Nonalcoholic fatty liver disease (NAFLD) is now recognized as the most common chronic liver disorder worldwide, encompassing a spectrum from simple steatosis to nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. A position statement from the European Association for the Study of the Liver (EASL) emphasized the growing global burden of NAFLD and its close association with cardiometabolic disorders, particularly type 2 diabetes mellitus (T2DM) [1].

Population-based studies using advanced imaging techniques suggest that hepatic steatosis affects 20–30% of adults in Western populations [2]. The pathogenesis is tightly linked to insulin resistance, which promotes hepatic triglyceride accumulation, as initially demonstrated by Marchesini et al. (1999), who found a strong correlation between NAFLD and insulin resistance in both diabetic and nondiabetic cohorts [3]. Similarly, Marceau et al. (1999) showed that liver pathology consistent with NAFLD was common in patients with metabolic syndrome and severe obesity [4].

Further evidence has established NAFLD as a hepatic manifestation of the metabolic syndrome. In a landmark study, Marchesini et al. (2001) demonstrated that nearly all components of metabolic syndrome — central obesity, dyslipidemia, hypertension, and glucose intolerance — were independently associated with NAFLD [5]. In India, Duseja (2010) reported that the prevalence of NAFLD is rising rapidly, paralleling the epidemic of diabetes and obesity, and highlighted the need for more regional data to guide clinical practice [6].

Metabolic syndrome is itself a constellation of cardiovascular risk factors, as defined by the National Cholesterol Education Program (NCEP) Adult Treatment Panel III, which identifies abdominal obesity, hypertension, dyslipidemia, and hyperglycemia as key diagnostic criteria [7]. Given that T2DM represents a central driver of this syndrome, diabetic patients are at particularly high risk for NAFLD and its progression to advanced liver disease.

Against this background, the present study was undertaken to determine the prevalence and clinical correlates of NAFLD in patients with T2DM, with special reference to liver function test abnormalities and radiological assessment using ultrasonography (USG) and Fibroscan.

Objectives

The primary objective of this study was to determine the prevalence of nonalcoholic fatty liver disease (NAFLD) in patients with type 2 diabetes mellitus (T2DM) using ultrasonography (USG) and Fibroscan.

The specific objectives were:

1. To grade the severity of NAFLD on the basis of ultrasonographic findings.
2. To assess the degree of hepatic fibrosis using Fibroscan elastography.
3. To analyze the relationship between liver function test (LFT) abnormalities and NAFLD severity.
4. To evaluate associations between clinical and metabolic factors (age, BMI, diabetes duration, hypertension) and NAFLD grades.
5. To compare and correlate findings obtained by USG and Fibroscan in T2DM patients.

Study Design and Setting

This was a cross-sectional observational study conducted in the Department of Medicine, Medica Superspeciality Hospital. The study protocol was approved by the institutional ethics committee, and written informed consent was obtained from all participants.

Participants

A total of 101 patients with type 2 diabetes mellitus (T2DM), aged 18–65 years, were enrolled. Diagnosis of T2DM was based on American Diabetes Association criteria.

Inclusion criteria:

• Diagnosed cases of T2DM
• Age 18–65 years
• Patients willing to provide informed consent

Exclusion criteria:

• History of significant alcohol consumption (>20 g/day for men, >10 g/day for women)
• Known chronic liver disease (viral hepatitis, autoimmune hepatitis, Wilson’s disease, hemochromatosis)
• Current use of hepatotoxic drugs (e.g., methotrexate, amiodarone)
• Secondary causes of fatty liver (parenteral nutrition, surgical procedures)
• Pregnant or lactating women

Clinical and Laboratory Assessment

Detailed demographic and clinical history, including age, sex, duration of diabetes, body mass index (BMI), and comorbidities (hypertension, dyslipidemia), was recorded. Physical examination included measurement of anthropometry, blood pressure, and presence of hepatomegaly or splenomegaly.

Venous blood samples were collected after overnight fasting for:

• Fasting plasma glucose
• HbA1c
• Lipid profile
• Liver function tests (serum bilirubin, SGOT/AST, SGPT/ALT, alkaline phosphatase, albumin)

Radiological Evaluation

• Ultrasonography (USG): Performed using a high-resolution B-mode ultrasound machine. Fatty liver was graded as:
• Grade 0: Normal echotexture
• Grade I: Slight increase in hepatic echogenicity with normal visualization of diaphragm and intrahepatic vessels
• Grade II: Moderate increase in echogenicity with slightly impaired visualization
• Grade III: Marked increase in echogenicity with poor visualization of diaphragm and intrahepatic vessels

• Fibroscan Elastography: Conducted using transient elastography to assess hepatic fibrosis, classified as:
• F0: No fibrosis (<5.5 kPa)
• F1: Mild fibrosis (5.5–7.0 kPa)
• F2: Moderate fibrosis (7.1–9.5 kPa)
• F3: Severe fibrosis (9.6–12.4 kPa)
• F4: Cirrhosis (≥12.5 kPa)

Statistical Analysis

Data were analyzed using SPSS software version 20.0. Continuous variables were expressed as mean ± standard deviation (SD), and categorical variables as proportions. Comparisons between groups were performed using Student’s t-test or one-way ANOVA for continuous data and chi-square test for categorical data. Pearson’s correlation coefficient was used to analyze the relationship between USG and Fibroscan grading. A p-value < 0.05 was considered statistically significant.

1.Patient Characteristics

A total of 101 patients with type 2 diabetes mellitus were included in the study. The mean age was 51.3 ± 11.2 years (range: 25–82), with a male predominance (63 males, 62.4%; 38 females, 37.6%). The mean BMI was 23.8 ± 1.8 kg/m², and the mean duration of diabetes was 4.05 ± 3.91 years.

Hypertension was present in 44% of patients, while dyslipidemia was noted in 36%. On clinical examination, hepatomegaly was observed in 23.7% and splenomegaly in 13.9% of cases. These baseline features are summarized in Table 1.

Table 1. Baseline demographic and clinical characteristics of study participants (n = 101)

2.Prevalence and Grading of NAFLD by Ultrasonography (USG)

Among the 101 patients evaluated, ultrasonography (USG) detected fatty liver in 80 individuals, corresponding to a prevalence of 79.2%. Of these, 54 (53.5%) were classified as Grade I, 23 (22.8%) as Grade II, and 3 (3%) as Grade III fatty liver. The remaining 21 patients (20.8%) had normal liver echotexture.

Advanced grades of NAFLD were more frequently associated with higher BMI, longer duration of diabetes, and presence of hypertension (p < 0.05). These findings are summarized in Table 2.

Table 2. Distribution of NAFLD grades by ultrasonography (n = 101)

3.Fibroscan Findings

Fibroscan elastography was performed in all 101 patients to assess hepatic fibrosis. Distribution across fibrosis stages was as follows: F0 in 10 patients (9.9%), F1 in 29 (28.7%), F2 in 23 (22.8%), F3 in 16 (15.8%), and F4 in 23 (22.8%).

Thus, 39 (38.6%) patients had significant fibrosis (≥F2), while 39 (38.6%) demonstrated advanced fibrosis (≥F3), including 23 patients with cirrhosis (F4). Higher fibrosis stages were significantly associated with increased BMI, longer diabetes duration, and presence of hypertension (p < 0.05).

These findings are presented in Table 3.

Table 3. Distribution of fibrosis stages by Fibroscan (n = 101)

4.Correlation Between USG and Fibroscan

A strong correlation was observed between the severity of fatty liver on ultrasonography and fibrosis staging on Fibroscan. Patients with higher USG grades (Grade II and III) more frequently demonstrated significant (≥F2) or advanced (≥F3) fibrosis. For example, 65% of patients with Grade II–III NAFLD on USG had ≥F2 fibrosis, compared with only 28% of those with Grade I.

Pearson’s correlation analysis confirmed a statistically significant positive correlation between USG grades and Fibroscan scores (r = 0.62, p < 0.001). This suggests that increasing echogenicity on USG parallels the progression of hepatic fibrosis detected by elastography.

These findings are summarized in Table 4, and the correlation is illustrated in Figure 1.

Table 4. Relationship between USG grade and Fibroscan fibrosis stage

Figure 1. Correlation between ultrasonographic fatty liver grade and Fibroscan fibrosis stage

Liver Function Test (LFT) Abnormalities

Serum transaminase levels showed a stepwise increase with advancing grades of NAFLD on ultrasonography. Mean SGOT (AST) levels rose from 29.3 IU/L in patients with normal echotexture to 75.0 IU/L in Grade III disease. Similarly, mean SGPT (ALT) increased from 22.3 IU/L to 103.6 IU/L across the same spectrum. These differences were statistically significant (p < 0.001).

The progressive rise in transaminases with higher grades of steatosis is summarized in Table 5 and illustrated in Figure 2.

Table 5. Mean transaminase levels across NAFLD grades on ultrasonography

Figure 2. Trends of SGOT (AST) and SGPT (ALT) across USG grades of NAFLD

Summary of Key Findings

In this cross-sectional cohort of 101 patients with type 2 diabetes mellitus, NAFLD was highly prevalent, detected in 79.2% of participants by ultrasonography. Most cases were of Grade I steatosis (53.5%), while 25.8% demonstrated Grade II or III disease.

Fibroscan elastography identified significant fibrosis (≥F2) in 38.6% and advanced fibrosis (≥F3) in 38.6%, including 22.8% with cirrhosis (F4). There was a strong positive correlation between USG grades and Fibroscan fibrosis stages (r = 0.62, p < 0.001).

Biochemically, serum transaminases (SGOT/AST and SGPT/ALT) increased progressively with higher USG grades, with ALT rising more steeply than AST. The associations of NAFLD severity with higher BMI, longer duration of diabetes, and hypertension were statistically significant.

No adverse events were recorded during imaging or laboratory evaluation.

In this cross-sectional study of 101 patients with type 2 diabetes mellitus (T2DM), the prevalence of nonalcoholic fatty liver disease (NAFLD) was found to be 79.2% on ultrasonography, with nearly one-quarter showing Grade II–III steatosis. Fibroscan revealed that 38.6% had significant fibrosis (≥F2) and an equal proportion demonstrated advanced fibrosis (≥F3), including cirrhosis in 22.8%. Elevated transaminases, particularly ALT, paralleled imaging severity, and NAFLD was significantly associated with higher BMI, longer duration of diabetes, and hypertension.

These findings are consistent with earlier work by Younossi et al. (2004), who reported NAFLD prevalence rates of up to 70% among diabetic patients, underscoring the close association between the two conditions [8]. In a meta-analysis, Younossi et al. (2016) demonstrated that the global prevalence of NAFLD is 25.2% in the general population, but significantly higher in patients with T2DM, often exceeding 60% [9]. Similarly, Park et al. (2006) documented a prevalence of 42% among Korean adults, with obesity and insulin resistance emerging as major determinants [10].

The strong association between NAFLD and obesity is well recognized. The World Health Organization (2000) has classified obesity as a global epidemic, highlighting its contribution to metabolic disorders including diabetes and NAFLD [11]. Regional considerations are particularly relevant, as Asian populations tend to develop metabolic complications at lower BMI values. The Asia-Pacific consensus report (2000) recommended lower BMI thresholds for defining overweight and obesity in Asians [12], and subsequent work by James et al. (2002) and the WHO expert consultation (2004) confirmed that BMI cut-offs of 23 kg/m² for overweight and 25 kg/m² for obesity are more appropriate for Asian cohorts [13,14]. Supporting this, Dudeja et al. (2001) demonstrated that conventional BMI thresholds underestimate adiposity and related risks in Asian Indians [16]. Our finding of mean BMI 23.8 kg/m² in patients with NAFLD aligns with this observation, reinforcing the need for ethnicity-specific definitions.

Misra et al. (2009) emphasized abdominal obesity as a more reliable marker of cardiometabolic risk in Indian populations, recommending its incorporation into diagnostic criteria [17]. This resonates with the clustering of metabolic syndrome in NAFLD patients, as described by Grundy et al. (2005) [19]. In our study, the coexistence of hypertension and dyslipidemia further supports NAFLD as a hepatic manifestation of the metabolic syndrome.

Pathophysiologically, Kotronen et al. (2008) demonstrated that increased hepatic fat content in T2DM is associated with impaired insulin clearance and tissue insulin resistance [20]. More recently, Jichitu et al. (2021) highlighted the bidirectional relationship between NAFLD and cardiovascular disease, wherein hepatic steatosis contributes to atherogenic dyslipidemia and systemic inflammation [21]. These mechanisms explain why our patients with advanced fibrosis also had higher rates of hypertension and longer diabetes duration.

Our data extend the current literature by providing regional evidence from an Indian cohort, with fibrosis rates that are notably high compared with Western series. This may reflect ethnic differences in susceptibility, dietary and lifestyle factors, or delayed diagnosis of NAFLD in routine diabetic care. Importantly, the observed strong correlation between USG and Fibroscan supports the combined use of these modalities for early detection and risk stratification

This study was limited by its single-centre design and modest sample size, which may restrict generalizability. Liver biopsy, the gold standard for diagnosing NAFLD and staging fibrosis, was not performed; instead, reliance on USG and Fibroscan, though practical and noninvasive, may introduce operator and technical variability. Additionally, the cross-sectional nature of the study precludes assessment of disease progression over time.

This study demonstrates a high prevalence of NAFLD (79.2%) among patients with Type 2 Diabetes Mellitus, with a significant proportion (38.6%) exhibiting clinically relevant liver fibrosis (≥F2) on Fibroscan. There was a strong correlation between ultrasonographic grading and fibrosis staging (r = 0.62, p < 0.001), supporting the use of combined non-invasive modalities for early identification and stratification of NAFLD severity in diabetic patients.

Clinically, this highlights the need for routine hepatic evaluation in T2DM patients—even in the absence of overt liver dysfunction—as part of comprehensive diabetes management. Early identification of fibrosis allows for timely lifestyle and pharmacologic interventions to mitigate progression toward cirrhosis or hepatocellular carcinoma. Given the asymptomatic nature of early NAFLD, integrating ultrasonography and transient elastography (Fibroscan) into diabetes care algorithms is both practical and impactful in resource-limited settings.

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