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)

Alcohol damages every organ and system in the body. The most important effects from a clinical point of view relate to diseases of the circulatory, nervous and hepato-gastrointestinal systems. In the digestive tract the effects range from increased intestinal transit time and gastrophaties, leading to classical early morning nausea and diarrhea, through to significant malabsorption and chronic pancreatitis. In this review the mechanisms of alcoholic damage have been evaluated with particular reference to alcoholic liver disease (ALD). In particular, the natural history, the influence due to host genetic susceptibility and due to cofactors (i.e. hepatitis C virus), the clinical features and the hepatocarcinogenesis mechanisms have been evaluated. Finally, a possible role of abstinence in association with pharmacological therapy in the course of steatohepatitis has also been evaluated.
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PMID:Alcoholic diseases in hepato-gastroenterology: a point of view. 1861 69

Growth failure is one of the most common problems in children with thalassemia with multiple etiologies. We present a case of celiac disease, an underdiagnosed cause of growth failure in a child with beta-thalassemia major. A 10-year-old boy on a hypertransfusion regimen was referred for early onset growth failure. Serology for hepatitis B, hepatitis C, and HIV was negative. Serum zinc levels were normal. Thyroid function tests and growth hormone secretion, evaluated with clonidine stimulation test were normal. Malabsorption syndrome was suspected, even in the absence of gastrointestinal symptoms. Tissue transglutaminase were highly raised >300 IU/mL (normal values <15 U/L). Characteristic mucosal lesions on jejunal biopsy confirmed the diagnosis of celiac disease. Institution of a gluten-free diet resulted in rapid gain in weight and improvement in height velocity.
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PMID:Celiac disease in a child with beta-thalassemia major: a need for improved screening and awareness. 1913 78

Familial hypercholesterolaemia (FH) is a common genetic disorder characterized by high plasma low-density lipoprotein (LDL)-cholesterol and premature coronary artery disease. Many factors, such as illness, high-dose statin therapy or a strict vegan diet can cause hypobetalipoproteinaemia (HBL). The more common secondary causes of HBL in the hospital setting include cachexia, intestinal malabsorption, malnutrition, severe liver disease and hyperthyroidism. We report a case of HBL in a 43-year-old man with previously demonstrated marked hypercholesterolaemia who attended a lipid disorders clinic for FH cascade screening. Surprisingly, a lipid profile taken at that time showed low plasma LDL-cholesterol and apolipoprotein B concentrations of 1.6 mmol/L and 0.61 g/L, respectively. He was not on lipid-lowering therapy. DNA sequencing showed that he was heterozygous for the LDLR gene mutation (C677R) present in other affected family members. Of interest, his serum transaminases were increased by approximately 3-fold and hepatitis serology and genotyping confirmed a diagnosis of hepatitis C virus (HCV) infection. In summary, we describe a case of HBL secondary to chronic HCV infection in a patient with FH, confirmed by mutational analysis.
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PMID:Hypobetalipoproteinaemia secondary to chronic hepatitis C virus infection in a patient with familial hypercholesterolaemia. 1948 12

Anemia is the most common complication of inflammatory bowel disease (IBD). Control and inadequate treatment leads to a worse quality of life and increased morbidity and hospitalization. Blood loss, and to a lesser extent, malabsorption of iron are the main causes of iron deficiency in IBD. There is also a variable component of anemia related to chronic inflammation. The anemia of chronic renal failure has been treated for many years with recombinant human erythropoietin (rHuEPO), which significantly improves quality of life and survival. Subsequently, rHuEPO has been used progressively in other conditions that occur with anemia of chronic processes such as cancer, rheumatoid arthritis or IBD, and anemia associated with the treatment of hepatitis C virus. Erythropoietic agents complete the range of available therapeutic options for treatment of anemia associated with IBD, which begins by treating the basis of the inflammatory disease, along with intravenous iron therapy as first choice. In cases of resistance to treatment with iron, combined therapy with erythropoietic agents aims to achieve near-normal levels of hemoglobin/hematocrit (11-12 g/dL). New formulations of intravenous iron (iron carboxymaltose) and the new generation of erythropoietic agents (darbepoetin and continuous erythropoietin receptor activator) will allow better dosing with the same efficacy and safety.
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PMID:Use of agents stimulating erythropoiesis in digestive diseases. 1978 31

Authors report a case of patient suffering from haemophilia A and hepatitis C virus infection acquired probably after blood transfusions and substitution factors application. He was treated with pegylated interferon alpha and ribavirin, with the development of malabsorption symptoms during the therapy. Celiac disease was established by histological, histochemical and serological examinations. oth, interferon alpha and ribavirin treatment as well as virus of hepatitis C may trigger coeliac disease in genetically predisposed individuals. The immunological mechanism of celiac disease include balance disruption between Th1 and Th2 immunological response with Th1 predominance. Only few similar cases have been published in the professional literature to date. Development of celiac disease during interferon alpha therapy with haemophilia A was not published until now (Fig. 3, Ref. 13).
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PMID:Celiac disease manifested during the treatment of chronic hepatitis C by pegylated alpha interferon and ribavirin. 2250 61

Hepatic and gastrointestinal disorders can produce a wide spectrum of neurologic complications both affecting the central nervous system (CNS) and the peripheral nervous system. These manifestations range in severity from coma in acute liver failure and acute pancreatitis, to minor cognitive changes in chronic portosystemic encephalopathy and hepatitis C. Cerebrovascular diseases can complicate hepatitis C infection and inflammatory bowel disease. Demyelinating disorders may co-exist with inflammatory bowel disease. Anti-tumor necrosis factor alpha drugs may induce demyelination. Ataxia may occur in malabsorption syndromes and in gluten related disorders. Characteristic movement disorders are key features of acquired hepatocerebral degeneration and of Whipple disease. Multiple types of neuropathy can be found in association with hepatitis, inflammatory bowel disease and gluten related disorders.
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PMID:Neurologic manifestations of gastrointestinal and liver diseases. 2517

The liver is a major organ and an essential component in maintaining an appropriate nutritional status in healthy individuals through metabolism of protein, carbohydrates, and fat. In individuals with chronic liver disease (CLD), along with a number of other essential functions that the liver serves, its role in nutrition maintenance is severely impaired. Common causes of CLD include hepatitis C, alcoholic liver disease, and non-alcoholic liver disease. Amongst this population, the most common manifestation of impaired nutritional maintenance is protein-calorie malnutrition. Aside from inherent abnormalities in metabolism, such as malabsorption and maldigestion, CLD can be associated with anorexia as well as increased metabolic requirements, all of which contribute to a state of malnutrition. Given the systemic implications and impact on prognosis of malnutrition, proper nutritional assessment is essential and can be achieved through a thorough history and physical, as well as biochemical investigations and anthropometry as needed. Following an appropriate assessment of a patient's nutritional status, an approach to management can be decided upon and is based on the extent of malnutrition which directly reflects the severity of disease. Management options can be grossly separated into enteral and parenteral nutrition. The former is usually sufficient in the form of oral supplements in less severe cases of malnutrition, but as the CLD worsens, parenteral nutrition becomes necessary. With appropriate assessment and early intervention, many of the complications of CLD can be avoided, and ultimately better outcomes can be achieved.
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PMID:Nutritional support in chronic liver disease and cirrhotics. 3038 61