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)

The indications for surgical intervention in chronic pancreatitis are suspicion of malignancy, local complications, and intractable pain. Chronic pancreatitis is a risk factor for development of pancreatic carcinoma, and carcinomas may present, initially with a clinical picture of chronic pancreatitis. Local complications of chronic pancreatitis such as common bile duct or duodenal obstruction and enlarging or symptomatic pseudocyst also mandate surgical intervention. Thrombosis of the splenic vein with left-sided portal hypertension is common and associated with a 10% incidence of gastric variceal hemorrhage, which requires splenectomy. The role of surgery in the management of pain associated with chronic pancreatitis is to provide relief. When the pain interferes substantially with the patient's quality of life or narcotics are required for pain relief, surgical intervention is indicated. Other factors that should be incorporated in assessing the need for surgical intervention are malnutrition due to the inability to eat or malabsorption, the need for frequent hospitalization, and the inability to work. The operation selected for chronic pancreatitis should correct or deal with all structural abnormalities, provide long-term pain relief, have a low mortality and morbidity rate, minimize subsequent exocrine and endocrine insufficiency, and have results independent of abstinence from alcohol. No single operation can provide an optimal solution to the management of pain or these diverse complications of chronic pancreatitis. The operation chosen must be individualized to treat the patient's needs.
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PMID:Current approach to the surgical management of chronic pancreatitis. 919 30

The effect of portal hypertension and chronic high venous pressure on the absorption of the small intestine was examined by constricting the suprahepatic and subdiaphragmatic inferior vena cava in rats. A group of rats with the constricted suprahepatic and subdiaphragmatic inferior vena cava comprised group 1 (n = 9) and another group of rats with only laparotomy comprised group 2 (n = 9). Two months after the operation, sugar absorption and other parameters were measured. The blood pressures of the infrahepatic inferior vena cava and the portal vein 8 wk after the operation in group 1 were significantly higher than those in group 2. The results of D-xylose absorption tests showed that the amount of excreted D-xylose in urine in group 1 was significantly lower than that of group 2, but the D-xylose everted sac test showed no significant differences between the two groups. The glucose everted sac test showed that the amount of glucose absorption in group 1 was significantly lower than that in group 2. These findings suggest that chronic high venous pressure caused by constriction of suprahepatic inferior vena cava may lead to sugar malabsorption. We conclude that portal hypertension with high venous pressure below the diaphragm can lead to sugar malabsorption in the intestine.
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PMID:Effect of portal hypertension caused by chronic high venous pressure on small-intestinal sugar absorption. 1067 32

Primary biliary cirrhosis (PBC) is a presumed autoimmune disease of the liver, which predominantly affects women once over the age of 20 years. Most cases are diagnosed when asymptomatic (60%). The antimitochondrial antibody is present in serum in most, but not in all, patients with PBC. The disease generally progresses slowly but survival is less than an age- and gender-matched general population. The symptomatic patient may have fatigue, generalized pruritus, portal hypertension, osteoporosis, skin xanthomata, fat soluble vitamin deficiencies, and/or recurrent asymptomatic urinary tract infections. Many nonhepatic autoimmune diseases are found in association with PBC and may prompt initial presentation. To date, immunosuppressive therapy has not been shown to prolong survival in PBC. The hydrophilic bile acid, ursodeoxycholic acid (UDCA), has been shown when given in a dose of 13 to 15 mg/kg daily for up to 4 years to delay the time to liver transplantation or death. This therapy also causes a significant improvement of all the biochemical markers of cholestasis but has no beneficial effects on any of the symptoms or associated disorders. Treatment with UDCA does not obviate the need for liver transplantation. Therapies to prevent complications arising from malabsorption, portal hypertension, and/or osteoporosis are required as well. Good control of pruritus can be achieved in most patients. PBC is diagnosed with increasing frequency, but the agent(s) responsible for this slowly progressive destruction of the interlobular bile ducts remains elusive and hence a specific therapy remains unavailable.
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PMID:Management of primary biliary cirrhosis. The American Association for the Study of Liver Diseases practice guidelines. 1073 59

Fistulae between the hepatic artery and portal vein, known as hepatoportal arteriovenous fistula (HPAVF), most commonly occur secondary to trauma or malignancy. Congenital HPAVF is an extremely rare anomaly and only 11 pediatric cases have been documented to date HPAVF causes portal hypertension with the reversal of flow in the portal circulation, leading to hyperemia and congestion of the bowel, causing severe ascites, gastrointestinal bleeding, anemia, and malabsorption. The diagnosis is first made by Doppler sonography, then confirmed by angiography. HPAVF is most effectively treated by performing either ligation of the hepatic artery or percutaneous transcatheter embolization. We describe herein the case of an 8-month-old boy diagnosed to have congenital HPAVF by duplex Doppler sonography and confirmed by digital subtraction angiography, who was successfully managed by percutaneous transcatheter embolization of the feeding right hepatic artery. A review of the previously reported 11 cases of infants with this unusual anomaly, examining presentation, management, and outcome, is also presented.
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PMID:Congenital hepatoportal arteriovenous fistula: report of a case. 1075 81

Recent studies have shown that involvement of the gastrointestinal tract is much more frequent than originally reported in patients with systemic mastocytosis. Seventy percent to 80% of patients with systemic mastocytosis are found to have gastrointestinal symptoms when a careful history is taken, and abnormalities in the gastrointestinal tract are frequently detected by endoscopic studies, functional studies of absorption, and barium studies. Because of the rarity of the disease, there are few prospective studies of gastrointestinal involvement, so the actual frequency of upper and lower gastrointestinal lesions is unknown. Furthermore, there have been no studies correlating endoscopic abnormalities of the lower gastrointestinal tract with the presence or absence of diarrhea, which is a frequent symptom (mean, 43% [range 14%-100%]). A review of gastric acid studies reveals that a proportion of patients develop gastric acid hypersecretion because of the hyperhistaminemia, which can result in ulcer disease that in turn can cause dyspeptic pain, small intestinal mucosal damage, and malabsorption. In some patients gastric acid hypersecretion in the range seen in Zollinger-Ellison syndrome can develop. A number of studies suggest that the prevalence of peptic ulcer disease has been underestimated in these patients and is certainly higher than the general population. The exact physiologic basis for the diarrhea or nondyspeptic abdominal pain remains largely unknown in these patients. Whereas some studies suggest small intestinal mucosal abnormalities are responsible for most cases of malabsorption not associated with gastric acid hypersecretion, this supposition also remains unproven. Hepatomegaly, portal hypertension, splenomegaly, and ascites occur frequently in patients with systemic mastocytosis, especially those with category II through IV disease. Whereas the histology of the liver and spleen and alterations in hepatic function studies have been well studied, the pathogenesis of each of these abnormalities has not been well studied, and almost all the information comes from a few well-studied case reports.
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PMID:Gastrointestinal abnormalities and involvement in systemic mastocytosis. 1090 42

Patients with chronic liver disease exhibit a progressive loss of fat and muscle mass leading to mixed protein-energy malnutrition. The severe loss of muscle mass and body cell mass have convincingly been shown to carry a grave prognosis. Cachexia is likely to progress due to increased requirements as a consequence of hypermetabolism on the one hand and reduced volitional food intake and malabsorption on the other. Hypermetabolism may be mediated by factors such as frequent episodes of endotoxinemia, an activation of the inflammatory cytokine and/or the beta-adrenergic system. Some of these factors may also be responsible for reduced appetite. Obviously, these mechanisms may also be operative in other disease entities but clearly, portal hypertension and portosystemic shunting pose the cirrhotic patient at a particular risk for such disturbances including that of malabsorption. Apart from the established value of providing sufficient nutritious substrate to meet requirements the use of beta-adrenergic blocking agents and endotoxinemia lowering strategies seem worthwhile options that merit further clinical evaluation.
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PMID:Cachexia in liver cirrhosis. 1216 12

The major complications of chronic pancreatitis are malabsorption, diabetes mellitus, pancreatic calcification and pseudocysts. Sinistral portal hypertension due to splenic vein thrombosis, obstructive jaundice and duodenal stricture have also been reported as complications of chronic pancreatitis. However, a case having all these three complications at the same time is relatively rare. We present a case of chronic alcoholic pancreatitis complicated with simultaneous multiple severe complications. Although biliary drainage is usually a useful treatment for reducing the bilirubin level in the patients with obstructive jaundice, jaundice was hardly improved by the percutaneous transhepatic cholangio-drainage (PTCD) in this case. We discussed the cause of the failure in reducing the jaundice and reviewed the previous reports of complications of pancreatitis.
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PMID:Alcoholic chronic pancreatitis with simultaneous multiple severe complications--extrahepatic portal obliteration, obstructive jaundice and duodenal stricture. 1600 77

Insulin-like growth factor I (IGF-I) is a polypeptide hormone secreted by multiple tissues in response to growth hormone (GH). It is partly responsible for GH activity, and also has glucose-lowering and anabolizing effects. Ninety percent of circulating IGF-I originates in the liver and has autocrine, paracrine, and endocrine effects, the latter on multiple tissues. Liver cirrhosis results in a progressive decline of hepatic IGF-I output, and this factor may become undetectable in advanced disease. Some cirrhosis complications, mainly those nutritional and metabolic in nature (insuline resistance, malnutrition, osteopenia, hypogonadism, intestinal disorders), may be at least partly related to this IGF-I deficiency, since some IGF-I effects represent a reverse image of cirrhosis complications. Despite this, IGF-I replacement therapy has been never suggested for cirrhosis. A number of experimental studies in cirrhotic rats showed that therapy using low-dose recombinant IGF-I exerts two types of effect on experimental cirrhosis: a) liver improvement driven by improved hepatocellular function, portal hypertension, and liver fibrosis; and b) cirrhosis-related extrahepatic disorder improvement driven by improved food efficiency, muscle mass, bone mass, gonadal function and structure, and intestinal function and structure, with a normalization of sugar and amino acid malabsorption, and improved intstinal barrier function, manifested by reduced endotoxemia and bacterial translocation. Subsequently, the first randomized, double-blind, placebo-controlled, pilot clinical trial in a small number of cirrhotic patients showed increased serum albumin and improved energy metabolism as a result of IGF-I use. Further clinical trials are needed to identify adequate IGF-I doses, administration duration and frequency, and the subgroup of cirrhotic patients who will benefit most from this replacement therapy.
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PMID:[Insulin-like growth factor I (IGF-I) and liver cirrhosis]. 1751 29

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

Congenital intrahepatic arterioportal fistula is a rare entity that most often presents with symptoms of portal hypertension and malabsorption. We discuss a patient who presented with distributive shock, congestive heart failure, pulmonary hypertension, ascites, and a history of severe constipation.
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PMID:An unusual presentation of a congenital intrahepatic arterioportal fistula in an infant with Down syndrome. 2123 80


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