Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0020104
Title: Progression of biopsy-measured liver fibrosis in untreated patients with hepatitis c infection: Non-markov multistate model analysis
Authors: Bacchetti P.
Boylan R.
Astemborski J.
Shen H. 
Mehta S.H.
Thomas D.L.
Terrault N.A.
Monto A.
Keywords: adolescent
adult
African American
age
article
controlled study
disease course
female
hepatitis C
high risk patient
human
Human immunodeficiency virus infection
liver biopsy
liver fibrosis
major clinical study
male
mixed infection
protection
risk factor
aging
biological model
biopsy
hepatitis C
liver
liver cirrhosis
middle aged
pathology
probability
sensitivity and specificity
time
Hepatitis C virus
Human immunodeficiency virus
Adolescent
Adult
Aging
Biopsy
Disease Progression
Hepatitis C
Humans
Liver
Liver Cirrhosis
Markov Chains
Middle Aged
Models, Biological
Risk Factors
Sensitivity and Specificity
Time Factors
Young Adult
Issue Date: 2011
Citation: Bacchetti P., Boylan R., Astemborski J., Shen H., Mehta S.H., Thomas D.L., Terrault N.A., Monto A. (2011). Progression of biopsy-measured liver fibrosis in untreated patients with hepatitis c infection: Non-markov multistate model analysis. PLoS ONE 6 (5) : e20104. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0020104
Abstract: Background: Fibrosis stages from liver biopsies reflect liver damage from hepatitis C infection, but analysis is challenging due to their ordered but non-numeric nature, infrequent measurement, misclassification, and unknown infection times. Methods: We used a non-Markov multistate model, accounting for misclassification, with multiple imputation of unknown infection times, applied to 1062 participants of whom 159 had multiple biopsies. Odds ratios (OR) quantified the estimated effects of covariates on progression risk at any given time. Results: Models estimated that progression risk decreased the more time participants had already spent in the current stage, African American race was protective (OR 0.75, 95% confidence interval 0.60 to 0.95, p = 0.018), and older current age increased risk (OR 1.33 per decade, 95% confidence interval 1.15 to 1.54, p = 0.0002). When controlled for current age, older age at infection did not appear to increase risk (OR 0.92 per decade, 95% confidence interval 0.47 to 1.79, p = 0.80). There was a suggestion that co-infection with human immunodeficiency virus increased risk of progression in the era of highly active antiretroviral treatment beginning in 1996 (OR 2.1, 95% confidence interval 0.97 to 4.4, p = 0.059). Other examined risk factors may influence progression risk, but evidence for or against this was weak due to wide confidence intervals. The main results were essentially unchanged using different assumed misclassification rates or imputation of age of infection. Discussion: The analysis avoided problems inherent in simpler methods, supported the previously suspected protective effect of African American race, and suggested that current age rather than age of infection increases risk. Decreasing risk of progression with longer time already spent in a stage was also previously found for post-transplant progression. This could reflect varying disease activity, with recent progression indicating active disease and high risk, while longer time already spent in a stage indicates quiescent disease and low risk. © 2011 Bacchetti et al.
Source Title: PLoS ONE
URI: https://scholarbank.nus.edu.sg/handle/10635/162048
ISSN: 19326203
DOI: 10.1371/journal.pone.0020104
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