Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LIVER”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 739 records · Page 41Linked to original sources

[Angiosarcoma of the liver as a rare cause of rapidly progressive liver failure].

BACKGROUND: Angiosarcoma of the liver is a rare, highly malignant and sometimes diffusely infiltrating vessel tumor with rapid progression and poor prognosis. CASE REPORT: A 46-year-old male patient with rapidly progressive liver failure, initially regarded as decompensation of known alcoholic liver cirrhosis, is reported. The patient was referred to the authors' center for evaluation of liver transplantation, but a massive weight loss despite long absence of any alcohol intake raised the suspicion of a malignant disease. The abdominal ultrasound examination showed a massive hepatomegaly with an extremely inhomogeneous echo structure as well as moderate ascites. A following MRI demonstrated diffuse focal contrast enhancement in the entire liver parenchyma, confirming diffuse infiltration of the organ by a malignant tumor. In addition, MRI was suspicious of bone metastases. The usual tumor markers were normal. Sonographically guided percutaneous liver biopsy established the diagnosis of a malignant vascular tumor with diffuse infiltration of the liver parenchyma. 3 days later the patient died of uncontrollable bleeding from esophageal varices. Macroscopic examination of the liver during autopsy showed multiple lacunae filled with blood. Therefore, the differential diagnosis of a peliosis hepatis was raised. However, histology confirmed the diagnosis of a malignant angiosarcoma with diffuse osseous metastases. CONCLUSION: A diffuse infiltration of the liver by an angiosarcoma in the absence of any definite lesions may lead to a substantial delay of the diagnosis. The only relevant differential diagnosis in this case is the equally rare peliosis hepatis.

Biopsy↗

Reassessment of monoethylglycinexylidide as preoperative liver function test in a rat model of liver cirrhosis and man.

It is known that lidocaine is rapidly metabolized by the hepatic cytochrome P-450 system to form monoethylglycinexylidide (MEGX), its primary metabolite. We analyzed serum MEGX levels experimentally and clinically by fluorescent polarization immunoassay to reassess preoperative liver microsome functions. EXPERIMENTAL STUDY: Liver cirrhosis was produced in rats by intra-abdominal injection of thioacetamide. MEGX, indocyanine green test (ICG), and liver biochemical variables were measured periodically. Then, survival rates were assessed after the rats received a 70% hepatectomy. CLINICAL STUDY: MEGX levels were measured in various human patients with chronic hepatitis or liver cirrhosis who underwent hepatectomy. Serum MEGX levels significantly dropped and ICG levels significantly rose with macroscopic and histologic progression of liver cirrhosis in rats. The MEGX levels correlated closely with albumin levels and ICG. Preoperative MEGX and ICG levels of the mortal group of rats differed significantly from those of the survival group with 70% hepatectomy. Furthermore, 100% of the rats with MEGX levels above 40 ng/ml and ICG levels below 1.0%. In the clinical study, MEGX levels were significantly lower in patients with chronic hepatitis or liver cirrhosis than in healthy volunteers and correlated significantly with liver function tests such as albumin, Fischer's ratio, prothrombin time, hepaplastin and ICG. A significant difference was found in MEGX levels between patients receiving lobectomy and those receiving subsegmentectomy or partial hepatectomy. All patients tolerated their operations. Our data indicate that the MEGX test combined with ICG test and Child-Pugh classification is a better predictor of residual liver reserve capacity, and the analysis of hepatic MEGX formation might prove useful for rapid and reliable assessment liver function and choice of surgical treatment.

Alanine Transaminase↗

Hepatocellular carcinoma and liver cell dysplasia in children with chronic liver disease.

The histology of 72 livers from 72 children who underwent liver transplantation was reviewed. Nine children (12.5%) had hepatocellular carcinoma (HCC) and/or liver cell dysplasia (LCD) in their native livers. Ages at the time of transplantation ranged from 2 months to 11 years. Primary liver diseases included tyrosinemia (3), biliary atresia (2), chronic active hepatitis B (1), chronic active non-A non-B non-C hepatitis (1), idiopathic neonatal hepatitis (1), and neonatal iron storage disease (1). Explanted livers showed large multifocal HCC in two cases, incidental HCC in three, and dysplastic nodules in four. LCD also was present in three cases in conjunction with HCC. All patients had cirrhosis. Alpha-fetoprotein was measured in six children and was elevated in all six (range, 300 to 1,770,000 ng/mL; normal, 0 to 15 ng/mL). Abdominal computed tomography, ultrasonography, and/or magnetic resonance imaging showed large masses in two cases, but did not detect the tumors of less than 2 cm or the dysplastic nodules in the other seven children. After a follow-up period of 2 months to 3 years (mean, 19.8 +/- 12.1 months), eight children are alive and have no evidence of recurrence. The patient with neonatal iron storage disease died 2 months after transplantation, without evidence of tumor recurrence. The authors conclude that children with end-stage liver disease of diverse causes referred for liver transplantation may have LCD and/or HCC. Serial determination of alpha-fetoprotein and images studies may detect early lesions curable by liver transplantation.

Carcinoma, Hepatocellular↗

Characterization of gamma-glutamyltransferase from neoplastic and non-neoplastic liver tissues in man and during rat liver hepatocarcinogenesis.

The activity and the affinity for concanavalin A-Sepharose (Con A) of liver gamma-glutamyltransferase (gamma GT) were investigated in man, under various clinical conditions and in rats during experimental hepatocarcinogenesis. In man, gamma GT activity was higher than normal in hepatomas and (except for 1 case of hemochromatosis) also higher in the surrounding cirrhotic liver. The proportion of gamma GT which did not bind to Con A (Con A- form) was also increased in the tumors and in the surrounding liver, yet (with the same exception as above) to a greater extent in the hepatomas. In rat, gamma GT activity was higher in fetal liver (15-fold) and in hepatocarcinomas (10-fold) than in normal adult liver; total liver gamma GT activity gradually increased during progression from foci of altered cells to neoplastic nodules and tumors. The proportion of the Con A- form of gamma GT in the early or late stage of the carcinogenic process did not significantly differ from that in normal adult or regenerating rat liver, i.e. about 20% of the total activity. By contrast, nearly all the gamma GT from fetal rat liver bound to Con A. This suggests that gamma GT expression in rat liver carcinoma does not correspond to so-called retrodifferentiation process.

Adolescent↗

Platelet-endothelial cell adhesion molecule-1 gene expression in liver sinusoidal endothelial cells during liver injury and repair.

BACKGROUND/AIMS: Platelet-endothelial cell adhesion molecule (PECAM)-1 is suggested to be critical for transmigration processes. It is a matter of debate whether PECAM-1 is expressed in liver sinusoids and whether it is involved in liver inflammation. METHODS: Indirect immunostaining and in situ hybridization was used to analyze PECAM-1 gene expression in normal and diseased rat and human livers as well as in isolated rat sinusoidal endothelial cells (SECs), hepatic stellate cells and hepatocytes. At various time points after the administration of CCl4 (6 h, 24 h, 48 h, and 72 h), PECAM-1 gene expression was analyzed in livers and in SECs by immunostaining, and Northern blot analysis. RESULTS: In normal rat or human livers PECAM-1 immunoreactivity was detected along the sinusoids in a pattern similar to ICAM-1 staining. PECAM-1 specific transcripts were detected in freshly isolated and cultured SECs. After a single CCl4-administration, PECAM-1 immunoreactivity did not increase along the sinusoids in contrast to the early increase of ICAM-1. Northern blot analysis indicated that PECAM-1 expression in liver tissue and in isolated SECs does not increase after a single administration of CCl4, whereas ICAM-1 steady-state level increased after 6 h. In diseased human livers PECAM-1 was detectable along the sinusoids, within inflammatory infiltrates and within fibrotic septa. Neither in acutely nor chronically diseased human livers was an obvious increase of PECAM-1 immunoreactivity detectable. CONCLUSIONS: PECAM-1 is expressed by SECs. In contrast to ICAM-1, PECAM-1 transcript level is not enhanced during liver damage.

Animals↗

Interaction of non-alcoholic fatty liver disease with other liver diseases.

Obesity-related steatosis is an increasingly common histological finding in liver biopsies and may co-exist with other chronic liver diseases. Although non-alcoholic fatty liver disease (NAFLD) without true steatohepatitis is generally a benign condition, when another liver disease is present, steatosis may exacerbate the liver damage. In this review, we discuss the interaction of obesity-related steatosis with chronic hepatitis C, alcoholic liver disease, disorders of hepatic iron storage and drug-induced liver disease. The role of weight reduction in minimizing liver injury in patients with chronic hepatitis C is discussed. Finally, we discuss the problems associated with orthotopic liver transplantation for patients with NAFLD.

Body Mass Index↗

Fatty liver in obesity: relation to Doppler perfusion index measurement of the liver.

BACKGROUND: The correlation of clinical and laboratory findings with various imaging techniques in obese patients is difficult. Colour duplex Doppler is of particularly limited value in fat individuals. The Doppler Perfusion Index (DPI) measures the ratio of hepatic arterial to total liver blood flow and seems to be more accurate in the study of hepatic hemodynamics. The aim of the present study was to investigate the clinical use of DPI measurement of the liver in obesity. METHODS: In the present prospective, open study we evaluated the DPI in 41 obese patients (body mass index (BMI) > 30 kg/m2) and 18 volunteers with normal or slightly increased weight. Thirty patients of the study group underwent liver biopsy during bariatric surgery. In these patients liver histology was assessed and age, BMI, waist to hip ratio (WHR), DPI, liver function tests and serum triglycerides were measured. RESULTS: Obese patients had significantly (P = 0.0036) higher DPI values (0.25 +/- 0.138) than the healthy volunteers (0.15 +/- 0.04). Multivariate analysis revealed that grade of fatty liver in the study group was inversely associated with DPI and positively depended on serum triglyceride and aspartate aminotransferase (ASAT) levels (fatty liver index = 1.03 x ASAT (IU/l) + 0.152 x triglyceride (mg%) - 49.75*DPI, with P < 0.0001 and r2 = 0.80). CONCLUSION: Grade of fatty liver in obese patients may be predicted from DPI, serum triglyceride and AST levels. The proposed index may be useful as a non-invasive diagnostic tool during the follow-up of patients with obesity-related fatty liver.

Adult↗

Human liver regeneration after major hepatectomy. A study of liver volume by computed tomography.

Regeneration of the remnant liver after major hepatectomy in humans was studied by computed axial tomography (CT) in 12 noncirrhotic and five cirrhotic patients. Liver volumes were measured by abdominal CT 3 days, 10 days, 3 months, 6 months, 1 year, and 1.5 years after resection. Of the 17 patients, liver remnant volume was increased in 21.2% +/- 6.7% and 30.6% +/- 12.7% at 3 months and 6 months after resection, respectively. Noncirrhotic livers were 28.4% +/- 9.5% and 48.4% +/- 17.8% larger at 3 and 6 months. For cirrhotic livers, the increase was 8.5% +/- 3.6% and 12.9% +/- 4.5%. In five patients with right hepatectomy (65% resection), the liver remnant volumes were increased 38.4% +/- 11.7%, 48.0% +/- 16.2% and 95.1% +/- 4.5% at 3 months, 6 months, and 1 year after resection, respectively. In seven patients with right partial hepatectomy (30% to 35% resection), the percentages were 7.4% +/- 3.2%, 21.8% +/- 8.4%, and 63.9% +/- 18.3% and in five patients with left lateral segmentectomy (15% resection), they were 15.6% +/- 8.2%, 27.8% +/- 12.2%, and 33.0% +/- 14.5% 3 months, 6 months, and 1 year after resections, respectively. Noncirrhotic livers showed better regeneration than cirrhotic livers. Complete regeneration took about 1 year. The noncirrhotic liver that underwent right lobectomy also needed 1 year to double its postresection volume.

Adult↗

Expression of factor VII in the liver of patients with liver disease: correlations with the disease severity and impairment in the hemostasis.

Factor VII (FVII) plasma levels in patients with liver disease may be below the normal range. However, no data are available on FVII expression in liver biopsies from patients with liver diseases other than cirrhosis. We have analyzed the expression of FVII by in situ hybridization in liver biopsies from 50 patients in comparison with the procoagulant activity of FVII, and with the plasma levels as activated FVII (FVIIa) and FVII antigen. The level of FVIIa was significantly lower in stage 4 liver fibrosis patients than in the remaining ones (P < 0.05). The percentage of hepatocytes expressing FVII was significantly lower in stage 4 liver fibrosis patients (4.1+/-1.3%) than in stage 3 (22.7+/-6.1%), stage 2 (31.5+/-6.1%), stage 1 (43.7+/-8.2%) and stage 0 patients (63.8+/-4.4%) (P < 0.001). These percentages correlated inversely in a statistically significant way with the histological activity index and the liver function tests. We have demonstrated that the FVIIa plasma levels in patients with chronic liver disease other than cirrhosis may be below the normal range in the absence of blood coagulation impairment. The percentage of hepatocytes expressing FVII decreases as the severity of liver damage increases.

Adult↗

N-acetylcysteine increases liver blood flow and improves liver function in septic shock patients: results of a prospective, randomized, double-blind study.

OBJECTIVE: In septic shock, decreased splanchnic blood flow is reported, despite adequate systemic hemodynamics. Aacetylcysteine (NAC) was found to increase hepatosplanchnic blood flow in experimental settings. In septic shock patients, NAC improved the clearance of indocyanine green and the relationship of systemic oxygen consumption to oxygen demand. We investigated the influence of NAC on liver blood flow, hepatosplanchnic oxygen transport-related variables, and liver function during early septic shock. DESIGN: Prospective, randomized, double-blind study. SETTING: Septic shock patients admitted to an interdisciplinary surgical intensive care unit. PATIENTS: We examined 60 septic shock patients within 24 hrs after onset of sepsis. They were conventionally resuscitated with volume and inotropes and were in stable condition. A gastric tonometer was inserted into the stomach and a catheter into the hepatic vein. Microsomal liver function was assessed by using the plasma appearance of monoethylglycinexylidide (MEGX). INTERVENTIONS: Subjects randomly received either a bolus of 150 mg/kg iv NAC over 15 mins and a subsequent continuous infusion of 12.5 mg/kg/hr NAC over 90 mins (n = 30) or placebo (n = 30). MEASUREMENTS AND MAIN RESULTS: Measurements were performed before (baseline) and 60 mins after beginning the infusion (infusion). After NAC, a significant increase in absolute liver blood flow index (2.7 vs. 3.3 L/min/m2; p = .01) and cardiac index (5.0 vs. 5.7 L/min/m2; p = .02) was observed. Fractional liver blood flow index (cardiac index-related liver blood flow index) did not change. The difference between arterial and gastric mucosal carbon dioxide tension decreased (p = .05) and MEGX increased (p = .04). Liver blood flow index and MEGX correlated significantly (r(s) = .57; p < or = .01). CONCLUSIONS: After NAC treatment, hepatosplanchnic flow and function improved and may, therefore, suggest enhanced nutritive blood flow. The increase of liver blood flow index was not caused by redistribution to the hepatosplanchnic area, but by an increase of cardiac index. Because of its correlation with liver blood flow index, MEGX may be helpful in identifying patients who benefit from NAC treatment in early septic shock.

Acetylcysteine↗

Hyperbilirubinemia and cholestatic liver injury in hepatitis C-infected liver transplant recipients.

OBJECTIVE: A cholestatic pattern of liver injury has been observed in liver transplant recipients with rapidly progressive hepatitis C. We assessed the frequency and causes of cholestasis in hepatitis C-infected liver transplant patients, and evaluated the clinical and pathological course of those with cholestatic hepatitis C. METHODS: Sixty-nine sequential liver transplant recipients who had detectable hepatitis C viremia were studied retrospectively. Records and diagnostic tests were examined from patients who developed hyperbilirubinemia. RESULTS: Hyperbilirubinemia occurred in 33 of 69 (48%) hepatitis C-infected liver transplant patients. A thorough evaluation including review of clinical and laboratory data, ultrasound with Doppler, cholangiogram, and liver biopsy identified causes of hyperbilirubinemia other than hepatitis C in 26 of 33 patients. Seven patients developed cholestatic hepatitis C characterized by histological features of recurrent hepatitis C and cholestatic liver injury with ballooning of centrilobular hepatocytes, bile ductular proliferation, and canalicular cholestasis, in the absence of other causes of cholestasis. Five progressed rapidly to bridging fibrosis and two died of complications related to liver failure. Four patients with cholestatic hepatitis C showed extended survival after the onset of hyperbilirubinemia. CONCLUSIONS: 1) Hepatitis C is a relatively infrequent cause of cholestasis in liver transplant recipients. 2) The diagnosis of cholestatic hepatitis C requires a multimodality approach to exclude other causes of cholestasis. 3) Cholestatic hepatitis C ranges in severity and is not always associated with rapid development of graft failure, although significant histological abnormalities are frequent.

Adult↗

Liver transplantation for chronic liver disease: advances and controversies in an era of organ shortages.

Since liver transplantation was first performed in 1968 by Starzl et al, advances in case selection, liver surgery, anaesthetics, and immunotherapy have significantly increased the indications for and success of this operation. Liver transplantation is now a standard therapy for many end stage liver disorders as well as acute liver failure. However, while demand for cadaveric organ grafts has increased, in recent years the supply of organs has fallen. This review addresses current controversies resulting from this mismatch. In particular, methods for increasing graft availability and difficulties arising from transplantation in the context of alcohol related cirrhosis, primary liver tumours, and hepatitis C are reviewed. Together these three indications accounted for 42% of liver transplants performed for chronic liver disease in the UK in 2000. Ethical frameworks for making decisions on patients' suitability for liver transplantation have been developed in both the USA and the UK and these are also reviewed.

Chronic Disease↗

Differential alterations of cytochrome P450 proteins in livers from patients with severe chronic liver disease.

To determine whether cytochrome P450 proteins were differentially altered in severe chronic liver diseases, we examined 50 livers removed at liver transplantation from patients with end-stage cirrhosis, including 18 with and 32 without cholestasis, and compared the results with 21 histologically normal livers. NADPH-cytochrome c reductase activities were unaltered in microsomes from cirrhotic livers. Total cytochrome P450 content was significantly reduced. The catalytic activities of four xenobiotic-metabolizing P450s and the level of the corresponding proteins were differentially altered. Thus, P450 3A-supported testosterone 6 beta-hydroxylase activity and 3A protein appeared to be reduced, but only in the subgroup without cholestasis was this change significant. In contrast, 2E1 and the related N,N-dimethylnitrosamine N-demethylase activity were clearly reduced in livers from patients with cholestatic forms of cirrhosis but appeared not to be changed in other cirrhotic livers. Similarly, P450 2C protein was reduced only in patients with severe chronic cholestasis. Finally, P450 1A2 and 1A2-supported ethoxyresorufin O-deethylase activity were significantly reduced in hepatic microsomes from patients with both types of advanced liver disease. In summary, these data demonstrate that cytochrome P450 proteins are selectively altered in severe chronic liver disease, some being profoundly decreased, others less so or not at all. Our results also suggest that there may be different patterns of altered hepatic P450 expression according to the presence or absence of cholestasis in patients with cirrhosis severe enough to require transplantation.

Adolescent↗

Ethanol-induced increase in cytosolic estrogen receptors in human male liver: a possible explanation for biochemical feminization in chronic liver disease due to alcohol.

The hepatic cytosolic estrogen receptor content was measured in liver samples from patients with normal livers and from patients with nonalcoholic cirrhosis, alcoholic cirrhosis and alcoholic hepatitis. The estrogen receptor content of normal liver was 5.2 +/- 3.5 fmoles per mg of cytosolic protein. Levels which were not significantly different from this were found in the samples from patients with nonalcoholic cirrhosis (2.1 +/- 2.0 fmoles per mg of cytosolic protein). The cytosolic estrogen receptor content in the livers of patients with alcoholic cirrhosis who were abstaining was 4.2 +/- 3.6 fmoles per mg of cytosolic protein, but it increased to 10.4 +/- 4.9 fmoles per mg of protein in the livers of patients with alcoholic cirrhosis who were drinking, to 17.3 +/- 8.7 fmoles per mg of protein in the livers of patients with alcoholic hepatitis with cirrhosis and to 22.7 +/- 15.7 fmoles per mg of protein in the livers of patients with alcoholic hepatitis without cirrhosis. Alcohol abuse appeared, therefore, to induce an increase in the estrogen receptor content of human liver, especially in patients who were drinking and had histological evidence of acute liver damage (alcoholic hepatitis). The increase in hepatic estrogen receptor which we have observed may be involved in the molecular mechanisms underlying the feminization of the liver in alcoholic males.

Aged↗

Monocrotaline promotes transplanted cell engraftment and advances liver repopulation in rats via liver conditioning.

Disruption of the hepatic endothelial barrier or Kupffer cell function facilitates transplanted cell engraftment in the liver. To determine whether these mechanisms could be activated simultaneously, we studied the effects of monocrotaline, a pyrollizidine alkaloid, with reported toxicity in liver sinusoidal endothelial cells and Kupffer cells. The effects of monocrotaline in Fischer 344 rats were examined by tissue morphology, serum hyaluronic acid levels, and liver tests (endothelial and hepatocyte injury) or incorporation of carbon and (99m)Tc-sulfur colloid (Kupffer cell damage). To study changes in cell engraftment and liver repopulation, Fischer 344 rat hepatocytes were transplanted into syngeneic dipeptidyl peptidase IV-deficient rats followed by histological assays. We observed extensive endothelial injury without Kupffer cell or hepatocyte damage in monocrotaline-treated rats. Monocrotaline enhanced transplanted cell engraftment without changes in transplanted cell numbers or induction of proliferation in native hepatocytes over 3 months. In monocrotaline-treated rats, transplanted cells integrated into the liver parenchyma and survived in vascular spaces. To determine whether native hepatocytes suffered inapparent damage after monocrotaline, we introduced further liver injury with carbon tetrachloride subsequent to cell transplantation. Monocrotaline sensitized the liver to carbon tetrachloride-induced necrosis, which advanced transplanted cell proliferation, leading to significant liver repopulation. During this process, we observed proliferation of bile duct cells and small epithelial cells, although transplanted hepatocytes did not appear to reconstitute bile ducts. The studies showed that perturbation of multiple liver cell compartments by monocrotaline promoted transplanted cell engraftment and proliferation. In conclusion, development of drugs with monocrotaline-like effects will help advance liver cell therapy.

Animals↗

Effect of Lactobacillus supplementation with and without arginine on liver damage and bacterial translocation in an acute liver injury model in the rat.

In acute liver failure following hepatitis, toxic insults, or after major liver surgery, there is an increased bacterial translocation from the gut. This may explain some of the infectious complications seen in these conditions. To elucidate mechanisms and find possible preventive measures, we investigated the effect of rectal administration of arginine and probiotic bacteria (Lactobacillus spp.) on bacterial translocation and the extent of liver failure. Sprague-Dawley rats were used and five different Lactobacillus strains (Lb. reuteri R2LC, Lb. rhamnosus DSM 6594 (= strain 271), Lb. plantarum DSM 9843 (= strain 299v), Lb. fermentum 8704:3 (= strain 245), and Lb. reuteri (= strain 108) were administered rectally once daily for 8 days with and without 2% arginine. Acute liver injury (ALI) was induced on the eighth day by intraperitoneal injection of D-galactosamine (1.1 g/kg body weight), and samples were collected after 24 and 48 hours. Bacterial translocation was evaluated by bacterial culture from portal and arterial blood, mesenteric lymph nodes, and liver tissue. Liver enzymes and bilirubin were evaluated in the serum. The bacterial load in the cecum and colon was determined and the liver histopathological changes were studied. There was no mortality at any time. The liver enzymes and bilirubin decreased in some of the groups supplemented with lactobacilli with and without arginine compared with the ALI control group. The incidence of bacterial translocation and the number of the translocated bacteria decreased significantly in some of the supplemented groups. Lb. plantarum + arginine administration significantly reduced the level of the released liver enzymes, hepatocellular necrosis and inflammatory cell infiltration, bacterial translocation, and the number of Enterobacteriaceae in the cecum and colon. Rectal administration of different Lactobacillus strains with and without arginine in an ALI model significantly modulates the extent of the liver failure and reduces bacterial translocation. Lb. plantarum DSM 9843 (= strain 299v) with or without arginine seemed superior to the other Lactobacillus strains. The beneficial effect of arginine administration alone indicates a possible role of nitric oxide and polyamines in this process, and the lactobacilli may execute their action via the same mechanisms or via bacterial antagonism and/or enhancement of systemic and intestinal mucosal immunity.

Alanine Transaminase↗

Expression of liver and placental alkaline phosphatases in Chang liver cells.

This paper presents evidence that a protein characteristic of differentiated liver cells, liver alkaline phosphatase is synthesized by the Chang liver cell line. Liver alkaline phosphatase was demonstrated by immunochemical assay, 32P-labeling and polyacrylamide gel electrophoresis, immunofluorescence microscopy, and the fluorescence-activated cell sorter. The synthesis of the liver enzyme by the Chang liver cells is interpreted to indicate fidelity of the Chang cells to their origin from human liver tissue. Chang liver cells also synthesize a phosphatase which is similar if not indentical to the placental alkaline phosphatase. Since a placental-type alkaline phosphatase has been observed in a number of non-trophoblastic cell lines and also in some neoplasms, it does not seem reliable as an index of the origins of the cell line. Because of the claims that Chang liver cells are actually HeLa cells, HeLa cells were studied in tandem with the Chang cells. The results showed that the HeLa cells do not make the liver type phosphatase. The data are discussed in relation to the question of HeLa cell contamination of the Chang cell line and the validity of criteria normally used to identify cell lines.

Alkaline Phosphatase↗

Liver volume in thalassaemia major: relationship with body weight, serum ferritin, and liver function.

BACKGROUND: It is not known whether body weight alone can adjust for the volume of liver in the calculation of the chelating dose in beta-thalassaemia major patients, who frequently have iron overload and hepatitis. OBJECTIVE: The hypothesis is that liver volume in children and adolescents suffering from beta-thalassaemia major is affected by ferritin level and liver function. MATERIALS AND METHODS: Thirty-five beta-thalassaemia major patients aged 7-18 years and 35 age- and sex-matched controls had liver volume measured by MRI. Serum alanine aminotransferase (ALT) and ferritin levels were obtained in the thalassaemia major patients. RESULTS: Body weight explained 65 and 86% of the change in liver volume in beta-thalassaemia major patients and age-matched control subjects, respectively. Liver volume/kilogram body weight was significantly higher (P < 0.001) in thalassaemia major patients than in control subjects. There was a significant correlation between ALT level and liver volume/kilogram body weight (r = 0.55, P = 0.001). Patients with elevated ALT had significantly higher liver volume/kilogram body weight (mean 42.9 +/- 12 cm3/kg) than control subjects (mean 23.4 +/- 3.6 cm3/kg) and patients with normal ALT levels (mean 27.4 +/- 3.6 cm3/kg). CONCLUSIONS: Body weight is the most important single factor for liver-volume changes in thalassaemia major patients, but elevated ALT also has a significant role. Direct liver volume measurement for chelation dose adjustment may be advantageous in patients with elevated ALT.

Adolescent↗