Which lab findings suggest nonalcoholic fatty liver disease (NAFLD)?

Updated: Apr 12, 2018
  • Author: Emily Tommolino, MD; Chief Editor: BS Anand, MD  more...
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Viral serologies for hepatitis C should be obtained to identify or exclude viral infection. In addition, iron levels and total iron-binding capacity (TIBC) should be measured, and abnormal results from liver function tests should be evaluated as indicated.

Elevations in serum ferritin or iron levels, decreased transferrin saturation, or both may occur in patients with NASH. Although iron overload occurs in a small proportion of patients with NASH, these patients have more severe disease. Evidence exists that a serum ferritin greater than 1.5 times the upper limit of the normal range in patients with NAFLD is associated with a higher NAFLD activity score (and thus, NASH) and with advanced hepatic fibrosis. [26] An iron index score may be ordered on a liver biopsy specimen to evaluate for phlebotomy. Hemochromatosis gene testing is recommended when the ferritin is significantly elevated. Simply eliminating dietary iron has been shown to improve fatty liver.

Autoimmune markers, such as antinuclear antibody (ANA) and anti–smooth muscle antibody (ASMA), are often slightly elevated in NASH. Positive antibodies are associated with more severe fibrosis levels. In the appropriate clinical setting, serum protein electrophoresis (SPEP) and anti–liver-kidney antibody may lead to a diagnosis of autoimmune liver disease.

Often, a clinical picture of obesity, hypertriglyceridemia, and elevated transaminases is enough to allow the clinician to conclude that a patient has NASH. However, underlying alcohol or other drug ingestion, as well as smoldering autoimmune disease or hemochromatosis, must be ruled out. Referral to a hepatologist with or without liver biopsy may help in staging and prognosis.

Serum beta-trophin level may have potential as a new marker for noninvasive evaluation of NAFLD and liver fibrosis, according to a study by Cengiz et al. [27] In their cohort of 69 patients with NAFLD and 69 healthy control subjects, serum beta-trophin levels were lower in the NAFLD group; those with mild fibrosis had elevated serum beta-trophin levels compared to those with significant fibrosis. In multivariate and ROC (receiver operating characteristic) analyses, levels of serum beta-trophin was, respectively, an independent predictor of significant fibrosis and was statistically significant in identifying significant fibrosis. [27]

Findings from the Multi-Ethnic Study of Atherosclerosis (MESA) appear to indicate that circulating interleukin-6 (IL-6) is a biomarker for coronary atherosclerosis in NAFLD. [99] IL-6 had an independent association with the prevalence and severity of subclinical atherosclerosis.

In a separate study, Abdel-Razik et al proposed mean platelet volume and the neutrophil-lymphocyte ratio as novel inexpensive and simple markers of inflammation to predict fibrosis in patients with NAFLD as well as to predict the presence of NASH. [28] The investigators noted that patients with NASH had elevated levels of mean platelet volume and neutrophil-lymphocyte ratio compared to those without NASH, as well as in patients with advanced fibrosis compared to those with early fibrosis. [28]

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