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PubMed1999

Pancreatitis-induced ascitic fluid and hepatocellular dysfunction in severe acute pancreatitis.

BACKGROUND: Multiple organ failure (MOF) is the most serious complication in severe acute pancreatitis, contributing to its high mortality. It has been suggested that changes of high-energy phosphates, intracellular pH, and intracellular cation homeostasis are closely related to hepatocellular injury associated with MOF. METHODS: Phosphorus metabolites, intracellular pH (pHi), and intracellular Na+ concentration ([Na+]i) were measured in rat livers in vivo using 31P and 23Na NMR spectroscopy after deoxycholic acid (DCA)-induced pancreatitis or intraperitoneal injection (ip) of pancreatitis-induced ascitic fluid (PAF). RESULTS: Two hours after induction of DCA-pancreatitis, the liver experienced significant intracellular acidosis (pHi = 6.99 +/- 0.16) and sodium loading (75 +/- 9 mM) and a reduction in its energy state (beta-ATP/Pi = 0.2 +/- 0.03 and Pi = 164 +/- 12). Although ip injection of PAF into healthy rats did not induce systemic hypotension, the livers under these conditions also developed severe disturbances in hepatocellular ion homeostasis and depletion of its bioenergetics. The longer the abdomen was exposed to the PAF, the worse the changes were. At 3 h after ip injection of PAF, hepatic [Na+]i significantly increased (42 +/- 3 mM) along with a significant decrease in pHi (7.30 +/- 0. 03). At 6 h after ip injection of PAF, the hepatic beta-ATP/Pi ratio decreased to 0.34 +/- 0.05 and Pi increased to 97 +/- 27. CONCLUSIONS: PAF induced severe hepatocellular acidosis, rapid accumulation of hepatic intracellular sodium, impaired hepatic cytosolic phosphorylation potential, and increased hepatic utilization of ATP. These effects may account for the eventual development of liver dysfunction associated with necrotizing pancreatitis.

Acute Disease↗
PubMed1978

Liver disease complicating the management of acute leukemia during remission.

Eight adults who developed persisting liver function abnormalities during remission from acute leukemia (6 acute nonlymphoblastic leukemia and 2 acute lymphoblastic leukemia) are reported. These patients constituted 20% of the adults with acute leukemia attaining remission over the time period studied. Although we were unable to be absolutely certain of the etiology of the liver dysfunction, the following findings characterize the problem: 1) onset following red blood cell and platelet transfusions in all cases; 2) minimal symptoms and signs except for transient episodes of jaundice; 3) fluctuating, but often marked, increases in liver transaminases; 4) no other consistent laboratory abnormalities; 5) liver biopsies showing varying degrees of inflammation; 6) a consistent decrease in transaminase levels following pulse chemotherapy; 7) absence of progression of abnormalities during the observation period. This group of patients did not have a worse prognosis than patients with normal liver function. We feel that it is important to recognize this entity and to not withhold antileukemic therapy.

Acute Disease↗
PubMed1998

Hepatitis C virus genotypes and the influence of the induction of immunosuppression with anti-thymocyte globulin (ATG) on chronic hepatitis in renal graft recipients.

Hepatitis C virus (HCV) exhibits a dramatic genetic variability and several mechanisms of immunological response are unable to control hepatic and extrahepatic replication. Genotype 1 b is associated with more severe clinical manifestations and is less responsive to interferon. In addition, we have reported an increase of HCV RNA viral load after renal transplantation. Anti-thymocyte globulin (ATG) is supposed to increase viral replication and liver dysfunction in chronically infected renal graft recipients. We evaluated the genotype profile in HCV+ patients of our Renal Transplant Unit and studied the effects of ATG, as part of the induction of immunosuppression, on viral load and liver enzymes abnormalities. From 726 renal graft recipients, 104 patients, with a mean follow up of 3.9 +/- 2.9 years, were anti-HCV+ by ELISA II. HCV RNA was measured by quantitative PCR. We correlated the viral load and biochemical liver parameters with genotype, exposure to ATG as induction therapy, early acute rejection episode and the duration of infection. Of the 81 patients tested, 72% were viraemic and genotype 1 b was the predominant viral strain (66%). The majority of these patients (65%) were coinfected by two or more strains. There was no correlation between HCV RNA blood levels and liver enzymes. We did not find higher viral load with genotype 1 b infection (68 +/- 88 mEq/ml vs 75.8 +/- 123 mEq/ml in the others) nor with ATG induction therapy (43.5 +/- 71.3 mEq/ml vs 64.1 +/- 110.5 mEq/ml). Early acute rejection and longer follow up were not associated with higher levels of HCV RNA. The biochemical liver profile showed no relationship with the variables studied. We concluded that genotype 1 b is the predominant strain in our HCV+ population and there is a great prevalence of coinfection with several genotypes. Our results did not confirm a deleterious effect of the use of ATG as induction therapy in these HCV-infected patients. Prospective randomised studies with liver biopsy evaluation are needed to answer more fully the remaining questions about the best immunosuppressive therapy in renal graft recipients with chronic HCV infection.

Genotype↗
PubMed1998

Increase in natural killer cell activity following living-related liver transplantation.

We monitored the serial changes of natural killer cell (NK) activity in eight recipients of living-related liver transplantation. The HLA types of all eight patients were haplotypically identical with those of their donors. Tacrolimus and methylprednisolone were used for immunosuppression. The NK activity before transplantation was 24.1 +/- 20.2% which is surprisingly low when compared with the value for normal individuals (67.7 +/- 13.2%, P < 0.01) or a liver dysfunction group (49.4 +/- 21.9%, P < 0.05). Serial changes in NK activity revealed a minimum of 6.1 +/- 3.6% 1 week after transplantation, gradually increasing to 49.2 +/- 12.5% at 2 months after transplantation. These results suggest that the diseased liver might play an important role in the suppression of NK activity.

Adolescent↗
PubMed1999

Acute liver injury associated with the use of ebrotidine, a new H2-receptor antagonist.

BACKGROUND/AIM: Ebrotidine is a new H2-receptor antagonist marketed in Spain in early 1997 and withdrawn in July 1998. We report 11 cases of acute liver injury related to ebrotidine and submitted to a Regional Registry of Hepatotoxicity between June 1997 and August 1998. METHODS: In all cases a structured protocol was used to ascertain the role of ebrotidine and to exclude other causes (viral, immunologic, metabolic) of liver injury. RESULTS: All patients showed clinical symptoms of acute hepatitis, with a marked increase in aminotransferase activities (ALT values ranging from 15 to 91 times the upper limit of normal). Total bilirubin values were also greatly increased (mean 16 mg/dl), and the liver injury was defined as hepatocellular. Features of hypersensitivity were absent. Liver biopsy was done in three patients. Histopathological examination revealed mainly centrozonal necrosis (two cases) or massive necrosis (one patient). Withdrawal of the drug was followed by a gradual improvement in liver dysfunction, except in one patient who developed fulminant hepatic failure and died. There was a positive response to rechallenge in one patient after an inadvertent drug administration. CONCLUSION: Ebrotidine therapy seems to be associated with severe acute liver injury, and therefore its benefit/risk ratio is unfavorable. The relative rareness and unpredictability of the injury, the lack of dose-relationship and the absence of hallmarks of drug allergy are suggestive of an idiosyncratic metabolic mechanism.

Acute Disease↗
PubMedDate not supplied

Case report: hepatic vein thrombosis (acute Budd-Chiari syndrome) in acute leukemia.

A 29-year-old female with acute promyelocytic leukemia presented with severe liver dysfunction and disseminated intravascular coagulation. Her condition rapidly deteriorated and she expired before any antileukemic therapy could be administered. At autopsy, she was found to have massive thrombosis of hepatic veins and their tributaries. Microscopic picture of liver was consistent with acute Budd-Chiari Syndrome, presumably due to the coexisting acute promyelocytic leukemia.

Adult↗
PubMed1991

[An autopsied case of chronic active Epstein-Barr virus (EBV) infection with various symptom].

A 19-year-old boy, who complained of fever and fatigue was hospitalized in November 1986. On physical examination, he had a temperature of 37 degrees C, cervical lymphadenopathy and hepatosplenomegaly. Serum transaminase was elevated moderately, while serum alkaline-phosphatase was elevated severely. Extremely elevated antibody titers to the EBV capsid antigen (IgG: 2560x, IgA: 160x), early antigen (IgG: 1280x, IgA: 160x) and nuclear antigen (160x) were noted. PPD and DNCB skin test were negative. Severe mobilization of Kupfer cells and mild proliferation of pseudoductule were seen in liver biopsied specimen. Cervical lymphnode biopsy showed necrotizing lymphadenitis associated with proliferation of histiocyte. In February 1987 his temperature was elevated to 40 degrees C and he had arthralgia and exanthema. Intravenous Acyclovir (500 mg every 8 hours) and Interferon alpha (6 million u/day) were administered together for 1 month. After that he improved for about a week. In March 1987 he had dyspnea. Arterial blood gas analysis in room air showed a PO2 of 51.8 mmHg, a PCO2 of 28.9 mmHg. A chest radiograph showed thickening of bilateral bronchial walls and obscurity of pulmonary vascular shadows. The effects of transfer factor and Interleukin-2 were unremarkable. High antibody titers to EBV, liver dysfunction and hypo-oxygenemia continued. He died of respiratory and heart failure on 24 October 1987. The most interesting finding of autopsied specimens was stenosis of pulmonary artery associated with interstitial pneumonitis. Hemophagocytosis was seen in liver, spleen and bone marrow.

Adult↗
PubMed1986

Biochemical and histologic pathology in an infant with cross-reacting material (negative) pyruvate carboxylase deficiency.

An infant with the acute neonatal form of pyruvate carboxylase deficiency (cross-reacting material negative) presented with severe intractable lactic acidosis within 4 h after birth. He also had hyperammonemia, hypercitrullinemia, and hyperlysinemia. Plasma glutamine was not elevated. He had a rapidly deteriorating clinical course with severe liver dysfunction, repeated septicemia and seizures; he was comatose and was on a ventilator throughout; death occurred at 8 wk of age. Skin fibroblast study confirmed the enzyme deficiency. Detailed biochemical parameters and histopathology of the brain and liver are presented. The evidence from this infant suggests that disturbances of intracellular oxaloacetate levels as a result of the primary enzyme defect might also contribute to deficiency in ATP generation which may explain the various other biochemical changes and liver pathology.

Acidosis↗
PubMedDate not supplied

Experimental and clinical studies on liver regeneration following transcatheter portal embolization.

BACKGROUND/AIMS: We studied compensatory hypertrophy following transcatheter portal embolization experimentally in dogs and clinically under the condition of cholestasis. METHODOLOGY: Experimental study: Sixteen dogs were used for this study. Transcatheter portal embolization was performed in the left lobes (70% of the total liver) using Gelfoam powder in dogs with 2-week obstructive jaundice. Liver weight, liver blood flow and the intracellular adenosine triphosphate content of isolated hepatocytes were measured after transcatheter portal embolization. Clinical Study: transcatheter portal embolization of the right portal branch was performed in 13 patients with cancer of the biliary tract and 3 patients with hepatocellular carcinoma before (extended) right lobectomy, using Gelfoam powder and thrombin. Six patients who had a total bilirubin level > 5 mg/dLunderwent a percutaneous transhepatic biliary drainage before transcatheter portal embolization. Liver function tests, a volumetric study with computed tomography and immunohistochemical staining for profilerating cell nuclear antigen and apoptosis in the resected livers were performed. RESULTS: Experimental study: The weight ratio of the non-embolized lobes to the total liver, 2 weeks after transcatheter portal embolization in the dogs with jaundice, was significantly lower than that of the normal dogs with transcatheter portal embolization (40.5 +/- 4.5% vs. 47.6 +/- 3.2%), but significantly larger than that of the dogs without transcatheter portal embolization. The cellular adenosine triphosphate content and tissue blood flow in the embolized lobes were significantly lower than those in the nonembolized lobes in the normal and cholestatic livers. Clinical study: The postoperative course in all patients was uneventful, with no serious complication or liver dysfunction. Extended right lobectomy with caudate lobectomy was equivalent to 65% before transcatheter portal embolization and to 56% after, transcatheter portal embolization owing to compensatory hypertrophy of the left lobe. However, there was no significant difference in liver volume in the patients with or without obstructive jaundice. Apoptosis was observed in the embolized lobe. CONCLUSIONS: Preoperative transcatheter portal embolization with percutaneous transhepatic biliary drainage for the purpose of liver regeneration would be useful for treating extended hepatectomy with obstructive jaundice.

Animals↗
PubMed2000

[Kidney transplant patients with hepatitis C virus infection:clinical, pathologic, and immunohistochemical study].

OBJECTIVE: To evaluate the clinical results of kidney transplant patients with hepatitis C virus (HCV) infection. METHODS: We tested the sera from 67 patients for anti-HCV and HCV RNA using second generation ELISA and Nest-PCR; HCV-NS3, NS5 were tested by immunohistochemistry LSAB. All patients were followed up for 1 year. RESULTS: The prevalence of anti-HCV was 50.75% (n = 34), and the rate of HCV RNA was 47.76% (n = 32). The HCV RNA positive group had a much longer duration of dialysis and had received more blood transfusion than HCV RNA negative group before transplantation. ALT levels and prevalence of liver dysfunction were significantly higher in HCV RNA positive group after transplantation; however, there was no difference in infection, rejection, graft survival and serum creatinine level. LSAB suggested that HCV-NS3, NS5 antigen of two from three liver bioptic specimens with HCV RNA positive patients were positive. CONCLUSIONS: HCV infection in renal transplant patients can result in liver disease, and is not significantly associated with infection, rejection, and graft survival within a short time. We consider HCV not a contraindication to renal transplantation.

Adult↗
PubMed2003

[The hemophagocytic syndrome (macrophage activation syndrome)].

The hemophagocytic syndrome (HPS) is an uncommon, often misdiagnosed life-threatening disorder of immune regulation, characterized by a widespread proliferation and multisystemic infiltration of non-malignant histiocytes that undergo uncontrolled hemophagocytosis in bone marrow and/or reticulo-endothelial system. The HPS immune dysfunction consists in a low or absent cytotoxic T and natural killercell activity and in hyperactivation of T lymphocytes and macrophages, with consequent proinflammatory cytokine storm. Clinically, HPS is characterized by high fever, lymphadenopathies, hepato-splenomegaly, liver dysfunction, (pan)cytopenia, hyperferritinemia, hypertriglyceridemia, hypofibrinogenemia, as well as coagulopathy and neurological manifestations in many cases. A hereditary/primary variant (familial hemophagocytic lymphohistiocytosis) and an acquired/secondary form (reactive HPS) are known. This latter may occur in several disorders, including infections, immunodeficiency states, malignancies, lymphoproliferative and autoimmune diseases. Without treatment, HPS fatally has an unfavourable prognosis. Recently, outcome improvements have been reported, due to better therapeutic strategies. The clinical and pathological features of this syndrome are reviewed.

Histiocytosis, Non-Langerhans-Cell↗
PubMed1986

[An autopsy case of adult T-cell leukemia with acute hepatic failure].

An autopsy case of ATL with acute hepatic failure is reported. A 39-year-old man born in Miyazaki Prefecture was admitted because of jaundice and general malaise of about 10 days' duration. Palpation of the abdomen revealed moderate hepatomegaly: the patient had clear consciousness. The white cell count was 62,500/mm3, with 34% abnormal lymphocytes having lobulated or convoluted nuclei. Marked liver dysfunction (TB 30.5 mg/dl; GOT 2,740 U; GPT 1,031 U; LDH 3,833 U) was noted. He developed hepatic coma and died of acute hepatic failure on the third hospital day. At autopsy, the enlarged liver weighed 2,000 g and was diffusely infiltrated by ATL cells.

Acute Disease↗
PubMed1993

Potential role of hepatic macrophages in neutrophil-mediated liver injury in rats with sepsis.

We investigated the pathogenesis of septic liver injury in rats caused by cecal ligation and puncture. In this model, numerous neutrophils accumulated in the liver in parallel with the development of liver dysfunction. The supernatants of hepatic macrophages isolated from these septic rats 24 hr after cecal ligation and puncture had enhanced chemotactic activities for human neutrophils. These results suggest that in sepsis, hepatic macrophages attract neutrophils to the liver. Human neutrophils preincubated in this macrophage supernatant had the following biological activities not seen in the sham-operated controls. (a) They became more adherent to cultured endothelial cells through up-regulation of adhesion molecules such as CD11b/CD18, (b) their chemiluminescence was markedly elevated. These functional changes of cecal ligation and puncture hepatic macrophages were the same as those in endotoxin-pretreated hepatic macrophages after isolation from normal rats. Therefore we suspect that hepatic macrophages are activated by portal vein endotoxin in sepsis. These activated hepatic macrophages secreted chemical mediators of inflammation, including leukotriene B4 and tumor necrosis factor. In conclusion, hepatic macrophages seem to interact closely with neutrophils and play an important role in the pathogenesis of septic liver injury.

Animals↗
PubMed1995

Alpha-fetoprotein-concanavalin A binding as a marker to discriminate between germ cell tumours and liver diseases.

In order to differentiate whether slight alpha-fetoprotein (AFP) increases observed in any patient are due to germ cell tumours (GCT) or to liver diseases (including hepatotoxicity of chemotherapy), we measured the binding ratio of the AFP to concanavalin A (ConA). A total of 218 serum samples were studied: 102 samples from 72 GCT patients and 116 from patients with liver diseases. Considering a cut-off value to be a ConA binding ratio of 15%, we distinguished AFP produced by GCT (> 15%) from AFP produced by tumoral and non-tumoral liver diseases (< or = 15%) with a sensitivity of 98% and specificity of 100%. The difference between mean ConA binding ratios was statistically significant (P < 0.0001). We did not distinguish AFP produced by tumoral and non-tumoral liver diseases. ConA binding ratio may be a sensitive index to distinguish whether an increase of AFP concentration as low as 15 U/ml in a GCT patient during the follow-up is produced by the tumour or by liver dysfunction (including hepatotoxicity of chemotherapy).

Biomarkers, Tumor↗
PubMed1997

Reduced radioactivity in the periphery of the liver in a patient with idiopathic portal hypertension.

The authors report a case of idiopathic portal hypertension in which radioaccumulation in the peripheral region of the liver decreased markedly. On dynamic CT, peripheral regional enhancement of the liver was seen in the arterial phase. The region was hypointense on T1-weighted MR images and hyperintense on T2-weighted images. On portograms via the superior mesenteric artery, markedly decreased portal venous perfusion was seen in the peripheral region of the liver. Tc-99m galactosyl human serum albumin (GSA) liver scintigrams showed decreased accumulation in the peripheral region and unchanged accumulation in the central region of the liver. Tc-99m GSA liver scintigraphy clearly showed localized liver dysfunction in the peripheral region.

Female↗
PubMed1999

Biochemical liver abnormalities in Turner's syndrome.

BACKGROUND: Turner's syndrome is a chromosomal abnormality (45X0) which may be associated with various autoimmune disorders and disease conditions; however, association with liver pathology has rarely been reported. OBJECTIVES: The aim of this work was to assess liver function abnormalities in a group of adult patients with Turner's syndrome. DESIGN AND METHODS: Liver function tests were performed in 16 women with Turner's syndrome all of whom had been previously treated with oestrogens. Patients with liver abnormalities were further studied with hepatic ultrasonography, serological markers of viral hepatitis and autoantibody determinations. RESULTS: Seven women (43.7%) presented with asymptomatic liver cholestasis; these patients were older than those with normal biochemical values (33.4+/-5.2 vs 24.7+/-5.7 years, P<0.05). Liver function abnormalities appeared 7.8+/-4.9 years after starting oestrogen therapy; however, no improvement of liver function was observed 20+/-17.7 months after stopping treatment. All of these women were anti-HCV and HBsAg negative, and autoimmune hepatitis was ruled out in all cases. Liver ultrasound only disclosed homogeneous liver enlargement in one case and cholelithiasis without bile duct abnormalities in another. Four patients underwent a percutaneous liver biopsy of which two were normal and two showed minimal non-specific changes. CONCLUSIONS: The incidence of biochemical liver cholestasis in this group of patients with Turner's syndrome is high. Oestrogen therapy and autoimmune disorders do not seem to be the responsible causes. It appears that this is a benign condition which does not seem to reflect any substantial liver dysfunction. The aetiology remains uncertain.

Adult↗
PubMed1996

Effects of chronic ethanol administration on the endocytosis of cytokines by rat hepatocytes.

The effects of chronic ethanol administration on the endocytosis of three representative cytokines were investigated in isolated rat hepatocytes. When hepatocytes were isolated from rats that were fed an ethanol liquid diet for 12 to 13 weeks, these cells exhibited a decreased ability to internalize and degrade transforming growth factor-alpha, tumor necrosis factor-alpha and interleukin-6, compared with hepatocytes from the pair-fed controls. This impaired endocytosis of all three cytokines was accompanied by significant decreases in the amount of hepatocyte surface-bound cytokine. Changes in cytokine binding to surface receptors and reduced rates of receptor-cytokine complex internalization into the cells seem to be major contributors to defective endocytosis in hepatocytes from the ethanol-fed rats. Impaired hepatocyte endocytosis could lead to altered steady-state levels of cytokines in the liver and modified physiological responses to cytokines. These changes could affect homeostasis among the various cell types in the liver and could contribute to liver dysfunction and injury.

Animals↗
PubMed2006

Resistin serum levels are associated with insulin resistance, disease severity, clinical complications, and prognosis in patients with chronic liver diseases.

OBJECTIVES: Hyperinsulinemia and insulin resistance are present in nearly all patients with liver cirrhosis. Resistin, a mainly adipose-derived peptide hormone, reduces insulin sensitivity in adipocytes, skeletal muscles, and hepatocytes. In experimental cirrhosis models, resistin expression is upregulated. We aimed to evaluate the potential clinical value of resistin in chronic liver diseases (CLD). METHODS: Serum resistin was measured in 82 non-diabetic CLD patients during evaluation for potential liver transplantation and 76 age- and sex-matched healthy controls. Patients were followed for 6 yr. RESULTS: Resistin serum levels were significantly elevated in patients with liver cirrhosis compared with healthy controls (p<0.001). Resistin increased with stage of liver cirrhosis as defined by Child-Pugh or model for end-stage liver disease (MELD) score. Serum resistin correlated with insulin secretion (C-peptide, p<0.001) and inversely with insulin sensitivity (HOMA-index, p=0.008) in CLD patients. Resistin also correlated inversely with markers of hepatic biosynthetic capacity and positively with markers of inflammation such as tumor necrosis factor alpha (TNF-alpha) or C-reactive protein (CRP), as well as with clinical complications, e.g., portal hypertension. Patients with elevated resistin had increased mortality in 6-yr-survival (p=0.005, Cox regression model). CONCLUSION: Resistin offers novel application potential as a clinical biomarker in the assessment of liver cirrhosis. Elevated resistin may contribute to insulin resistance in advanced liver dysfunction.

Adult↗