Home MRI-diagnosed Nonalcoholic Fatty Liver Disease Is Correlated to Insulin Resistance in Adolescents
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MRI-diagnosed Nonalcoholic Fatty Liver Disease Is Correlated to Insulin Resistance in Adolescents

Rationale and Objectives

To evaluate the presence of nonalcoholic fatty liver disease (NAFLD) in eutrophic and obese adolescents with magnetic resonance imaging (MRI) and its relationship to insulin resistance and other potential biomarkers.

Materials and Methods

A total of 50 adolescents (aged 11–17 years), including 24 obese and 26 eutrophic adolescents, were evaluated using MRI exams for NAFLD diagnosis. Blood analysis was performed to measure glucose, insulin, total cholesterol, high-density lipoprotein cholesterol, triglycerides, fibrinogen, aminotransferases, alkaline phosphatase, gamma-gt, and C-reactive protein. The Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) index was also calculated. Laboratory test results and anthropometric assessment were statistically analyzed to determine potential correlation with NAFLD prevalence.

Results

The prevalence of NAFLD among the obese was significantly higher (83.3%; CI 95: 64.5–94.5%) than that of the eutrophic group (19.2%; CI 95: 7.4–37.6%). In multivariate analysis, only HOMA-IR was an independent risk factor for diagnosis NAFLD using MRI. Compared to eutrophic adolescents, the obese adolescents had significantly higher levels for all parameters measured except for total and high-density lipoprotein cholesterol, which were significantly lower.

Conclusion

The prevalence of NAFLD was 19.2% among eutrophic patients and 83.3% among obese patients. Only HOMA-IR was determined to be an independent risk factor for NAFLD.

Nonalcoholic fatty liver disease (NAFLD), a subset of hepatic steatosis, was first described in adult patients in 1980 by Ludwig et al. as a clinicopathologic condition that presents histology findings that correspond with alcoholic hepatitis, but in people who do not drink . Cases of NAFLD that can progress to its most severe nonalcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma, have risen drastically in the United States, with estimates of 80–100 million Americans currently being affected . In Europe, growth in the percentage of the population afflicted with NAFLD has grown by 10–40% in the past 10 years .Geographically, NAFLD prevalence is particularly high in the United States .

Recent studies have shown an association between NAFLD and childhood obesity , with estimated prevalence rates being lower than 10% for the general population, but 70–75% for the obese juvenile population .

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Materials and methods

Study Population

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Anthropometric Measurements

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Laboratory Tests

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MRI of the Liver

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Figure 1, Demonstrating the in-phase (IP) and out-of-phase (OP) signal intensity, the chemical shift, and the regions of interest. Fat fraction 21.8%. (a) Magnetic resonance images (MRI) IP of a patient with nonalcoholic fatty liver disease (IP: 475.8). (b) MRI OP: 269.8. (Color version of figure is available online).

Figure 2, Demonstrating the in-phase (IP) and out-of-phase (OP) signal intensity, the chemical shift, and the regions of interest. Fat fraction 1.4%. (a) Magnetic resonance images (MRI) IP of a patient without nonalcoholic fatty liver disease (IP:2144). (b) MRI OP: 199.9. (Color version of figure is available online).

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Statistical Analysis

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Results

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Table 1

Clinical and Laboratory Characteristics of Obese and Eutrophic Study Groups

Variables ∗ Eutrophic ( n = 26) Obese ( n = 24)P Age (y) 14.7 ± 2.0 14.2 ± 1.9 .379 Male 8 (30.8) 17 (70.8) .011 BMI (kg/m²) 21.1 ± 2.6 32.6 ± 3.8 <.001 AC (cm) 65.8 (15.4) 111.5 (15.8) <.001 Glucose (mg/dL) 86.9 ± 8.4 94.3 ± 7.0 .001 Insulin (μUI/mL) 6.0 (5.3–8.4) 14.9 (11.9–18.5) <.001 Total C (mg/dL) 165.7 ± 28.3 159.7 ± 25.0 .435 HDL C (mg/dL) 49.5 ± 9.7 39.7 ± 8.0 <.001 Fibrinogen (g/L) 2.01 (1.78–2.37) 2.53 (1.93–3.00) .002 Alkaline protein (U/L) 123.5 (96.3–107.3) 215.5 (111.5–295) .020 Gamma GT (U/L) 18 (17–22) 27.5 (20–29) .011 C-reactive protein (mg/L) 0.55 (0.2–1.6) 3.4 (1.08–5.45) .003 Oxaloacetic 16.5 (14–19.8) 20 (16.3–25.5) .011 Triglycerides (mg/dL) 60.5 (47–95) 89 (57.5–129.3) .103 Hepatic FF NMRI 2.95 (1.38–4.35) 7.10 (5.05–12.9) <.001 NAFLD 5 (19.2) 20 (83.3) <.001 HOMA IR 1.21 (1.10–1.89) 3.47 (2.83–4.37) <.001

AC, abdominal circumference; AP, alkaline phosphatase; BMI, body mass index; FF, fat fraction; gamma GT, γ-glutamyl transpeptidase; GOT, glutamic oxaloacetic transaminase; HDL C, high-density lipoprotein cholesterol; HOMA IR, Homeostatic Model Assessment of Insulin Resistance; total C, total cholesterol; NAFLD, nonalcoholic fatty liver disease.

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Table 2

The Clinical and Laboratory Characteristics of Adolescents with and without NAFLD

Variables ∗ with NAFLD ( n = 25) without NAFLD ( n = 25)P Age (y) 14.2 ± 2.0 14.8 ± 1.9 .275 Male 14 (56.0) 11 (44.0) .572 BMI (kg/m²) 31.1 ± 5.1 22.1 ± 4.6 <.001 AC (cm) 101 (14.0) 71 (12.0) <.001 Glucose (mg/dL) 94.2 ± 6.2 86.6 ± 9.0 .001 Insulin (μUI/mL) 15.2 (12.6–18.3) 5.9 (5.2–7.2) <.001 Total C (mg/dL) 165.1 ± 23.2 160.7 ± 30.0 .564 HDL C (mg/dL) 41.3 ± 9.4 48.3 ± 9.8 .014 Fibrinogen (g/L) 2.5 (2.0–2.95) 1.9 (1.75–2.33) .001 Alkaline P (U/L) 195 (112.5–295) 113 (93.5–227.5) .014 Gamma GT (U/L) 26 (18–29) 20 (17.5–26) .139 C-reactive protein (mg/L) 2.2 (0.45–5.0) 0.7 (0.2–3.4) .113 Oxaloacetic 19 (15.5–23) 17 (14–22) .083 Triglycerides (mg/dL) 88 (58 – 134.5) 60 (46–97) .042 HOMA IR 3.48 (2.87 – 4.34) 1.20 (1.09–1.48) <.001

AC, abdominal circumference; AP, alkaline phosphatase; BMI, body mass index; FF, fat fraction; gamma GT, γ-glutamyl transpeptidase; GOT, glutamic oxaloacetic transaminase; HDL C, high-density lipoprotein cholesterol; HOMA IR, Homeostatic Model Assessment of Insulin Resistance; total C, total cholesterol; NAFLD, nonalcoholic fatty liver disease.

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Table 3

Multivariate Poisson Regression to Evaluate Predictors Independently Associated with NAFLD

Variables Model 1 Model 2 PR (CI 95%)P PR (CI 95%)P Obese 1.47 (0.73–2.99) .283 NE NE High AC NE NE 1.91 (0.94–3.89) .074 Triglycerides 1.002 (1.000–1.004) .071 1.002 (1.000–1.005) .063 HOMA >2 13.7 (1.40–142.9) .024 13.0 (1.52–111) .019 HDL 1.01 (0.99–1.03) .157 1.01 (0.99–1.04) .214 Fibrinogen 1.12 (0.90–1.41) .316 1.08 (0.89–1.33) .436 AP 1.00 (0.99–1.00) .364 1.001 (0.99–1.003) .214 Aminotransferase 0.99 (0.98–1.01) .306 0.99 (0.97–1.00) .109

AP, alkaline phosphatase; AT, aminotransferase; HDL, high-density lipoprotein; NE, not evaluated, PR, prevalence ratios.

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Figure 3, Evaluation of nonalcoholic fatty liver disease in obese and eutrophic patients according to their Homeostatic Model Assessment of Insulin Resistance classification.

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Discussion

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Dual-Echo, Chemical Shift Gradient-Echo MRI to Quantify Hepatic Steatosis: Implications for Living Liver Donation

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Limitations

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Acknowledgments

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