge of this particular pathological entity is important as it can mimic a well differentiated adenocarcinoma of the rectum and therefore could lead to unnecessary surgical resection. We present a case of colitis cystica profunda misdiagnosed as adenocarcinoma based on their similar clinical picture and histological features.
Background/Aims: Intermediate filament proteins contain few aggregates as their main component. Among those, Mallory-Denk bodies (MDBs) are by far the best recognized component. To identify the presence of MDBs in individuals having chronic liver disease and to evaluate the correlation among MDBs and steatosis as well as the severity and zonal distribution of hepatocyte balloon degeneration. Tertiary reference hospital. Materials and Methods: Three hundred consecutive liver specimens derived from our patients with chronic liver disease were included in the current study. Immunohistochemistry analysis was conducted on frozen liver biopsies fixed at room temperature with acetone anti-rabbit antibody to ubiquitin. In addition, histological activity was evaluated by the routine staining of liver biopsy sections with hematoxylin-eosin and periodic staining by acid-Schiff stain, reticulin, Masson trichrome, and iron. The presence of MDBs, steatosis, severity, and the zonal distribution of hepatocyte balloon degeneration were evaluated in every patient. Results: Histopathologic diagnosis were chronic hepatitis B (n=219), alcoholic steatohepatitis (n=23), non-alcoholic steatohepatitis (n=20), chronic hepatitis C (n=20), overlap syndrome (n=10), and primary biliary cirrhosis (n=8). The distribution of MDBs stained positive for ubiquitin was 80% in the overlap syndrome, 86% in chronic hepatitis B, and 100% in alcoholic steatohepatitis, NASH, chronic hepatitis C, and primary biliary cirrhosis. There was a correlation between the severity of steatosis and ubiquitin positivity, particularly in zone 2. A conspicuous correlation existed between the severity of hepatocyte balloon degeneration and ubiquitin positivity. Conclusion: These findings have demonstrated that the observation of MDB together with ubiquitin positivity will be helpful in the evaluation of the models of diagnosis, staging, and therapy in patients with chronic liver disease.
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