Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Significant differences exist in the prevalence of most gastroenterological emergencies in tropical compared with temperate countries. Both ethnic and environmental (often clearly defined geographically) factors are relevant. The major oesophageal lesions which can present acutely in tropical countries are varices and carcinoma; bleeding and obstruction are important sequelae. Peptic ulcer disease (and its complications), often associated (not necessarily causally) with Helicobacter pylori infection, has marked geographical variations in incidence. Emergencies involving the small intestine are dominated by severe dehydration, and its sequelae, resulting from secretory diarrhoea, most notably cholera. However, enteritis necroticans ('pig bel' disease), paralytic ileus (sometimes caused by antiperistaltic agents) and obstruction (secondary to luminal helminths, volvulus and intussusception) are other important problems, especially in infants and children. Enteric fever is occasionally complicated by perforation and haemorrhage; the former (which is notoriously difficult to manage) is accompanied by significant mortality. Ileocaecal tuberculosis is a major cause of right iliac fossa pathology--sometimes associated with malabsorption; amoeboma is an important clinical differential diagnosis. The colon can be involved in invasive Entamoeba histolytica infection (which, like complicated enteric fever, is difficult to manage if the fulminant form, with perforation, ensues), shigellosis, volvulus and intussusception. Acute colonic dilatation occasionally follows Salmonella sp., Shigella sp., Campylobacter jejuni, Yersinia enterocolitica and rarely E. histolytica infections. Acute hepatocellular failure is a major cause of morbidity and mortality in the tropics and subtropics. It usually results from viral hepatitis (HBV, sometimes complicated by HDV, and HCV), but there is a long list of differential diagnoses. Hepatotoxicity resulting from herbs, chemotherapeutic agents or alcohol also occurs not infrequently. Chronic liver disease and its sequelae (often long-term results of viral hepatitis) are commonplace. Haematemesis and hepatocellular failure are usually very difficult to manage due to a lack of sophisticated support techniques in developing countries. Invasive hepatic amoebiasis usually responds well to medical management; however, spontaneous perforation can occur and the consequences of this are serious. Pyogenic liver abscess, although far less common than amoebic 'abscess', carries a bad prognosis whatever the method(s) of management. Hydatidosis and schistosomiasis also involve the liver, and helminthiases are important in the context of biliary tract disease. Gall stones are unusual in most tropical settings. Acute pancreatitis is overall unusual, but chronic calcific pancreatitis can present as an acute abdominal emergency.
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PMID:Gastroenterological emergencies in the tropics. 176 26

Since antimitochondrial antibodies (AMA) specific to primary biliary cirrhosis (PBC) recognise enterobacterial proteins and can be induced by R(rough)-mutants of enterobacteriaceae a study was done to find out the prevalence of enterobacterial R-forms in stool samples of patients with chronic inflammatory liver diseases. Liver biopsy specimens were also examined for lipid A, a common antigenic component of the cell wall in gram-negative bacteria. In all stool samples from the 21 patients with PBC Escherichia coli R-forms constituted up to half of the total amount of E coli. In contrast E coli R-forms were detectable in the stools of only 1 healthy control (n = 20), and in 25% of patients with other cholestatic diseases (n = 10), chronic hepatitis type B (n = 15), type non-A, non-B hepatitis (n = 15), or chronic pancreatitis and fat malabsorption (n = 8). An immunoblot technique showed that E coli R-forms isolated from patients' stools contained PBC-specific AMA-reactive proteins with molecular weights of 70-80 kD and 50 kD. Deposits of lipid A, located primarily in the cytoplasm of hepatocytes, were found in 11 patients with PBC but not in the liver of patients with chronic viral hepatitis. Circulating antibodies against lipid A were found rarely and in low titres. The data support the hypothesis that intestinal enterobacterial R-forms are aetiologically important in PBC and that antigens released from the bacterial cell wall contribute to the pathogenesis of the disease.
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PMID:Relation between Escherichia coli R(rough)-forms in gut, lipid A in liver, and primary biliary cirrhosis. 257 61

Patients with chronic cholestasis, particularly those with associated cirrhosis, are susceptible to infectious complications. A predictable consequence of cholestasis is malabsorption of fat-soluble vitamins and free radical scavengers. On the other hand, it has been postulated that cholestasis affects polymorphonuclear leukocytes function by impeding chemotaxis, phagocytosis and superoxide anion release in experimental animals. This work is aimed to evaluate the antioxidant status and phagocytic activity of neutrophils in chronic liver disease patients. 15 primary biliary cirrhosis (PBC) patients, 15 primary sclerosing cholangitis (PSC) patients, 15 chronic viral hepatitis C (HCV) patients, and 15 healthy individuals (control group) were included in this study. Levels of catalase (Cat), superoxide dismutase (SOD), reduced glutathione (GSH), glutathione peroxidase (GPx) and malondialdehyde (MDA) were assessed in both serum and neutrophils homogenates. Neutrophils function was estimated by nitroblue tetrazolium (NBT) reduction assay. A marked decrease in the antioxidant status was observed in serum and neutrophils' homogenate of patients with chronic liver diseases compared to healthy subjects. Significant elevation of lipid peroxides was found in all groups of liver disease patients. The majority of patients had reduced value in NBT reduction assay, which suggested a lack of response to infection by neutrophils. In conclusion, deficient antioxidant defense mechanisms may lead to excess oxygen free radicals formation that promote the pathological process in the liver. The use of free radicals scavengers by chronic liver patients may potentiate the antioxidant defense system against oxidative stress.
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PMID:Study of antioxidant enzymes level and phagocytic activity in chronic liver disease patients. 1571 21

Anemia of diverse etiology is a common complication of chronic liver diseases. The causes of anemia include acute or chronic gastrointestinal hemorrhage, and hypersplenism secondary to portal hypertension. Severe hepatocellular disease predisposes to hemorrhage because of impaired blood coagulation caused by deficiency of blood coagulation factors synthesized by hepatocytes, and/or thrombocytopenia. Aplastic anemia, which is characterized by pancytopenia and hypocellular bone marrow, may follow the development of hepatitis. Its presentation includes progressive anemia and hemorrhagic manifestations. Hematological complications of combination therapy for chronic viral hepatitis include clinically significant anemia, secondary to treatment with ribavirin and/or interferon. Ribavirin-induced hemolysis can be reversed by reducing the dose of the drug or discontinuing it altogether. Interferons may contribute to anemia by inducing bone marrow suppression. Alcohol ingestion is implicated in the pathogenesis of chronic liver disease and may contribute to associated anemia. In patients with chronic liver disease, anemia may be exacerbated by deficiency of folic acid and/or vitamin B12 that can occur secondary to inadequate dietary intake or malabsorption.
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PMID:Spectrum of anemia associated with chronic liver disease. 1978 28