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The galactose elimination capacity and mortality in 781 Danish patients with newly-diagnosed liver cirrhosis: a cohort study.

Jepsen P, Vilstrup H, Ott P, Keiding S, Andersen PK, Tygstrup N - BMC Gastroenterol (2009)

Bottom Line: Cox regression was used to adjust the association between GEC and all-cause mortality for confounding by age, gender and comorbidity, measured by the Charlson comorbidity index.Among the 75% of patients with a decreased GEC (<1.75 mmol/min), GEC was a strong predictor of 30-day, 1-year, and 5-year mortality, and this could not be explained by confounding (crude hazard ratio for a 0.5 mmol/min GEC increase = 0.74, 95% CI 0.59-0.92; adjusted hazard ratio = 0.64, 95% CI 0.51-0.81).Among the 25% of patients with a GEC in the normal range (>or= 1.75 mmol/min), GEC was only weakly associated with mortality (crude hazard ratio = 0.79, 95% CI 0.59-1.05; adjusted hazard ratio = 0.80, 95% CI 0.60-1.08).

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark. pj@dce.au.dk

ABSTRACT

Background: Despite its biologic plausibility, the association between liver function and mortality of patients with chronic liver disease is not well supported by data. Therefore, we examined whether the galactose elimination capacity (GEC), a physiological measure of the total metabolic capacity of the liver, was associated with mortality in a large cohort of patients with newly-diagnosed cirrhosis.

Methods: By combining data from a GEC database with data from healthcare registries we identified cirrhosis patients with a GEC test at the time of cirrhosis diagnosis in 1992-2005. We divided the patients into 10 equal-sized groups according to GEC and calculated all-cause mortality as well as cirrhosis-related and not cirrhosis-related mortality for each group. Cox regression was used to adjust the association between GEC and all-cause mortality for confounding by age, gender and comorbidity, measured by the Charlson comorbidity index.

Results: We included 781 patients, and 454 (58%) of them died during 2,617 years of follow-up. Among the 75% of patients with a decreased GEC (<1.75 mmol/min), GEC was a strong predictor of 30-day, 1-year, and 5-year mortality, and this could not be explained by confounding (crude hazard ratio for a 0.5 mmol/min GEC increase = 0.74, 95% CI 0.59-0.92; adjusted hazard ratio = 0.64, 95% CI 0.51-0.81). Further analyses showed that the association between GEC and mortality was identical for patients with alcoholic or non-alcoholic cirrhosis etiology, that it also existed among patients with comorbidity, and that GEC was only a predictor of cirrhosis-related mortality. Among the 25% of patients with a GEC in the normal range (>or= 1.75 mmol/min), GEC was only weakly associated with mortality (crude hazard ratio = 0.79, 95% CI 0.59-1.05; adjusted hazard ratio = 0.80, 95% CI 0.60-1.08).

Conclusion: Among patients with newly-diagnosed cirrhosis and a decreased GEC, the GEC was a strong predictor of short- and long-term all-cause and cirrhosis-related mortality. These findings support the expectation that loss of liver function increases mortality.

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All-cause mortality after 30 days, 1 year, and 5 years by GEC for the 781 included cirrhosis patients. The gray lines connect each GEC-decile's median GEC with its observed mortality, and the black lines are lowess smoothings of the gray lines.
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Figure 1: All-cause mortality after 30 days, 1 year, and 5 years by GEC for the 781 included cirrhosis patients. The gray lines connect each GEC-decile's median GEC with its observed mortality, and the black lines are lowess smoothings of the gray lines.

Mentions: GEC was a strong predictor of short- and long-term mortality, particularly among the 75% of patients with a GEC below 1.75 mmol/min (Figure 1). For example, patients with a GEC of 1.75 mmol/min had a lower mortality than patients with a GEC of 1.25 mmol/min: 5% vs. 14% after 30 days, 22% vs. 35% after 1 year, and 48% vs. 61% after 5 years (Figure 1), and adjustment for potential confounders strengthened the GEC-mortality association (crude hazard ratio = 0.74, 95% CI 0.59–0.92; adjusted hazard ratio = 0.64, 95% CI 0.51–0.81), primarily because male gender was a risk factor for death and also associated with a high GEC (Table 1). Among the patients with a GEC above 1.75 mmol/min, the association between GEC and mortality was weaker and unaffected by confounding (crude hazard ratio = 0.79, 95% CI 0.59–1.05; adjusted hazard ratio = 0.80, 95% CI 0.60–1.08) (Figure 1 and Table 1).


The galactose elimination capacity and mortality in 781 Danish patients with newly-diagnosed liver cirrhosis: a cohort study.

Jepsen P, Vilstrup H, Ott P, Keiding S, Andersen PK, Tygstrup N - BMC Gastroenterol (2009)

All-cause mortality after 30 days, 1 year, and 5 years by GEC for the 781 included cirrhosis patients. The gray lines connect each GEC-decile's median GEC with its observed mortality, and the black lines are lowess smoothings of the gray lines.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2721849&req=5

Figure 1: All-cause mortality after 30 days, 1 year, and 5 years by GEC for the 781 included cirrhosis patients. The gray lines connect each GEC-decile's median GEC with its observed mortality, and the black lines are lowess smoothings of the gray lines.
Mentions: GEC was a strong predictor of short- and long-term mortality, particularly among the 75% of patients with a GEC below 1.75 mmol/min (Figure 1). For example, patients with a GEC of 1.75 mmol/min had a lower mortality than patients with a GEC of 1.25 mmol/min: 5% vs. 14% after 30 days, 22% vs. 35% after 1 year, and 48% vs. 61% after 5 years (Figure 1), and adjustment for potential confounders strengthened the GEC-mortality association (crude hazard ratio = 0.74, 95% CI 0.59–0.92; adjusted hazard ratio = 0.64, 95% CI 0.51–0.81), primarily because male gender was a risk factor for death and also associated with a high GEC (Table 1). Among the patients with a GEC above 1.75 mmol/min, the association between GEC and mortality was weaker and unaffected by confounding (crude hazard ratio = 0.79, 95% CI 0.59–1.05; adjusted hazard ratio = 0.80, 95% CI 0.60–1.08) (Figure 1 and Table 1).

Bottom Line: Cox regression was used to adjust the association between GEC and all-cause mortality for confounding by age, gender and comorbidity, measured by the Charlson comorbidity index.Among the 75% of patients with a decreased GEC (<1.75 mmol/min), GEC was a strong predictor of 30-day, 1-year, and 5-year mortality, and this could not be explained by confounding (crude hazard ratio for a 0.5 mmol/min GEC increase = 0.74, 95% CI 0.59-0.92; adjusted hazard ratio = 0.64, 95% CI 0.51-0.81).Among the 25% of patients with a GEC in the normal range (>or= 1.75 mmol/min), GEC was only weakly associated with mortality (crude hazard ratio = 0.79, 95% CI 0.59-1.05; adjusted hazard ratio = 0.80, 95% CI 0.60-1.08).

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark. pj@dce.au.dk

ABSTRACT

Background: Despite its biologic plausibility, the association between liver function and mortality of patients with chronic liver disease is not well supported by data. Therefore, we examined whether the galactose elimination capacity (GEC), a physiological measure of the total metabolic capacity of the liver, was associated with mortality in a large cohort of patients with newly-diagnosed cirrhosis.

Methods: By combining data from a GEC database with data from healthcare registries we identified cirrhosis patients with a GEC test at the time of cirrhosis diagnosis in 1992-2005. We divided the patients into 10 equal-sized groups according to GEC and calculated all-cause mortality as well as cirrhosis-related and not cirrhosis-related mortality for each group. Cox regression was used to adjust the association between GEC and all-cause mortality for confounding by age, gender and comorbidity, measured by the Charlson comorbidity index.

Results: We included 781 patients, and 454 (58%) of them died during 2,617 years of follow-up. Among the 75% of patients with a decreased GEC (<1.75 mmol/min), GEC was a strong predictor of 30-day, 1-year, and 5-year mortality, and this could not be explained by confounding (crude hazard ratio for a 0.5 mmol/min GEC increase = 0.74, 95% CI 0.59-0.92; adjusted hazard ratio = 0.64, 95% CI 0.51-0.81). Further analyses showed that the association between GEC and mortality was identical for patients with alcoholic or non-alcoholic cirrhosis etiology, that it also existed among patients with comorbidity, and that GEC was only a predictor of cirrhosis-related mortality. Among the 25% of patients with a GEC in the normal range (>or= 1.75 mmol/min), GEC was only weakly associated with mortality (crude hazard ratio = 0.79, 95% CI 0.59-1.05; adjusted hazard ratio = 0.80, 95% CI 0.60-1.08).

Conclusion: Among patients with newly-diagnosed cirrhosis and a decreased GEC, the GEC was a strong predictor of short- and long-term all-cause and cirrhosis-related mortality. These findings support the expectation that loss of liver function increases mortality.

Show MeSH
Related in: MedlinePlus