Study Design: Observational
Conditions: Liver Diseases
Division: DDN
Duration: 09/2004 – 09/2009
# Recruitment Centers: 8
Available Genotype Data: No
Image Summary: No
Transplant Type: None
Does it have dialysis patients: No
Data Package Version Number: 4 (Updated on: March 25, 2024)
DOI: 10.58020/p1k3-eb54
How to cite this dataset: Tonascia, James (2024). Nonalcoholic Fatty Liver Disease (NAFLD) Pediatric Database (V4) [Dataset]. NIDDK Central Repository. https://doi.org/10.58020/p1k3-eb54
Data availability statement: Data from the Nonalcoholic Fatty Liver Disease (NAFLD) Pediatric Database [(V4)/https://doi.org/10.58020/p1k3-eb54] reported here are available for request at the NIDDK Central Repository (NIDDK-CR) website, Resources for Research (R4R), https://repository.niddk.nih.gov/.
Nonalcoholic fatty liver disease (NAFLD) is the most common cause of liver disease in the preadolescent and adolescent age groups in the United States. Despite the prevalence of pediatric NAFLD, overweight, obesity, and related conditions remain underdiagnosed by health care providers. Because of the risk and expense of liver biopsies, it would be advantageous to identify clinical predictors of histologic severity so that children at greatest risk for progression could be identified. The Nonalcoholic Steatohepatitis Clinical Research Network (NASH CRN) was initiated by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) in 2002 to conduct multicenter, collaborative studies on the etiology, contributing factors, natural history, complications, and treatment of NASH.
Demographic data was obtained via structured interview and questionnaires. Height, weight, waist, and hip measurements, Tanner staging, and the presence and severity of acanthosis nigricans were assessed. Biopsy specimens were evaluated for the following according to the validated histologic NASH CRN scoring system: steatosis, portal inflammation, lobular inflammation, ballooning degeneration, and fibrosis. A NAFLD activity score (NAS) was tabulated by summing scores for steatosis, lobular inflammation, and ballooning degeneration.
To evaluate whether simple, readily available clinical and laboratory measures have predictive power with respect to the histologic pattern or severity of NAFLD among children.
Patients between 2 to 17 years old were eligible for inclusion if they had baseline clinical data within six months of liver biopsy.
Exclusion criteria:
Certain components of routine laboratory tests are predictive of NAFLD pattern and fibrosis severity, but do not have adequate discriminate power to replace liver biopsy in evaluating pediatric NAFLD.