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PubMedDate not supplied

The impact of dengue haemorrhagic fever on liver function.

The impact of dengue haemorrhagic fever (DHF) on liver function was studied by measuring serum transaminase levels on 45 patients with DHF confirmed by virus isolation and serodiagnosis in 1995. Abnormal levels of AST and ALT were observed in 97.7 and 37.3% of the patients, respectively. The fact that the level of AST was higher than that of ALT and that the elevation of transaminases was mild to moderate in most cases (< 5-fold greater than the normal upper limit for AST and ALT) showed that liver involvement was also mild to moderate in most cases of DHF. The results of transaminases did not differ significantly between cases with and without hepatitis B or hepatitis C virus infection, nor between primary and secondary cases of infection, but a significantly higher elevation of AST and ALT was observed in DHF patients with gastrointestinal haemorrhage. Two patients with dengue encephalopathy (in 1992) and one patient with dengue encephalopathy who died of massive gastrointestinal haemorrhage (in 1995) had unusually high transaminase levels as a sign of acute liver failure. It is concluded that DHF may cause mild to moderate liver dysfunction in most cases; only some patients may suffer from acute liver failure leading to encephalopathy and death.

Alanine Transaminase↗
PubMed1990

Acute hepatitis after tetrahydroaminoacridine administration for Alzheimer's disease.

Tetrahydroaminoacridine administration has been proposed as a treatment for Alzheimer's disease. Although recent studies have shown that tetrahydroaminoacridine administration can be associated with mild or moderate liver dysfunction, to our knowledge, no case of symptomatic hepatitis with severe liver lesions has heretofore been reported. We describe a patient who developed jaundice after receiving tetrahydroaminoacridine for three weeks. Histologic examination showed extensive hepatocellular necrosis. Tetrahydroaminoacridine withdrawal was followed by the disappearance of jaundice within a few days and complete recovery within 5 weeks. This case shows that tetrahydroaminoacridine administration can induce marked liver cell necrosis resulting in symptomatic acute hepatitis.

Acute Disease↗
PubMed1998

Effect of partial HLA class I match on acute rejection in viral pre-infected human liver allograft recipients.

BACKGROUND: Acute rejection in liver transplants is one of the commonest causes of liver dysfunction in the early postoperative period. However, the factors involved in liver graft rejection are still unknown. Our study was aimed at ascertaining whether the degree of HLA class I and class II compatibility or pretransplant viral infection have any influence on early acute liver graft rejection. METHODS: We reviewed clinical and laboratory data in 190 consecutive patients who underwent a liver transplant. HLA-A, HLA-B, and HLA-DR typing for the establishment of an HLA match score was performed by a standard microcytotoxicity method. The existence of pretransplant viral infection was investigated in sera and biopsy tissue by serologic (hepatitis B virus, hepatitis C virus) and polymerase chain reaction (cytomegalovirus) techniques, respectively. The influence of these two factors in acute rejection and the interaction between them was also analyzed. RESULTS: A strong association between viral infection and acute rejection in the group with partial class I matching was found (odds ratio=7.75; P<0.0009), whereas no correlation was observed in the group with zero class I matching (odds ratio=0.98; P=0.81). The rejection percentage in the group in which partial class I match and viral infections coexisted was 60%, whereas in the partially class I-matched group without pretransplant viral presence it was 16%. CONCLUSIONS: These findings suggest a participation of partial HLA class I compatibility in triggering acute rejection in recipients suffering preoperative viral infections and support the idea that HLA class I antigen matching could play a role as a linking element between the MHC-restricted T cell-mediated response to viral infection and the allogenic response in liver transplantation.

Adolescent↗
PubMed2006

Variable degree of liver involvement in siblings with PiZZ alpha-1-antitrypsin deficiency-related liver disease.

PiZZ alpha-1-antitrypsin deficiency is the commonest genetic cause of chronic liver disease, but only 10-15% of PiZZ individuals develop liver disease in childhood. Studies have demonstrated varying patterns of disease progression within siblings with the PiZZ phenotype. We retrospectively analysed the case-notes of all patients diagnosed with PiZZ A1ATD between 1978-2002 and compared the pattern of liver disease between affected siblings. We identified 29 families with more than 1 child with the PiZZ phenotype. Twenty-one (72%) PiZZ siblings of the 29 probands had liver disease, which was concordant for severity in 6 (29%), while 8 (28%) had no liver involvement. Five of 7 children requiring liver transplantation had siblings with no persistent liver dysfunction. This study suggests that there is a variable degree of liver involvement in siblings with PiZZ A1ATD-related liver disease and environmental and/or other genetic factors must be involved in determining disease severity.

Aspartate Aminotransferases↗
PubMed1975

Quantitative liver imaging using 131-I Rose Bengal as an index of liver function and prognosis.

A technique for assessing quantitatively hepatic function by direct measurement of liver parenchymal cell uptake of 131I Rose Bengal using a scintillation camera with a digital store and retrieval system is described. Ninety-four studies were performed on 84 patients with a variety of hepatic disorders over a two-year period, the diagnosis in each case being established by liver biopsy or laparotomy. The results were compared with the clinical, biochemical and histological assessment of the patients. A good correlation was found between the half-time for hepatic uptake of 131I Rose Bengal and the histological changes, as well as with clinical prognosis measured in terms of clinical improvement or deterioration to death. The rate of liver uptake was found to be a better index than the clearance of radioisotope from the blood and was superior to conventional biochemical investigations in both icteric and anicteric patients. The test was not shown to be of clinical value in discriminating between intra- and extrahepatic causes of jaundice. It is suggested that this technique may provide a safe and sensitive method for assessing the severity of liver dysfunction and also for monitoring clinical progress, especially in situations where liver biopsy may be unreliable or hazardous.

Biopsy↗
PubMed2006

New management options for end-stage chronic liver disease and acute liver failure: potential for pediatric patients.

The management of children with end-stage chronic liver disease and acute liver failure mandates a multidisciplinary approach and intense monitoring. In recent years, considerable progress has been made in developing specific and supportive medical measures, but studies and publications have mainly concerned adult patients. Therapeutic approaches to complications of end-stage chronic liver disease and acute liver failure (e.g. refractory ascites, hepatorenal syndrome, encephalopathy, and cerebral edema) that may be applied to children are reviewed in this article.Mild-to-moderate ascites should be managed by modest salt restriction and oral diuretic therapy in the first instance. Large volume paracentesis associated with colloid volume expansion and diuretic therapy may be effective for acute relief. Treatment of hepatorenal syndrome type 1 with vasopressin analogs (terlipressin) is recommended prior to liver transplantation in order to improve renal function. Prevention and treatment of chronic hepatic encephalopathy are directed primarily at controlling the events that may precipitate hepatic encephalopathy and at reducing ammonia generation and increasing its detoxification or removal. In addition to reduction of gut ammonia production using non-absorbable disaccharides such as lactulose and/or antibacterials such as neomycin, sodium benzoate may be used on a long-term basis to prevent, stabilize, or improve hepatic encephalopathy. The management of hepatic encephalopathy in acute liver failure is considerably more unsatisfactory; treatment is aimed at preventing brain edema and intracranial hypertension. Extracorporeal liver support devices are now used commonly in critically ill children with acute renal failure, advanced hepatic encephalopathy, cerebral edema, intracranial hypertension, and severe coagulopathy. Continuous renal replacement therapy could potentially help support patients until liver transplantation is performed or liver regeneration occurs. The Molecular Adsorbent Recirculating System (MARS or albumin dialysis) is the liver support system most frequently used worldwide in adults and appears to offer distinct advantages over hepatocyte-based systems. There are no specific medical therapies or devices that can correct all of the functions of the liver. Apart from a few metabolic diseases presenting with severe liver dysfunction for which specific medical therapies may preclude the need for liver transplantation, liver transplantation still remains the only definitive therapy in most instances of end-stage chronic liver disease and acute liver failure. Future research should focus on gaining a better understanding of the mechanisms responsible for liver cell death and liver regeneration, as well as developments in hepatocyte transplantation and liver-directed gene therapy.

Ascites↗
PubMed2002

[A case report of primary hepatic carcinoid with lymph node metastasis--treatment of hepatic arterial infusion to post-reoperative liver and radiation to metastasis of para-aortic lymph nodes].

We report a case of primary liver carcinoid. A 50-year-old woman had undergone left nephrectomy six years earlier for renal cell carcinoma. She developed abdominal pain. CT scans showed a low-density area in the lateral segment of the liver and lymph node swelling to the left of the abdominal aorta. Angiography showed a hypovascular tumor. After lateral segmentectomy and examination of the gastrointestinal tract, we diagnosed primary liver carcinoid. Unfortunately, the tumor recurred at multiple sites in the residual liver about 9 months after the first operation. She underwent further liver resection and microwave coagulation therapy. At that time, lymph node biopsy confirmed metastatic carcinoid. We began hepatic arterial chemotherapy for the residual liver and radiation therapy for the para-aortic lymph nodes (total 45 Gy). During chemotherapy, no recurrence was seen. At 11 months after reoperation, however, multiple liver metastases occurred with severe liver dysfunction and jaundice. She died about 24 months after the first liver resection.

Carcinoid Tumor↗
PubMed1992

[A case of simple hepatic cyst accompanied with dilatation of the intrahepatic bile duct].

Here we report a rare case of simple hepatic cysts causing dilatation of the intrahepatic bile duct. A 75-year old female was admitted to Kyushu University Hospital because of liver dysfunction. Ultrasonogram and CT scan showed two neighboring cysts in the liver (S2, S4), and dilatation of the peripheral bile duct in left lateral segment of the liver. Echo-guided percutaneous aspiration of cyst fluid showed the elevated levels of CA19-9, but malignant cell were not seen. These findings suggested that the compression by these neighboring simple hepatic cysts caused the stenosis of the bile duct. The dilatation of the bile duct disappeared after the percutaneous ethanol sclerosing therapy for cyst.

Aged↗
PubMed1991

[Clinical evaluation of per-rectal scintigraphy using I-123 IMP--evaluation of the portal hemodynamic changes after TAE].

Per-rectal portal scintigraphy using I-123 IMP was performed before and after TAE in 29 patients with hepatoma. Index of porto-systemic shunt (PSS index) was obtained by lung/(lung + liver) uptake ratio at 30 min after administration of IMP. The influence of TAE on portal circulation was evaluated by using this PSS index. PSS index increased 16 of 29 patients (55.2%) after TAE. PSS index increased after TAE especially in cases of severe liver dysfunction before TAE, marked portal involvement, and embolization of a larger liver volume. PSS index also increased when there was deterioration of esophageal varices, ascites, and hepatic coma after TAE. PSS index is useful for evaluation of portal circulation after TAE.

Amphetamines↗
PubMed1989

Renal tubular dysfunction in pancreatic cancer and chronic pancreatitis.

Urinary excretion of alpha-glucosidase (AGL), gamma-glutamyltransferase (GGT) and ribonuclease (RNase), and serum amylase and immunoreactive trypsin (IRT) were determined in 38 control subjects, 48 patients with pancreatic cancer, 77 with chronic pancreatitis and 47 with extrapancreatic diseases in order to ascertain the presence of a renal tubular damage and to investigate its etiology. A significantly increased frequency of pathological results for all urinary enzymes was documented in the various groups of patients as compared to controls. Significant correlations were detected among AGL, GGT and RNase. Considering the subjects as a whole, GGT and RNase excretions correlated with serum IRT and amylase; the two urinary enzymes were found to be higher when jaundice was present. In chronic pancreatic disease enzymuria was related to increased serum pancreatic enzymes; in extrapancreatic diseases it was associated to hyperbilirubinemia. The vast majority of patients with pancreatic cancer and elevated urinary enzymes presented hepatic metastases and/or jaundice. We can conclude that an anatomical and functional tubular impairment is detectable in some patients with chronic pancreatic and extrapancreatic diseases. Tubular damage seems to least in part to be related to pancreatic inflammation and necrosis in chronic pancreatic disease, while jaundice may be found to play an important role in diseases of the hepatobiliary tract. In pancreatic cancer, liver dysfunction (presence of liver metastases and/or extrahepatic cholestasis) also appears to be involved in altering tubular cells.

Adult↗
PubMed1980

Acute liver disease with encephalopathy and renal failure in late pregnancy and the early puerperium -- a study of fourteen patients.

Fourteen patients, aged 18 to 38 years, presented in the last trimester of pregnancy, or immediately post partum, with severe acute hepatic dysfunction. Liver biopsy confirmed the presence of acute fatty liver in six patients; the cause of hepatic dysfunction was presumed viral hepatitis in five patients, pre-eclampsia in two, and gram-negative septicaemia in one. There was one set of twins and the perinatal mortality was 33 per cent; there were three maternal deaths (21 per cent). Two survivors with acute fatty liver subsequently had successful pregnancies without evidence of hepatic dysfunction.

Acute Disease↗
PubMed2006

Risk factors of acute renal failure after liver transplantation.

The objective of this study was to determine the risk factors of postoperative acute renal failure (ARF) in orthotopic liver transplantation (OLT). We reviewed 184 consecutive OLT. Postoperative ARF was defined as a persistent rise of 50% increase or more of the S-creatinine (S-Cr). The patients were classified as early postoperative ARF (E-ARF) (first week) and late postoperative ARF (L-ARF) (second to fourth week). Preoperative variables were age, sex, comorbidity, indication for OLT, Child-Pugh stage, united network for organ sharing status, analysis of the blood and urine, and donor's data. Intraoperative variables were systolic arterial pressure, mean arterial pressure, pulmonary capillary wedge pressure, cardiac index, and systemic vascular resistance index. Surgical technique, number of blood products transfused, need for adrenergic agonist drugs, and intraoperative complications were also important. Postoperative variables were duration of stay in the intensive care unit, time on mechanic ventilation, liver graft dysfunction, need for adrenergic agonist drugs, units of blood products infused, episodes of acute rejection, re-operations, and bacterial infections. Firstly we carried out a univariate statistical analysis, and secondly a logistic regression analysis. The risk factors for E-ARF were: pretransplant ARF (odds ratio (OR)=10.2, P=0.025), S-albumin (OR=0.3, P=0.001), duration of treatment with dopamine (OR=1.6, P=0.001), and grade II-IV dysfunction of the liver graft (OR=5.6, P=0.002). The risk factors for L-ARF were: re-operation (OR=3.1, P=0.013) and bacterial infection (OR=2.9, P=0.017). The development of E-ARF is influenced by preoperative factors such as ARF and hypoalbuminemia, as well as postoperative factors such as liver dysfunction and prolonged treatment with dopamine. The predicting factors of L-ARF differ from E-ARF and correspond to postoperative causes such as bacterial infection and surgical re-operation.

Acute Kidney Injury↗
PubMed2006

Sepsis-induced cholestasis, steatosis, hepatocellular injury, and impaired hepatocellular regeneration are enhanced in interleukin-6 -/- mice.

OBJECTIVE: Hepatic dysfunction is an important but poorly understood component of sepsis. In severe sepsis, liver dysfunction is characterized by cholestasis, steatosis, hepatocellular injury, impaired regeneration, a decreased response to the cytokine interleukin-6, and high mortality. To determine whether loss of interleukin-6 activity caused hepatic dysfunction and mortality, we induced sepsis in wild-type (interleukin-6 +/+) and interleukin-6 knockout (interleukin-6 -/-) mice. We hypothesized that sepsis in interleukin-6 -/- mice would increase cholestasis, steatosis, hepatocellular injury, and mortality and impair hepatocyte regeneration. DESIGN: Randomized prospective experimental study. SETTING: University medical laboratory. SUBJECTS: Male adolescent C57Bl6 interleukin-6 +/+ and interleukin-6 -/- mice. INTERVENTIONS: Mild sepsis was induced using cecal ligation and single puncture (CLP). Severe, lethal sepsis was induced using cecal ligation and double puncture (2CLP). Some mice received recombinant human interleukin-6 at the time of CLP/2CLP. All animals were fluid resuscitated at the time of surgery and every 24 hrs thereafter. In survival cohorts, mortality at 16, 24, 48, and 72 hrs was recorded. In separate cohorts, surviving animals were killed at 24 and 48 hrs, and liver tissue was harvested. A separate cohort of mice received bromodeoxyuridine for detection of regeneration. MEASUREMENTS AND MAIN RESULTS: 2CLP was 100% fatal within the first 12 hrs in interleukin-6 -/- mice. Mortality from 2CLP in interleukin-6 +/+ mice before 24 hrs was nil but was 90% by 72 hrs. At 72 hrs, CLP was 40% fatal in interleukin-6 +/+ mice but 90% in interleukin-6 -/- mice. CLP induced cholestasis, steatosis, and hepatocellular injury in interleukin-6 -/-, but not interleukin-6 +/+, mice. Regeneration was absent following CLP in interleukin-6 -/- animals but occurred in interleukin-6 +/+ mice. Early administration of recombinant human interleukin-6 did not reverse abnormalities in interleukin-6 -/- mice. CONCLUSIONS: The absence of interleukin-6 is an important determinant of hepatic dysfunction and mortality in sepsis.

Animals↗
PubMed2001

Organ dysfunction following stem cell transplantation: relationship to plasma cytokine concentrations.

Patients receiving high-dose preparation for stem cell transplantation are at risk for organ dysfunction (OD). Signs of early OD include hypoxia, mental status changes, and liver dysfunction. These early signs have not been correlated with potential cytokine mediators. We compared plasma concentrations of IL-6, TNF-alpha, and IL-10 in OD patients and controls. Cytokines were measured before preparation, 5 days before OD, day of OD, and 5 days after OD. TNF-alpha and IL-10 were not measurable prior to preparation. IL-10 was more likely to be measurable in OD patients than in controls 5 days prior to onset of OD (P = 0.039), on the day of OD (P = 0.023), and 5 days later (P < 0.0001). TNF-alpha was more likely to be measurable only on the day of OD (P = 0.0035). IL-6 was significantly elevated in OD patients at all time points. Patients who had measurable IL-6 on admission were 5.1 times more likely to develop OD (95% CI = 1.4-17.9; P = 0.011). Five days prior to OD for each 100 pg/ml increase in IL-6, patients were 2.75 times more likely to develop OD (95% CI = 1.3-5.8; P = 0.0087). The early elevation of IL-6 in patients who develop OD may help identify a high risk group where preventive therapies can be evaluated.

Acute Kidney Injury↗
PubMedDate not supplied

Altered platelet function in cirrhosis of the liver: impairment of inositol lipid and arachidonic acid metabolism in response to agonists.

Hemorrhagic disorders are common in patients with liver cirrhosis and result from several factors including impaired platelet function. We evaluated platelet aggregation and arachidonic acid metabolism in response to standard agonists in platelet-rich plasma from 12 cirrhotic patients with mild impairment of liver function (Child A), 12 patients with severe liver dysfunction (Child B and C) and 12 healthy subjects. Platelet aggregation and thromboxane A2 production were consistently reduced in patients with severe liver impairment. To determine whether the platelet dysfunction is due to an intrinsic platelet defect or a circulating inhibitor, we measured platelet aggregation and thromboxane A2 synthesis on washed platelets in healthy subjects and in Child B and C patients. The aggregating response of washed platelets in response to thrombin, collagen and arachidonic acid was markedly reduced, suggesting an intrinsic platelet defect. The biochemical events underlying platelet aggregation were investigated by prelabeling platelets with [1-14C]arachidonic acid. Thrombin-induced activation of phospholipase C (measured as the release of [1-14C]phosphatidic acid) and phospholipase A2 (measured as the release of [1-14C]arachidonic acid and its metabolites) was greatly impaired in platelets from patients with severe liver impairment. We conclude that in advanced cirrhosis there is a severe reduction in platelet aggregatory response to physiologic agonists due to an intrinsic platelet defect which is related to an impairment of the platelet transmembrane signaling mechanism induced by receptor stimulation.

Adenosine Diphosphate↗
PubMed2004

Growth hormone/insulin-like growth factor 1 axis recovery after liver transplantation: a preliminary prospective study.

Many studies on cirrhotic patients have shown that insulin-like growth factor 1 (IGF-1) plasma levels are related to the severity of liver dysfunction. This result suggests that IGF-1 is probably useful for monitoring liver function in the perioperative course of orthotopic liver transplantation (OLT). Growth hormone (GH), IGF-1 plasma levels, and routine liver function tests were measured in 15 adult cirrhotic patients undergoing OLT. Measurements were made at the beginning of the operation; during OLT; 24 hours after reperfusion; and in the morning on days 7, 30, and 90. Twenty age-matched healthy volunteers with normal liver function served as controls. The study group had significantly higher GH levels and lower IGF-1 levels in the preoperative period compared with the controls. All patients achieved a complete functional hepatic recovery 1 month after OLT, although in 6 of them, the graft had an initial poor function (Group-IPF). GH and IGF-1 levels achieved near normal range within 1 week after OLT, and they had no significant correlations with other routine biochemistry tests in this period. IGF-1 levels in Group-IPF rose more slowly than in the group with a normal recovery of graft function. Surprisingly, 24 hours after reperfusion, IGF-1 levels were higher in Group-IPF than in the group with normal graft function. In conclusion, the severe GH/IGF-1 axis impairment found in patients with end-stage cirrhosis reverted very rapidly in the first days after successful OLT. Such a quick, postoperative modulation of IGF-1 plasma level by the graft suggests that this hormone has the potential to become one of the early indicators of post-OLT liver function recovery.

Adult↗
PubMed1993

Autopsy case of hepatocellular carcinoma associated with lupoid hepatitis and complicated by malignant lymphoma.

An 81-year-old woman in whom liver dysfunction had been pointed out 3 years previously was diagnosed as having liver cirrhosis due to lupoid hepatitis. Considering the poor prognosis of cirrhosis and her age, immunosuppressive therapy was not adopted. Nine months later, a small liver tumor was found by ultrasonography and was diagnosed as hepatocellular carcinoma (HCC). The tumor was treated with transcatheter arterial embolization, but grew continuously. She also developed gingival lymphoma that was successfully treated. Three years after initial diagnosis of lupoid hepatitis, she died of hepatic failure. An autopsy was performed and confirmed the clinical diagnosis, liver cirrhosis with HCC. HCC is regarded as a rare complication of lupoid hepatitis, but cases of HCC complicating lupoid hepatitis may increase with progress in treatment methods and elongation of survival. The present case suggests that any malignancy can be developed in long-term surviving patients with lupoid hepatitis.

Aged↗
PubMed1992

Incidence of liver toxicity associated with the use of flutamide in prostate cancer patients.

PURPOSE: The incidence of flutamide-related liver toxicity was studied in 1,091 consecutive patients treated for stage C or D prostate cancer with the antiandrogen flutamide and the luteinizing hormone-releasing factor (LHRH) agonist [D-Trp6, des-Gly-NH2(10)] LHRH ethylamide. PATIENTS AND METHODS: Liver function tests, namely measurement of serum aspartate amino-transferase (AST) and alanine aminotransferase (ALT), total bilirubin, alkaline phosphatase, gamma-glutamyl transpeptidase (gamma-GT), and prothrombin and thromboplastin times, were performed at 4, 8, and 12 weeks and every 3 months thereafter. Clinical signs and symptoms of liver dysfunction were also sought. The causal link between the antiandrogen used and liver injury was assessed on the basis of the temporal relationship with the use of the drug in the absence of other possible causes and, in two patients, through rechallenge of the putative causative drug after a period of normalization of liver function. RESULTS: An increase in AST and ALT at fourfold or more above upper normal limits was observed in only four patients (0.36%). Total serum bilirubin and alkaline phosphatase were elevated in only one patient at 126 mmol/L and 640 IU/L, respectively. Among the four patients, only two developed clinical manifestations of liver disease (0.18%). Biopsy was performed in one patient, and the histopathologic findings showed a mixed pattern of cytotoxic and cholestatic changes. All clinical and biologic manifestations of liver toxicity rapidly disappeared upon discontinuation of flutamide alone. No sequelae were observed in the long-term follow-up at 18, 22, 31, and 62 months. The 1,087 remaining patients experienced no or mild (less than fourfold upper normal limit) and transient elevation in aminotransferase serum levels during the first 6 months of treatment, with normalization at later time intervals. CONCLUSION: Despite the fact that the cases reported so far, along with our large series, indicate that the incidence of flutamide-induced liver toxicity is very low, we recommend serial blood aminotransferase measurements at 2 and 4 weeks of treatment in order to detect early signs of possible flutamide-induced hepatic injury, thus avoiding the low potential risk of clinically significant liver toxicity.

Adenocarcinoma↗