Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intolerance of gluten, resposible for Coeliac disease, is essentially shown by an auto-immune enteropathy, even if the cutaneous manifestation (herpetiform dermatitis) and perhaps certain neurological signs (cerebral syndrome, peripheral neuropathy) may be independent as well as associated with the intestinal illness. This affection is of immunological nature, occuring in a genetic field that predisposes to the illness (familial form: concordance of 70% in homozygote twins; 90% of patients show an HLA molecule of type DQ2, DQ8 in almost all the other cases. The exogenous factor is the gluten content contained in wheat, rye and barley, more precisely by the intermediary "the prolamines" which are the "reactive" element that induces a the same time an inflammatory reaction of type TH11 locally (expressed by the histological aspect of a duodenal biopsy evolving as villous atrophy) and a humoral response with production of anti-gliadine and anti-transglutaminase antibodies (the role of the latter enzyme is intervention in the local transformation of antigens to make them antigenic). It is an illness of adults as well as children and this point must now be emphasized. Recent epidemiological studies insist on a high prevalence (1/300 in Europe). Clinical expression, at the start very polymorphic and so misleading, before the appearance of the more classical signs of malabsorption and development, always feared, towards a lymphoma. These signs are haematological (anemia of various types, hyper platelets by hyposplenism, haemorrhagic signs) cutaneous (herpetiform dermatitis, cutaneous vasculitis) mucosal (aphtose), hepatic (cytolysis), neurophysical (fatigue, troubles of behaviour, cerebral syndrome, neuropathy) and osteo-articulitis (osteopenia, arthralgias, diffuse pains). The association of certain auto-immune illnesses must be emphasized (diabetes, Hashimoto thyroiditis, Gougerot disease, primitive biliary cirrhosis). To think early of the possibility of intolerance to gluten, is to give the means of a very easy diagnosis (measurement of anti-gliadin, anti-endomysium and anti-transglutaminase, and secondarily duodenal biopsy if necessary), and it is early elimination of gluten food which will make the various clinical manifestations disappear and so prevent the risk of evolution to a tumoral pathology.
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PMID:[A great imitator for the allergologist: intolerance to gluten]. 1513 80

Multidetector computed tomography (MDCT) angiography has provided excellent opportunities for advancement of computed tomography (CT) technology and clinical applications. It has a wide range of applications in the abdomen including vascular pathologies either occlusive or aneurysmal; enables the radiologist to produce vascular mapping that clearly show tumor invasion of vasculature and the relationship of vessels to mass lesions. MDCTA can be used in preoperative planning for hepatic resection, preoperative evaluation and planning for liver transplantation. MDCTA can also provide extremely valuable information in the evaluation of ischemic bowel disease, active Crohn disease, the extent and location of collateral vessels in cirrhosis.
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PMID:Multidetector computed tomography angiography of the abdomen. 1538 Aug 46

Rifaximin (4-deoxy-4'-methylpyrido[1',2'-1,2]imidazo- [5,4-c]-rifamycin SV) is a synthetic antibiotic designed to modify the parent compound, rifamycin, in order to achieve low gastrointestinal (GI) absorption while retaining good antibacterial activity. Both experimental and clinical pharmacology clearly show that this compound is a nonsystemic antibiotic with a broad spectrum of antibacterial action covering Gram-positive and Gram-negative organisms, both aerobes and anaerobes. Being virtually nonabsorbed, its bioavailability within the GI tract is rather high with intraluminal and fecal drug concentrations that largely exceed the minimal inhibitory concentration values observed in vitro against a wide range of pathogenic organisms. The GI tract represents, therefore, the primary therapeutic target and GI infections the main indication. The appreciation of the pathogenic role of gut bacteria in several organic and functional GI diseases has increasingly broadened its clinical use, which is now extended to hepatic encephalopathy, small intestine bacterial overgrowth, inflammatory bowel disease and colonic diverticular disease. Potential indications include the irritable bowel syndrome and chronic constipation, Clostridium difficile infection and bowel preparation before colorectal surgery. Because of its antibacterial activity against the microorganism and the lack of strains with primary resistance, some preliminary studies have explored the rifaximin potential for Helicobacter pylori eradication. Oral administration of this drug, by getting rid of enteric bacteria, could also be employed to achieve selective bowel decontamination in acute pancreatitis, liver cirrhosis (thus preventing spontaneous bacterial peritonitis) and nonsteroidal anti-inflammatory drug (NSAID) use (lessening in that way NSAID enteropathy). This antibiotic has, therefore, little value outside the enteric area and this will minimize both antimicrobial resistance and systemic adverse events. Indeed, the drug proved to be safe in all patient populations, including young children. Although rifaximin has stood the test of time, it still attracts the attention of both basic scientists and clinicians. As a matter of fact, with the advancement of the knowledge on microbial-gut interactions in health and disease novel indications and new drug regimens are being explored. Besides widening the clinical use, the research on rifaximin is also focused on the synthesis of new derivatives and on the development of original formulations designed to expand the spectrum of its clinical use.
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PMID:Rifaximin, a poorly absorbed antibiotic: pharmacology and clinical potential. 1585 48

Patients with cirrhosis are at increased risk of developing infections due to bacterial translocation. This process depends on three principal factors: bacterial overgrowth, immunodepression, and altered intestinal permeability. Intestinal barrier functions may be disturbed in cirrhosis, related to the toxic effects of alcohol (on mucosa and biological membranes) and portal hypertensive enteropathy. Few studies on the assessment of intestinal permeability in cirrhotic patients are available, and contradictory results may be explained by methodological differences. However, four studies using a differential sugar absorption test (lactulose-mannitol test, a combination of an oligosaccharide and a monosaccharide) showed an increased intestinal permeability in cirrhotic patients. The recurrence of spontaneous bacterial peritonitis can be appreciated only by one similar case history, a low rate of protides in ascites (<10 g/L), bilirubinemia > 55 micromol/L, and thrombocytopenia<98.000/mm3. These results suggest that primary antibiotherapy prophylaxis should be recommended, but this recommendation is limited by the risk of bacterial resistant selection and by the fact that no patient survival benefits was shown. Intestinal permeability could be another predictive factor to justify preventive antibiotherapy; but more studies are needed and methods should be standardized (technique used to measure permeability, patient groups involved).
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PMID:[Intestinal permeability and cirrhosis]. 1663 14

The paper describes the results of studying the immune status of 1,960 patients with stomach, pancreas, liver, gall bladder, small and large intestine disorders, who were treated in the Central Research Institute of Gastroenterology. The results of the study demonstrate that alimentary system diseases are concomitant with changes in the functional activity of the immune system and development of the systemic immune response aimed at the neutralization and elimination of pathogenic agents. Impaired regulatory and efferent lymphocyte capacities, increased synthesis of cytokines, immunoglobulins, heterologous (anti-viral, anti-bacterial or antigliadin), autologous (to parietal cells, microsome mitochondria, tissue transglutaminase) antibodies, formation of immune complexes, autoimmune reactions and secondary immunodeficiency are specific immune mechanisms of the pathological process development, its synchronization and progression in patients with alimentary system diseases. Changes in the immunological status indices are expressed in varying degree depending on the organ involved, etiological factor, clinical course and stage of the disease, as well as treatment used. The immunological status indices have maximal values in cases of chronic hepatitis, hepatic cirrhosis, peptic or duodenal ulcer, cholelithiasis, chronic pancreatitis, gluten-sensitive enteropathy and minimal values in cases of chronic gastritis, gastroesophageal disease, steatohepatitis and irritable bowel syndrome. These data are sufficient for developing an algorithm of immune diagnostics for a number of alimentary system diseases. The study of immune status indices is of great diagnostic and prognostic value as it defines the etiological factor, intensity of inflammatory, infectious and autoimmune processes as well as disease stage and activity, its forecast and the efficacy of treatment of alimentary system diseases.
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PMID:[Diagnostic and prognostic value of humoral immune status indices for alimentary system diseases]. 1753 52

Syndromic diarrhea (SD), also known as phenotypic diarrhea (PD) or tricho-hepato-enteric syndrome (THE), is a congenital enteropathy presenting with early-onset of severe diarrhea requiring parenteral nutrition (PN). To date, no epidemiological data are available. The estimated prevalence is approximately 1/300,000-400,000 live births in Western Europe. Ethnic origin does not appear to be associated with SD. Infants are born small for gestational age and present with facial dysmorphism including prominent forehead and cheeks, broad nasal root and hypertelorism. Hairs are woolly, easily removed and poorly pigmented. Severe and persistent diarrhea starts within the first 6 months of life (</= 1 month in most cases) and is accompanied by severe malabsorption leading to early and relentless protein energy malnutrition with failure to thrive. Liver disease affects about half of patients with extensive fibrosis or cirrhosis. There is currently no specific biochemical profile, though a functional T-cell immune deficiency with defective antibody production was reported. Microscopic analysis of the hair show twisted hair (pili torti), aniso- and poilkilotrichosis, and trichorrhexis nodosa. Histopathological analysis of small intestine biopsy shows non-specific villous atrophy with low or no mononuclear cell infiltration of the lamina propria, and no specific histological abnormalities involving the epithelium. The etiology remains unknown. The frequent association of the disorder with parental consanguinity and/or affected siblings suggests a genetic origin with an autosomal recessive mode of transmission. Early management consists of total PN. Some infants have a rather milder phenotype with partial PN dependency or require only enteral feeding. Prognosis of this syndrome is poor, but most patients now survive, and about half of the patients may be weaned from PN at adolescence, but experience failure to thrive and final short stature. DISEASE NAME AND SYNONYMS: Syndromic diarrhea - Phenotypic diarrhea - Tricho-hepato-enteric syndrome - Intractable diarrhea of infancy with facial dysmorphism - Trichorrhexis nodosa and cirrhosis - Neonatal hemochromatosis phenotype with intractable diarrhea and hair abnormalities - Intractable infant diarrhea associated with phenotypic abnormalities and immune deficiency.
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PMID:Syndromic (phenotypic) diarrhea in early infancy. 1830 70

Abnormalities of liver function are one of the manifold extraintestinal manifestations of celiac disease. Although the spectrum of liver manifestations associated with celiac disease is particularly wide, two main forms of liver damage namely, cryptogenic and autoimmune, appear to be strictly related to gluten-sensitive enteropathy. The most frequent finding is represented by a cryptogenic hypertransaminasemia, observed in about a half of untreated celiac patients, as an expression of a mild liver dysfunction with a histological picture of nonspecific reactive hepatitis (celiac hepatitis) reverting to normal after 6-12 months of a strict gluten-free diet. In a few cases, when celiac disease is diagnosed, a more severe liver injury, characterized by a cryptogenic chronic hepatitis or liver cirrhosis, is present. In these patients, liver damage can still improve after a gluten-free diet institution. Moreover, a close association between celiac disease and autoimmune liver disorders has been widely demonstrated. Indeed, celiac disease has been found in 3-7% of patients with primary biliary cirrhosis, in 3-6% with autoimmune hepatitis, and in 2-3% with primary sclerosing cholangitis. Differently from cryptogenic liver injury, autoimmune liver dysfunction, found in celiac disease, does not usually improve after a gluten-free diet. Presently, it is difficult to establish if the two main kinds of liver injury found in celiac disease (cryptogenic and autoimmune) are discrete entities with a different pathogenesis or if they are an expression of the same disorder where genetic factors and the duration of gluten exposure may determine the severity and the pattern of liver injury.
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PMID:Pathogenesis and clinical significance of liver injury in celiac disease. 1849 73

Although the spectrum of liver abnormalities associated with celiac disease is particularly wide, two main forms of liver damage, namely cryptogenic and autoimmune, appear to be strictly related to gluten-sensitive enteropathy. The most frequent occurrence is a cryptogenic hypertransaminasemia, present in about a half of untreated celiac patients, as an expression of a mild liver impairment characterised by a histological picture of non specific reactive hepatitis (celiac hepatitis) reverting to normal after a few months of gluten withdrawal. In a few cases, a more severe liver injury leading to chronic hepatitis or liver cirrhosis is present. In these patients liver damage can still improve after a gluten-free diet institution. In addition, a close association between celiac disease and autoimmune liver disorders has been largely demonstrated. Indeed, 3%-7% of patients with primary biliary cirrhosis, 3%-6% with autoimmune hepatitis and 2-3% with primary sclerosing cholangitis are affected by celiac disease. Autoimmune liver dysfunction, found in celiac disease, does not usually improve after gluten-free-diet. Presently, it is difficult to establish if the two main kinds of liver injury found in celiac disease (cryptogenic and autoimmune) are discrete entities with a different pathogenesis or if they are an expression of the same disorder where genetic factors and duration of gluten exposure may determine the severity and the pattern of liver injury.
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PMID:Liver dysfunction in celiac disease. 1903 59

There is limited data about the mucosal lesions of portal hypertensive enteropathy (PHE) detected by capsule endoscopy, and there is no scoring system to evaluate their severity. Our aim is to create a reliable scoring system for PHE, and to explore the possible usefulness of using transient elastograhy (TE) in that field. We compared the medical records of 31 patients with liver cirrhosis and portal hypertension with 29 control patients. We found that the mucosal lesions compatible with PHE were significantly more common in cirrhotic patients than in control patients (67.7% vs 6.9%, p<0.001). Cirrhotic patients with high TE score (p = 0.018), high Child-Pugh grade, large esophageal varices (EV), portal hypertensive gastropathy, and history of endoscopic variceal injection sclerotherapy or ligation (EIS/EVL) were significantly associated with PHE. Using our scoring system, we found that patients with higher TE score (p = 0.004), high Child-Pugh score (p = 0.011), larger EV (p = 0.006), and prior EIS/EVL (p = 0.006) were significantly associated with higher PHE score. We concluded that using our scoring system might be helpful in grading PHE severity, and TE might be a new non-invasive method for detecting the presence and severity of PHE in cirrhotic patients.
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PMID:Evaluation of portal hypertensive enteropathy by scoring with capsule endoscopy: is transient elastography of clinical impact? 2066 29

Paper is devoted to the study of the clinical features of the course diseases of gastrointestinal tract and liver in the formation of osteopenia and osteoporosis. Given frequencies of occurrence of infringements of mineral density of bone at patients with chronic pancreatitis, cirrhosis, cholelithiasis, inflammatory bowel disease as well as diseases that are accompanied by malabsorption syndromes (celiac enteropathy syndrome of short small intestine). Established populational (age, sex, lower body mass index, menopause), clinical and laboratory factors indicating high risk of lower bone mineral density in these patients.
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PMID:[Features of bone metabolism in patients with chronic diseases of digestive system]. 2262 81


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