Hepatitis: Henrion J

Colle I, Adler M, Brenard R, Henrion J, Langlet P, Michielsen P, Orlent H, Reynaert H, Sprengers D, Stärkel P, Van Damme P, Verslype C, Delwaide J, Anonymous00199. · Department of Hepatology and Gastroenterology, Ghent University Hospital, Ghent, De Pintelaan 185, 9000 Gent, Belgium. · Acta Gastroenterol Belg. · Pubmed #18330099 No free full text.

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Robaeys G, Buntinx F, Bottieau E, Bourgeois S, Brenard R, Colle I, De Bie J, Matheï C, Mulkay JP, Van Damme P, Van Ranst M, Verrando R, Michielsen P, Bourgeois N, Brenard R, de Galocsy Ch, Delwaide J, Henrion J, Horsmans Y, Michielsen P, Reynaert H, Robaeys G, Sprengers D, Anonymous00401. · Department of Gastroenterology and Hepatology, Ziekenhuis Oost Limburg, Genk, Schiepse Bos, 6, B-3600 Genk, Belgium. · Acta Gastroenterol Belg. · Pubmed #15832586 No free full text.

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Michielsen P, Brenard R, Bourgeois N, De Galocsy Ch, Delwaide J, Henrion J, Horsmans Y, Nevens F, Reynaert H, Robaeys G, Sprengers D, Van Vlierberghe H, Anonymous00046. · Department of Hepatogastroenterology, University Hospital Antwerp, Wilrijkstraat 10, 2650 Edegem. · Acta Gastroenterol Belg. · Pubmed #12812144 No free full text.

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Henrion J. · Service d'hépato-gastroentérologie, Département de médecine interne, Hôpital de Jolimont, Haine Saint Paul. · Acta Gastroenterol Belg. · Pubmed #17715637 No free full text.

Abstract: Hypoxic hepatitis better known under the terms of ischemic hepatitis or shock liver is the clinical manifestation of an acute liver cell necrosis consecutive to liver hypoxia. The clinical syndrome is defined as a massive but rapidly resolutive increase in serum aminotransferase activities (AT) occurring in a clinical setting of hemodynamic failure. Actually, when confronted to a case of massive increase in serum AT in the setting of cardiac or respiratory failure, the diagnosis of HH may be assumed without liver biopsy if another cause of hepatocyte necrosis such as viral hepatitis or drug induced hepatitis may be excluded. To our opinion, in these patients often aged and in poor general condition, it is particularly important to exclude herpes simplex virus infection and paracetamol intoxication. In case of doubt, a mere ultrasonography of the liver will be helpful. Indeed the majority of these patients will have a dilation of hepatic veins due to passive congestion of the liver. There is no specific liver therapy and the prognosis is poor depending on the severity of the underlying condition. In this point of view, we report what could be of interest for the hospital clinician.

Verslype C, Michielsen P, Adler M, Orlent H, Sprengers D, Delwaide J, D'heygere F, Langlet P, Brenard R, Colle I, Reynaert H, Stärkel P, Henrion J, Anonymous00136. · Department of Hepatology, University Hospital Gasthuisberg, Leuven, Belgium. · Acta Gastroenterol Belg. · Pubmed #16268417 No free full text.

Abstract: Infection with the hepatitis C virus (HCV) represents an important public health problem and is a leading cause of chronic hepatitis, cirrhosis and hepatocellular carcinoma. Chronic hepatitis C is a heterogeneous disease. Many patients have mild disease at presentation but not all of them will develop advanced liver disease. However, the identification of these patients with mild hepatitis C who will show progressive disease is difficult and is based on histological criteria and the assessment of co-factors (age, alcohol intake, steatosis). In addition, serum transaminases that are persistently normal on several occasions during 18 months may point to a more benign course. Patients with mild hepatitis C should not be excluded "a priori" from the possibility of being treated, as treatment with pegylated interferon and ribavirin is safe and effective in this group. Overall, the decision to initiate therapy should be individualized and based on the severity of the disease by liver biopsy, the potential of serious side effects, the probability of response and the motivation of the patient.

Henrion J. · Département de médecine interne, unité d'hépato-gastroentérologie, Hôpital de Jolimont, Haine-Saint-Paul, B-7100 Belgium. · Acta Gastroenterol Belg. · Pubmed #11233516 No free full text.

Abstract: For the last decade, numerous experimental studies have demonstrated that the main part of liver injury caused by low or no flow states does not occur at the time of hypoxia, but during reperfusion. These experimental studies have a crucial clinical impact, because ischemia/reperfusion injury is involved in situations such as temporary vascular exclusion during liver surgery for trauma or tumors, preservation injury before liver transplantation, and liver cell necrosis observed in hypoxic (ischemic) hepatitis. The aim of the present review is to clarify the sequence of pathophysiological events responsible for ischemia/reperfusion injury of the liver, and to examine the potential contribution of liver ischemia/reperfusion injury to the syndrome of human hypoxic hepatitis.

Henrion J. · Hôpital de Jolimont, Département de Médecine Interne, Haine-Saint-Paul. · Acta Clin Belg. · Pubmed #10555386 No free full text.

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Brouwer JT, Nevens F, Bekkering FC, Bourgeois N, Van Vlierberghe H, Weegink CJ, Lefebvre V, Van Hattum J, Henrion J, Delwaide J, Hansen BE, Schalm SW, For The Benelux Study Group On Treatment Of Chronic Hepatitis C. · Department of Hepatogastroenterology, Erasmus Medical Center, Rotterdam, The Netherlands. · J Hepatol. · Pubmed #15030987 No free full text.

Abstract: BACKGROUND/AIMS: Treatment of chronic hepatitis C with interferon can be ineffective due to relapse. We aimed to reduce the 40% relapse rate of 6 months interferon-ribavirin combination therapy by prolonging treatment to 18 months. METHODS: Three hundred patients with treatment-naive hepatitis C, were randomized to 18 months combination therapy with interferon (3MU tiw) and ribavirin (1000-1200 mg/day), 18 months interferon combined with placebo, or 6 months combination therapy with interferon and ribavirin, in a double blinded manner. All 295 patients who received at least one dose of treatment were included in the intention to treat analysis. RESULTS: At the end of treatment, HCV RNA was undetectable in 55 and 49% of those on 6 and 18 months combination therapy, respectively, versus 26% of those on monotherapy (P<0.001). The relapse rate was 38% for 6 months combination therapy, 38% for 18 months monotherapy, and only 13% for 18 months combination treatment (P=0.002). The sustained response rates were 34% for 6 months combination therapy, 16% for 18 months monotherapy and 43% for 18 months combination therapy (P<0.05). CONCLUSIONS: Reduction of relapse rates to 15% or less is feasible by prolongation of interferon-ribavirin treatment to 18 months.

Van Vlierberghe H, Leroux-Roels G, Adler M, Bourgeois N, Nevens F, Horsmans Y, Brouwer J, Colle I, Delwaide J, Brenard R, Bastens B, Henrion J, de Vries RA, de Galocsy C, Michielsen P, Robaeys G, Bruckers L. · Department of Gastroenterology and Hepatology, Ghent University Hospital, Ghent, Belgium. hans.vanvlierberghe@rug,ac.be · J Viral Hepat. · Pubmed #14633181 No free full text.

Abstract: 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.

Deuffic-Burban S, Deltenre P, Louvet A, Canva V, Dharancy S, Hollebecque A, Boitard J, Henrion J, Yazdanpanah Y, Mathurin P. · CTRS-INSERM U795, CHRU Lille, Lille, France. · J Hepatol. · Pubmed #18538441 No free full text.

Abstract: BACKGROUND/AIMS: In France, two recent studies enabled modeling of the impact of viral eradication on HCV mortality. METHODS: The French HCV population was simulated from infection to death using a computer-based model. We took into account the impact of alcohol, present screening and antiviral therapy to predict 2006--2025 HCV mortality and to assess the impact of viral eradication. RESULTS: In 2006, the model estimated that among HCV-RNA+, 55% were F0-F1, 18% F2, 22% F3-F4 and 6% had liver complications. The mortality ratio was 11-fold higher in alcoholic patients 40-65 years old. Current therapy will save 14,400 (95% CI, 13,900-15,000) lives compared to absence of therapy. Sensitivity analyses did not change the main results. Contrary to guidelines, if patients F<2 were treated in the same proportions as those with F> or = 2,700 (95% CI, 700-750) lives would be saved. If screening were to reach 75% in 2010, 4 years earlier than model expectation, 950 (95% CI, 900-1000) lives would be saved. If a new molecule improving eradication for genotype 1/4 by 40% were to become available in 2010, 1500 (95% CI, 1400-1600) lives would be saved. CONCLUSIONS: Current therapy is reducing HCV mortality. Therapeutic guidelines must take into account their impact on HCV mortality.

De Maeght S, Henrion J, Bourgeois N, de Galocsy C, Langlet P, Michielsen P, Reynaert H, Robaeys G, Sprengers D, Orlent H, Adler M. · CH Jolimont, Haine Saint Paul. · Acta Gastroenterol Belg. · Pubmed #18396742 No free full text.

Abstract: AIM OF THE STUDY: There is a lack of epidemiological data on hepatitis C (HCV) infected patients in Belgium. Therefore our purpose was to address this important question and to evaluate the feasibility of a national HCV observatory. PATIENTS AND METHODS: From November 2003 to November 2004, every new patient prospectively seen for HCV antibody positivity in 9 Belgian hospital centres was recorded and a standardised 10-items questionnaire was completed during the consultation, including a Quality of Live (QOL) visual analogue scale. RESULTS: Three hundred and eighteen consecutive patients were recruited. Fifty five percent were male with a median age of 45 y (11-87 y). The main risk factors for infection were IV drug use (27%), blood transfusion (23%), and invasive medical procedure (11%). On the QOL scale, ranging from 0 and 100, mean value was 61 +/- 31. Transaminases were abnormal in 66% with a median elevation 2 times above normal value. HCV RNA was positive in 87% with a viral load above 800 000 IU/ml in 42%. Genotype 1 was predominant (59%), followed by genotypes 3 (19%) and 4 (14%). A liver biopsy was performed in 190 patients, with minimal fibrosis (METAVIR F0-F1) in 43%, moderate fibrosis (F2) in 35% and advanced stages (F3-F4) in 22%. Antiviral treatment was not considered in 53% because of normal ALT (30%), old age (7%), minimal histological stage (6%) or patient refusal (4%). CONCLUSIONS: This study highlights the feasibility of a national HCV survey using a simple questionnaire. This pilot study could be generalised throughout Belgium, and, if repeated, could allow a regular assessment of the changes in epidemiology and management of HCV infection in our country.

Cadranel JF, Lahmek P, Causse X, Bellaiche G, Bettan L, Fontanges T, Medini A, Henrion J, Chousterman M, Condat B, Hervio P, Periac P, Eugène C, Moindrot H, Grasset D, Nouel O, Pilette C, Szostak-Talbodec N, Cayla JM, Si-Ahmed SN, Dumouchel P, Pariente A, Lesgourgues B, Denis J. · Hepato-gastroenterology and Diabetology Section, Centre Hospitalier Laennec, 60109 Creil, France. · Aliment Pharmacol Ther. · Pubmed #17661760 No free full text.

Abstract: BACKGROUND: Epidemiological data concerning hepatitis B are scarce in France. AIM: To describe epidemiological, clinical, virological and histological features of HBsAg-positive patients followed at non-academic hospitals in France. METHODS: Clinical, biological, virological and histological data of all HBsAg-positive consecutive patients observed from April 1, 2001 to May 31, 2002 in participating centres were recorded prospectively. Multivariate analyses of factors associated with significant fibrosis and cirrhosis were performed. RESULTS: Nearly 1166 HBsAg-positive patients were seen in the 58 centres: 671 males and 495 females from metropolitan France (32%) and from outside metropolitan France (68%); mean age 41 +/- 15 years. Twenty-nine percent of patients were probable HBsAg inactive carriers, while 50% had chronic hepatitis; 43% of these were HBeAg-positive and 57% HBeAg-negative. Liver biopsy had been performed in 558 (51%) patients; 205 (17.6%) patients had cirrhosis. By multivariate analysis, factors associated with significant fibrosis were: age >40 years (P < 0.05), HBeAg-negative status (P < 0.02) and histological activity (P < 0.0001). Factors associated with cirrhosis: age (P < 0.0001), platelet count <150 000/mm(3) (P < 0.0001) and viral co-infection (P < 0.03). CONCLUSION: HBV infection represents a significant workload for hepatogastroenterologists at non-academic hospitals in France.

Thevenot T, Boruchowicz A, Henrion J, Nalet B, Moindrot H, Anonymous00276. · Service d'Hépatologie et de Soins Intensifs Digestifs, Hôpital Universitaire Jean Minjoz, Boulevard Fleming, 25030, Besançon, France. · Dig Dis Sci. · Pubmed #17372827 No free full text.

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Deltenre P, Henrion J, Canva V, Dharancy S, Texier F, Louvet A, De Maeght S, Paris JC, Mathurin P. · Services d'Hépato-Gastroentérologie, Hôpital Huriez, CHRU Lille, France. · J Hepatol. · Pubmed #15336450 No free full text.

Abstract: BACKGROUND/AIMS: The benefit of amantadine combination therapy, either with interferon (IFN) alone (double therapy) or with ribavirin and IFN (triple therapy) is unknown. METHODS: We analyzed the effect of amantadine on the end-of-treatment virological response and the sustained response using meta-analysis of 31 randomized controlled trials. RESULTS: Overall analysis revealed a significant effect of amantadine. Triple therapy was the best regimen for improving the sustained response (mean difference: 8.4%, 95% CI: 2.4-13.8%, P=0.002). In subgroup analysis, amantadine did not have a significant effect upon naive patients or relapsers. In non-responders, combination therapy with amantadine was associated with a significant effect on the sustained response (mean difference: 8.3%, 95% CI: 1.9-14.6%, P=0.01). In sensitivity analysis, double therapy did not improve virological responses. Conversely, triple therapy tended to improve the end-of-treatment virological response and was associated with a significant effect upon the sustained response (mean difference: 12.7%, 95% CI: 3.8-21.6%, P=0.005). CONCLUSIONS: Combination therapy with amantadine is of no effect upon naive patients or relapsers. In non-responders, triple therapy with amantadine improved the sustained response. New randomized controlled trials are required to confirm this meta-analysis.

Henrion J, Schapira M, Luwaert R, Colin L, Delannoy A, Heller FR. · Department of Internal Medicine, Hôpital de Jolimont-Lobbes, Haine-Saint-Paul, Belgium. · Medicine (Baltimore). · Pubmed #14663289 No free full text.

Abstract: The centrilobular liver cell necrosis observed in hypoxic hepatitis is generally attributed to failure of hepatic blood perfusion. Accordingly, this injury of the liver is commonly recognized under the terms "shock liver" or "ischemic hepatitis." During a 10-year period, 142 episodes of hypoxic hepatitis were consecutively identified in the intensive care unit of a general hospital, and the clinical, biological, and hemodynamic parameters were prospectively collected on individual files. We conducted the current study to assess retrospectively the role of the hemodynamic mechanisms of tissue hypoxia: ischemia, passive venous congestion, and hypoxemia. Among the 142 episodes of hypoxic hepatitis, 138 were separated in 4 main groups based on clinical features: decompensated congestive heart failure (80 cases), acute cardiac failure (20 cases), exacerbated chronic respiratory failure (19 cases), and toxic/septic shock (19 cases). An elementary hemodynamic evaluation, including blood pressure, central venous pressure, and arterial blood gas analysis, was carried out in every episode and a more complete hemodynamic assessment through pulmonary artery catheterization was performed in 61 episodes.The hemodynamic mechanisms responsible for hypoxic hepatitis were different in the 4 groups. In congestive heart failure and acute heart failure, the hypoxia of the liver resulted from decreased hepatic blood flow (ischemia) due to left-sided heart failure and from venous congestion secondary to right-sided heart failure. In chronic respiratory failure, liver hypoxia was mainly due to profound hypoxemia. In toxic/septic shock, oxygen delivery to the liver was not decreased but oxygen needs were increased, while the liver was unable to use oxygen properly. In all conditions underlying hypoxic hepatitis, except toxic/septic shock, a shock state was observed in only about 50% of the cases. Therefore, the expressions "shock liver" or "ischemic hepatitis" are misleading and should be replaced by the more general term "hypoxic hepatitis."

Henrion J, Libon E, De Maeght S, Deltenre P, Schapira M, Ghilain JM, Maisin JM, Heller FR. · Unité d'Hépato-Gastroentérologie, Centre Hospitalier de Jolimont-Lobbes, Belgique. · Gastroenterol Clin Biol. · Pubmed #12843918 links to  free full text

Abstract: OBJECTIVES: To assess the feasibility and efficiency of the screening for hepatocarcinoma in a cohort of cirrhoseis mainly of alcoholic origin. PATIENTS AND METHODS: 293 patients with cirrhosis, among them 186 (63.5%) from alcoholic origin, were included in a surveillance programme for hepatocarcinoma by carrying out liver ultrasonography and alpha-foetoprotein dosage every 6 months. Results were analyzed with a mean follow-up of 60 months. Seventeen hepatocarcinoma discovered through the surveillance programme ("screened HCC") were compared with 40 hepatocarcinoma discovered outside the surveillance programme during the same period ("incidental HCC"). RESULTS: The alcoholic origin of the cirrhosis was a predictive factor of poor compliance to the surveillance programme. Among the 186 patients with alcoholic cirrhosis, 129 (69%) were lost during the surveillance programme due to lack of compliance (97 cases) or death (32 cases). By comparison, among the 65 patients with hepatitis C-related cirrhosis, 18 were lost by lack of compliance (11 cases) or death (7 cases) (P<0.001). Moreover, sustained or relapsing alcohol abuse after inclusion in the surveillance programme were also related to the quality of the compliance. Seventeen hepatocarcinoma were discovered through the surveillance giving an annual incidence of 2% for the emergence of hepatocarcinoma. The comparison between screened (n=17) and incidental (n=40) hepatocarcinoma showed that screened HCC were more often asymptomatic (P<0.01), were more often a solitary nodule less than 5 cms (P<0.001) and underwent more often curative treatment (P=0.02). However, the survival between screened and incidental hepatocarcinoma was not different. CONCLUSIONS: Screening for hepatocarcinoma in patients with alcoholic cirrhosis is a difficult task due to poor compliance and early death. According to our results, a surveillance every 6 months is sufficient to detect early lesions accessible to curative treatment by surgical resection or transcutaneous ablation.

Henrion J, De Maeght S, Deltenre P, Ghilain JM, Maisin JM, Schapira M, Heller F. · Hôpital de Jolimont, B-7100 Haine St Paul, Belgium. · Acta Gastroenterol Belg. · Pubmed #12148443 No free full text.

Abstract: In a consecutive series of 411 patients with cirrhosis attending the outpatient liver clinics of 3 general hospitals located in the southern part of Belgium, hepatitis C virus infection accounted for 20% of the cases, far behind alcohol (63%). However, in a consecutive series of 57 hepatocarcinoma superimposed on cirrhosis, hepatitis C virus infection was the main aetiological factor accounting for 44% of the cases.

Henrion J, Libon E, De Maeght S, Schapira M, Ghilain JM, Maisin JM, Heller FR. · Département de Médecine Interne, Hôpital de Jolimont, Haine-Saint-Paul, Belgium. · Acta Gastroenterol Belg. · Pubmed #10907311 No free full text.

Abstract: Surveillance for early detection of hepatocarcinoma (HCC) in patients with cirrhosis is widely accepted. In a cohort of 141 patients with cirrhosis collected during the year 1995, we conducted a surveillance program by performing liver ultrasonography and blood alpha-foetoprotein measurement every 6 months. The median follow-up was 34 months. This study addressed to two questions: the compliance to the surveillance schedule according to the aetiology of cirrhosis and the results in terms of emergence of HCC and outcome. Aetiology of cirrhosis was alcohol-induced in 86 (61%), HCV-related in 30 (21%) and from other origins in 25 (18%). Compliance to the program schedule was good in patients with HCV-related cirrhosis (29/30--97%) and patients with cirrhosis of "other origins" (20/25--80%) but was poor in patients with alcoholic cirrhosis (45/86--52%). The lack of compliance was significantly linked to the failure to achieve alcohol abstinence. During follow-up, 6 HCC lesions were observed in 6 male patients with median age of 68 years. All 6 HCC were single nodule, less than 4 cm and accessible to percutaneous acetic acid injection. Nevertheless, the outcome was disappointing, four patients dying 3-15 months later (median: 8 months), two of them with extensive HCC. One of the two patients still alive developed extensive HCC, 36 months after percutaneous acetic acid injection.

Hautekeete ML, Horsmans Y, Van Waeyenberge C, Demanet C, Henrion J, Verbist L, Brenard R, Sempoux C, Michielsen PP, Yap PS, Rahier J, Geubel AP. · Department of Hepatogastroenterology, University Hospital Gent, Gent, Belgium. · Gastroenterology. · Pubmed #10535882 No free full text.

Abstract: 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.

Henrion J, Minette P, Colin L, Schapira M, Delannoy A, Heller FR. · Department of Internal Medicine, Hôpital de Jolimont, Haine St. Paul, Belgium. · Hepatology. · Pubmed #9918919 No free full text.

Abstract: 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).