Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033774 (pruritus)
 14,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An exceptional case of early onset and prolonged postpartum course of intrahepatic cholestasis of pregnancy is described. Contrary to other drugs tested, ursodeoxycholic acid administered after the 29th week of gestation improved pruritus and decreased bile acid levels both in serum and amniotic fluid. Labour was induced at 36 weeks, and a female weighing 2.050 g and with an Apgar score of nine was born. Ursodeoxycholic acid, by decreasing the passage of bile acids to the foetus, may have improved the outcome of the pregnancy.
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PMID:Unusual case of severe cholestasis of pregnancy with early onset, improved by ursodeoxycholic acid administration. 948 68

Ursodeoxycholic acid (UDCA) has been shown to be both an effective and well-tolerated treatment of primary biliary cirrhosis, a model chronic cholestatic liver disease. Beneficial effects of UDCA have also been observed in other cholestatic disorders such as primary sclerosing cholangitis, cystic fibrosis, or intrahepatic cholestasis of pregnancy. Liver transplantation is the treatment of choice in end stage chronic cholestatic liver disease. Symptomatic therapeutic concepts include the treatment of cholestasis-associated problems such as pruritus, osteopathy and vitamin deficiency.
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PMID:[Cholestasis: therapeutic options]. 954 51

Liver transplantation is a highly effective treatment for patients with advanced primary biliary cirrhosis and primary sclerosing cholangitis. Transplantation is indicated when the patient's survival with transplantation is better than without or, earlier than this, if the patient's quality of life is intolerable from intractable fatigue or pruritus. Medical therapies for chronic cholestatic liver diseases are very limited. Ursodeoxycholic acid therapy in primary biliary cirrhosis reduces cholestasis and prolongs transplant-free survival; no other drugs are of proven efficacy in primary biliary cirrhosis, and none have any benefit on the disease progression of primary sclerosing cholangitis. Aggressive endoscopic therapy may produce symptomatic and biochemical improvement in primary sclerosing cholangitis but should be done without the expectation of retarding disease progression. Bilirubin is one of five criteria of the Child-Turcotte-Pugh score, which is necessary for the United Network for Organ Sharing listing for orthotopic liver transplantation. In addition, it is a major prognostic indicator in all the predictive models for primary biliary cirrhosis. Bilirubin reduction with ursodeoxycholic acid therapy in primary biliary cirrhosis appears to parallel disease severity, and prognostic models utilizing bilirubin retain their predictive power for survival even in treated patients. In summary, medical therapies for chronic cholestatic liver disease have very little effect on disease progression and, subsequently, on the timing or selection for transplantation. Liver transplantation is the only definitive therapy for primary biliary cirrhosis and primary sclerosing cholangitis.
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PMID:Liver transplantation for primary biliary cirrhosis and primary sclerosing cholangitis: does medical treatment alter timing and selection? 974 89

Ursodeoxycholic acid, employed in treatment of intrahepatic cholestasis as seen in primary biliary cirrhosis, primary sclerosing cholangitis, and chronic hepatitis; does not have marketing approval for prescription during pregnancy because of lack of data. In 3 cases of gravidic cholestasis, we administered oral ursodeoxycholic acid 1 g a day from the 34th week of amenorrhea to delivery. In each case, it took 3 days of treatment for the pruritus to regress incompletely and for plasma levels of biliary acid and transaminases to decrease. The infants, born between the 36th and 38th week of amenorrhea, presented with no problem. Forty-eight cases of gravidic cholestasis treated by ursodeoxocholic acid (0.4 to 1 g a day) have been reported in the literature; 18 cases belonging to 2 randomized studies. In 46 cases pruritus disappeared generally 3 days after treatment onset, and plasma level of biliary acid and transaminase decreased in one week. Only two patients experienced persisting pruritus despite biological improvement. No foetal adverse effect is reported. Ursodeoxycholic acid seems to be an efficient treatment of gravidic cholestasis. Long term observation of fetuses exposed in utero to this treatment is required to assess safety.
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PMID:[Ursodeoxycholic acid: prospect for treatment of gravidic cholestasis? Report of 3 cases]. 985 26

Intrahepatic cholestasis is characterized by a decrease in bile flow in the absence of overt bile duct obstruction, resulting in the accumulation of bile constituents in the liver and blood. Various etiological factors have been incriminated including drugs, total parenteral nutrition, sepsis, pregnancy, graft-versus-host disease and systemic disorders such as sarcoidosis, amyloidosis and Hodgkin's disease. The pathogenesis of cholestasis is unclear and several mechanisms have been hypothesized, without convincing evidence that any of these play a role in clinical cholestasis. Despite the uncertainty about the pathophysiology of intrahepatic cholestasis, several forms of therapy have been employed. Ursodeoxycholic acid may relieve pruritus and lethargy, and in some cases may modify disease progression. If cholestasis persists, supportive therapy is important to maintain optimal physical and nutritional well-being. In patients with advanced liver disease associated with hepatocellular failure, liver transplantation is the only viable option.
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PMID:Intrahepatic cholestatic syndromes: pathogenesis, clinical features and management. 1043 57

Intrahepatic cholestasis of pregnancy is characterized by pruritus and raised maternal aminotransferases and bile acid in serum. It is correlated to increased risk of meconium staining of amniotic fluid, stillbirth and premature labour. A case of treatment with ursodeoxycholic acid from 26. to 36. week gestation is described. Ursodeoxycholic acid is an effective treatment of intrahepatic cholestasis of pregnancy, but the effect seems to decrease after a period.
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PMID:[Intrahepatic cholestasis in pregnancy treated with ursodeoxycholic acid]. 1055 57

This report describes two patients who developed jaundice within two weeks of receiving an amoxycillin-clavulanate potassium combination. Causes of jaundice, other than drug administration, were excluded. The patients' jaundice and clinical symptoms did not respond to stopping the drug. Ursodeoxycholic acid (750 mg/day) led to a prompt and sustained improvement in their hyperbilirubinaemia and symptoms such as pruritus and fatigue. These cases suggest that ursodeoxycholic acid may be an effective treatment for drug-associated cholestasis.
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PMID:Ursodeoxycholic acid (UDCA) for the treatment of amoxycillin-clavulanate potassium (Augmentin)-induced intra-hepatic cholestasis: report of two cases. 1075 Jun 60

Cholestasis is decrease or absence of bile flow into the duodenum. It can be either or in combination pathology of hepatocytes, intrahepatic bile ducts or extrahepatic bile ducts. Hepatocyte with their bile secretory apparatus and tight junction between hepatocytes are of specific importance in this. Bile is formed by several different energy-dependent transport processes. Secretion of bile is a complex metabolic process, which depends upon multiple structural and functional components in the hepatocytes and bile duct cells. The regulation of bile flow is regulated by many hormones. Bile is secreted in bile ducts having pressure of 15-25 cm of water. Rise in pressure in these bile ducts of more than 35 cm of water result suppression of bile flow and jaundice. A rise of conjugated serum bilirubin above the value of 400-500 mumol/L finds an alternate excretory pathway like urine. Various conditions are responsible for infantile cholestasis and can have different outcome of chronic cholestasis. These can be extrahepatic or intrahepatic and acute or chronic. Pathological consequences of infantile cholestasis are mainly because of malabsorption of fat and fat-soluble vitamins and hepatocellular dysfunctions. A battery of tests are required to diagnose the early infantile cholestasis. In the management of cholestasis diet rich in MCT is needed. Further, a high caloric intake up to 200 kcal/day to get adequate weight gain is desirable. Phototherapy, phenobarbitone and rifampicin is helpful in the pruritus of cholestasis by enhancing the excretion of bile. Ursodeoxycholic acid is specifically helpful in the cholestasis. A number of anti-inflammatory and immunosuppressive agents and a new compound, FK 506 has specific role in the management.
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PMID:Infantile cholestasis--advances in its understanding: new concepts. 1091 May 52

Intrahepatic cholestasis of pregnancy is one of the primary disorders of the liver that adversely affects maternal well-being and fetal outcome. Early identification of this condition, careful interdisciplinary monitoring, and prompt delivery at fetal maturity can improve outcomes in the mother and child. Although the cause is unclear, IHCP probably arises from a genetic predisposition for increased sensitivity to estrogens and progestogens and altered membrane composition and expression of bile ducts, hepatocytes, and canalicular transport systems. As a result, the elevations in maternal levels of bile acids and their molar ratios seen in healthy pregnancy rise further in IHCP patients. Also, as the normal fetal-to-maternal transfer of bile acids across the trophoblast is impaired, the excess bile acids with abnormal profiles accumulate and are toxic to the fetus. The management of IHCP is dictated by the increased risks of fetal distress, spontaneous preterm delivery, and sudden death, as well as by alleviating pruritus in the mother. These risks to the fetus rise progressively to delivery, regardless of serum levels of bile acids and ALT. Close monitoring of these markers is essential but does not prevent sudden fetal distress and death. Provision should be made to induce labor as soon as fetal lung maturity has been established. Ursodeoxycholic acid is the only therapy that has proven effective, albeit in small studies, in alleviating pruritus and restoring towards normal the abnormal profiles of bile acids and sulfated steroids in serum and other body fluids. Ursodeoxycholic acid seems to have no obvious adverse effects on the fetus, but experience is insufficient to draw conclusions regarding teratogenicity and prevention of adverse outcomes.
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PMID:Intrahepatic cholestasis of pregnancy. 1129 Dec 41

Hyperlipidemia with a marked increase of low-density lipoprotein (LDL) and high- density lipoprotein (HDL) cholesterol levels is a common feature in patients with chronic cholestatic liver disease. Excess morbidity and mortality from cardiovascular disease has not been reported in these patients. This may be due to the particular lipoprotein pattern observed during chronic cholestasis, characterized by elevated serum HDL cholesterol, which may have a cardioprotective effect. However, in a subgroup of patients with chronic cholestasis, hyperlipidemia is characterized by markedly elevated LDL levels with normal or low HDL levels, probably reflecting hypercholesterolemia with coexisting familial and nutritional origins. Ursodeoxycholic acid, the only drug approved for the treatment of chronic cholestatic liver diseases, has been shown to slightly decrease serum cholesterol concentrations. However, the extent of LDL reduction by ursodeoxycholic acid may be insufficient to protect this subgroup of patients from increased cardiovascular risk. Patients in this subgroup probably would benefit from dietary modification, weight loss, and the administration of specific lipid-lowering drugs. Cholestyramine, which is the first-line treatment for pruritus in chronic cholestasis, may be also indicated for its cholesterol-lowering capacity in patients with hypercholesterolemia who complain of pruritus. Administration of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (simvastatin or pravastatin, 20 mg/d) should be limited to hypercholesterolemic patients with mild chronic cholestatic liver diseases in whom HDL serum levels are below the protective range or if additional risk factors for cardiovascular diseases are present.
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PMID:Hyperlipidemia in Chronic Cholestatic Liver Disease. 1146 68


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