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Am J Gastroenterol. 2017 Aug;112(8):1277-1286. doi: 10.1038/ajg.2017.140. Epub 2017 May 30.

Low Birthweight Increases the Likelihood of Severe Steatosis in Pediatric Non-Alcoholic Fatty Liver Disease.

Author information

1
Division of Gastroenterology, Department of Medical Sciences, University of Turin, Turin, Italy.
2
Unit of Endocrinology and Diabetes, "Bambino Gesù" Children's Hospital, IRCCS (Instituto di Ricovero e Cura a Carattere Scientifico), Rome, Italy.
3
Hepato-Metabolic Disease Unit, "Bambino Gesù" Children's Hospital, IRCCS (Instituto di Ricovero e Cura a Carattere Scientifico), Rome, Italy.
4
Liver Reseach Unit, "Bambino Gesù" Children's Hospital, IRCCS (Instituto di Ricovero e Cura a Carattere Scientifico), Rome, Italy.
5
Neonatal Surgery Unit, "Bambino Gesù" Children's Hospital, IRCCS (Instituto di Ricovero e Cura a Carattere Scientifico), Rome, Italy.
6
Department of Laboratory Medicine, "Bambino Gesù" Children's Hospital, IRCCS (Instituto di Ricovero e Cura a Carattere Scientifico), Rome, Italy.
7
Medical Directorate, "Bambino Gesù" Children's Hospital, IRCCS (Instituto di Ricovero e Cura a Carattere Scientifico), Rome, Italy.

Abstract

OBJECTIVES:

Small for gestational age (SGA) is associated with an increased risk of non-alcoholic fatty liver disease (NAFLD). Our aim was to investigate the correlation of birthweight with the severity of liver damage in a large cohort of children with NAFLD.

METHODS:

Two hundred and eighty-eight consecutive Caucasian Italian overweight/obese children with biopsy-proven NAFLD were included in the study. We examined the relative association of each histological feature of NAFLD with metabolic alterations, insulin-resistance, I148M polymorphism in the patatin-like phospholipase domain-containing protein 3 (PNPLA3) gene, and birthweight relative to gestational age.

RESULTS:

In the whole NAFLD cohort, 12.2% of patients were SGA, 62.8% appropriate for gestational age (AGA), and 25% large for gestational age (LGA). SGA children had a higher prevalence of severe steatosis (69%) and severe portal inflammation (14%) compared with the AGA and LGA groups. Notably, severe steatosis (>66%) was decreasing from SGA to AGA and LGA, whereas the prevalence of moderate steatosis (33-66%) was similar in three groups. The prevalence of type 1 NAFLD is higher in the LGA group with respect to the other two groups (25% vs.5.2% vs.9.4%), whereas the SGA group shows a higher prevalence of overlap type (85.8%) with respect to the LGA group (51.4%) but not compared with the AGA group (75%). At multivariable regression analysis, SGA at birth increased fourfold the likelihood of severe steatosis (odds ratio (OR) 4.0, 95% confidence interval (CI) 1.43-10.9, P=0.008) and threefold the likelihood of NAFLD Activity Score (NAS)≥5 (OR 2.98, 95% CI 1.06-8.33, P=0.037) independently of homeostasis model assessment of insulin resistance and PNPLA3 genotype. The PNPLA3-CC wild-type genotype was the strongest independent predictor of the absence of significant fibrosis (OR 0.26, 95% CI 0.13-0.52, P=<0.001).

CONCLUSIONS:

In children with NAFLD, the risk of severe steatosis is increased by SGA at birth, independent of and in addition to other powerful risk factors (insulin-resistance and I148M variant of the PNPLA3 gene).

PMID:
28555633
DOI:
10.1038/ajg.2017.140
[Indexed for MEDLINE]
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