Abstract
The prevalence of nonalcoholic fatty liver disease (NAFLD) has increased significantly over the last few decades mirroring the increase in obesity and type II diabetes mellitus. NAFLD has become one of the most common indications for liver transplantation. The deleterious effects of NAFLD are not isolated to the liver only, for it has been recognized as a systemic disease affecting multiple organs through protracted low-grade inflammation mediated by the metabolic activity of excessive fat tissue. Extrahepatic manifestations of NAFLD such as cardiovascular disease, polycystic ovarian syndrome, chronic kidney disease, and hypothyroidism have been well described in the literature. In recent years, it has become evident that patients suffering from NAFLD might be at higher risk of developing various infections. The proposed mechanism for this association includes links through hyperglycemia, insulin resistance, alterations in innate immunity, obesity, and vitamin D deficiency. Additionally, a risk independent of these factors mediated by alterations in gut microbiota might contribute to a higher burden of infections in these individuals. In this narrative review, we synthetize current knowledge on several infections including urinary tract infection, pneumonia, Helicobacter pylori, coronavirus disease 2019, and Clostridioides difficile as they relate to NAFLD. Additionally, we explore NAFLD's association with hidradenitis suppurativa.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the United States and worldwide
E hallmark feature of NAFLD is the aberrant and excessive storage of macrovesicular fat due to alterations in the homeostatic balance between the fat synthesis and its utilization [1,2,3]. This seemingly benign fat accumulation in hepatocytes triggers inflammation leading to nonalcoholic steatohepatitis (NASH), liver fibrosis, cirrhosis, and/or development of hepatocellular carcinoma. e progression from NAFLD to these more severe entities is multifactorial and depends on an individual’s genetic factors, environmental factors, and abnormal activation of the innate immune system [1,2,3,4,5]
Abnormal activation of the innate immune system leads to persistent low-grade inflammation which leads to tissue injury and fibrosis and has an important role in carcinogenesis [1,2,3,4,5]
Summary
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the United States and worldwide. E hallmark feature of NAFLD is the aberrant and excessive storage of macrovesicular fat (in >5% of hepatocytes) due to alterations in the homeostatic balance between the fat synthesis and its utilization [1,2,3]. In some individuals, this seemingly benign fat accumulation in hepatocytes triggers inflammation leading to nonalcoholic steatohepatitis (NASH), liver fibrosis, cirrhosis, and/or development of hepatocellular carcinoma. While the role of the immune system is well recognized in the pathogenesis of NAFLD and its complications, it is less known how the presence of NAFLD influences an individual’s risk for the development of various bacterial, fungal, and viral infections. Obesity and type II DM (T2DM) have been previously recognized as risk factors for the development of various infections [7,8,9,10]
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