Alcoholic cirrhosis in Denmark – population-based incidence, prevalence, and hospitalization rates between 1988 and 2005: A descriptive cohort study-0

Ce rates are per 1,000,000 population. The Danish per adult (>14 years) alcohol consumption increased from 7 to 12 liters from 1965 to 1975, was 12 liters from 1975 to 2001, and 11 liters thereafter.<p><b>Copyright information:</b></p><p>Taken from "Alcoholic cirrhosis in Denmark – population-based incidence, prevalence, and hospitalization rates between 1988 and 2005: A descriptive cohort study"</p><p>http://www.biomedcentral.com/1471-230X/8/3</p><p>BMC Gastroenterology 2008;8():3-3.</p><p>Published online 9 Feb 2008</p><p>PMCID:PMC2275281.</p><p></p

Alcoholic cirrhosis in Denmark – population-based incidence, prevalence, and hospitalization rates between 1988 and 2005: A descriptive cohort study-1

Ce rates are per 1,000,000 population. The Danish per adult (>14 years) alcohol consumption increased from 7 to 12 liters from 1965 to 1975, was 12 liters from 1975 to 2001, and 11 liters thereafter.<p><b>Copyright information:</b></p><p>Taken from "Alcoholic cirrhosis in Denmark – population-based incidence, prevalence, and hospitalization rates between 1988 and 2005: A descriptive cohort study"</p><p>http://www.biomedcentral.com/1471-230X/8/3</p><p>BMC Gastroenterology 2008;8():3-3.</p><p>Published online 9 Feb 2008</p><p>PMCID:PMC2275281.</p><p></p

Incidence rate (IR) of primary osteoarthritis of the hip or knee in Danish cirrhosis patients and age- and gender-matched reference persons from the general population.

<p>Incidence rate (IR) of primary osteoarthritis of the hip or knee in Danish cirrhosis patients and age- and gender-matched reference persons from the general population.</p

Hazard ratio (HR) for primary osteoarthritis for cirrhosis patients vs. reference persons by gender, age on index date, ascites, cirrhosis etiology, and site.

<p>Hazard ratio (HR) for primary osteoarthritis for cirrhosis patients vs. reference persons by gender, age on index date, ascites, cirrhosis etiology, and site.</p

Supplemental material for Terlipressin for variceal bleeding induces large plasma sodium fluctuations in patients without cirrhosis

<p>Supplemental material for Terlipressin for variceal bleeding induces large plasma sodium fluctuations in patients without cirrhosis by Peter Lykke Eriksen, Anne Luise Hartkopf-Mikkelsen, Peter Ott, Hendrik Vilstrup and Niels Kristian Aagaard in United European Gastroenterology Journal</p

Time course of compromised urea synthesis in patients with alcoholic hepatitis

<p><b>Objectives</b>: Alcoholic hepatitis (AH) markedly decreases the urea synthesis capacity. We aimed to investigate the time course of this compromised essential liver function in patients with AH and its relation to treatment and survival.</p> <p><b>Materials and methods</b>: Thirty patients with AH were included in a prospective cohort study. We measured the substrate-independent urea synthesis capacity, i.e., the functional hepatic nitrogen clearance (FHNC), in the patients at study entry and again at three months (survivors/available: <i>n</i> = 17). Patients with severe disease (Glasgow Alcoholic Hepatitis Score ≥9, <i>n</i> = 17) were randomized to receive either prednisolone or pentoxifylline and were in addition examined after 14 days (<i>n</i> = 9).</p> <p><b>Results</b>: FHNC (normal range = 25–45 L/h) was markedly decreased at study entry (median = 5.6 (IQR = 3.0–9.6) L/h) and increased by three-fold in survivors at three months (15.1 (12.0–22.9) L/h; <i>p</i> < .001). In patients with severe AH, FHNC was also increased after 14 days of pharmacologic treatment and showed the greatest increase in the patients taking prednisolone (prednisolone 25.4 (20.6–26.2) L/h vs. pentoxifylline 12.3 (8.0–15.3) L/h; <i>p</i> = .05). FHNC at study entry was lower in 90-day non-survivors than in survivors (<i>p</i> = .04).</p> <p><b>Conclusions</b>: The decrease in the urea synthesis capacity in patients with AH was the most marked in short-term non-survivors and partly recovered in survivors at three months. In patients on pharmacologic treatment, recovery was observed already after 14 days, and it was nearly complete in those on prednisolone. Thus, metabolic liver failure in AH seems to be prognostically important, is potentially reversible, and may recover more rapidly following treatment with prednisolone.</p

Unexplained cholestasis in adults and adolescents: diagnostic benefit of genetic examination

<p><b>Objectives:</b> A few adult and adolescent patients with even severe cholestatic liver disease remain unexplained after standard diagnostic work-up. We studied the value of genetic examination in such patients and developed a panel of eight genes with known cholestatic associations.</p> <p><b>Materials and methods:</b> Thirty-three patients with unexplained cholestasis despite a thorough clinical work-up were examined for sequence variations in the coding regions of the <i>ABCB4, ABCB11, ABCC2, ABCG5, ATP8B1, JAG1, NOTCH2,</i> and <i>UGT1A1</i> genes and the promoter region of <i>UGT1A1</i> by massive parallel sequencing of DNA extracted from whole blood. Hepatologists and clinical geneticists evaluated the causal potential of genetic variants.</p> <p><b>Results:</b> In 9/33 patients (27%), we identified genetic variants as a certain causal factor and in further 9/33 (27%) variants as a possible contributing factor. In most cases, a detailed family history was necessary to establish the importance of genetic variants. Genetic causes were identified in 6/13 women (46%) with intrahepatic cholestasis during pregnancy and persisting abnormal biochemistry after delivery.</p> <p><b>Conclusions:</b> Our study suggests that a small number of well-known genetic variants are involved in at least 27–54% of patients with unexplained cholestasis. An expanded panel will likely explain more cases. This motivates genetic testing of these patients. Genetic testing, however, cannot stand alone but should be combined with a clinical genetic work-up in collaboration between hepatologists and clinical geneticists.</p

Relationship between the functional hepatic nitrogen clearance and galactose elimination capacity.

<p>Relationship between the functional hepatic nitrogen clearance (FHNC) and galactose elimination capacity (GEC) in patients with non-severe (hollow circles) (GAHS<9, N = 8) and severe (circles) (GAHS≥9, N = 10) alcoholic hepatitis. No significant correlation was observed between the FHNC and GEC.</p

Relationship between the functional hepatic nitrogen clearance and Model for End-Stage Liver Disease score.

<p>Relationship between the functional hepatic nitrogen clearance (FHNC) and Model for End-Stage Liver Disease (MELD) score in patients with non-severe (hollow circles) (GAHS<9, N = 9) and severe (circles) (GAHS≥9, N = 11) alcoholic hepatitis. The linear regression line shows the correlation (rho = -0.49; P<0.05).</p

Baseline characteristics of the patients with alcoholic hepatitis and healthy controls.

<p>Baseline characteristics of the patients with alcoholic hepatitis and healthy controls.</p