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PubMed1981

Urinary and fecal keto bile acids in liver cirrhosis.

The urinary and fecal bile acids of thirteen male patients with liver cirrhosis were analyzed by gas chromatography and gas chromatography-mass spectrometry to obtain information on their keto bile acid excretion. 3 alpha-Hydroxy-12-keto-5 beta-cholanoic, 3 alpha,12 alpha-dihydroxy-7-keto-5 beta-cholanoic, 3 alpha,7 alpha-dihydroxy-12-keto-5 beta-cholanoic and 3 alpha-hydroxy-7,12-diketo-5 beta-cholanoic acids were found in the urine of ten patients. In four of these patients, keto bile acids were the main bile acids excreted in the urine. However, the ratios of fecal keto bile acids to the total fecal bile acids in these four patients were similar to those in the other six patients whose urinary excretion of keto bile acids was low. Three of the four patients had clinical abnormalities, such as ascites, esophageal varices or a history of hepatic encephalopathy, that may indicate advanced liver dysfunction and/or presence of collateral circulation. These findings suggest that the occurrence of keto bile acids in the urine might be ascribed to the escape of these acids from reduction to hydroxy-forms in the liver, not to bacterial over-production in the intestine. However, the mechanism and significance of the presence of keto bile acids in the urine are still unknown.

Adult↗
PubMed1993

Localization of the cystic fibrosis transmembrane conductance regulator in human bile duct epithelial cells.

BACKGROUND: Liver dysfunction is a common manifestation of cystic fibrosis (CF), a disease caused by mutations affecting the CF transmembrane conductance regulator (CFTR). The aim of this study was to examine the distribution and role of CFTR in liver. METHODS: CFTR messenger RNA was detected in cryosections of human liver by in situ hybridization. CFTR immunoreactivity was detected using antibodies raised against two CFTR peptides. RESULTS: The predominant site of CFTR messenger RNA and immunoreactivity in liver is the intrahepatic bile duct. CFTR is not detected in hepatocytes of normal liver or in livers exhibiting bile duct proliferation. Within bile duct cells, CFTR is localized at or near the apical plasma membrane. CONCLUSIONS: The apical localization of CFTR in bile duct cells suggests a model explaining how the CFTR-associated Cl- channel contributes to normal biliary secretion. This model suggests that if CFTR expression could be promoted in intrahepatic duct cells by somatic gene therapy, this might prevent the occurrence of liver disease in CF.

Antiporters↗
PubMed2005

Decrease in hepatic circulation induces hepatic fibrosis in a neonatal piglet model with short bowel syndrome.

BACKGROUND: Regarding the complications associated with short bowel syndrome (SBS), progressive liver failure is one of the most severe complications known to occur: Although several studies have suggested that many factors interactively influence this clinical condition we investigated the relationship between hepatic circulation and hepatic fibrosis using a neonatal piglet SBS model. MATERIALS AND METHODS: This study used the following 4 groups of neonatal piglets: a group with an 80% resection of the small bowel (SBS group), a group with a bypass operation of the small bowel (functional SBS group), a group with only a laparotomy as a sham operation (sham group), and a no operative treatment group (control group). We measured the hepatic circulation just before and after the reconstruction of the intestine, as well as on the 7th and 14th postoperative day. In addition, both blood and hepatic tissue samples were collected to investigate them both biochemically and morphologically. RESULTS: Regarding the biochemical liver function and the tissue blood flow of liver, there were no significant differences among all groups on any investigated days. However, on both the 7th and 14th postoperative days, the portal venous flow in the SBS group was significantly lower than that in other groups. According to a histological analysis, only hepatic samples on the 14th postoperative day showed mild hepatic fibrosis in the SBS group. Regarding the alpha-smooth muscle actin staining findings that expresses active stellate cells, numerous positive cells were found to be distributed in the perisinusoidal space on the 14th postoperative day in the SBS group. CONCLUSION: Based on our data, a decrease in the hepatic circulation, especially in the portal venous flow, after a massive resection of the intestine may cause progressive liver dysfunction because of the activation of hepatic stellate cells.

Animals↗
PubMed1996

Leukocyte adhesion and hepatic microvascular responses to intestinal ischemia/reperfusion in rats.

BACKGROUND & AIMS: Although it has been reported that gut ischemia/reperfusion (I/R) elicits neutrophil-dependent liver dysfunction, little is known about the kinetics of leukocyte accumulation in the hepatic microcirculation after gut I/R. The aim of this study was to determine the temporal relationship between leukocyte sequestration and oxidative stress in rat liver after occlusion (30 minutes) and reperfusion (60 minutes) of the superior mesenteric artery and assess the effects of neutrophil depletion or immunoneutralization of either intercellular adhesion molecule 1 (ICAM-1) or the leukocyte adhesion glycoprotein CD11/CD18 on the hepatic microvascular responses to gut I/R. METHODS: Leukocyte accumulation, number of nonperfused sinusoids, and autofluorescence of reduced nicotinamide adenine dinucleotide (NADH) were monitored using intravital videomicroscopy both before and after gut I/R. RESULTS: The number of adherent leukocytes in both midzonal and pericentral regions after gut I/R was elevated. Autofluorescence of NADH increased after reperfusion (indicating hypoxia), particularly in the pericentral region. Neutrophil depletion or antibodies to either ICAM-1 or CD11/CD18 blunted the gut I/R-induced increases in NADH autofluorescence in the pericentral region, leukocyte adherence, and nonperfused sinusoids. CONCLUSIONS: Leukocytes accumulate in the liver after gut I/R via interaction of CD11/CD18 and ICAM-1. The leukocytes appear to mediate an oxidative stress, occurring in proximity to nonperfused sinusoids, that may contribute to liver injury.

Animals↗
PubMed1990

Systemic lipid peroxidation and inflammation induced by thermal injury persists into the post-resuscitation period.

We determined the time course of the oxidant-induced systemic lipid peroxidation seen after burn injury. Twelve sheep were given a 15% of total body surface third-degree burn and monitored for 3 or 5 days. Circulating lipid peroxides were monitored by both malondialdehyde (MDA) and conjugated dienes (CD). Lung and liver tissue MDA was also measured and compared to controls. A significant but transient increase in circulating MDA and CD was noted several hours after burn. Venous plasma levels increased again 3-5 days postburn with onset of wound inflammation. Oxygen consumption, VO2, also increased by 35 +/- 12% at this time. Lung MDA, which increased to 64 +/- 5 from a control of 45 +/- 4 nMol/gm, at 12 hours after burn was still increased 3 days after injury. Marked lung inflammation was present early after injury and persisted for the 5-day study period. Liver MDA also increased from control value of 110 +/- 20 to 252 +/- 25 at 12 hours and remained increased over the 5-day period. Serum alkaline phosphatase was also increased. Burn biopsies revealed no infection to explain the ongoing lipid peroxidation process, i.e., bacterial content was less than 10(5) organisms/gram burn tissue. We conclude that an initial system lipid peroxidation occurs immediately after burn injury, and that this process continues well into the post-resuscitation period, corresponding in time with increased VO2, lung inflammation, and evidence of liver dysfunction. The ongoing oxidant changes with the presence of a burn may explain the accentuated organ dysfunction seen with an additional septic insult in burned patients.

6-Ketoprostaglandin F1 alpha↗
PubMed2000

Isolated liver transplant and sequential small bowel transplantation for intestinal failure and related liver disease in children.

Liver dysfunction is a well-recognized complication of intestinal failure in children. Advances in total parenteral nutrition (TPN) have allowed these children to survive while their intestinal tract gradually adapts. Unfortunately TPN may lead to cholestatic liver disease particularly in the young children. Progression of liver disease is associated with a poor prognosis and is an indication for small bowel transplantation. We report our experience of orthotopic liver transplantation in four children with short gut and sequential liver and small bowel transplantation in one child. All children had TPN-related liver failure. Causes of intestinal failure included necrotising enterocolitis (n=2), gastroschisis (n=1), intestinal atresia (n=1), and megacystic, microcolon syndrome (n=1). At the time of liver transplantation the children's mean age was 10.9 months (2.5-24) and weight 6.7 kg (4.8-10.1). The mean serum bilirubin was 522 micromol/liter (299-823), aspartate transaminase 423 IU/liter (49-1024) and international normalized ratio 2.8 (2-3.9). There were two deaths both from respiratory failure secondary to adenovirus pneumonia including the child who received a sequential small bowel transplant. Three children with isolated liver grafts are alive and off TPN at 20 months (mean) follow up (range 6-35). Isolated orthotopic liver transplantation has a role in selected children with intestinal failure, particularly those with short but normally functioning gut and progressing with satisfactory intestinal adaptation but developing liver disease. Those children with TPN-related liver disease and unadapted gut or irreversible intestinal disease need combined liver and small bowel transplantation. Sequential small bowel transplantation is feasible after orthotopic liver transplantation and may provide an option for the child with terminal liver and small bowel failure.

Adolescent↗
PubMed1995

Results of long-term deferiprone (L1) therapy: a report by the International Study Group on Oral Iron Chelators.

This report updates the combined experience of four centres involved in the long-term treatment of transfusional iron overload in 84 patients with the oral iron chelator deferiprone (L1) over 167 patient-years. The source of L1 was variable, including two university research laboratories and three pharmaceutical firms. Compliance was rated as excellent in 48%, intermediate in 36%, and poor in 16% of patients. On a mean L1 dose of 73-81 mg/kg/d, urinary iron excretion was stable, at around 0.5 mg/kg/d, with no indication of a diminishing response with time. Serum ferritin showed a very steady decrease with time from an initial mean +/- 1 SD of 4207 +/- 3118 to 1779 +/- 1154 micrograms/l after 48 months (P < 0.001). 17 patients abandoned L1 therapy. Major complications of L1 requiring permanent discontinuation of treatment included agranulocytosis (three), severe nausea (four), arthritis (two) and persistent liver dysfunction (one). The remaining patients abandoned treatment because of low compliance (three) and conditions unrelated to L1 toxicity (four). Lesser complications permitting continued L1 treatment included transient mild neutropenia (four), zinc deficiency (12), transient increase in liver enzymes (37), moderate nausea (three) and arthropathy (17). There was no treatment-related mortality. Although the complications associated with L1 treatment are significant and require close monitoring, they do not preclude effective long-term therapy in the vast majority of patients. Further well-controlled prospective studies of L1 are required in order to enable proper judgement of its suitability for general long-term clinical use.

Adult↗
PubMed1985

Effect of toxic doses of progesterone on hepatotoxic effects of tetracycline.

The combined effects of high doses of tetracycline and progesterone on parameters indicative for liver function (serum transaminases and urea, serum and liver triglycerides and cholesterol) have been studied in mice. Apart from disturbance of cholesterol metabolism tetracycline-induced liver dysfunction was not aggravated by progesterone.

Alanine Transaminase↗
PubMed1969

Effect of oestrogens and progestogens on liver function in the puerperium.

A modified bromsulphthalein test has been used to detect alterations in liver function in puerperal women taking either a synthetic oestrogen, stilboestrol, or a pure progestogen, megestrol acetate. The oestrogen appreciably reduced the ability of the liver to excrete dye into the bile. It also reduced significantly the equivalent liver volume and the plasma clearance of dye. The progestogen did not have this effect. In so far as these results represent liver dysfunction they are due to the oestrogen component of the combined preparation.

Bile↗
PubMed1985

Increased ethanol consumption and blood ethanol levels in rats with portacaval shunts.

In a series of experiments, it was demonstrated that male rats with end-to-side portacaval shunts (PCS) consumed more ethanol and exhibited higher blood ethanol levels than sham-operated control animals in chronic tests with 2% ethanol and water ad libitum. Ethanol intake in the 6 h prior to blood sampling was 2-5 times and blood ethanol 10-50 times higher in PCS than control rats. These effects were not due to the feminization of male rats occurring after a PCS, since female PCS rats exhibited comparable increases of ethanol intake and blood ethanol. In both sexes ethanol elimination rate and alcohol dehydrogenase activity per total liver were lower after PCS than in control rats, explaining the disproportionate increase in blood ethanol relative to ethanol intake. Interestingly, ethanol intake was not abnormal in PCS rats fed a low-protein, low-tryptophan diet (corn) alone or as a supplement to the usual chow diet. Such dietary modulation of ethanol preference in this animal model of chronic liver dysfunction merits further attention.

Alcohol Drinking↗
PubMed1994

Impact of leukocyte-endothelial cell interaction in hepatic ischemia-reperfusion injury.

To clarify the in vivo relevance of leukocyte-endothelial cell interactions in the manifestation of hepatic ischemia-reperfusion (I/R) injury, we studied leukocyte flow behavior in sinusoids and postsinusoidal venules of postischemic hepatic tissue in rats using intravital microscopy. Reperfusion following either 20 min (n = 9) or 60 min (n = 9) of left hepatic lobar ischemia resulted in a significant increase of the number of stagnant leukocytes in sinusoids and adherent cells in postsinusoidal venules compared with sham-operated controls (n = 10). Transmission electron microscopy revealed the extravasation of leukocytes from both sinusoids (into the space of Disse) and postsinusoidal venules. In parallel, hepatic I/R was associated with increased serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities and reduced bile flow. Linear regression estimates revealed significant (P < 0.01) correlations between serum ALT (r = 0.76) and AST (r = 0.65) activities, bile flow (r = -0.62), and the number of adherent leukocytes in postsinusoidal venules. In contrast, parameters of hepatocellular integrity and function did not directly correlate with the number of stagnant leukocytes in liver sinusoids. We conclude that hepatic I/R induces accumulation, adherence, and extravasation of leukocytes in both hepatic sinusoids and postsinusoidal venules. However, the adherence of leukocytes to the endothelial lining of venules, rather than of sinusoids, may determine the manifestation of hepatocellular damage and liver dysfunction.

Alanine Transaminase↗
PubMed1982

The pharmacokinetics of theophylline in an infant with hepatic failure.

In a 6 1/2-month-old infant with hepatic failure secondary to hereditary tyrosinemia, the theophylline clearance rate of 0.016 liter/kg/h was reduced for age and the serum half-life was prolonged to 18.0 h. Theophylline, 3.4 micrograms/ml, and caffeine, 2.2 micrograms/ml, were identified in a urine sample obtained 48 h after the test dose of theophylline, but no 1-methyluric acid, 1,3-dimethyluric acid or 3-methylxanthine were detected. This is the first infant with liver dysfunction and impaired theophylline disposition to be reported.

Female↗
PubMed2000

[Autoimmune cholangitis (AIC) associated with myositis in monozygotic twins].

A 53-year-old female suffered from joint pain and muscle weakness in all extremities in 1991. Laboratory data showed increased creatine phosphokinase (CK) and aldolase. Liver dysfunction and weakness of proximal muscles also appeared and polymyositis (PM) was suspected. Two years later, she was diagnosed with dermatomyositis (DM) through skin and muscle biopsy. Because elevation of biliary enzymes and transaminases were continued, liver biopsy was performed in 1997. Histopathological findings of her liver were compatible with primary biliary cirrhosis (PBC). Similar conditions were noticed in her identical twin as well. DM associated with PBC is unusual and cases of monozygotic twins with both conditions are very rare. The difference between PBC and autoimmune cholangitis (AIC) which has recently reported and the genetic influence on the pathogenesis of DM and AIC are also discussed.

Autoimmune Diseases↗
PubMedDate not supplied

Hepatotoxicity of the opioids morphine, heroin, meperidine, and methadone to cultured human hepatocytes.

Adult human hepatocytes in chemically defined culture conditions were incubated with morphine, heroin, meperidine, and methadone to investigate their potential hepatotoxicity to human liver. Cytotoxic effects were observed at about 100 times the plasma concentrations required to produce analgesia in human nonaddicts. Concentrations of 1 mM morphine, heroin, and meperidine reduced the glycogen content by 50%, while even 0.2 mM methadone produced a depletion of 70% after 24 h of treatment. Concentrations of 0.8 mM morphine and heroin, 0.4 mM meperidine, and 0.005 mM methadone inhibited the albumin synthesis by about 50% after 24 h of pretreatment. Intracellular glutathione was reduced to 50% of that of controls after 2-3 h of incubation with 2 mM morphine and 1 mM heroin, while 1 mM meperidine and 0.2 mM methadone produced a reduction of about 30% after 6 h incubation. The results show that therapeutic doses of the opioids is unlikely to produce irreversible damage to human hepatocytes, but opiate doses during tolerance or abuse may be a cause of liver dysfunction.

Cell Survival↗
PubMed1995

[Ultrasonic and laboratory studies on fatty liver in white-collar workers].

Ultrasonic and laboratory studies were performed in 816 white-collar workers over 35 years old who received health examination. Prevalence of fatty liver diagnosed by ultrasonography was 17.9% in all subjects and was maximum (24.4%) in males 45-49 years of age. Obesity index and body mass index were higher in fatty liver than in normal controls. Serum levels of glutamate pyruvate transaminase (GPT), cholinesterase, glutamate oxaloacetate transaminase (GOT), gamma-glutamyl transpeptidase (gamma-GTP), triglyceride, total cholesterol, uric acid, HbA1c and glucose were significantly higher, and a serum level of HDL-cholesterol was significantly lower in males with fatty liver than in controls with obesity. Prevalence of abnormal laboratory findings in fatty liver was also shown, and prevalence of fatty liver was prominently high in males with severe obesity or with mild elevation of GPT. A major cause of fatty liver was considered as obesity. In conclusion, fatty liver was a common cause of liver dysfunction and was closely related to risk factors for atherosclerosis especially in white-collar workers.

Adult↗
PubMed1996

Effect of growth hormone administration on serum somatomedin-C levels in bilharzial and liver disorders patients.

This work was designed in an attempt to clarify the effect of growth hormone injection on the serum somatomedin-C (SM-C) levels in Egyptian children with (1) urinary bilharziasis, (2) advanced bilharzial hepatic fibrosis, and (3) children suffering from chronic hepatitis, in comparing with 11 healthy age- and sex-matched children,, served as controls. SM-C levels were studied prior and after injection of human growth hormone (hGH). The basal and hGH-stimulated SM-C levels were significantly reduced in bilharzial patients compared with controls. Patients with hepatitis had significantly lower serum SM-C values prior or post hGH administration. Liver tests carried out for bilharzial patients showed impaired function both on admission and after treatment. It can concluded from this work that shortness in children with bilharzial hepatic fibrosis may be result of hepatic and endocrinal factors and nutritional. Also, our results suggested that the delayed skeletal maturation in chronic hepatitis cases is probably secondary to liver dysfunction, malnutrition and associated endocrinopathies.

Adolescent↗
PubMed1996

[Intraoperative EEG monitoring in hemihepatectomies].

End-stage liver diseases are correlated with specific EEG changes. In chronic liver diseases normal EEG excludes hepatic encephalopathy. To date, it is not known at what time EEG changes appear in liver dysfunction and whether they are to be seen during the unhepatic phase in hemihepatectomies. To clarify this, we analyzed EEGs in 10 patients during hemihepatectomies with the CATEEM system. During the hemihepatectomies an occlusion of the liver hilus for 20-38 minutes (on average 28 minutes) was necessary. During and after the occlusion we found no changes in EEG. We conclude that brief failure of liver function under general anaesthesia is tolerated without danger to the central nervous system.

Adult↗
PubMed1998

[HELLP syndrome. Hepatic subcapsular hematoma and infarction. 2 cases reports].

Two patients with HELLP syndrome are presented and hepatic subcapsular haematoma and infarction were documented. The first clinical manifestation in both cases was hypotension. A surgical pregnancy interruption was required. These patients also presented leukocytosis, renal insufficiency, severe hepatic failure and the presence of hepatic encephalopathy (grade III-IV). One patient died in spite of medical intervention with multiple organ failure. The other patient is still alive but with minor liver dysfunction.

Abortion, Induced↗