In a representative population sample of 905 persons we examined the prevalence of raised levels of liver-derived enzymes and its possible association with self-reported alcohol consumption adjusted for smoking and BMI applying logistic regression analyses. A large proportion of 12% (women 8%; men 16%) presented raised liver-derived enzymes. Below 21 units per week (one unit equals 12 grams of alcohol) there was no association with self-reported alcohol consumption. However, the risk of abnormal liver enzymes increased with higher consumption for both sexes; if the intake was above 28 units per week, the odds ratio for raised liver enzymes increased dramatically. Whether this subclinical biochemical liver condition is an early marker of alcohol-related liver damage remains to be seen, but the long-term consequences of the reported alcohol consumption and the frequency of raised liver enzymes require follow-up.
BACKGROUND: Based on the increased consumption of alcohol in Denmark the aim of this study was to measure prevalence of abnormal liver-derived enzymes in a homogeneous Danish population and possible associations with alcohol consumption, smoking and body mass index (BMI). METHOD: In a representative population sample of 905 people (aged 30-50) from the baseline survey of the Ebeltoft Health Promotion Project in Denmark, we examined prevalence of abnormal liver-derived enzymes and its possible association with self-reported alcohol consumption, smoking and BMI, applying logistic regression analyses. RESULTS: In a significant proportion, 12% (women 8%; men 16%) of the cohort we found raised levels of liver-derived enzymes associated with moderate self-reported alcohol intake adjusted for BMI and smoking. If the intake was higher than moderate, i.e. > 28 units per week (one unit equals 12 g of alcohol), the odds ratio (OR) for raised liver enzymes increased further; S-gamma-glutamyltransferase (GGT) (OR: for women 24.4; men 18.4). S-aspartate-aminotransferase (ASAT) (24.2; 5.8) and S-alanine-aminotransferase (ALAT) (27.2; 3.0). Furthermore, daily smoking increased the risk of raised liver enzymes in women (OR: 3.4-4.2), and obesity (BMI > or = 30 kg/m2) in men showed a positive association with all three enzymes (OR: 3.0-9.0). CONCLUSIONS: The occurrence of raised liver-derived enzymes was frequent in the Danish population sample and associated with moderate self-reported alcohol consumption adjusted for BMI and smoking.
BACKGROUND: The association between alcohol intake and liver disease is well known, but little is known about alcohol consumption and changes in liver-derived enzymes within 1 year. In a 1-year follow-up study we examined changes in liver-derived enzymes and their association with self-reported alcohol consumption. METHODS: We recorded liver-derived enzyme values, self-reported alcohol consumption, and potential confounder variables at base line and at a 1-year follow-up in a representative sample of 822 persons (aged 30-50 years) from the survey of The Ebeltoft Health Promotion Project in Denmark, by using questionnaires, health examinations, and blood samples. RESULTS: The prevalence of increased liver-derived enzyme values was 11.1% at base line and 11.8% at the 1-year follow-up. The incidence rate of increased liver-derived enzyme values was 5.1 per 100 person-years, and 34% of the cases of increased liver-derived enzyme values returned to normal within I year. We found an odds ratio of 4.0 for men and 8.0 for women of developing increased liver-derived enzyme values if alcohol consumption was more than 21 units a week. The risk seemed to be dose-dependent. CONCLUSIONS: The prevalence of increased liver-derived enzyme values in the population was high and increased slightly during the study period. There was a strong association between the incidence rate of increased liver-derived enzyme values and self-reported alcohol consumption in a dose-dependent relationship, also when adjusted for confounding by smoking and obesity. The persons with persistently increased enzyme values had a higher weekly alcohol consumption than the rest of the study population.
Alcoholic fatty liver disease comprises alcoholic pure steatosis and alcoholic steatohepatitis. These diseases are prevalent, but their prognostic outcome is uncertain, particularly regarding the impact of hepatic inflammation. The paucity of data based on liver biopsy diagnoses contributes to this uncertainty.
To examine the cirrhosis and mortality risks of Danish men and women with biopsy-verified alcoholic pure steatosis or steatohepatitis.
In this registry-based historical cohort study we combined liver biopsy diagnoses with hospital discharge diagnoses from nationwide healthcare registries to identify all Danish citizens with alcoholic pure steatosis (N = 136) or alcoholic steatohepatitis (N = 58) during 1997-2008. We enrolled a reference cohort of 100 gender- and age-matched persons from the general population for each patient and compared cirrhosis and mortality risks through 2010.
The 5-year cirrhosis risks were 6.9% (95% CI: 3.4-12.2%) for patients with alcoholic pure steatosis and 16.0% (95% CI: 7.8-26.8%) for patients with alcoholic steatohepatitis, their 5-year mortality risks were 16.7% (95% CI: 11.3-24.2%) and 25.1% (95% CI: 15.7-38.9%), respectively. Patients with steatohepatitis had a higher liver-related mortality than patients with pure steatosis. In the reference cohort, the 5-year cirrhosis and mortality risks were 0.3% and 4.3%, respectively.
Patients with alcoholic fatty liver disease had markedly increased cirrhosis and mortality risks compared with a matched reference cohort. The cirrhosis risk was more than twice as high for the patients with steatohepatitis than for those with pure steatosis; and was higher for women than for men.
We estimated the validity, i.e., whether the diagnostic criteria were fulfilled for the patients registered with the diagnosis of liver cirrhosis in a Danish hospital discharge registry, and the completeness, i.e., whether all patients with liver cirrhosis were included in the registry. Information in the regional hospital discharge registry in the Country of Aarhus, Denmark was compared with hospital records and information in a pathology registry. 85.4% of the patients registered with a diagnosis of liver cirrhosis fulfilled the diagnostic criteria for the diagnosis (validity). 93.2% of the patients registered with biopsy proven liver cirrhosis in the pathology registry were found in the discharge registry (completeness) with a diagnosis of liver cirrhosis. The hospital discharge registry showed relatively few misclassifications and the Danish National Registry of Patients (NRP), which is based on the regional registries, may provide a unique study base for future research.
OBJECTIVES: To evaluate the influence of established liver cirrhosis on muscle strength and muscle contents of magnesium (Mg), potassium (K) and sodium, potassium pumps (Na,K-pumps) in chronic alcoholic patients. DESIGN: An open cross-sectional study. SETTING AND SUBJECTS: Forty consecutive chronic alcoholics (18 with cirrhosis and 22 without cirrhosis) admitted to the Department of Hepatology, Aarhus University Hospital, Denmark, or to a collaborating alcoholism treatment centre, and 36 healthy control subjects. MAIN OUTCOME MEASURES: Evaluation of participant's subjective physical ability and measurement of maximum isokinetic muscle strength and muscle mass, as well as measurements of Mg, K and Na,K-pumps in skeletal muscle. RESULTS: Maximum isokinetic muscle strength and muscle mass were equally reduced in patients with and without cirrhosis (P
Patients with liver cirrhosis are at increased risk of serious bacterial infections carrying a high case fatality rate. Case reports have suggested an association between liver cirrhosis and pyogenic liver abscess.
To estimate the risk and case fatality rate of pyogenic liver abscess in Danish patients with liver cirrhosis compared with the background population.
Identification of all patients with liver cirrhosis and pyogenic liver abscess over a 17 year period in the National Registry of Patients. Information on death was obtained from the Danish Central Person Registry.
We identified 22 764 patients with liver cirrhosis and 665 patients with pyogenic liver abscess, of whom 21 were cirrhotics and 644 were non-cirrhotics. The crude incidence rate of liver abscess in cirrhotics was 23.3 (95% CI 14.4-35.6) per 100 000 person years. The age adjusted risk of liver abscess was increased 15-fold in patients with cirrhosis compared with the background population. The 30 day case fatality rates in patients with liver abscess and cirrhosis were 38.5% (13.9-68.4) in alcoholic cirrhosis and 62.5% (24.5-91.5) in non-alcoholic cirrhosis compared with 26.9% (23.5-30.5) in liver abscess patients from the background population. After adjustment for sex, age, and comorbidity, the relative risk of death was increased more than fourfold in alcoholic cirrhosis and non-alcoholic cirrhosis compared with the background population.
Liver cirrhosis is a strong risk factor for pyogenic liver abscess associated with a poor prognosis.
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The prognosis for transplant-free survivors of paracetamol-induced acute liver failure remains unknown.
To examine whether paracetamol-induced acute liver failure increases long-term mortality.
We followed up all transplant-free survivors of paracetamol-induced acute liver injury, hospitalized in a Danish national referral centre during 1984-2004. We compared age-specific mortality rates from 1 year post-discharge through 2008 between those in whom the liver injury led to an acute liver failure and those in whom it did not.
We included 641 patients. On average, age-specific mortality rates were slightly higher for the 101 patients whose paracetamol-induced liver injury had caused an acute liver failure (adjusted mortality rate ratio = 1.70, 95% CI 1.02-2.85), but the association was age-dependent, and no survivors of acute liver failure died of liver disease, whereas suicides were frequent in both groups. These observations speak against long-term effects of acute liver failure. More likely, the elevated mortality rate ratio resulted from incomplete adjustment for the greater prevalence of substance abuse among survivors of acute liver failure.
Paracetamol-induced acute liver failure did not affect long-term mortality. Clinical follow-up may be justified by the cause of the liver failure, but not by the liver failure itself.
Obesity is associated with metabolic derangement and non-alcoholic fatty liver disease (NAFLD). Macrophages are involved in liver inflammation and fibrosis, and soluble (s)CD163 is a macrophage activation marker.
To associate sCD163 with parameters of paediatric obesity and NAFLD, as well as changes in these parameters during lifestyle intervention.
We studied 117 obese children during a 10-week lifestyle intervention; 71 completed the 12-month follow-up. We recorded clinical and biochemical data, and performed liver ultrasonography.
Baseline sCD163 was higher in children with elevated alanine transaminase (ALT) (2.3?±?0.7 vs. 2.0?±?0.6?mg?L(-1), P?=?0.03), steatosis (2.3?±?0.7 vs. 2.0?±?0.6?mg?L(-1), P?=?0.01) and high paediatric NAFLD fibrosis index (2.3?±?0.7 vs. 1.9?±?0.6?mg?L(-1) , P?=?0.03). Baseline sCD163 was independently associated with ALT, cholesterol and high-sensitivity C-reactive protein (hs-CRP). The change in sCD163 during lifestyle intervention was associated with changes in ALT, homeostatic model assessment of insulin resistance (HOMA-IR), hs-CRP and cholesterol, and inversely associated with the change in high-density lipoprotein cholesterol.
sCD163 was associated with markers of liver injury and metabolic parameters in obese children, and changes in these parameters during lifestyle intervention. This may suggest that activated macrophages play a role in NAFLD and sCD163 may serve as a marker of liver disease severity and treatment effect.