High prevalence of vitamin A deficiency and vitamin D deficiency in patients evaluated for liver transplantation

Abstract

Background Deficiencies in vitamins A, D and E have been linked to night blindness, bone health, and post-liver transplant reperfusion injury. Aims To determine the prevalence and predictive factors of fat soluble vitamin deficiencies in liver transplantation candidates. Methods We reviewed medical records of liver transplantation candidates at our center from 1/2008–9/2011. Etiology of cirrhosis, MELD scores, Child Pugh class, BMI, vitamin A, vitamin E, and vitamin 25-OH-D levels were recorded. Patients were excluded for incomplete laboratory data, short gut syndrome, celiac disease, pancreatic insufficiency, or prior liver transplantation. Results Sixty three patients were included. The most common etiologies of liver disease were alcohol (23), hepatitis C (19), and NASH (5). Vitamin A and D deficiency was noted in 69.8% and 80.9%, respectively. Only 3.2% of patients were vitamin E deficient. There were no documented cases of night blindness. Of 55 patients with bone density measurements, 25 had osteopenia and 10 had osteoporosis. Four patients had vertebral fractures. There was one case of post-transplant reperfusion injury in a patient with vitamin E deficiency. In a multivariate analysis, there were no statistically significant predictors for vitamin D deficiency. Child Pugh class (OR=6.84 {1.52–30.86};p = 0.012), elevated total bilirubin (OR=44.23{5.02–389.41}; p < .001), and elevated BMI (OR=1.17{1.00–1.36};p = 0.045) were found to be predictors of vitamin A deficiency. Conclusions The majority of liver disease patients evaluated for liver transplantation at our center had vitamin A and D deficiency. Presence or absence of cholestatic liver disease did not predict the deficiency, whereas Child Pugh class, bilirubin level, and elevated BMI predicted vitamin A deficiency.

Hypovitaminosis D is associated with increased whole body fat mass and greater severity of non‐alcoholic fatty liver disease

“…In addition, only NASH and the presence of diabetes mellitus independently predicted lower vitamin D levels. These data along with those from others emphasize the importance of insulin resistance on vitamin D levels and that low vitamin D levels can accelerate advanced stages of liver disease. The liver injury associated with low vitamin D concentration may be explained, in part, by a recent study that reported a TGFβ1/Smad3 mediated increase in hepatic profibrotic genes .…”

Nutrition in the Management of Cirrhosis and its Neurological Complications

“…Fat soluble vitamin deficiencies are common manifestations of malnutrition and liver disease. 19,20 A retrospective study reported that the majority of liver disease patients being considered for liver transplantation present with vitamin A and D deficiencies. 19 Vitamin A Vitamin A (retinol) is implicated in ocular retinoid metabolism, tissue repair and immunity, and is principally stored in hepatic stellate cells.…”

“…19,20 A retrospective study reported that the majority of liver disease patients being considered for liver transplantation present with vitamin A and D deficiencies. 19 Vitamin A Vitamin A (retinol) is implicated in ocular retinoid metabolism, tissue repair and immunity, and is principally stored in hepatic stellate cells. As quiescent stellate cells become activated, they lose their vitamin A stores and are then capable of producing collagen and subsequent fibrosis.…”

Calcidiol Deficiency in End-Stage Organ Failure and after Solid Organ Transplantation: Status quo

“…Thus, it is not surprising that the degree of liver dysfunction correlates with calcidiol levels [3] and that the prevalence of vitamin D insufficiency is particularly high in patients with chronic liver disease [29,30,31,32]. At the time of transplantation, between 80% and 95% of the patients with end-stage liver failure were reported to have hypovitaminosis D, with varying prevalence of severe vitamin D deficiency (ranging from 3% up to 50%) [15,33,34,35]. Notably, in one study, more than one fifth of the patients had serum calcidiol below the detection limit of 6.8 ng/mL [15].…”