[Treatment of chronic liver diseases with a total liver extract by oral and parenteral routes].
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Humans↗
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Chronic liver disease: value of volumetry of liver and spleen with computed tomography.
Volumetric comparisons of portions of liver and spleen were performed in patients with chronic liver diseases to determine their diagnostic value. Volumetric ratios of liver and spleen were determined by CT examination in 34 normal subjects and 125 consecutive patients with histologically proved liver cirrhosis, chronic active hepatitis, chronic persistent hepatitis, acute hepatitis, or fatty liver. Ratios of caudate lobe, spleen, and lateral segment of the left lobe of the liver to the remainder of the liver, right lobe and medial segment of the left lobe (RL+LM), were calculated. The product of caudate lobe/RL+LM and spleen/RL+LM was of value in differentiating liver cirrhosis from other liver disease, with a sensitivity of 60%, specificity of 98%, and accuracy of 86%. The same ratios differentiated liver cirrhosis and chronic active hepatitis from other liver diseases with a sensitivity of 79%, specificity of 100%, and accuracy of 90%. Volumetric ratio measurements are useful in the diagnosis of cirrhosis and chronic active hepatitis.
Acute Disease↗
Blood manganese correlates with brain magnetic resonance imaging changes in patients with liver disease.
BACKGROUND: Chronic liver failure is associated with high signal abnormalities in the basal ganglia on T1-weighted magnetic resonance imaging of the brain. These abnormalities are strikingly similar to those seen following manganese intoxication. As dietary manganese is normally cleared by the liver, we hypothesize that hepatic dysfunction could lead to manganese overload and account for the MRI abnormalities seen in patients with chronic liver disease. METHODS: We measured blood manganese concentrations in eleven patients with biopsy-proven hepatic cirrhosis and eleven healthy age and sex-matched controls. We also performed semi-quantitative measures of T1 signal abnormalities on MRI in the patients with chronic liver disease. RESULTS: Patients with cirrhosis had significantly higher blood manganese concentrations (20.6 +/- 10.2 mcg/L) than controls (7.2 +/- 2.7, p = .0013). In addition, semi-quantitative scores of T1-weighted signal hyperintensity on MRI correlated with blood manganese concentration in patients with cirrhosis (r = .65, p = .029). CONCLUSIONS: These findings demonstrate that chronic liver disease is associated with manganese overload and suggest that manganese is responsible for the T1-weighted signal hyperintensity seen on MRI of patients with liver disease. As manganese intoxication is known to cause parkinsonism and an encephalopathy similar to those which occur with chronic liver disease, it is possible that manganese toxicity contributes to the development of these symptoms in liver damaged patients and that therapies which prevent or reduce manganese overload may have clinical benefit.
Adult↗
Surgery for adult polycystic liver disease.
Adult polycystic liver disease, commonly associated with polycystic kidney disease, can result in massive hepatomegaly and debilitating symptoms. Surgical intervention for symptomatic polycystic liver disease, such as cyst fenestration or liver resection has been associated with significant morbidity and inconsistent long-term palliation. However, selected patients with severe symptoms benefit from liver resection and extensive fenestration with acceptable morbidity and mortality. Total hepatectomy and orthotopic liver transplantation may be considered for patients with severe adult polycystic liver disease.
Adult↗
Hemostasis in liver disease.
Patients with liver disease have a wide range of coagulation problems. Patients with parenchymal liver disease are likely to have reduced synthesis of proteins and inhibitors (Table 1), whereas dysfibrinogenemia and hyperplenism develop in cirrhosis. Patients with cholestasis without cirrhosis often have elevated levels of fibrinogen, Factors V and VIII, probably due to reduced clearance of proteins (Table 1). The hemostatic defects in liver disease are complex and multifactorial. They are often unpredictable and the mechanisms elusive. Developments in molecular genetics and immunology have shown that both qualitative and quantitative abnormalities of coagulation proteins and protein inhibitors contribute to the abnormalities in liver disease. Future research will certainly result in a better understanding of these defects and more effective therapy.
Adult↗
Autoimmune liver disease.
Autoimmune liver disorders are inflammatory liver diseases characterised histologically by a dense mononuclear cell infiltrate in the portal tract and serologically by the presence of non-organ and liver specific autoantibodies and increased levels of immunoglobulin G (IgG), in the absence of a known etiology. They usually respond to immunosuppressive treatment, which should be instituted as soon as diagnosis is made. The onset is variable and often mimics acute hepatitis. The previously accepted requirement of six month duration of symptoms before a diagnosis of autoimmune disease could be made has been abandoned.
Child↗
Higher neutrophil infiltration mediated by osteopontin is a likely contributing factor to the increased susceptibility of females to alcoholic liver disease.
Alcoholic liver disease (ALD) is a major public health problem in the United States and women are known to be more susceptible to ALD. However, the precise mechanism for increased susceptibility of females to ALD is not completely understood. The present study is based on the hypothesis that induction of osteopontin (OPN), a matricellular protein, is the likely contributing factor for higher neutrophil recruitment in females during alcoholic steatohepatitis (ASH). ASH was induced in male and female Sprague-Dawley rats by feeding them a Lieber-DeCarli diet containing ethanol (EtOH) for 6 weeks, followed by a single injection of lipopolysaccharide (LPS, 10 mg/kg, ip). Liver injury, measured by plasma transaminase elevations and confirmed by haematoxylin and eosin-stained liver sections, revealed approximately 25-fold higher liver injury in the female ASH model compared with the males. Although steatosis, necrosis, and neutrophil infiltration were evident in both male and female rats, hepatic neutrophilic necrotic foci were noted as early as 2 h after LPS injection in the EtOH-treated female rats. Hepatic neutrophil infiltration correlated with higher expression of cleaved (cOPN) and uncleaved OPN in the EtOH + LPS-treated female rats compared with the males. OPN secretion was localized predominantly in the biliary epithelium and females had significantly higher OPN mRNA than their male counterparts in the ASH model. The ability of OPN to attract neutrophils was further confirmed in vivo, in a peritonitis rat model, and by neutralizing OPN (nOPN) antibody experiments. Hepatic neutrophil infiltration was largely inhibited ( approximately 50%) by nOPN antibody. Flow cytometry experiments revealed OPN-mediated up-regulation of the CD11b neutrophil adhesion molecule. In conclusion, these data suggest that higher hepatic expression of OPN is the likely reason for higher and early hepatic neutrophil infiltration making females more susceptible to ALD during ASH.
Animals↗
Germline mutations in PRKCSH are associated with autosomal dominant polycystic liver disease.
Polycystic liver disease (PCLD, OMIM 174050) is a dominantly inherited condition characterized by the presence of multiple liver cysts of biliary epithelial origin. Fine mapping established linkage to marker D19S581 (Z(max) = 9.65; theta = 0.01) in four large Dutch families with PCLD. We identified a splice-acceptor site mutation (1138-2A-->G) in PRKCSH in three families, and a splice-donor site mutation (292+1G-->C) in PRKCSH segregated completely with PCLD in another family. The protein encoded by PRKCSH, here named hepatocystin, is predicted to localize to the endoplasmic reticulum. These findings establish germline mutations in PRKCSH as the probable cause of PCLD.
Base Sequence↗
Hepatography patterns following rectal administration of radioiodine as seen in chronic liver disease and other liver disorders.
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Blood Pressure↗
[Liver resection in patients with polycystic liver disease].
OBJECTIVES: Polycystic liver disease is sometimes responsible for chronic symptoms linked to hepatomegaly which can result in acute complications such hemorrhage or infection of cysts. The aim of this retrospective study was to evaluate the results of partial hepatic resection in patients with symptomatic or complicated polycystic liver disease. METHODS: Twelve patients (11 women and one man, mean age 49) with diffuse polycystic liver disease were treated by partial liver resection (left lateral lobectomy in 7, left hepatectomy in 4, and extended right hepatectomy in 1). Four patients had terminal renal failures and three had chronic haemodialysis. Median follow-up was 34 months. RESULTS: Ascites occurred postoperatively in 10 patients (83%) and was long-lasting (> 2 weeks) in 5; all patients with end-stage renal failure had long-lasting ascites. One of them died on the 40th postoperative day of ascites infection. Another patient with end-stage renal failure died two years postoperatively from chronic disabling ascites and malnutrition while awaiting kidney transplantation. The 10 other patients were markedly improved after partial liver resection, including a marked decrease in hepatomegaly, and the disappearance of chronic symptoms and cystic complications. This beneficial effect was incomplete in the two surviving patients with end-stage renal failure until kidney transplantation was performed. CONCLUSION: These results suggest that partial liver resection is a highly effective treatment in patients with symptomatic polycystic liver disease, preferably before the onset of end-stage renal failure.
Adult↗
Low birth weight: a possible risk factor also for liver diseases in adult life?
Birth weight is a popular topic, because it is precisely recorded, a major determinant of infant survival, associated with infant mortality, and health outcomes later in life. Low birth weight (LBW) is a predisposing factor for metabolic abnormalities such as atherosclerosis, renal disease, non-insulin diabetes mellitus, asthma, low IQ, hypertension, obesity, psychological distress. They have all been reported to be more common among those who were small at birth. Due to lack of studies suggesting a linkage between LBW and diseases of liver; evidences, which support the hypothesis on the creation of a link between LBW, an indicator of unfavourable intrauterine environment, and liver diseases emerging in the adult life, and possible direct associations of LBW with liver diseases, e.g., hepatitis, non-alcoholic fatty liver disease, cirrhosis, hepatoblastoma, or hepatocellular carcinoma were discussed. The associations between LBW and hepatitis vaccination as well as paediatric parental nutrition were also noted.
Cholestasis↗
Relation between zinc status and hepatic functional reserve in patients with liver disease.
Patients with liver disease may be at risk of zinc depletion. We measured polymorphonuclear cell, mononuclear cell, plasma, and erythrocyte zinc values, and erythrocyte carbonic anhydrase activity to assess zinc status in 17 patients with non-alcoholic liver disease (primary biliary cirrhosis and chronic active hepatitis) and 13 patients with alcoholic liver disease. The plasma zinc concentration was reduced in both patient groups and correlated strongly with the plasma albumin concentration. The mean polymorphonuclear cell zinc value in both groups was similar to that of controls but when results were combined and grouped according to hepatic functional reserve, patients with more severe liver damage (grade C) had a lower polymorphonuclear cell zinc value (mean (SD) 0.86 (0.24) nmol/mg protein) than patients with grade A (1.44 (0.43) nmol/mg protein, p less than 0.01) or grade B liver damage (1.08 (0.30) nmol/mg protein, p less than 0.05), or control subjects (1.26 (0.28) nmol/mg protein, p less than 0.001). The polymorphonuclear cell zinc value did not correlate with other indices of zinc status. The mononuclear cell zinc value was normal in all patients and was unrelated to hepatic damage. The erythrocyte zinc value and carbonic anhydrase activity were raised in alcoholic patients only. Since the polymorphonuclear cell zinc concentration is low in human experimental zinc deficiency and also correlates with tissue zinc, we suggest that our results provide evidence of progressive leucocyte zinc depletion in patients with liver disease.
Adult↗
Role of liver biopsy in the assessment of non-alcoholic fatty liver disease.
Assessments of liver biopsies are important in the diagnosis and management of non-alcoholic fatty liver disease. Histology remains the 'gold standard' for making the important distinction between simple steatosis, which is generally non-progressive and readily reversible, and steatohepatitis, which has the potential to progress to severe fibrosis or cirrhosis. Liver biopsy may also identify other causes of liver disease in patients thought to have fatty liver disease and vice versa. Histological grading and staging of fatty liver disease require further study but these are potentially important approaches for studying disease severity and progression, particularly in the context of clinical trials to assess novel therapeutic approaches.
Alcoholism↗
Relationship between liver biochemical tests and dietary intake in patients with liver disease.
Relationships between liver biochemical test values and reported frequency of consumption of various foods were examined using a principal-component analysis of data from 42 patients with chronic liver disease. The statistical procedure identified relationships among biochemical and dietary variables. One relationship included the variables albumin, bilirubin, and frequency of intake of fruits and vegetables, starch, and meats. A relationship was also found between serum alkaline phosphatase (ALP) levels and fat/oil intake. Data from patients with primary biliary cirrhosis (PBC) and noncholestatic liver disease were compared using a correlational analysis. In patients with PBC, serum ALP levels were positively correlated with frequency of intake of fat/oil (r = 0.59, p < 0.01) and meats (r = 0.46, p < 0.05), whereas serum bilirubin (Bili) and aspartate aminotransferase (AST) levels were significantly correlated with frequency of intake of dairy products (rs = 0.48 and 0.45, ps < 0.05 for Bili and AST, respectively), meats (rs = 0.59 and 0.65, ps < 0.01), and fat/oil (r = 0.54, p < 0.02 and r = 0.48, p < 0.05). In patients with noncholestatic liver disease, Bili levels were correlated with frequency of intake of fat/oil (r = 0.58, p < 0.01), and fruits and vegetables (r = 0.68, p < 0.01). These results suggest that the degree of elevation of some liver biochemical tests in patients with liver disease may be affected by dietary intake.
Alkaline Phosphatase↗
Electrophoretic studies in liver disease. I. Comparison of serum and plasma electrophoretic patterns in liver disease, with special reference to fibrinogen and gamma globulin patterns.
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Blood Proteins↗
[Evolutive liver disease and liver-protective drugs].
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Folic Acid↗
Expression of neural cell adhesion molecule in human liver development and in congenital and acquired liver diseases.
In the liver, neural cell adhesion molecule (NCAM) is a marker of immature cells committed to the biliary lineage and is expressed by reactive bile ductules in human liver diseases. We investigated the possible role of NCAM in the development of intrahepatic bile ducts and aimed at determining whether immature biliary cells can contribute to the repair of damaged bile ducts in chronic liver diseases. Therefore, we performed immunohistochemistry for NCAM and bile duct cell markers cytokeratin 7 and cytokeratin 19 on frozen sections of 85 liver specimens taken from 14 fetuses, 10 donor livers, 18 patients with congenital liver diseases characterized by ductal plate malformations (DPMs), and 43 cirrhotic explant livers. Duplicated ductal plates and incorporating bile ducts during development showed a patchy immunoreactivity for NCAM, while DPMs were continuously positive for NCAM. Bile ducts showing complete or patchy immunoreactivity for NCAM were found in cirrhotic livers, with higher frequency in biliary than in posthepatitic cirrhosis. Our results suggest that NCAM may have a function in the development of the intrahepatic bile ducts and that NCAM-positive immature biliary cells can contribute to the repair of damaged bile ducts in chronic liver diseases.
Biomarkers↗
[Pseudocystic metastases of carcinoma of the uterine cervix mimicking polycystic liver disease].
Pseudocystic liver metastases are rare and mainly described in neuroendocrine or ovarian tumors. We report the case of a 46-year-old woman who presented with multiple hepatic metastases mimicking polycystic liver disease. Carcinoma of the uterine cervix had been diagnosed 9 years earlier, and initially treated by radiumtherapy and surgery. Although histological post mortem examination of the pseudocystic liver metastases was not characteristic, they were related to the uterine cervix carcinoma for the following reasons: no other primary tumor was discovered, especially carcinoid or ovarian tumors: immunostains were positive for epithelial cells and negative for the neuroendocrine panel: the cystic cerebellum metastasis had a typical histologic aspect. Uterine cervical carcinoma must thus be included in the list of tumors which may form cystic hepatic metastases.
Carcinoma, Squamous Cell↗