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J Henrion

Publications and source records attributed to J Henrion.

At least 19 recordsLinked to original sources
PubMed2005

Review article: the treatment of non-alcoholic steatohepatitis with thiazolidinediones.

It is generally accepted that non-alcoholic fatty liver disease will be the most frequent liver disease in the near future and that the management of patients with non-alcoholic fatty liver disease will be a challenge for hepatologists in the next decades. Non-alcoholic fatty liver disease is considered the hepatic manifestation of the metabolic syndrome, in which insulin resistance plays a crucial role. Although steatosis will often not progress to severe liver disease, in some patients, it results in cirrhosis and even hepatocellular carcinoma. Therefore, it is important to identify those patients at risk for developing fibrosis. Age, diabetes, obesity and hypertriglyceridaemia are independent risk factors for fibrosis in patients with elevated serum alanine aminotransferase levels and steatosis on ultrasound. The presence of multiple metabolic disorders increases the risk. Apart from diet, exercise and correction of underlying metabolic abnormalities, no specific treatment is available at the moment. Theoretically, thiazolidinediones are an attractive way to treat non-alcoholic fatty liver disease, because they improve insulin resistance. Some preliminary studies with thiazolidinediones were encouraging, as steatosis, inflammation and fibrosis improved in a substantial number of patients. Although no serious side effects occurred in the pilot studies, we should look vigilantly for hepatotoxicity, as the first generation thiazolidinediones proved to be toxic for the liver.

Chemical and Drug Induced Liver Injury↗
PubMed2005

Transjugular intrahepatic portosystemic shunt in refractory ascites: a meta-analysis.

UNLABELLED: Transjugular intrahepatic portosystemic shunt (TIPS) is a more effective treatment for refractory ascites than large volume paracentesis (LVP), but the magnitude of its effect in terms of control of ascites, encephalopathy and survival has not been established. AIM: This meta-analysis compare TIPS to LVP in terms of control of ascites at 4 and 12 months, encephalopathy and survival at 1 and 2 years. RESULTS: Five randomized controlled trials involving 330 patients were included. In the TIPS group, control of ascites was more frequently achieved at 4 months (66% vs 23.8%, mean difference: 41.4%, 95% confidence interval (CI): 29.5-53.2%, P < 0.001) and 12 months (54.8% vs 18.9%, mean difference: 35%, 95% CI: 24.9-45.1%, P < 0.001), whereas encephalopathy was higher (54.9% vs 38.1%, mean difference: 17%, 95% CI: 7.3-26.6%, P < 0.001). Survival at 1 year (61.7% vs 56.5%, mean difference: 3.2%, 95% CI: -14.7 to 21.9%) and 2 years (50% vs 42.8%, mean difference: 6.8%, 95% CI: -10 to 23.6%) were not significantly different. CONCLUSIONS: TIPS is a more effective treatment for refractory ascites than LVP. However, TIPS increase encephalopathy and does not improve survival.

Aged↗
PubMed2003

Daily induction combination treatment with alpha 2b interferon and ribavirin or standard combination treatment in naive chronic hepatitis C patients. A multicentre randomized controlled trial.

The standard treatment for patients with chronic hepatitis C is a 6-12-month combination therapy with interferon alpha and ribavirin. Induction treatment could result in a faster early decline of the hepatitis C virus (HCV) load and a better response rate. Naive chronically infected HCV patients (n = 454) were randomized into two arms to receive either induction treatment with interferon alpha 2b 5 million units (MU) subcutaneously (s.c.) daily during a period of 8 weeks (arm A); or treatment with interferon alpha 2b 5 MU s.c. three times a week (TIW) for a period of 8 weeks (arm B). After week 8, interferon treatment in both arms was 3 MU s.c. TIW for a total period of 12 months. In both arms, ribavirin (1000-1200 mg orally per day) was added at week 4. Induction treatment resulted in a higher virological response at week 8 of treatment (66%vs 47%; P < 0.01). However, response at the end of treatment and at 6 months follow-up was not different (53%vs 50%, 41%vs 33%). The occurrence of adverse events and the drop-out rate were similar in both arms. Although an early virological response is observed more frequently in the induction treatment, end of treatment response and sustained responses did not differ.

Adolescent↗
PubMed2003

Hepatocellular carcinoma associated with precocious puberty and oral contraceptives. A case report.

A 36-year-old woman presented with sudden abdominal pain and vomiting. Computed tomography showed a tumour of the right hepatic lobe with possible signs of acute haemorrhage. Her medical history revealed precocious puberty when she was a 5-year-old and the use of oral contraceptives for 18 years. Bisegmentectomy was performed and histological examination revealed hepatocellular carcinoma. The role of male and female sex hormones in the development of hepatic tumours has been well documented but, to our knowledge, association with precocious puberty has not yet been described.

Adult↗
PubMed2001

Haptoglobin phenotype 2-2 overrepresentation in Cys282Tyr hemochromatotic patients.

BACKGROUND/AIMS: Patients with genotypic Cys282Tyr homozygous hemochromatosis differ largely in phenotypic presentation. The HFE mutation on itself does not explain the different manifestations of hemochromatosis. We hypothesized that the genetic haptoglobin (Hp) polymorphism, because of its effect on iron metabolism, could be a modifying factor that influences the clinical presentation of hereditary hemochromatosis. METHODS: In 167 Cys282Tyr homozygous hemochromatotic patients, the frequencies of Hp types (1-1, 2-1 and 2-2) and alleles (Hp1, Hp2) were compared with those in 918 healthy subjects. Clinical and laboratory indices of iron overload were incorporated in the analysis. RESULTS: The Hp 2-2 type was overrepresented in the patient group (P<0.01). Male patients carrying Hp 2-2 had higher serum iron (P=0.003) and ferritin levels (P=0.03) than those with a Hp 1-1 or 2-1 type. The amount of iron removed with phlebotomy was also higher in Hp 2-2 patients (P=0.03). CONCLUSIONS: The Hp 2-2 type is overrepresented among Cys282Tyr homozygous hemochromatotic patients. At diagnosis, iron overload was more pronounced in male patients carrying Hp 2-2. Our data suggest that Hp polymorphism affects iron metabolism in hereditary hemochromatosis.

Adult↗
PubMed1999

Hypoxic hepatitis caused by acute exacerbation of chronic respiratory failure: a case-controlled, hemodynamic study of 17 consecutive cases.

Out of a prospective series of 142 consecutive episodes of hypoxic (ischemic) hepatitis (HH), we identified 17 episodes associated with an acute exacerbation of chronic respiratory failure (CRF) without left cardiac failure. In the aim to evaluate the role of arterial hypoxemia in the pathogenesis of HH associated with respiratory failure, these 17 episodes of HH (study group) were hemodynamically compared with a control group of 17 episodes of HH associated with congestive heart failure (CHF) (control group 1) and a group of 16 episodes of acute respiratory failure (ARF) not complicated by HH (control group 2). Arterial hypoxemia was significantly more severe in the study group (arterial blood tension in O2 [PaO2], 34 mm Hg) than in control group 1 (PaO2, 70 mm Hg; P <.0001) and control group 2 (PaO2, 45.5 mm Hg; P =.002). The role of arterial hypoxemia, however, appeared weakened by comparable degrees of systemic hypotension and liver passive congestion in episodes of HH associated with CRF and episodes of HH associated with CHF. Finally, the causative role of arterial hypoxemia emerged from hemodynamic measurements of cardiac index (CI), systemic vascular resistances (SVR), and oxygen transport: systemic hypotension in HH associated with CHF (control group 1) was the result of a fall in CI (median, 2. 33 L/min. m2; range, 1.21-3.14 L/min. m2) associated with high SVR (median, 2,492 dyn. s/cm5. m2; range, 1,382-4,053 dyn. s/cm5. m2), whereas in HH associated with respiratory failure (study group), systemic hypotension was the result of a fall in SVR (median, 1,053 dyn. s/cm5. m2; range, 646-3,148 dyn. s/cm5. m2), resulting in high CI (median, 4.23 L/min. m2; range, 1.9-5.32 L/min. m2) (P =.0087 and. 0038 for cardiac index and SVR, respectively). Moreover, measurements of oxygen transport in patients with HH associated with respiratory failure showed low values of O2 delivery (DO2) (median, 376 mL/min. m2; range, 253-427 mL/min. m2) as a result of extreme arterial hypoxemia despite high CI. In conclusion, these hemodynamic results and additional measurements of hepatic blood flow (HBF) by the method of galactose clearance at a low concentration suggest that in the setting of HH associated with respiratory failure, the liver is not "ischemic," despite hypotension, but rather "hypoxic" as a result of the combination of severe arterial hypoxemia and elevated central venous pressure (CVP).

Aged↗
PubMed1999

HLA association of amoxicillin-clavulanate--induced hepatitis.

BACKGROUND & AIMS: Drug-induced immunoallergic hepatitis typically affects a minority of patients exposed to a particular drug. Its rarity is believed to be due to metabolic or immunologic idiosyncrasy. The presence of an immunologic idiosyncrasy might imply an HLA association. Previous studies reporting an HLA association of drug-induced hepatitis included only small numbers of patients and used serological HLA typing. METHODS: We studied 35 patients with biopsy-documented amoxicillin-clavulanate-induced hepatitis. HLA-A and -B were typed using alloantisera and compared with those of 300 controls (volunteer bone marrow donors). HLA-DRB and -DWB were typed by polymerase chain reaction-line probe assay, with 60 volunteer bone marrow donors serving as controls. RESULTS: The study group was characterized by a higher frequency of DRB1*1501-DRB5*0101-DQB1*0602 haplotype (57.1% vs. 11.7% in controls, P < 0.000005; after correction for the large number of comparisons, P < 0.0002). Patients with DRB1*1501-DRB5*0101-DQB1*0602 haplotype were more likely than patients without it to have a cholestatic (70% vs. 60%) or mixed (30% vs. 13%) than a hepatocellular pattern of hepatitis (0% vs. 27%) (P < 0.05). CONCLUSIONS: Amoxicillin-clavulanate-induced hepatitis is associated with the DRB1*1501-DRB5*0101-DQB1*0602 haplotype. The data support the view that an immunologic idiosyncrasy, mediated through HLA class II antigens, plays a role in the pathogenesis of drug-induced immunoallergic hepatitis. HLA association has a limited impact on the expression of hepatitis.

Adult↗
PubMed1997

Hypoxic hepatitis caused by severe hypoxemia from obstructive sleep apnea.

Cardiac and circulatory failure are the main causes of hypoxic hepatitis. In a prospective study of 142 cases of hypoxic hepatitis collected during a 10-year period, we encountered two cases resulting from extreme arterial hypoxemia without congestive heart failure, cor pulmonale, or circulatory failure. Both patients were morbidly obese women admitted to the intensive care unit for carbonarcosis. Oxygen arterial saturation was very low, less than 35% in both patients, but there was no history of cardiac or respiratory failure and no clinical evidence of circulatory failure. Cardiac function, evaluated by isotopic scintigraphy, was normal. After the episode of hypoxic hepatitis, a diagnosis of obstructive sleep apnea was made clinically and confirmed by performing nocturnal oximetry, which showed multiple episodes of oxygen desaturation in both patients. Polysonography could be performed in one case and was typical of obstructive sleep apnea. Liver ischemia is the main mechanism leading to hypoxic hepatitis. More recently, the role of passive congestion of the liver has been emphasized. Arterial hypoxemia, however, is generally considered to be a minor factor. Our two cases support the hypothesis that severe arterial hypoxemia may lead to hypoxic hepatitis even in the absence of cardiac and circulatory failure.

Aged↗
PubMed1996

[Fulminant or sub-fulminant hepatocellular failure caused by metastatic invasiveness of the liver: an other cause of hypoxic hepatitis?].

OBJECTIVES: The purpose of this retrospective study was to report a series of 9 new cases of fulminant hepatic failure due to metastatic liver disease and to identify signs to support a theory of hypoxia. METHODS: In these 9 cases and in 38 previously published cases of fulminant or subfulminant liver failure, we looked for clinical (shock, sepsis, and cutaneous signs of circulatory failure), laboratory (marked increase in serum aminotransferases levels) and histological (cell necrosis) parameters compatible with liver hypoxia. RESULTS: Cutaneous signs of circulatory failure or shock were observed in 3 of the 9 cases in this study, and were not due to cardiogenic or septic shock. A marked increase in serum aminotransferases levels, 10 times above the upper limit of normal, was observed in 8 of the 9 cases in the present study and in 23 of 37 cases of the literature. Liver cell necrosis was observed in 6 of the 7 autopsied patients in this series and in 20 of 34 cases in the literature. Generally, liver cell necrosis was more severe than tumor cell necrosis and was related to the degree of sinusoidal involvement by tumoral cells. In one case, hepatic blood flow was decreased despite a high level of cardiac blood flow suggesting impairment of circulation in the liver. CONCLUSIONS: These 9 cases and a review of the literature support the hypothesis of hypoxic liver cell necrosis leading to acute liver failure in cases of metastatic liver disease. However, liver hypoxia cannot explain all the reported cases and was never due to circulatory failure from cardiac or septic causes, but to the sinusoidal involvement by tumor cells.

Adult↗
PubMed1995

[Lipoprotein (a) in liver diseases. Correlation between low levels and liver function].

OBJECTIVES: To analyze the role of the liver function on the serum levels of lipoprotein(a) (Lp(a)), a lipoprotein considered to be a risk factor for atherosclerosis. METHODS: To measure the Lp(a) levels in patients with liver disease (n = 68) due to various causes and in patients with no liver disease and of similar age and sex-ratio (n = 62) and to analyze the relationship between Lp(a) levels on one hand and liver function and lipid and apoprotein levels on the other hand. RESULTS: Patients with liver disease had significantly lower levels of Lp(a). Lp(a) levels were significantly lower in patients with more severe liver disease (Child Turcotte classification) and significantly correlated with liver function tests, in particular those related to the microsomal function and the synthetic capacity of the liver (albumin, coagulation tests, apoprotein A-II). In patients with liver disease, mean Lp(a) levels were not significantly different between those with and those without chronic alcohol intake. CONCLUSIONS: Patients with liver disease have low levels of Lp(a) that are related to reduced synthetic capacity of this organ and are not linked to a specific cause of liver disease, in particular excess alcohol intake.

Adult↗
PubMed1995

Liver injury related to amoxycillin-clavulanic acid: interlobular bile-duct lesions and extrahepatic manifestations.

We report eight cases of liver injury related to amoxycillin-clavulanate. Liver biopsy performed in seven patients revealed varying degrees of injury to interlobular bile ducts in all cases. Lesions included irregularity of the nuclei, vacuolization of the cytoplasm, lymphocytic infiltration, destruction and endothelialization of the bile duct epithelium. Ductopenia was not observed. In two patients liver injury was accompanied by prominent extrahepatic manifestations (acute interstitial nephritis in one and acute lacrimal gland inflammation and sialadenitis with prolonged xerostomia in the other). We conclude that interlobular bile-duct lesions of varying severity are a common feature in liver injury related to amoxycillin-clavulanate. Side effects of the drug include acute interstitial nephritis and sialadenitis.

Aged↗
PubMed1995

Severe hepatotoxicity related to benzarone: a report of three cases with two fatalities.

We report three cases of severe hepatotoxicity related to benzarone, a benzofuran derivative. Our cases include a 35-year-old woman with (sub)fulminant hepatitis, a 67-year-old woman with macronodular cirrhosis, and a 68-year-old man with severe chronic active hepatitis and cirrhosis, with positivity of anti-smooth muscle antibodies. Two patients died. We stress the potential of benzarone to cause hepatotoxicity, which usually resembles severe chronic active hepatitis. Our cases constitute the most severe cases of benzarone hepatotoxicity reported so far, and comprise the first cases of (sub)fulminant hepatitis and cirrhosis related to benzarone.

Adult↗
PubMed1994

Hypoxic hepatitis in patients with cardiac failure: incidence in a coronary care unit and measurement of hepatic blood flow.

The incidence of hypoxic hepatitis was prospectively studied for 1 year in a group of high-risk patients suffering from low cardiac output in a coronary care unit. Hypoxic hepatitis, defined as an increase in serum aminotransferase activity of at least 20 times the upper limit of normal without any other cause for hepatic necrosis, was observed in 20 patients. This represents 2.6% of the 766 patients admitted to the unit during this period and 21.9% of the 91 patients suffering from low cardiac output. Clinical, biological and hemodynamic data were compared between 20 patients with low cardiac output and hypoxic hepatitis, and 48 patients with low cardiac output but without hypoxic hepatitis who survived more than 24 h. In these two groups of patients, hepatic blood flow was measured by galactose clearance at low concentration. Patients with hypoxic hepatitis exhibited a higher central venous pressure (90% versus 38%-p < 0.001) as well as a lower hepatic blood flow (867 +/- 377 ml/min versus 1429 +/- 644 ml/min-p = 0.001). In conclusion, although it is considered a rare hepatic disorder, hypoxic hepatitis is frequent in patients with low cardiac output admitted to the coronary care unit, and is associated with a decrease in hepatic blood flow and passive hepatic venous congestion.

Adult↗