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Co-existence of non-alcoholic fatty liver disease and inflammatory bowel disease: A review article

View Article: PubMed Central - PubMed

ABSTRACT

Emerging data have highlighted the co-existence of non-alcoholic fatty liver disease (NAFLD) and inflammatory bowel disease; both of which are increasingly prevalent disorders with significant complications and impact on future health burden. Cross-section observational studies have shown widely variable prevalence rates of co-existing disease, largely due to differences in disease definition and diagnostic tools utilised in the studies. Age, obesity, insulin resistance and other metabolic conditions are common risks factors in observational studies. However, other studies have also suggested a more dominant role of inflammatory bowel disease related factors such as disease activity, duration, steroid use and prior surgical intervention, in the development of NAFLD. This suggests a potentially more complex pathogenesis and relationship between the two diseases which may be contributed by factors including altered intestinal permeability, gut dysbiosis and chronic inflammatory response. Commonly used immunomodulation agents pose potential hepatic toxicity, however no definitive evidence exist linking them to the development of hepatic steatosis, nor are there any data on the impact of therapy and prognosis in patient with co-existent diseases. Further studies are required to assess the impact and establish appropriate screening and management strategies in order to allow early identification, intervention and improve patient outcomes.

No MeSH data available.


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Potential pathogenic factors contributing to the coexistence of non-alcoholic fatty liver disease and inflammatory bowel disease. NAFLD: Non-alcoholic fatty liver disease; IBD: Inflammatory bowel disease.
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Figure 1: Potential pathogenic factors contributing to the coexistence of non-alcoholic fatty liver disease and inflammatory bowel disease. NAFLD: Non-alcoholic fatty liver disease; IBD: Inflammatory bowel disease.

Mentions: NAFLD in IBD patients was predicted by disease-specific factors in the aforementioned studies which included disease activity and duration, along with prior IBD related or small bowel surgery, steroid and possibly anti-TNFα use. The etiology of IBD and factors provoking exacerbation are still partially understood. Intestinal microbiota have emerged as a key player in the pathogenesis of IBD. Alteration of gut microbiota has been associated with disease activity[27]. On the same line, NAFLD is associated with increased intestine permeability, and this abnormality is related to the increased prevalence of small bowel bacterial overgrowth in these patients. As such, alteration of gut microbiota may act as a pathogenic link between IBD and NAFLD. This makes one suspect that an active inflammatory process could drive fatty infiltration of the liver. Similar association have been made between psoriasis and NAFLD[28]. Duration of IBD was another independent predictor of development of NAFLD in the aforementioned Bessissow et al[22] study. Longer disease duration exposes patients to multiple risk factors for NAFLD, including chronic relapsing inflammation, alteration of gut microbiota and hepatotoxic drugs. In particular, oxidative stress from reactive oxygen species may also be the common pathogenic factor contributing the consistence of NAFLD and IBD. Along the same lines, prior surgery was also independently associated with incident NAFLD. This is most likely a surrogate marker of the severity of the disease with a more active inflammatory condition. Those patients will also tend to be exposed to hepatotoxic medications repeatedly. NASH development following extensive small bowel resection in non-IBD patients has also been previously described and may be related to nutritional deficiencies akin to those patients with bariatric bypass procedures[29]. Table 2 summarises the reported risk factors for NAFLD in IBD and Figure 1 depicts the hypothesized pathogenic factors of NAFLD in IBD.


Co-existence of non-alcoholic fatty liver disease and inflammatory bowel disease: A review article
Potential pathogenic factors contributing to the coexistence of non-alcoholic fatty liver disease and inflammatory bowel disease. NAFLD: Non-alcoholic fatty liver disease; IBD: Inflammatory bowel disease.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5016371&req=5

Figure 1: Potential pathogenic factors contributing to the coexistence of non-alcoholic fatty liver disease and inflammatory bowel disease. NAFLD: Non-alcoholic fatty liver disease; IBD: Inflammatory bowel disease.
Mentions: NAFLD in IBD patients was predicted by disease-specific factors in the aforementioned studies which included disease activity and duration, along with prior IBD related or small bowel surgery, steroid and possibly anti-TNFα use. The etiology of IBD and factors provoking exacerbation are still partially understood. Intestinal microbiota have emerged as a key player in the pathogenesis of IBD. Alteration of gut microbiota has been associated with disease activity[27]. On the same line, NAFLD is associated with increased intestine permeability, and this abnormality is related to the increased prevalence of small bowel bacterial overgrowth in these patients. As such, alteration of gut microbiota may act as a pathogenic link between IBD and NAFLD. This makes one suspect that an active inflammatory process could drive fatty infiltration of the liver. Similar association have been made between psoriasis and NAFLD[28]. Duration of IBD was another independent predictor of development of NAFLD in the aforementioned Bessissow et al[22] study. Longer disease duration exposes patients to multiple risk factors for NAFLD, including chronic relapsing inflammation, alteration of gut microbiota and hepatotoxic drugs. In particular, oxidative stress from reactive oxygen species may also be the common pathogenic factor contributing the consistence of NAFLD and IBD. Along the same lines, prior surgery was also independently associated with incident NAFLD. This is most likely a surrogate marker of the severity of the disease with a more active inflammatory condition. Those patients will also tend to be exposed to hepatotoxic medications repeatedly. NASH development following extensive small bowel resection in non-IBD patients has also been previously described and may be related to nutritional deficiencies akin to those patients with bariatric bypass procedures[29]. Table 2 summarises the reported risk factors for NAFLD in IBD and Figure 1 depicts the hypothesized pathogenic factors of NAFLD in IBD.

View Article: PubMed Central - PubMed

ABSTRACT

Emerging data have highlighted the co-existence of non-alcoholic fatty liver disease (NAFLD) and inflammatory bowel disease; both of which are increasingly prevalent disorders with significant complications and impact on future health burden. Cross-section observational studies have shown widely variable prevalence rates of co-existing disease, largely due to differences in disease definition and diagnostic tools utilised in the studies. Age, obesity, insulin resistance and other metabolic conditions are common risks factors in observational studies. However, other studies have also suggested a more dominant role of inflammatory bowel disease related factors such as disease activity, duration, steroid use and prior surgical intervention, in the development of NAFLD. This suggests a potentially more complex pathogenesis and relationship between the two diseases which may be contributed by factors including altered intestinal permeability, gut dysbiosis and chronic inflammatory response. Commonly used immunomodulation agents pose potential hepatic toxicity, however no definitive evidence exist linking them to the development of hepatic steatosis, nor are there any data on the impact of therapy and prognosis in patient with co-existent diseases. Further studies are required to assess the impact and establish appropriate screening and management strategies in order to allow early identification, intervention and improve patient outcomes.

No MeSH data available.


Related in: MedlinePlus