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PubMed2002

Unique imaging issues in pediatric liver disease.

In many clinical scenarios, liver imaging does not differ as greatly in children as in adults. Common indications for liver imaging in children include trauma, suspected mass, pre-transplantation studies, monitoring after liver transplantation, jaundice, or liver dysfunction. This article highlights areas in which pathology or imaging approach in children differs from that seen in adults. Topics covered include imaging of a suspected hepatic mass, neonatal jaundice, and segmental liver transplantation.

Child↗
PubMed1991

Impact of malnutrition and its therapy on liver transplantation.

The consequences of malnutrition and impact of nutritional support on the liver transplant patient have not been adequately addressed in clinical research studies. As we have gained experience in assessing patients for transplantation surgery, the risks of malnutrition have been realized. Part of the success of liver transplantation today is related to improved timing of surgery, patient selection, and perioperative management. Malnutrition is one of the adverse risk factors that is potentially reversible and therefore specialized nutritional support techniques should be able to improve postsurgical outcome. However, the performance and interpretation of nutritional research has been impeded by difficulties in separating the effects of liver dysfunction from disturbances secondary to nutritional deficiencies; for example, hypoproteinemia would be a consequence of both. Through the use of multivariate prognostic formulas and development of better nutritional indices for patients with liver disease, it should be possible to identify those patients who will receive the greatest benefit from preoperative and perioperative nutritional support. Furthermore, the kinds of nutritional supplementation having the greatest impact could then be determined.

Diet Therapy↗
PubMedDate not supplied

L-selectin blockade and liver function in rats after uncontrolled hemorrhagic shock.

Hemorrhagic shock (HS) and resuscitation can be seen as a global body ischemia-reperfusion (I/R) injury characterized by neutrophil infiltration and organ damage. Liver dysfunction occurs early after HS. Adhesion molecules are needed for the first steps ofneutrophil migration. Thus, the purpose of this study was to investigate the role of L-selectin in the liver after uncontrolled HS and resuscitation. Forty-eight Sprague Dawley rats were subjected to uncontrolled HS and resuscitation. Animals were divided into three groups: sham, uncontrolled HS and resuscitation, and uncontrolled HS and resuscitation with anti-L-selectin treatment. At 6 we evaluated liver injury tests, liver tissue myeloperoxidase (MPO), and liver histology. Survival was followed for 3 days and compared between groups. Statistical analysis included Fisher's exact test and one-way analysis of variance. Survival significantly increased from 30% in the control group to 60% in the treated group (p < .05). Hepatocellular and structural injury as well as neutrophil infiltration was significantly decreased in treated animals (p < .05). Thus, blockade of L-selectin resulted in decreased hepatocellular injury and increased survival in our model of uncontrolled HS. Selectins may be important therapeutic targets for blockade in the treatment of HS.

Animals↗
PubMed1992

Hepatic encephalopathy mimicking stroke. A case report.

This case demonstrates focal neurologic deficit mimicking stroke with underlying hepatic encephalopathy. Unilateral weakness in patients with hepatic encephalopathy has not been previously described in the English language literature. A 46-yr-old white woman was admitted to an acute care hospital for left shoulder manipulation, underwent general anesthesia and appeared to have had a right cerebrovascular accident. At transfer to the rehabilitation hospital, in addition to the left hemiparesis, there were inconsistencies in the neurologic examination and signs of cognitive impairment and liver failure. The patient's response to an intensive, multidisciplinary inpatient rehabilitation program along with treatment of the liver dysfunction led to resolution of left-sided weakness and flapping tremor with independence in ambulation and activities of daily living. Relevant literature is reviewed. A thorough history and physical examination with liver function assessment should always be performed in patients with cerebrovascular accident and unusual recovery.

Brain↗
PubMed2001

Spontaneous disappearance of a hepatic cyst.

The spontaneous disappearance of a hepatic cyst is described. A 62-year-old woman presented with symptoms of general fatigue in August 1992. Her past medical history was significant for chronic hepatitis, which was diagnosed in 1990 but not treated. Initial laboratory tests revealed mild liver dysfunction with a positive serologic test for hepatitis C. In August 1992, ultrasonography and computed tomography disclosed a cystic lesion along the middle hepatic vein in the right anterior segment of the liver, which was 40 mm in diameter. Repeat radiologic studies in June 1994 demonstrated that the size of the cyst was unchanged. In May 1995, the cyst was only 25 mm in diameter, and it continued to decrease in size thereafter, to 10 mm in September 1995 and 7 mm in September 1996. No hepatic cyst was visualized in December 1996, though the region in which the cyst existed was hyperechoic. Laboratory data were essentially unchanged from August 1992 to December 1996. Clinically the patient remained asymptomatic.

Cysts↗
PubMedDate not supplied

Hyperbilirubinemia induced by endoscopic variceal ligation for esophageal varices in a patient with primary biliary cirrhosis: a case report.

We describe the case of a 51-year-old woman with primary biliary cirrhosis who developed hyperbilirubinemia with transient liver dysfunction after undergoing endoscopic variceral ligation to control hemorrhaging from esophageal varices. After undergoing a variceal ligation, the serum total bilirubin increased from 4.0 mg/dL to 9.5 mg/dL, and the degree of liver failure worsened. She finally had to undergo a liver transplant. We discuss the mechanism of hyperbilirubinemia after endoscopic variceal ligation.

Endoscopy↗
PubMedDate not supplied

Liver ferritin subunit ratios in neonatal hemochromatosis.

Neonatal hemochromatosis is an enigmatic disease. Little is known about iron metabolism in this disease, including the tissue concentration of ferritin or its H and L subunit ratio. The authors report the tissue iron, ferritin, and ferritin subunit content of a child who died at 5 weeks of neonatal hemochromatosis. The child was born at 29 weeks gestation to a mother with lupus, sickle cell trait, and gestational diabetes. The child's severe liver dysfunction led to the clinical diagnosis of neonatal hemochromatosis at 1 week of age. Despite aggressive support, including red cell transfusions and chelation, the child died of an intracranial hemorrhage. Autopsy showed liver fibrosis and iron staining characteristic of neonatal hemochromatosis. Autopsy liver tissue was compared to age-matched control tissue. Soluble protein was analyzed by the Bradford method. Soluble iron (over 90% of total iron) was analyzed by the o-phenanthroline complex. Tissue ferritin and human ferritin controls (Calzyme) were analyzed by Western blotting after SDS-PAGE, identified with sheep anti-human ferritin antibodies (The BindingSite) secondary antibody-fluorescence for detection, and quantified using the Molecular Dynamics Storm 840 phosphorimager and ImageQuant software. Protein, iron, and total ferritin were similar in the normal and neonatal hemochromatosis liver tissues. Ferritin subunits, however, showed an increased H/L-subunit ratio compared to an age-matched control. This first report of a marked increase in the ferritin H/L-subunit ratio may point to an underlying mechanism of disease in this enigmatic disorder.

Biopsy↗
PubMed1995

[Liver transplantation in the treatment strategy of portal hypertension].

We reviewed 1000 consecutive liver transplants over a 10 year period with special attention to a pre-transplant history of portal hypertension revealed by variceal hemorrhage. Of 730 primary transplanted patients with chronic liver disease 186 (26%) experienced variceal bleeding prior to transplantation of which 130 (70%) required interventional therapy to palliate the bleeding. Sclerotherapy was performed in 93 (50%), surgical portal diversion in 27 (15%) and TIPSS in 10 (5%) patients. Moderate to severe liver dysfunction accounted for 91% of the patients with bleeding complications. The impact of both bleeding and treatment modality utilized in the pre-transplant period was analyzed in a way to integrate liver transplantation into the multimodality treatment of portal hypertension. The overall survival for all patients was 76% at five years. Previous history of variceal bleeding did not affect the outcome of patients following liver transplantation. The patients treated by initial sclerotherapy demonstrated no difference with either graft or patient survival. The patients who had TIPSS to control hemorrhage had lower, but insignificant, graft and patient survival. The group of patients with variceal hemorrhage who had prior surgical shunt did, however, demonstrate a significant increased survival of 96% when compared to the non-shunted group which had a 73% survival (p < 0.007). The strategy in treating these potential transplant patients is critical to the success of the subsequent transplant.

Adult↗
PubMed1997

[Hepatic diseases caused by drugs].

Drug-induced hepatotoxicity covers the clinical and pathological expressions of almost any acute or chronic liver disease. Liver damage is due to intrinsic toxicity of the drug (paracetamol) and/or immunoallergic mechanisms (halothane). Acute injury may be cytotoxic or cholestatic. Cytotoxic injury is characterized by necrosis (paracetamol, halothane) or steatosis (valproate). Cholestatic injury can be associated with immune-mediated portal inflammation (chlorpromazine) or solely attributed to inhibition of transport systems (cyclosporin A). Chronic drug-induced disorders include chronic active hepatitis (methyldopa), autoimmune hepatitis (tienilic acid), alcoholic steatohepatitis-like reactions (amiodarone), indolent fibrosis (methotrexate), chronic cholestatic diseases, vascular lesions, and hepatic neoplasms. The clinical and morphological picture of many drug-induced liver diseases is nonspecific. Diagnosis is based on thorough drug history, temporal relationship, time-course of liver dysfunction, and the exclusion of other causes. Treatment consists of instant withdrawal of the suspected drug and administration of acetylcysteine as early as possible in case of paracetamol intoxication. Drug-induced liver diseases are usually reversible, but prolonged treatment leads to progression and liver cirrhosis.

Chemical and Drug Induced Liver Injury↗
PubMed2002

Human fetuin/alpha2HS-glycoprotein level as a novel indicator of liver cell function and short-term mortality in patients with liver cirrhosis and liver cancer.

OBJECTIVE: Human fetuin/alpha2HS-glycoprotein (AHSG) is synthesized by hepatocytes. We intended to determine whether liver dysfunction or acute phase reaction is dominant in the regulation of its serum concentrations and to see if decreased AHGS levels are associated with short-term mortality. DESIGN: We determined the serum AHSG levels in patients with acute alcoholic, acute A, B, and Epstein-Barr virus hepatitis, alcoholic cirrhosis, and hepatocellular cancer and correlated them to conventional laboratory parameters of inflammation and liver function. Patients were followed for 1 month. METHODS: Serum AHSG was determined by radial immunodiffusion. RESULTS: Compared to controls, significantly lower AHSG levels were found in patients with liver cirrhosis and hepatocellular cancer but not the acute viral hepatitides. Strong positive correlation with serum transferrin, albumin and prothrombin was found. Febrile episodes were not associated with significantly decreased AHSG levels. Concentrations below 300 microg/ml were associated with high mortality rate (52.0%; relative risk, 5.497; 95% confidence interval, 2.472-12.23; P < 0.0001). Of all laboratory parameters studied serum AHSG levels showed the greatest difference between deceased and survived patients with cirrhosis and cancer. Moreover, other acute phase reactants did not differ significantly. The multiple logistic regression analysis indicated that the decrease of serum AHSG is independent of all other variables that were found decreased in deceased patients. CONCLUSIONS: Decreased serum AHSG concentration is due rather to hepatocellular dysfunction than the acute phase reaction and is an outstanding predictor of short-term mortality in patients with liver cirrhosis and liver cancer.

Acute-Phase Reaction↗
PubMed1991

Clinical presentation of metabolic liver disease.

Some clinical clues should alert paediatricians to the possibility of metabolic liver diseases. They can be classified into three categories: (i) Manifestations due to hepatocellular necrosis, acute or subacute, which can reveal galactosaemia, hereditary fructose intolerance, tyrosinaemia type I, Wilson disease and alpha 1-antitrypsin deficiency. Symptoms and signs suggestive of Reye syndrome should lead to a study of fatty acid oxidation and urea cycle enzymes. All these manifestations may necessitate a rapid diagnosis and treatment when liver dysfunction is severe. (ii) Cholestatic jaundice can reveal alpha 1-antitrypsin deficiency, Byler's disease, cystic fibrosis, Niemann-Pick disease and some disorders of peroxisome biogenesis. (iii) Hepatomegaly can reveal disorders with liver damage but also storage diseases such as glycogen storage diseases, cholesteryl ester storage disease and, when associated with splenomegaly, lysosomal storage diseases. Appropriate investigations for recognizing all these entities are proposed.

Child↗
PubMed2003

Structural and metabolic characteristics of liver acini in dogs with acute cholecystitis.

Structural and metabolic changes in liver tissue in dogs with acute cholecystitis were studied by histological, histoenzymatic, and biochemical methods. It was found that the development of destructive inflammatory processes in the gallbladder wall induces morphological damage to the liver tissue, which correlates with metabolic disorders in this organ and leads to liver dysfunction.

Animals↗
PubMed1989

Vitamin A in parenteral nutrition: uptake and distribution of retinyl esters after intravenous application.

Short-term parenteral application of vitamin A was examined in rats. Retinyl margarinate, which is chemically similar to physiological retinyl esters, was used in vitamin A-depleted rats to study uptake, distribution, and storage of retinyl esters in tissues. Vitamin A-depleted and Vitamin A-sufficient rats were infused with a micellar suspension of retinyl margarinate for 7 h and then killed at different times. Retinyl margarinate was directly taken up by all tissues examined. It appears that infusion of retinyl esters in micellar form provides a direct way to supply vitamin A to peripheral, vitamin A-dependent tissues. Therefore, a short-term infusion of retinyl esters with an emulsifier may be an effective means of preventing development of vitamin A-deficiency during long-term application of TPN, particularly in cases of liver dysfunction.

Animals↗
PubMed1997

Depletion of hepatocyte nuclear estrogen receptor expression is associated with promotion of tamoxifen induced GST-P foci to tumours in rat liver.

The expression of hepatocyte nuclear estrogen receptor (ER) in putative preneoplastic foci, adenomas and carcinomas, induced by the rat liver carcinogen tamoxifen, has been examined immunohistologically. ER staining of normal rat liver shows between 30-50% of hepatocyte nuclei to be positive, depending on fixation. Depletion of ER was defined as <10% of cells in foci or tumours staining for nuclear ER. A proportion of all but the smallest glutathione-S-transferase, placental form (GST-P) expressing foci had depleted expression of nuclear ER. The percentage of GST-P expressing foci with depletion of nuclear ER increased with the size of the foci. The liver adenomas and carcinomas induced by tamoxifen showed a high incidence (90%) of depletion of ER. This suggests that abnormal expression of the ER is associated with the promotion of putative preneoplastic foci to adenomas and carcinomas in tamoxifen exposed rat livers. Dysfunction of the ER could contribute to selective continued stimulation of initiated cells that would be consistent with a role for modification of the ER in target cells and the promotion stage of liver cancer. Liver tumours induced by other carcinogens in both sexes of rat were also found to have a high incidence of ER depletion, indicating that this could be a general regulatory mechanism for rat liver tumour promotion, irrespective of the possible estrogen like action of individual carcinogens.

Adenoma↗
PubMed1994

Comparison of different assays for the quantitation of FK 506 levels in blood or plasma.

In a prospective study, we evaluated the analytical performance of different assays for the quantitation of FK 506 in blood and plasma. The new whole blood IMX assay was compared with four modifications (liquid/liquid or solid/liquid extraction of blood or plasma respectively) of the standard enzyme-linked immunosorbent assay (ELISA). Both assays utilize the same monoclonal antibody for detection of FK 506. Using isolated FK 506 metabolites generated in vitro, this antibody was shown to recognize not only the unmodified parent drug but also FK 506 metabolites. In stable liver-grafted patients, sensitivity of both modifications of the whole blood ELISA was adequate. In contrast, in some stable patients, plasma ELISA was not able to detect FK 506; this was observed mainly after liquid/liquid extraction of FK 506. Sensitivity of the IMX assay was also low; in six of 10 stable liver-grafted patients, IMX levels were below the limit of detection. In all assays, FK 506 levels were found to be elevated during episodes of liver dysfunction; a possible explanation for this effect would be that of accumulation of cross-reacting FK 506 metabolites. As FK 506 metabolites are known to be less immunosuppressive than the parent drug, liver function should always be taken into account if IMX or ELISA levels are used for drug monitoring.

Antibodies, Monoclonal↗
PubMed2002

Temporary auxiliary liver transplantation from a living donor to an adult recipient with familial amyloid polyneuropathy.

A 33-year-old patient with familial amyloid polyneuropathy (FAP) underwent temporary auxiliary partial orthotopic liver transplantation (APOLT) from a living donor with a small-for-size graft. The auxiliary left lobar graft, which weighed only 230 g, was orthotopically transplanted after resection of the recipient's left lobe. The right portal vein was transected to induce compensatory hypertrophy of the left lobar graft. Posttransplant computed tomography showed atrophy of the native liver and hypertrophy of the graft, the volume of which had increased to 446 ml by postoperative day 41. The remnant native liver was removed 6 weeks after APOLT, and there were no signs of liver dysfunction during the postoperative course. Our experience with this case suggests that temporary APOLT is the treatment of choice, guaranteeing a sufficient margin of safety for both donor and recipient, in living donor liver transplants for FAP where the donor's left lobe is disproportionately small.

Adult↗
PubMedDate not supplied

Choice of treatments for small hepatocellular carcinoma: hepatectomy, embolization or ethanol injection.

The results of hepatectomy, percutaneous ethanol injection therapy and transcatheter arterial embolization for small hepatocellular carcinoma (HCC) of 3 cm or less in diameter from the published literature were compared with the authors' experiences with surgical treatment. The survival rates for those treated by hepatectomy and ethanol injection were almost the same, being more than 90% at 1 year and 70% at 3 years. The overall results achieved by embolization were inferior to those achieved by the other two therapeutic modalities, although the 1 year survival rate was not worse. The cancer-free survival rates after hepatectomy and ethanol injection were also similar. Most of the patients with small HCC had associated liver cirrhosis or chronic active hepatitis, but the degree of liver dysfunction and the level of hepatic reserve varied. Anatomically, the number, size, and location of the cancer also varies. Choice of treatment for small HCC should be made based upon the degree of liver function and the anatomic status of the cancer. For example, a patient with multiple (more than four) cancer nodules is a good candidate for embolization. Ethanol injection is indicated for a small HCC, deeply seated in a severely diseased liver. Hepatectomy is the first choice for a small HCC situated near the surface of a liver with relatively good liver function.

Carcinoma↗
PubMed1977

Tissue distribution and blood levels of gamma-glutamyl transferase in the horse.

In the horse, gamma-glutamyl transferase (GGT) was found to be mainly located in the kidneys, liver and pancreas. As renal lesions are followed by a urinary escape of enzyme, it can be assumed that if there are raised serum enzyme levels then the source will be chiefly from the liver and pancreas. In the blood, GGT can be measured either in plasma or serum. Its mean level in 58 horses was 12 U/L. This level was not affected by moderate dilution or slight haemolysis and its activity was only slightly decreased by storage at--30 degrees C. The relative hepatic specificity of this enzyme and its easy measurement make it a potentially very useful measure of liver dysfunction in the horse.

Animals↗