Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008370 (cholestasis)
 9,378 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Children with end-stage liver disease have been found to have cognitive deficits. The aim of this study was to examine whether cholestatic jaundice causes spatial deficits in rats and if these cognitive deficits are reversed by biliary drainage. Rats were randomly divided into three groups. In the first group, the bile duct was ligated for 3 weeks (BDL group); in the second group, the proximal bile duct was ligated with a Broviac CV catheter for 2 weeks followed by a tube bilioduodenostomy (TBD group); in the third group, a sham operation was performed (SHAM group). All the surviving rats were assessed for spatial learning and memory (a major cognitive function in rats) by the Morris water maze task about 3 weeks after the first operation. Blood was aspirated by cardiocentesis and assayed for total bilirubin, albumin, ammonia, and hemoglobin levels on the day following the water maze task. During the four consecutive acquisition trial days of the Morris water maze, jaundiced rats (BDL group) had a significant longer latency to escape than the SHAM group ( p < 0.05). Rats that underwent biliary decompression for 1 week (TBD group) showed improved status of the spatial deficit, as they required less time to reach the escape platform, approaching the performance of the SHAM group. The BDL group had a significantly higher serum ammonia level, higher bilirubin level, and lower hemoglobin level than the other two groups. After biliary decompression for 1 week, the serum albumin concentration in the TBD group still did not return to the level of the SHAM group. The results of this study suggest that long-term cholestasis results in spatial memory deficits in rats that correlate with anemia and hyperbilirubinemia encephalopathy. Early biliary decompression of obstructive jaundice improves spatial memory deficits, possibly related to the recovery of the serum ammonia and hemoglobin levels.
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PMID:Obstructive jaundice in rats: cause of spatial memory deficits with recovery after biliary decompression. 1496 Nov 95

Forty-one patients undergoing total parenteral nutrition (TPN), were studied in a prospective manner. We found that patients with low serum albumin were more likely to develop cholestasis than patients with normal serum albumin. None of the patients with normal serum albumin developed cholestasis. Fifty-one per cent of patients with low serum albumin (< 3.0 g/dl) developed cholestasis (p < 0.05). In those who developed cholestasis there was a significant, correlation (r = 0.816, p < 0.001) between the serum albumin and the number of days after start of TPN when cholestasis appeared.
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PMID:The role of hypoalbuminemia in the development of the TPN-associated cholestasis. 1683 69

30 cecum-ligated rats were divided into 3 groups: group OS fed with stock diet; group HTPN (high-energy total parenteral nutrition) infused with 260 kcal/kg/d of non-protein energy (NPE), which was isoenergetic to the first group; and group LTPN (low-energy total parenteral nutrition) infused with 160 kcal/kg/d. All rats received approximately 1.4 g/kg/d of nitrogen. Positive nitrogen balances were obtained in all 3 groups, although the values were lower in group LTPN. Serum albumin remained normal. Total bilirubin, lipoprotein-X, alkaline phosphatase (AKP), gamma-glutamyl trans-peptidase (gamma-GT) and glutamic-pyruvic transminase (GPT) were significantly lower in group LTPN than in group HTPN. Histological examination with both light and electron microscopy revealed more severe bile stasis in the canaliculi in group HTPN than in group LTPN. In a separate clinical study, lasting more than 4 weeks, two groups of surgical patients received isonitrogenous TPN regimes containing different amounts of energy (40 kcal/kg/d and 30 kcal/kg/d, respectively). 40% of the NPE was infused as fat. The patients were matched for age, clinical condition and nutritional support technique. There were no differences between the groups in nitrogen balance or serum albumin. However serum AKP and gamma-GT increased in the HTPN group after 2 weeks of nutritional support, whilst in the LTPN group the increase did not occur until the fourth week. Our results suggest that TPN-induced cholestasis can be prevented or delayed by reducing the intake of NPE.
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PMID:Prevention of total parenteral nutrition-induced cholestasis by low non-protein energy supply: an animal experiment and clinical study. 1684 91

Fracturing after liver transplantation (OLT) occurs due to the combination of preexisting low bone mineral density (BMD) and early posttransplant bone loss, the risk factors for which are poorly defined. The prevalence and predictive factors for hepatic osteopenia and osteoporosis, posttransplant bone loss, and subsequent bone gain were studied by the long-term posttransplant follow-up of 360 consecutive adult patients with end-stage primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC). Only 20% of patients with advanced PBC or PSC have normal bone mass. Risk factors for low spinal BMD are low body mass index, older age, postmenopausal status, muscle wasting, high alkaline phosphatase and low serum albumin. A high rate of spinal bone loss occurred in the first 4 posttransplant months (annual rate of 16%) especially in those with younger age, PSC, higher pretransplant bone density, no inflammatory bowel disease, shorter duration of liver disease, current smoking, and ongoing cholestasis at 4 months. Factors favoring spinal bone gain from 4 to 24 months after transplantation were lower baseline and/or 4-month bone density, premenopausal status, lower cumulative glucocorticoids, no ongoing cholestasis, and higher levels of vitamin D and parathyroid hormone. Bone mass therefore improves most in patients with lowest pretransplant BMD who undergo successful transplantation with normal hepatic function and improved gonadal and nutritional status. Patients transplanted most recently have improved bone mass before OLT, and although bone loss still occurs early after OLT, these patients also have a greater recovery in BMD over the years following OLT.
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PMID:Bone mineral density before and after OLT: long-term follow-up and predictive factors. 1693 32

Biliary atresia is the leading cause of chronic infantile cholestasis which eventually leads to cirrhosis. Re-establishment of biliary drainage by Kasai portoenterostomy and liver transplantation for end-stage liver disease has favorably altered the clinical outcome. However, growth failure, one of the major complications of chronic liver disease, remains a major problem. The aim of the study is to evaluate growth, nutritional status and serum growth factor IGF-1 in children with biliary atresia after Kasai operation and at comparing these data between the groups with successful and unsuccessful operation. Fifty-four children with postoperative biliary atresia were evaluated for their clinical outcome, height, blood biochemistry related nutritional status and serum IGF-1. Height and serum IGF-1 were expressed as standard deviation score (SDS) to minimize the influence of age. With 44.4% of the enrolled patients the operation had been unsuccessful and jaundice persisted. The mean age of children with jaundice in comparison with the jaundice free groups was not significantly different (42.0 and 49.9 months, p = 0.458). In jaundice-free patients, hematocrit, serum albumin, calcium and phosphorus were normal and significantly higher. In the successful Kasai group, the height SDS and serum IGF-1 SDS were within the normal range and significantly higher (height SDS 0.2 +/-1.0 vs. -0.9 +/- 1.2, p < 0.01 and IGF-1 SDS 0.5 +/- 2.2 vs. -1.3 +/- 1.0, p < 0.01). The mean IGF-1 SDS in the failed Kasai group was less than -1. Children with good outcome of postoperative biliary atresia showed better growth, better nutritional status and higher serum IGF-1 levels when compared to those with unsuccessful operation.
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PMID:Insulin-like growth factor-1 (IGF-1) in children with postoperative biliary atresia: a cross-sectional study. 1859 30

North American Aboriginal populations are at increased risk for developing immune-mediated disorders, including autoimmune hepatitis. In the present study, the demographic, clinical, biochemical, serological, radiological and histological features of autoimmune hepatitis were compared in 33 First Nations (FN) and 150 predominantly Caucasian, non-FN patients referred to an urban tertiary care centre. FN patients were more often female (91% versus 71%; P=0.04), and more likely to have low serum albumin (69% versus 36%; P=0.0006) and elevated bilirubin (57% versus 35%; P=0.01) levels on presentation compared with non-FN patients. They also had lower hemoglobin, and complement levels, more cholestasis and higher serum immunoglobulin A levels than non-FN patients (P=0.05 respectively). Higher histological grades of inflammation and stages of fibrosis, and more clinical and radiological evidence of advanced liver disease were observed in FN patients, but the differences failed to reach statistical significance. The results of the present study suggest that in addition to being more common, autoimmune hepatitis may be more severe in FN populations, compared with predominantly Caucasian, non-FN populations.
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PMID:Autoimmune hepatitis in a North American Aboriginal/First Nations population. 1892 7

Cornerstones of the diagnostic investigations of disturbances in liver function are analysis and sophisticated evaluation of serum liver enzymes, bilirubin and ammonia. Coagulation factors, serum albumin and cholinesterase levels are indicators of the hepatic metabolic capacity. Dynamic assessment of complex liver functions allows quantification of the hepatic metabolic activity and excretory function. Imaging techniques permit visualization of the size and texture of the liver, the vascular supply and perfusion as well as an assessment of the gall bladder and the extra-hepatic and intra-hepatic bile ducts. Manifold causes for cholestasis and/or liver dysfunction are known, such as ventilation with high pressure, total parenteral nutrition, shock, hypoxia and certain drugs. Obstructive cholestasis requires reconstitution of bile duct drainage, while non-obstructive cholestasis primarily requires treatment of the causative disease. The symptomatic therapy of liver insufficiency is rarely possible via direct treatment of the cause, but mostly requires specific management of secondary organ dysfunctions related to hepatic dysfunction including circulatory failure, hepatorenal syndrome and hepatic encephalopathy. In rare cases a temporary liver surrogate is necessary. The molecular absorbent recirculating system (MARS), a form of extracorporeal albumin dialysis, is introduced as a modality for the treatment of liver failure.
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PMID:[Cholestasis and liver dysfunction in critical care patients]. 1898 50

The physiological changes in liver function in pregnancy are commonly transient, rarely permanent. Disorders arising in pregnancy, such as pre-eclampsia and eclampsia, acute fatty liver of pregnancy (AFLP), haemolysis, elevated liver enzyme and low platelets (HELLP) syndrome, cholestasis, hyperemesis gravidarum and isolated cases of raised liver enzymes can have serious implications. Proper interpretation of liver function tests (LFTs) at an early stage can lead to timely management and may reduce complications in both mother and fetus. Normal LFTs do not always mean that the liver is normal. A number of pitfalls can be encountered in the interpretation of basic blood LFTs. The commonly used LFTs primarily assess liver injury rather than hepatic function. Abnormal LFTs may indicate that something is wrong with the liver, and they can provide clues to the nature of the problem but this is not always the case. The various biochemical tests, their pathophysiology, and an approach to the interpretation of abnormal LFTs are discussed in this review. Commonly available tests include alanine transaminase, aspartate transaminase, alkaline phosphatase, bile acid, serum bilirubin, serum albumin and prothrombin time.
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PMID:Liver function test and pregnancy. 1933 Jul 14

The urinary ratio of 6 beta-hydroxycortisol/cortisol (6 beta-OHC/C) as a biomarker of CYP3A4 metabolizing activity has been studied in Egyptian patients with chronic liver cirrhosis associated with previous hepatic Schistosomiasis infection to determine any possible alteration in enzyme activity. The ratio of 6-beta OHC/C was determined in morning urine samples collected from 8:00 a.m. to 12:00 p.m. in healthy adults (n = 36) and patients with liver cirrhosis (n = 57). The median age for control was 27 years (range: 18-50 years) and 50 years (range: 27-75 years) for patients. 6 beta-OHC was detected in urine by ELIZA kits (Stabiligen, France). Patients with liver cirrhosis were categorized according to Child Pugh Classification into Child B (n = 28) and Child C (n = 29) classes. Cholestasis was observed in 9/28 of Child B class and 8/29 of Child C class of patients. The control subjects showed gender-related difference in the urinary ratio of 6 beta-OHC/C. A significant reduction (P < 0.001) in 6 beta-OHC/C ratio was observed only in Child C patients in comparison with control subjects. Regression analysis showed a significant correlation (P < 0.05) between 6 beta-OHC/C ratio and serum albumin. The influence of cholestasis on the urinary ratio of 6-beta OHC/C was observed on cirrhotic patients of Child B class. In conclusion, patients with chronic liver cirrhosis might have a reduction of metabolizing activity of CYP3A4 enzymes which could be identified by measuring the urinary ratio of 6 beta-OHC/C. This reduction is more apparent in severe liver injury (Child C class). Therefore, it is important to understand the metabolic fate of drugs metabolized by 3A4 enzymes in patients with liver cirrhosis to avoid drug accumulation that might lead to development of drug toxicity.
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PMID:Study of the Urinary Ratio of 6 beta-Hydroxycortisol/Cortisol as a Biomarker of CYP3A4 Activity in Egyptian Patients with Chronic Liver Diseases. 1969 Jun 46

Abnormalities of liver function (notably rise in alkaline phosphatase and fall in serum albumin) are common in normal pregnancy, whereas rise in serum bilirubin and aminotransferase suggest either exacerbation of underlying pre-existing liver disease, liver disease related to pregnancy or liver disease unrelated to pregnancy. Pregnant women appear to have a worse outcome when infected with Hepatitis E virus. Liver diseases associated with pregnancy include abnormalities associated hyperemesis gravidarum, acute fatty liver disease, pre-eclampsia, cholestasis of pregnancy and HELLP syndrome. Prompt investigation and diagnosis is important in ensuring a successful maternal and foetal outcome. In general, prompt delivery is the treatment of choice for acute fatty liver, pre-eclampsia and HELLP syndrome and ursodeoxycholic acid is used for cholestasis of pregnancy although it is not licenced for this indication.
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PMID:Liver abnormalities in pregnancy. 2409 Sep 43


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