4.7 Article

Association Between Puberty and Features of Nonalcoholic Fatty Liver Disease

Journal

CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
Volume 10, Issue 7, Pages 786-794

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.cgh.2012.01.020

Keywords

Sexual Development; Nonalcoholic Steatohepatitis; Obesity; Sex Hormones; QUICKI

Funding

  1. National Center for Research Resources (NCRR) [UL1RR024128]
  2. National Institutes of Health (NIH)
  3. NIH Roadmap for Medical Research
  4. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [U01DK061718, U01DK061728, U01DK061731, U01DK061732, U01DK061734, U01DK061737, U01DK061738, U01DK061730, U01DK061713]
  5. National Institute of Child Health and Human Development (NICHD)
  6. General Clinical Research Centers or Clinical and Translational Science Awards in NASH CRN Studies [UL1RR024989, M01RR000750, M01RR00188, UL1RR02413101, M01RR000827, UL1RR02501401, M01RR000065, M01RR020359]
  7. NIH/NIDDK K23 Career Development award [K23-DK06211]

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BACKGROUND & AIMS: Physiological changes that occur during puberty might affect pathologic features of nonalcoholic fatty liver disease (NAFLD). We investigated associations between pubertal development and clinical and histopathologic features of NAFLD. METHODS: We studied 186 children (age <18 years, 143 boys) with biopsy-proven NAFLD. The population was divided into 3 groups on the basis of Tanner stage (prepuberty, puberty, and postpuberty). Clinical characteristics and histologic features were compared among groups. Multivariable regression models were used to adjust for potential confounders. RESULTS: After adjusting for other factors, hyperuricemia and low levels of high-density-lipoprotein cholesterol were more prevalent among children who entered puberty with lower levels of quantitative insulin sensitivity check index (P < .05). The degree of steatosis, numbers of Mallory-Denk bodies, and diagnostic categories of NAFLD differed among groups (P < .05). There were potential sex differences in associations between stages of puberty and lobular inflammation, hepatocyte ballooning, and borderline steatohepatitis of zone 3; these were therefore not included in multivariable analyses of the overall population. After adjustment for different sets of confounders, patients at or beyond puberty were less likely to have high-grade steatosis, severe portal inflammation, borderline steatohepatitis (zone 1), or a high stage of fibrosis than patients who had not entered puberty (P < .05). On the contrary, the prevalence of Mallory-Denk body was greater among postpuberty subjects (P = .06). CONCLUSIONS: Steatosis, portal inflammation, and fibrosis are less severe during or after puberty than before puberty among subjects with NAFLD. Postpubescent individuals have a lower prevalence of borderline steatohepatitis of zone 1 but are more likely to have Mallory-Denk bodies. These findings indicate that puberty affects the pathologic features of NAFLD.

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