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Abstract
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Non-alcoholic fatty liver disease (NAFLD) has emerged as the most prevalent chronic liver disease globally, representing a significant public health challenge that encompasses a spectrum of histological conditions ranging from simple hepatic steatosis to non-alcoholic steatohepatitis (NASH), advanced fibrosis, and potentially hepatocellular carcinoma [1]. The global burden of NAFLD has increased dramatically over the past decades, with current estimates indicating that approximately 38% of the global adult population is affected by this condition [2]. In the Middle East and North Africa (MENA) region, the prevalence of NAFLD is particularly alarming, with recent meta-analyses reporting rates as high as 39.43% in the general population and 68.71% among patients with type 2 diabetes [3].
The epidemiological landscape of NAFLD in Iraq, particularly in Salah Aldden Governorate, reflects the broader regional trends observed across the MENA region. The prevalence of NAFLD in this region exceeds 40% in many areas, making it one of the highest globally [4]. This elevated prevalence is attributed to the complex interplay of genetic predisposition, rapid urbanization, dietary changes characterized by increased consumption of processed foods and refined carbohydrates, sedentary lifestyle patterns, and the rising prevalence of metabolic syndrome components including obesity, type 2 diabetes mellitus, and dyslipidemia [5]. The socioeconomic transformations in post-conflict Iraq have further exacerbated these risk factors, with changes in food security, stress-related metabolic dysfunction, and reduced access to preventive healthcare contributing to the increasing burden of metabolic liver disease.
The pathogenesis of NAFLD involves complex molecular mechanisms where inflammatory cytokines play pivotal roles in disease initiation, progression, and outcomes. Among the numerous cytokines implicated in NAFLD pathophysiology, interleukin-1β (IL-1β) and transforming growth factor-β (T
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