Abstract
Subjects with chronic liver disease are susceptible to hypovitaminosis A due to several factors. Therefore, identifying patients with vitamin deficiency and a requirement for vitamin supplementation is important. Most studies assessing vitamin A in the context of hepatic disorders are conducted using cirrhotic patients. A cross-sectional study was conducted in 43 non-cirrhotic patients with chronic hepatitis C to evaluate markers of vitamin A status represented by serum retinol, liver retinol, and serum retinol-binding protein levels. We also performed the relative dose-response test, which provides an indirect estimate of hepatic vitamin A reserves. These vitamin A indicators were assessed according to the stage of liver fibrosis using the METAVIR score and the body mass index. The sample study was predominantly composed of male subjects (63%) with mild liver fibrosis (F1). The relative dose-response test was <20% in all subjects, indicating vitamin A sufficiency. Overweight or obese patients had higher serum retinol levels than those with a normal body mass index (2.6 and 1.9 µmol/L, respectively; P<0.01). Subjects with moderate liver fibrosis (F2) showed lower levels of serum retinol (1.9 vs 2.5 µmol/L, P=0.01) and retinol-binding protein levels compared with those with mild fibrosis (F1) (46.3 vs 67.7 µg/mL, P<0.01). These results suggested an effect of being overweight on serum retinol levels. Furthermore, more advanced stages of liver fibrosis were related to a decrease in serum vitamin A levels.
Highlights
The liver plays a major role in vitamin A metabolism
A reference value was not defined for free liver retinol. *Evaluated in 42 patients; **Evaluated in 41 patients
Knowledge regarding vitamin A metabolism and liver disease is mainly based on studies that included patients with severe liver disease, and whose diverse etiologies were evaluated together [12,13,14]
Summary
The liver plays a major role in vitamin A (retinol) metabolism This organ is involved in serum retinol uptake after intestinal absorption from nutritional sources, as well as its storage and continuous supply to target tissues. HSCs become activated, losing their retinoid content, and produce an extracellular matrix, which is responsible for liver fibrosis [2]. Other factors, such as decreased vitamin intake or absorption, and excessive alcohol consumption, may place cirrhotic patients at risk for hypovitaminosis A, which could benefit from vitamin supplementation. When hepatic retinol storage is not depleted, prolonged vitamin A supplementation in subjects with liver disease may induce hepatotoxicity [3]. Estimating vitamin A status is important to distinguish between subjects that have retinol deficiency and those for whom vitamin supplementation is not recommended
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