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PubMed1992

Influence of hepatic dysfunction on cyclosporine metabolism in the pig.

Cyclosporine (CyA) is eliminated from the body via biliary excretion at a rate directly proportional to bile production and the functional status of the liver. Previous reports demonstrated that disturbances in the hepatic excretory function with a rise in the plasma bilirubin level are positively correlated with high blood concentrations of CyA and CyA plus metabolites (CyA + M). Less information is available about the blood concentrations of the CyA parental substance or CyA metabolites in the case of liver dysfunction when there was no elevation of serum bilirubin content. To answer this question, we compared the pharmacokinetic profile of CyA in a cholestatic and in a ischemic model in pigs. Our results show that in pigs receiving a single dose of CyA after liver ischemia, the blood concentrations of CyA and CyA + M are significantly increased independently of the serum bilirubin concentration, probably through a slow down of CyA metabolism by impairment of cytochrome P450 III A.

Alanine Transaminase↗
PubMed1998

Prevention of hypoxic liver cell necrosis by in vivo human bcl-2 gene transfection.

Prevention of hypoxic cell death is a key to successful liver transplantation. We developed a new method for preventing liver hypoxic cell death by introducing an anti-cell death gene directly into rat livers. When the human bcl-2 gene (hbcl-2) was directly transfected into rat livers together with non-histone chromosomal protein high mobility group 1 (HMG1) by the hemagglutinating virus of Japan (Sendai virus; HVJ)-liposome method, human Bcl-2 protein (hBcl-2) was efficiently expressed. Electron microscopy and fluorescence microscopy revealed that hepatocytes expressing exogenous hBcl-2 were almost completely protected the hypoxic cell necrosis. The expression of the hBcl-2 also inhibited activation of caspase-3 (-like) proteases and liver dysfunction. Thus, we conclude that transfection of the hbcl-2 gene through HVJ-liposome method is useful to prevent liver cell necrosis induced by hypoxia. This finding could lead to new strategies to avoid the hypoxic cell death, the major problem in liver transplantation.

Animals↗
PubMed1997

A comparison of EMIT and FPIA methods for the detection of cyclosporin A blood levels: does impaired liver function make a difference?

OBJECTIVE: Apparent cyclosporin A (CSA) blood levels, as determined by fluorescence polarization immunoassay (FPIA) and enzyme-multiplied immunoassay technique (EMIT), were compared in CSA-treated patients with various degrees of liver dysfunction. METHODS: FPIA and EMIT were performed in parallel according to test manufacturer instructions in blood from kidney (n = 82), liver (n = 96) and heart transplant (n = 20) patients. RESULTS: The precision of both techniques was greatest in patients with the highest blood levels, and at each blood level greater for the FPIA than for the EMIT. Apparent CSA blood levels, as determined by EMIT, were typically approximately 70% of those determined by FPIA, indicating greater cross-reaction of the antibody in the FPIA with CSA metabolites. However, the ratio of values determined with EMIT and FPIA was very similar in kidney, liver and heart transplant patients. Among liver transplant patients it was also very similar in those without major alterations of hepatic function and in those with impaired excretory (increased bilirubin and gamma GT) or synthetic (i.e., reduced thromboplastin time) function. Extended storage of blood samples for up to 10 days did not affect apparent CSA blood level estimates by EMIT in a clinically relevant manner. CONCLUSIONS: We conclude that the greater specificity of the antibody in the EMIT for the CSA parent compound does not translate into a clinically relevant advantage for CSA monitoring.

Cyclosporine↗
PubMed1998

Mixed malignant germ cell tumour of the liver.

Germ cell tumours of the liver are rare neoplasms, with fewer than 20 cases reported in the literature following presentation as teratomas, choriocarcinomas or yolk sac tumours. We report a 52-year-old patient who complained of upper abdominal pain and anorexia. Ultrasonography and computed tomography of the abdomen revealed a large hepatic mass. Among the laboratory values we found elevated levels of alpha-fetoprotein and beta-chorionic gonadotropin. Repeated biopsies via CT scan, laparoscopy and laparotomy disclosed a poorly differentiated adenocarcinoma. Subsequently liver function deteriorated and, on the basis of clinical data highly suggestive of a malignant germ cell tumour, a modified chemotherapeutic protocol (PEI) was initiated. The elevated levels of alpha-fetoprotein and beta-chorionic gonadotropin declined rapidly, but the patient died 10 days later of liver dysfunction and bronchopneumonia. Subsequent autopsy confirmed the initial clinical diagnosis of a multilocular extragonadal malignant germ cell tumour of the liver with components of choriocarcinoma and embryonal carcinoma.

Chorionic Gonadotropin, beta Subunit, Human↗
PubMed1990

Clinical utility of liver biopsy in patients with serum antibodies to the human immunodeficiency virus.

PURPOSE: Patients with the acquired immunodeficiency syndrome (AIDS) frequently have liver dysfunction, which may be due to a number of causes. Determination of the patients who are likely to benefit from liver biopsy, an invasive procedure, is therefore important. In this study, the results of liver biopsy in patients with AIDS were compared to those in human immunodeficiency virus (HIV)-infected patients without AIDS. PATIENTS AND METHODS: Thirty-six consecutive patients with antibodies to HIV present in the serum underwent liver biopsy from 1984 through 1988 at the Bronx Municipal Hospital. Twenty (56%) of the patients had AIDS diagnosed prior to the liver biopsy. Indications for the liver biopsy were unexplained fever in 83%, and abnormal serum levels of biochemical parameters of liver function in 89%. RESULTS: Liver biopsy was diagnostic in 18 cases (50%), including findings of hepatic infection by mycobacteria in 15, cytomegalovirus in two, and schistosoma in one; these infections had been previously detected at an extrahepatic site in only two cases. Helpful clinical information in 10 others included findings of granulomas of undetermined etiology in four, cirrhosis in five, and chronic persistent hepatitis in one. Patients with a diagnostic biopsy, as compared to patients with a nondiagnostic biopsy, had a statistically significant increase in the frequency of having AIDS diagnosed before the biopsy, longer duration of AIDS (in patients with AIDS diagnosed before the biopsy), greater number of different prior opportunistic infections, and a more elevated serum alkaline phosphatase level. For example, 70% of patients with AIDS, as compared to 25% of patients with serum antibodies to HIV but without AIDS, had diagnostic liver biopsies. Patients with a diagnostic biopsy also had statistically significantly more frequent pulmonary symptoms, possibly due to more frequent occurrence of Pneumocystis carinii pneumonia. In particular, the 15 patients with hepatic mycobacterial infection, as compared to the other patients, had a statistically significant increase in the frequency of having AIDS diagnosed prior to the biopsy, longer duration of AIDS, more frequent prior opportunistic infections, more severe leukopenia, and a more elevated serum alkaline phosphatase level. Liver biopsy was more sensitive than bone marrow aspiration and biopsy at detecting mycobacterial infection. CONCLUSION: Liver biopsy, when indicated, is useful to detect opportunistic infection in HIV-infected patients who are not known to have AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Liver damage in patients with colony-stimulating factor-producing tumors.

PURPOSE: We have demonstrated that colony-stimulating factor (CSF)-producing tumor cell lines produce not only CSF but also interleukin-1 (IL-1) and interleukin-6 (IL-6). Clinically, we have observed that patients bearing such tumors present with liver dysfunction and fever in addition to marked leukocytosis. The purpose of this study was to determine whether or not the liver damage was specifically related to CSF-producing tumors. PATIENTS AND METHODS: Clinicopathologic examinations were performed in six autopsied patients with CSF-producing tumors. We also transplanted two tumor cell lines (KHC287 and CHU-2), which produce granulocyte (G)-CSF, IL-1, and IL-6, to nude mice. RESULTS: Of the six patients, five had G-CSF- and one had granulocyte/macrophage (GM)-CSF-producing tumors. IL-1 and IL-6 concentrations in plasma or culture supernatant were elevated in these patients. Biochemical examinations revealed high serum enzyme levels of the biliary system in contrast to normal or slight increases in transaminase levels in all patients studied. Serum direct bilirubin was elevated in five of the six patients. Three common pathologic changes of the liver were found: (1) focal necrosis associated with neutrophil infiltration in the centrilobular zones, (2) fibrous change and enlargement of the portal area associated with neutrophil infiltration, and (3) intrahepatic cholestasis. The same pathologic changes, except for cholestasis, were reproduced in the liver of mice transplanted with KHC287 or CHU-2. CONCLUSION: These results indicate that patients with CSF-producing tumors have characteristic liver damage, and suggest a new paraneoplastic syndrome of leukocytosis and liver damage.

Aged↗
PubMed2001

Indications for pediatric intestinal transplantation: a position paper of the American Society of Transplantation.

Parenteral nutrition represents standard therapy for children with short bowel syndrome and other causes of intestinal failure. Most infants with short bowel syndrome eventually wean from parenteral nutrition, and most of those who do not wean tolerate parenteral nutrition for protracted periods. However, a subset of children with intestinal failure remaining dependent on parenteral nutrition will develop life-threatening complications arising from therapy. Intestinal transplantation (Tx) can now be recommended for this select group. Life-threatening complications warranting consideration of intestinal Tx include parenteral nutrition-associated liver disease, recurrent sepsis, and threatened loss of central venous access. Because a critical shortage of donor organs exists, waiting times for intestinal Tx are prolonged. Therefore, it is essential that children with life-threatening complications of intestinal failure and parenteral nutrition therapy be identified comparatively early, i.e. in time to receive suitable donor organs before they become critically ill. Children with liver dysfunction should be considered for isolated intestinal Tx before irreversible, advanced bridging fibrosis or cirrhosis supervenes, for which a combined liver and intestinal transplant is necessary. Irreversible liver disease is suggested by hyperbilirubinemia persisting beyond 3-4 months of age combined with features of portal hypertension such as splenomegaly, thrombocytopenia, or prominent superficial abdominal veins; esophageal varices, ascites, and impaired synthetic function are not always present. Death resulting from complications of liver failure is especially common during the wait for a combined liver and intestinal transplant, and survival following combined liver and intestinal Tx is probably lower than following an isolated intestinal transplant. The incidence of morbidity and mortality following intestinal Tx is greater than that following liver or kidney Tx, but long-term survival following intestinal Tx is now at least 50-60%. It is probable that outcomes shall improve in the future with continued refinements in operative technique and post-operative management, including immunosuppression.

Child↗
PubMed2001

Are there histopathologic characteristics particular to fulminant hepatic failure caused by human herpesvirus-6 infection? A case report and discussion.

An 8-month-old boy was admitted to a neighboring hospital for severe liver dysfunction and drowsiness 4 days after a diagnosis of exanthem subitum. A diagnosis of fulminant hepatic failure was made, and liver biopsy was performed during the acute stage. The presence of human herpesvirus-6 variant B (HHV-6B) DNA was shown in liver tissue by polymerase chain reaction (PCR) and in the endothelium of the portal vein by in situ hybridization (ISH). Histologic examination showed microvesicular steatosis resembling that of Reye's syndrome, even though aspirin had not been prescribed. We considered HHV-6 to be the causative agent in this case and report what is perhaps the first precise histologic description of fulminant hepatic failure caused by HHV-6.

DNA Primers↗
PubMed1991

Morbidity and mortality of short bowel syndrome in infancy and childhood.

This report concerns 59 infants and children with short bowel syndrome, most commonly caused by necrotizing enterocolitis in this study. Resection of atretic or gangrenous bowel was performed in 53 patients, tapering enteroplasty and primary anastomosis was performed in 13 patients, and temporary enterostomies were performed in 40 patients. Second-look laparotomy was useful in two of four cases of questionable bowel viability. The ileocecal valve was resected in 32 patients and remained intact in 27. The mean length of the remaining bowel was 58.4 cm. All patients received total parenteral nutrition and early enteral feedings. Home hyperalimentation was attempted when 50 per cent of the calorie intake was enteral. Intestinal adaptation required from 3 to 14 months. Frequent setbacks were related to catheter sepsis, rotavirus infection, carbohydrate intolerance, and liver dysfunction. The overall survival rate was 80 per cent with mortality due to sepsis associated with total parenteral nutrition and liver failure.

Adaptation, Physiological↗
PubMed1976

Study of an epidemic of venoocclusive disease in India.

Twenty-five cases of rapidly developing ascites occurring in an epidemic form were observed in a tribal district in Central India during August 1972-May 1973. Eleven of the patients died. Six patients were brought to hospital and studied for periods of two to 17 months. Necropsy was performed on one patient who died. The clinical features suggested an outflow tract obstruction such as a Budd-Chiari-like syndrome or venoocclusive disease. Radiographic and haemodynamic studies demonstrated a combination of post and perisinusoidal blocks. Liver dysfunction was indicated by the presence of a marked bromsulphthalein retention and mild to moderate hypoalbuminaemia. Histological examination of the liver biopsies showed changes that ranged from centrizonal haemorrhagic necrosis to an extensive centrilobular fibrosis associated with central vein occlusion. The disease was apparently caused by a food toxin, and the possible nature of this is discussed.

Adolescent↗
PubMed1973

Serum D-glutamyl transferase following myocardial infarction.

D-glutamyl transferase (GMT) activity was measured in 49 patients with proven myocardial infarction. Twenty-three patients had normal GMT activity and 26 had increased GMT activity. Most of the patients with increased GMT had evidence of liver dysfunction and it is suggested that any increases in serum GMT activity following myocardial infarction are a result of secondary liver damage rather than a release of GMT from cardiac tissue.

Alanine Transaminase↗
PubMed2000

[A case of biloma caused by early complications of hepatic artery infusion chemotherapy].

We report a 70-year-old male who had biloma as an early complication of hepatic artery infusion chemotherapy. The patient had a history of subtotal gastrectomy for a advanced gastric cancer. Two years after the primary operation on the stomach, a solitary metastatic liver tumor was indicated by follow-up abdominal CT, and a segmental hepatectomy was performed. Soon after the hepatectomy, intraarterial catheter placement was performed via the left subclavian artery for preventive chemotherapy. Infusion chemotherapy of 10.5 g 5-FU and 75 mg CDDP was administered for a month, during which time the patient had liver dysfunction, fever, tenderness, and abdominal fullness. Abdominal CT revealed a large low density mass at a lateral segment of the liver which could not be seen on the previous CT image. Also, extravasation of contrast media was identified by angiography via the reservoir catheter. Using an interventional technique, percutaneous transhepatic drainage for biloma and extubation of the reservoir catheter were performed. The present case is thought to be of an early and rare complication of hepatic artery infusion chemotherapy. The etiology is discussed herein.

Aged↗
PubMed2005

Platelet activation in patients with alcoholic liver disease.

OBJECTIVE: To elucidate the mechanisms of thrombocytopenia in alcoholic liver diseases, we investigated activation status of platelets in patients with alcoholic fatty liver (Al-FL), alcoholic liver cirrhosis (Al-LC) or hepatitis-C liver cirrhosis C (C-LC). METHODS: Platelet activation was evaluated by flow cytometry using monoclonal antibodies against P-selectin (CD62P) and the fibrinogen receptor (PAC-1), both specific for platelet activation, and anti-CD61 antibody for the presence of microparticles (PMP) in seven patients with Al-FL, thirteen patients with Al-LC and, as a non-alcoholic liver disease control, nine patients with C-LC. As a normal control, seventeen healthy subjects without liver dysfunction were also evaluated. RESULTS: Compared with the healthy controls, the platelet count was significantly decreased in patients with alcoholic liver diseases or C-LC. Ten days after discontinuation of alcohol intake, the platelet count was significantly higher in both the Al-FL and Al-LC groups than that measured on admission. There was an inverse correlation between the platelet count and PMP, a marker of platelet activation. The Al-FL, Al-LC and C-LC groups showed significantly higher percentages of platelets positive for CD62P than the healthy controls. The PAC-1 positivity was increased only in the C-LC group. PMP were significantly increased in the Al-FL, Al-LC and C-LC groups compared to that in the healthy group. In the Al-LC group, PMP were significantly decreased 10 days after discontinuation of alcohol intake from that measured on admission. CONCLUSION: Patients with alcoholic liver diseases have increased platelet activation, which may contribute to the occurrence of thrombocytopenia. The formation of PMP might be one of the important factors of thrombocytopenia in alcoholic liver diseases.

Aged↗
PubMed2007

[A case of recurrent gastric cancer with obstructive jaundice successfully treated by docetaxel].

Recently, treatment by taxane regimen for advanced gastric cancer as second-line chemotherapy has been increasingly reported. A 58-year-old man underwent distal gastrectomy for advanced gastric cancer on November 25, 2002. There was permeation through the duodenum side, and a Billroth II operation was done for repair. Although a relapse was not clear from the picture image, due to the tumor marker increase since July 2004, chemotherapy using TS-1 100 mg/day was given. On February 2005, liver dysfunction and obstructive jaundice appeared, and the patient was diagnosed with a recurrence in the hilar lymph node of the liver through PET and CT. Because of the Billroth II operation for repair, ERBD was impossible, and we performed PTCD to decrease jaundice. Treatment by docetaxel 60 mg/m(2) every three weeks was given since March 15. After two courses of chemotherapy with docetaxel, the insertion of the guide wire was possible from the part of PTCD. Implantation of the stent became possible after four courses. PTCD could be removed, and the patient QOL has effectively improved. Outpatient treatment became possible for him in January 2006.

Adenocarcinoma↗
PubMed1991

[Analysis of hemostatic abnormality in various disease using molecular-I. Liver disease].

We examined the hemostatic abnormality of liver disease using hemostatic molecular markers, i.e. TAT, FPA and SFMC for coagulation, B beta 15-42, FDP, D dimer and PIC for fibrinolysis, t-PA and TM for vessel wall. The molecular markers for coagulation were generally increased in cases of liver disease, which was most sensitively reflected by FPA. On the other hand, it was postulated that SFMC was a marker reflecting the complication of DIC in these cases. Hyperfibrinolysis of liver disease was sensitively reflected by the increase of B beta 15-42, and an occasional increase of SFMC or FDP was thought to indicate the complication of DIC in these cases. A high correlation was found between t-PA and TM. It was postulated that the increase of the both markers in liver disease was due to deteriorated clearance by liver dysfunction, although TM is regarded as a marker reflecting endothelial injury. It was expected that visualization of hemostatic disorder of liver disease was made practical with the use of radar chart of these molecular markers.

Antifibrinolytic Agents↗
PubMed1994

[A case of allograft rejection induced by the interferon-alpha therapy to hepatitis type C after renal transplantation].

We report a case of renal allograft rejection induced by the administration of interferon-alpha for hepatitis type C in a 36-year-old male. In September 1986, renal transplantation from his brother was performed after a 6-month delay because of his liver dysfunction. In October 1992, under the diagnosis of chronic active hepatitis type C, interferon alpha therapy was administered. Although his liver function was normalized during the treatment, proteinuria turned positive after 8 weeks of the therapy. Fourteen weeks after the start of interferon alpha therapy, the serum creatinine level was elevated, which was diagnosed clinically as a rejection reaction. We first discontinued the medication of interferon alpha and administered steroid pulse injection. As the renal disfunction did not respond to our first treatment, we changed mizoribine to azathioprine and added horse antilymphocyte immunoglobulin. Two weeks later, the creatinine level improved from 2.5 mg/dl to 2.0 mg/dl. The pathological findings of the transplanted kidney were acute on chronic type rejection.

Adult↗
PubMedDate not supplied

Hepatic tissue microcirculation, oxygenation and energy charge in ischemia-reperfusion subjected cirrhotic rat liver.

BACKGROUND/AIMS: The hemodynamic disturbances in the cirrhotic liver following severe variceal bleeding and subsequent restoration by blood transfusion is an ischemia/reperfusion injury event which represents the clinical situation of liver dysfunction. Therefore, the aim of this study was to evaluate the microcirculation, oxygenation and energy charge of the cirrhotic rat liver after ischemia/reperfusion. METHODOLOGY: In eight carbon tetrachloride-induced cirrhotic rats and an equal number of controls subjected to 30 minutes of ischemia and 60 minutes of reperfusion by hepatoduodenal ligament clamping, the following parameters were assessed: hepatic microcirculation by laser-Doppler fluxmetry, hepatic tissue oxygenation by a Clark-type electrode, hepatic energy charge by tissue sampling and adenine-nucleotides determination by means of high-performance liquid chromatography. RESULTS: At baseline, liver microcirculation was found to be significantly decreased in the cirrhotics versus controls groups. Ischemia led to a reduction in both groups, while reperfusion improved microcirculation, but not to the baseline level. Oxygenation was reduced during ischemia and restored after reperfusion in both groups. Hepatic energy charge was reduced in the cirrhotics versus controls at baseline, and significantly decreased during ischemia in both groups. At reperfusion, a further reduction was found in the cirrhotic group, while in the control group it was restored to baseline. CONCLUSION: Hepatic microcirculation, oxygenation and energy charge are subjected to different degrees of diminution after ischemia/reperfusion in the cirrhotic rat liver.

Adenine Nucleotides↗
PubMedDate not supplied

Total parenteral nutrition-related liver disease.

Administration of parenteral nutrition to the small infant has decreased morbidity but is associated with the development of cholestasis and liver dysfunction in a high proportion of infants. In this review, contributing factors of the etiopathogenesis of parenteral nutrition-associated liver disease will be outlined, forming the basis for a unifying theory of its pathogenesis. It is proposed that oxidant stress and stimulation of hepatic Kupffer cells by bacterial cell wall products absorbed from the injured intestine are major factors leading to cholestasis and liver injury during prolonged parenteral nutrition. Improved outcome in patients has been related to the early introduction of feedings. New proposed therapeutic modalities have included antibiotics and probiotics to prevent bacterial overgrowth of the small intestine, enterally-administered ursodeoxycholic acid and intravenous cholecystokinin. Improved understanding of the fundamental mechanisms producing liver injury and fibrosis during parenteral nutrition will lead to new preventative and treatment measures in the future.

Cholestasis↗