ABSTRACT
INTRODUCTION: Acute necrosis of the esophagus, frequently referred to as black esophagus is a rare clinical entity. CASE REPORT: We here report a case of an acute necrosis of the esophagus secondary to hemodynamic compromise after total hip replacement. Past medical history of our 72-year-old patient was remarkable for coronary heart disease, obstructive arteriopathy of the lower limbs, diabetes mellitus and hypertension. He was referred for hematemesis and epigastric pain one day after the surgical intervention was performed. Gastric endoscopy showed necrosis of the esophagus. Treatment consisted on intravenous proton pump inhibitor, parenteral renutrition, and red blood cell transfusion. Fours days later, endoscopy found complete disappearance of necrosis. CONCLUSION: Black esophagus develops in debilitated patients during hypoperfusion and stress. The outcome is usually favourable in the absence of comorbidities.
Subject(s)
Esophagus/pathology , Aged , Arthroplasty, Replacement, Hip , Erythrocyte Transfusion , Humans , Male , Necrosis/diagnosis , Necrosis/therapy , Parenteral Nutrition , Postoperative Complications , Proton Pump Inhibitors/therapeutic useABSTRACT
In order to establish a relationship between Hepatitis C virus (HCV) chronic infection and autoimmune thyroiditis, 97 untreated patients with biopsy-proven HCV chronic hepatitis and 97 controls were studied. An ultrasound examination of the thyroid and an assay of serum thyroid-stimulating hormone (TSH), thyroid hormones and anti-thyroid antibodies were performed in all cases. The overall prevalence of thyroid abnormalities was higher in patients than in controls (17 vs. 4%, P<0.01) and the prevalence of anti-thyroid antibodies was significantly different between the two groups (P<0. 02). HCV patients with (n=13) compared to HCV patients without anti-thyroid antibodies (n=84) were older, predominantly female, and more frequently had increased serum TSH levels or a hypoechogenic pattern of the thyroid gland, while Knodell's score and prevalence of cirrhosis were similar. Latent autoimmune thyroiditis is more frequent in untreated HCV patients than in controls. This finding raises questions about the mechanism of autoimmunity induced by HCV and provides an explanation for the high rate of overt autoimmune thyroiditis during interferon treatment in these patients.
Subject(s)
Hepatitis C, Chronic/complications , Thyroiditis, Autoimmune/complications , Adult , Aged , Autoantibodies/blood , Autoimmunity , Case-Control Studies , Female , Hepatitis C, Chronic/immunology , Humans , Male , Middle Aged , Thyroid Gland/immunology , Thyroiditis, Autoimmune/etiology , Thyroiditis, Autoimmune/immunology , Thyrotropin/bloodABSTRACT
BACKGROUND/AIMS: Severe alcoholic hepatitis occurs mainly in patients with cirrhosis, and has a high death rate. Corticosteroid therapy has been particularly advocated as reducing mortality in patients with severe histologic lesions. However, identification of these patients is difficult, requiring transvenous liver biopsy. Extracellular matrix serum markers have been proposed as non-invasive diagnostic tools in alcoholic liver disease. The aim of this study was to determine the accuracy of 5 extracellular matrix serum markers, i.e. laminin (Lam), N-terminal peptide of type III procollagen (PIIINP), type I (CI), type III (CIII) and type IV (CIV) collagens in identifying patients with severe histologic alcoholic hepatitis from among those with cirrhosis and suspected alcoholic hepatitis. METHODS: We studied 80 consecutive patients with alcoholic cirrhosis and clinical suspicion of alcoholic hepatitis referred for transvenous liver biopsy. Clinical severity of alcoholic hepatitis was assessed according to Maddrey's score. Histological severity was scored using the sum of the 3 following items: polynuclear infiltration (0-3); hepatocytes alterations (0-3); Mallory bodies (0-2). According to this score, patients were divided into 3 groups: mild (1-3), moderate (4-6), and severe (7-8) alcoholic hepatitis. Serum levels of the 5 extracellular matrix serum markers were measured at the time of biopsy using radioimmunoassays. Diagnostic value for histologically severe alcoholic hepatitis of the 5 extracellular matrix serum markers was assessed using receiver operating characteristic curves. RESULTS: Histological alcoholic hepatitis was present in 67 patients (mean alcoholic hepatitis score: 3.4+/-2.3). Maddrey's score was 66% sensitive and 69% specific for the diagnosis of severe histologic alcoholic hepatitis. The serum Lam and CIV concentrations were the most accurate in identifying correctly patients with severe histologic alcoholic hepatitis. At a cut-off of 4.1 UI/ml, Lam was 90% sensitive and 77% specific, whereas at a cut-off of 150 ng/ml, CIV was 89% sensitive and 77% specific. Combination of markers did not result in improved diagnostic value. CONCLUSION: In patients with cirrhosis, determination of serum Lam or CIV could represent a simple and accurate non-invasive method for identification of patients with histologically severe alcoholic hepatitis eligible for corticosteroid treatment.
Subject(s)
Collagen/blood , Hepatitis, Alcoholic/blood , Hepatitis, Alcoholic/complications , Laminin/blood , Liver Cirrhosis/complications , Adult , Biomarkers/blood , Diagnosis, Differential , Female , Hepatitis, Alcoholic/diagnosis , Hepatitis, Alcoholic/pathology , Humans , Male , Middle Aged , Peptide Fragments/blood , Procollagen/blood , Severity of Illness IndexABSTRACT
OBJECTIVES: Giant-cell hepatitis is rare in adults and its significance has not been clarified. We report the clinical and histological characteristics and outcome in a group of adult patients with giant-cell hepatitis. METHODS: Seventeen patients with giant-cell hepatitis, hospitalized in our unit between 1976 and 1992, were studied retrospectively. Giant-cell hepatitis was defined as at least two hepatocytes with four or more nuclei per cell on liver biopsy. Clinical and biochemical parameters, liver histology, and the serological profile of HAV, HBV, HCV, HIV, HSV, EBV, CMV, and paramyxovirus were evaluated. Paramyxovirus immunochemistry was performed in 6 liver biopsies. RESULTS: There were 11 females and 6 males, an average of 48 years old (range: 29-80). Four patients had a well-defined etiology: acute hepatitis B infection with a favorable outcome in 2 cases, clometacine induced-hepatitis resulting in death from liver failure in one case, and chronic hepatitis B and C in one patient with AIDS. Among the 13 patients in which the etiology could not be determined, histologically defined acute hepatitis was observed in 8 and chronic hepatitis in 5. Nine patients were treated with immunosuppressive drugs. One patient was lost to follow-up. Eight patients responded to treatment, but 5 patients progressed to cirrhosis between 5 months and 7 years. Two of the 4 patients with unexplained liver disease who did not receive any treatment died of liver failure. CONCLUSION: In patient with acute or chronic hepatitis without an identified cause (with or without autoimmune abnormalities), the presence of giant-cell hepatitis seems to have a similar evolution as active autoimmune hepatitis. The poor prognosis of these patients suggests that early immunosuppressive treatment is justified.
Subject(s)
Giant Cells/pathology , Hepatitis/physiopathology , Adult , Aged , Aged, 80 and over , Analgesics/poisoning , Chemical and Drug Induced Liver Injury/drug therapy , Chemical and Drug Induced Liver Injury/pathology , Chemical and Drug Induced Liver Injury/physiopathology , Female , Giant Cells/virology , Hepatitis/drug therapy , Hepatitis/pathology , Hepatitis, Viral, Human/drug therapy , Hepatitis, Viral, Human/pathology , Hepatitis, Viral, Human/physiopathology , Humans , Immunosuppressive Agents/therapeutic use , Indoleacetic Acids/poisoning , Male , Middle Aged , Retrospective StudiesABSTRACT
BACKGROUND/AIMS: A 4977-base pair deletion has been detected in the hepatic mitochondrial DNA of alcoholic patients with microvesicular steatosis, a lesion ascribed to impaired mitochondrial beta-oxidation. However, only a single deletion had been looked for in this previous study, and it could not be determined whether the deletion was preexisting or acquired. Alcohol abuse increases the formation of reactive oxygen species in hepatic mitochondria. If this effect accelerates the oxidative aging of mitochondrial DNA, several other mutations would be expected. METHODS: The mtDNA region extending from nucleotide 8167 to nucleotide 14246 was screened for the presence of large mitochondrial DNA deletions in 58 alcoholic patients and 67 age-matched non-alcoholic controls. Hepatic DNA was subjected to polymerase chain reactions that amplified non-deleted and deleted mitochondrial DNA, respectively, and the boundaries of the mitochondrial DNA deletions were sequenced. RESULTS: Only 3% of the non-alcoholic controls carried a mitochondrial DNA deletion, whereas 24% of all alcoholic patients and 85% of the 13 alcoholic patients with microvesicular steatosis exhibited either single or multiple 4977, 5385, 5039 and 5556-base pair mitochondrial DNA deletions. No deletion(s) were observed, however, in 13 patients with microvesicular steatosis due to other causes. CONCLUSIONS: Diverse mitochondrial DNA rearrangements are observed in alcoholic patients with microvesicular steatosis. We suggest that alcohol abuse leads to premature oxidative aging of mitochondrial DNA. Hypothetically, oxidative damage to mitochondrial constituents (DNA, proteins and lipids) may favor microvesicular fat deposition.
Subject(s)
Aging/metabolism , Alcoholism/genetics , DNA, Mitochondrial/genetics , Mitochondria, Liver/genetics , Sequence Deletion , Adult , Aged , Aging/genetics , Alcoholism/complications , Alcoholism/metabolism , DNA Damage , DNA, Mitochondrial/metabolism , Fatty Liver, Alcoholic/etiology , Fatty Liver, Alcoholic/genetics , Fatty Liver, Alcoholic/metabolism , Humans , Liver/metabolism , Male , Middle Aged , Mitochondria, Liver/metabolism , Oxidation-Reduction , Polymerase Chain ReactionABSTRACT
Although autoantibodies have been found in the serum of patients with chronic hepatitis C virus (HCV) there has been no convincing evidence of the presence of antimitochondrial antibodies, until now. Sera from 460 untreated patients with chronic hepatitis C were tested for antimitochondrial antibodies, using an indirect immunofluorescence technique; and if they tested positive for the antibodies (titer more than 1:50), they also were treated by Western blot analysis. Seven (1.5%) sera were positive. None of the patients had biological or histological evidence of primary biliary cirrhosis. Antimitochondrial antibodies recognized one of the oxo-dehydrogenase multienzyme complexe's epitopes by Western blot assay in three patients only. All seven patients were then treated by interferon alpha for six months. None showed exacerbation of liver disease during treatment. HCV-RNA disappeared from the serum in one patient who became negative for anti-M2 antibodies. The four patients who did not respond to interferon-alpha therapy, and the two who relapsed after treatment withdrawal, had sustained positive antimitochondrial antibodies. These data suggest that: 1) antimitochondrial antibodies present in patients with chronic hepatitis C do not always recognize the same epitopes as in primary biliary cirrhosis; 2) these antibodies may disappear after eradication of HCV, suggesting that the production of antimitochondrial antibodies is linked to the presence of the virus and 3) the clinical and biological course of chronic hepatitis C, and the response to interferon-alpha therapy, does not seem to be different in patients who are positive for antimitochondrial antibodies.
Subject(s)
Antibodies/blood , Hepatitis C/virology , Mitochondria/immunology , 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide) , Adult , Aged , Antibodies/analysis , Antibodies, Antinuclear/blood , Biopsy , Blotting, Western , Female , Fluorescent Antibody Technique , Hepacivirus/genetics , Hepacivirus/metabolism , Histocytochemistry , Humans , Interferon-alpha/pharmacology , Interferon-alpha/therapeutic use , Ketone Oxidoreductases/immunology , Liver/pathology , Liver/virology , Male , Middle Aged , Molecular Weight , Multienzyme Complexes/immunology , Muscle, Smooth/immunology , Polymerase Chain ReactionABSTRACT
OBJECTIVES AND METHODS: Extrahepatic manifestations have been reported in hepatitis C virus infection. To assess the relationship between diabetes mellitus and hepatitis C virus, we studied 152 patients with chronic hepatitis C and 152 controls hospitalized during the same period with hepatitis B virus (n = 51) or alcohol-induced (n = 101) liver diseases matched for age, sex, and the presence of cirrhosis (prevalence: 58%). Patients with jaundice, ascites, encephalopathy, prothrombin activity < 65%, or serum albumin < 35 g/L were excluded. RESULTS: Diabetes, defined by fasting serum glycemia > 1.4 g/L on at least two separate occasions or previously treated overt diabetes, was present in 38 patients with chronic hepatitis C (24%) and in 13 patients in the control group (9%, P < 0.002). In the 51 diabetic patients, irrespective of serum anti-hepatitis C virus status, 41 (81%) had non insulin dependent diabetes and 45 (88%) had cirrhosis. Family history of diabetes or obesity was observed in 2 (5%) of the diabetic patients with chronic hepatitis C and in 6 (46%) of the diabetic controls (P = 0.002). Plasma C-peptide (855 +/- 448 pmol/L versus 1,152 +/- 491 pmol/L, NS) and insulin levels (83 +/- 40 pmol/L versus 184 +/- 86 pmol/L, NS), assayed in 17 diabetic patients with chronic hepatitis C and in 9 diabetic controls, were lower in the former. The prevalence of HLA B8, DR3 or DR4 antigens, which was searched for in 77 patients with chronic hepatitis C, was not different in diabetic and non diabetic patients, and, was similar to the reference population. Serum islet-cell antibodies were found in 5 patients with chronic hepatitis C (3 with diabetes) and in 2 controls. CONCLUSION: Diabetes mellitus is more prevalent in patients with chronic hepatitis C than in patients with other liver diseases, and usually occurs in the absence of predisposing factors. These results suggest a role of hepatitis C virus infection in the pathogenesis of diabetes.
Subject(s)
Diabetes Complications , Hepatitis C/complications , Adult , Chronic Disease , Diabetes Mellitus/blood , Diabetes Mellitus/immunology , Female , Hepatitis B/blood , Hepatitis B/immunology , Hepatitis C/blood , Hepatitis C/immunology , Humans , Liver Cirrhosis, Alcoholic/blood , Liver Cirrhosis, Alcoholic/immunology , Liver Diseases, Alcoholic/blood , Liver Diseases, Alcoholic/immunology , Male , Middle AgedSubject(s)
Actins/immunology , Antibodies/isolation & purification , Antiviral Agents/adverse effects , Hepatitis C/therapy , Interferon-alpha/adverse effects , Muscle, Smooth/immunology , Antiviral Agents/therapeutic use , Female , Humans , Immune System Diseases/chemically induced , Interferon-alpha/therapeutic use , Male , Middle AgedABSTRACT
Acute fatty liver of pregnancy occurs in some women. As other cases of microvesicular steatosis are due to impaired mitochondrial oxidation of fatty acids, we investigated the effects of female sex hormones on liver mitochondria in female mice. Three hours after administration of both estradiol (36 mumol/kg) and progesterone (150 mumol/kg), the in vitro beta-oxidation of [U-14C]palmitic acid and the activity of the tricarboxylic acid cycle decreased 49 and 54%, whereas the in vivo oxidation of [U-14C]palmitic acid decreased 38%. One week of treatment with both sex hormones produced ultrastructural lesions of mitochondria, decreased the recovery of mitochondrial proteins by 34%, increased state 4 respiration by 54-77%, and decreased the activities per gram of liver of several enzymes involved in the activation, mitochondrial uptake, and oxidation of fatty acids by 34-54%. We conclude that female sex hormones have deleterious effects on liver mitochondria and suggest that these effects, together with other factors, may contribute to the development of acute fatty liver of pregnancy in some women.
Subject(s)
Estradiol/pharmacology , Fatty Liver/etiology , Mitochondria, Liver/drug effects , Pregnancy Complications/etiology , Progesterone/pharmacology , Acute Disease , Animals , Dose-Response Relationship, Drug , Female , Mice , Mice, Inbred Strains , Mitochondria, Liver/physiology , Mitochondria, Liver/ultrastructure , Pregnancy , Time FactorsABSTRACT
BACKGROUND/AIMS: Alcohol abuse may lead to microvesicular steatosis, a lesion ascribed to impaired mitochondrial function. Because alcohol abuse leads to reactive oxygen species in the hepatic mitochondria, it may damage mitochondrial DNA. The aim of this study was to look for the presence of the "common" 4977-base pair deletion in the hepatic mitochondrial DNA of alcoholic patients and age-matched, nonalcoholic controls. METHODS: Hepatic DNA was subjected to two polymerase chain reactions that amplified non-deleted and deleted mitochondrial DNA, respectively. RESULTS: The deletion was found in 6 of 10 alcoholics with microvesicular steatosis, 2 of 17 alcoholic patients with macrovacuolar steatosis, but in none of 12 patients with acute alcoholic hepatitis, 11 patients with alcoholic cirrhosis, or 62 nonalcoholic patients of comparable ages with various other liver diseases or normal liver histology. In all patients with the deletion, restriction fragments of deleted mitochondrial DNA co-migrated with those of reference Pearson bone marrow-pancreas syndrome patients with the common mitochondrial DNA deletion. CONCLUSIONS: The common deletion is frequent in the hepatic DNA of alcoholic patients with microvesicular steatosis. Alcohol-induced mitochondrial DNA damage may contribute to the occurrence of this lesion in some alcoholics.
Subject(s)
Alcoholism/complications , Alcoholism/genetics , DNA, Mitochondrial/genetics , Fatty Liver/complications , Gene Deletion , Liver/metabolism , Adult , Base Sequence , DNA, Mitochondrial/metabolism , Female , Humans , Liver Circulation , Male , Microcirculation , Middle Aged , Molecular Probes/genetics , Molecular Sequence Data , Reference ValuesABSTRACT
The HMG-CoA reductase inhibitor, lovastatin, is known to induce asymptomatic liver dysfunction in a few patients. We report the case of an adult who suffered from clinical hepatitis three months after the onset of lovastatin administration. Manifestations included asthenia, jaundice, and increased aminotransferase and alkaline phosphatase activities. Histologic examination showed centrilobular necrosis, centrilobular cholestasis, and infiltrates with mononuclear and polymorphonuclear cells, including eosinophils. Withdrawal of lovastatin was followed by complete normalization of liver tests within two months.
Subject(s)
Chemical and Drug Induced Liver Injury/etiology , Lovastatin/adverse effects , Acute Disease , Biopsy , Chemical and Drug Induced Liver Injury/pathology , Humans , Hypercholesterolemia/drug therapy , Male , Middle AgedABSTRACT
Two cases of sclerosing cholangitis after oily arterial chemoembolization are reported. In one patient angiocholitis with liver abscesses, in the other patient gradual cholestasis were the main clinical features. In both cases, endoscopic retrograde cholangiogram showed a stricture of the common hepatic bile duct and, in one case, irregularities of intrahepatic biliary tree. Histologic examination of the liver in the two patients pointed out the involvement of small bile ducts and arteriolar endarteritis obliterans. Ischaemia is likely to be the main mechanism of these two cases of sclerosing cholangitis as well as in those described after FUDR intra-arterial chemotherapy. The prevalence of sclerosing cholangitis after arterial oily chemoembolization is probably underestimated because of a non specific clinical presentation and need to be precise by further study.
Subject(s)
Cholangitis, Sclerosing/etiology , Embolization, Therapeutic/adverse effects , Iodized Oil/adverse effects , Carcinoma, Hepatocellular/therapy , Cholangiopancreatography, Endoscopic Retrograde , Cholangitis, Sclerosing/diagnostic imaging , Cholangitis, Sclerosing/pathology , Endarteritis/etiology , Endarteritis/pathology , Fatal Outcome , Female , Hepatic Duct, Common/diagnostic imaging , Humans , Ileal Neoplasms/pathology , Liver Neoplasms/secondary , Liver Neoplasms/therapy , Male , Middle AgedABSTRACT
OBJECTIVES: The prevalence and significance of antiorganelle antibodies in the serum of patients with chronic hepatitis C is a subject of controversy. We studied prospectively these characteristics in patients with chronic hepatitis C. METHODS AND RESULTS: Among 156 patients (age: 55 +/- 14 years; 83 females), 30 (19%) had significant titers of antiorganelle antibodies: anti-nuclear antibodies in 18, anti-smooth muscle antibodies in 8 (no anti-actin or anti-vimentine subtypes), anti-LKM1 in 2, type 2 anti-mitochondrial antibodies in 2 patients. Anti-organelle antibodies were not detected in 126 patients. Patients with anti-organelle antibodies were significantly older but no difference was found between the two groups for sex ratio, serum amino-transferases or gammaglobulins, histopathological liver activity or prevalence of lymphocytic sialadenitis. The presence of anti-organelle antibodies was not related to HLA phenotype, especially B8 DR3, or DR4. Response to alpha interferon, estimated by serum aminotransferase levels after six months of treatment, was the same in both groups. CONCLUSIONS: These results suggest that serum anti-organelle antibodies are prevalent in during chronic hepatitis C but do not indicate a distinct autoimmune mechanism. Furthermore, the typing of anti-smooth muscle antibodies might help distinguish chronic hepatitis C from type 1 autoimmune chronic hepatitis.
Subject(s)
Antibodies, Antinuclear/immunology , Hepatitis C/immunology , Hepatitis, Chronic/immunology , Muscle, Smooth/immunology , Adult , Aged , Aged, 80 and over , Autoantibodies/immunology , Female , Humans , Male , Middle Aged , Mitochondria, Muscle/immunology , Prospective StudiesSubject(s)
Hepatitis A/complications , Porphyria Cutanea Tarda/etiology , Adult , Humans , Male , Time FactorsABSTRACT
Severe impairment of the beta-oxidation of fatty acids, as a consequence of a single factor or a combination of different causes, leads to microvesicular steatosis of the liver. In an effort to understand the mechanism(s) leading to the development of acute fatty liver of pregnancy in some women, we determined the effects of pregnancy on the mitochondrial oxidation of fatty acids in mice. In vivo, the rate of oxidation of the whole fatty-acid chain length was determined by measuring the rate of exhalation of [14C]CO2 after intragastric administration of a tracer dose of [U-14C]palmitic acid. [14C]CO2 exhalation was not significantly decreased at 14 days of gestation, but it had declined by 40% at 18 days of gestation (i.e., 24 to 48 hr before delivery). The rate of first beta-oxidation cycle was assessed by measuring the rate of [14C]CO2 exhalation after administration of [1-14C]octanoic acid, [1-14C]butyric acid or [1-14C]palmitic acid. [14C]CO2 exhalation had declined by 60%, 46%, and 24% after administration of [1-14C]octanoic acid, [1-14C]butyric acid and [1-14C]palmitic acid, respectively, in 18-day-pregnant mice. Total hepatic lipids and triglycerides, expressed per gram of liver, remained unchanged in 18-day-pregnant mice. In vitro, the rate of mitochondrial beta-oxidation (expressed per milligram of protein) had decreased by 47% at 18 days' gestation with [U-14C]palmitic acid as substrate and by 33% with [1-14C]octanoic acid but remained unchanged with [1-14C]palmitic acid. The activity of the tricarboxylic acid cycle, assessed by the formation of [14C]CO2 from [1-14C]acetic acid, had decreased by 24%. We conclude that the mitochondrial oxidation of fatty acids decreased during late-term pregnancy in mice as a consequence of both decreased mitochondrial beta-oxidation of medium-chain fatty acids, and decreased activity of the tricarboxylic acid cycle. We suggest that this effect, in combination with other factors, may contribute to the development of fatty liver of pregnancy in some pregnant women.
Subject(s)
Fatty Acids, Nonesterified/metabolism , Fatty Liver/physiopathology , Mitochondria, Liver/metabolism , Oxygen Consumption , Pregnancy Complications/physiopathology , Pregnancy, Animal/metabolism , Repressor Proteins , Saccharomyces cerevisiae Proteins , Acyl-CoA Dehydrogenase , Animals , Body Weight , Carbon Radioisotopes , Carnitine O-Palmitoyltransferase/metabolism , Coenzyme A Ligases/metabolism , Fatty Acid Desaturases/metabolism , Fatty Liver/metabolism , Female , Isoenzymes/metabolism , Liver/anatomy & histology , Liver/ultrastructure , Male , Mice , Mice, Inbred ICR , Microscopy, Electron , Mitochondria, Liver/ultrastructure , Organ Size , Oxidation-Reduction , Pregnancy , Pregnancy Complications/metabolism , Radioisotope Dilution Technique , Reference ValuesABSTRACT
The aim of this study was to compare 6 potential serum markers for hepatic fibrosis in patients with alcoholic liver disease. Ninety-three patients (50 +/- 11 years old, 62 males) with biopsy-proven alcoholic liver disease were included in the study. A liver biopsy and serum assays of type I, type III and type IV collagens, N-terminal peptide of type III procollagen, laminin (by radioimmunoassays) and apolipoprotein A1 (by nephelometry) were performed in all patients. A histological score of hepatic fibrosis was established. Alcoholic hepatitis lesions and perisinusoidal fibrosis were assessed separately. A significant correlation was found between the score of hepatic fibrosis and serum levels of type I collagen (r = 0.44, P < 10(-3)), type III collagen (r = 0.36, P < 10(-2)), N-terminal peptide of type III procollagen (r = 0.50, P < 10(-3)), type IV collagen (r = 0.44, P < 10(-3)), laminin (r = 0.50, P < 10(-3)), and apolipoprotein A1 (r = 0.21, P < 0.05). After adjustment for the presence of lesions of alcoholic hepatitis and perisinusoidal fibrosis (partial correlation), serum levels of type I collagen, type III collagen, N-terminal peptide of type III procollagen, type IV collagen, and laminin remained significantly correlated with the score of hepatic fibrosis; in contrast, correlation with serum apolipoprotein A1 was no longer significant. Serum levels of N-terminal peptide of type III procollagen, type IV collagen and laminin were significantly higher in patients with perisinusoidal fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
Subject(s)
Collagen/analysis , Hepatitis, Alcoholic/blood , Liver Cirrhosis, Alcoholic/blood , Liver Diseases, Alcoholic/blood , Peptide Fragments/analysis , Procollagen/analysis , Adult , Apolipoprotein A-I/analysis , Female , Hepatitis, Alcoholic/complications , Humans , Laminin/analysis , Liver Cirrhosis, Alcoholic/complications , Male , Middle Aged , Retrospective StudiesABSTRACT
We described the case of a 56 year-old man with cirrhosis due to hemochromatosis and who had undergone a surgical terminolateral portocaval shunt 17 years previously. The patient was admitted for jaundice. Ultrasonography initially suggested multiple intrahepatic tubular structures, interpreted as enlarged intrahepatic bile ducts. Pulsed Doppler ultrasonography demonstrated that this spectral waveform corresponded to the intrahepatic extension of a diffuse portal cavernoma. Cavernomatous transformation of portal vein should be suspected when intrahepatic tubular structures are associated with long standing portal vein thrombosis.