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Our purpose was to test the hypothesis that liver disease may disrupt B12 distribution. Results: Severe liver disease initiates highly elevated B12 levels in plasma and a lowered liver tissue total B12 concentration. Total B12 and B12 distributed to TC are lower in diseased liver tissue.
Conclusion: Severe alcoholic liver disease involves leakage of total B12 from liver tissue into the plasma. However, plasma holo TC II B12 distribution is decreased, indicating that there is a depression of exogenous B12 entering the plasma and tissues. In severe liver disease, liver tissue B12 binding and storage by TC is disrupted and causes B12 to leak out of the liver into the circulation.
Eventually liver disease could produce enough severe tissue B12 deficits to cause metabolic dysfunction despite elevated plasma total B12. Elevation of plasma B12, accompanied by a lowering of holo TC II distribution, seemed to be a useful index of liver disease severity suggesting preventive treatmen.
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D serum vitamin B12 level is frequently seen in cirrhosis due to excess release and/or reduced clearance, and thus has been proposed as a marker to differentiate cryptogenic cirrhosis from non-cirrhotic portal hypertension.
The aim of the study is to evaluate the utility of serum vitamin B12 level as a diagnostic marker to predict cirrhosis in patients with chronic liver disease. Methods: We designed a retrospective cohort study including patients seen at a tertiary referral hospital in Miami FL, USA between January 2013 and April 2014. Data on demographics, etiology of liver disease, and serum markers (AST, ALT, platelets, and vitamin B12) was obtained.
Ast/ALT ratio and APRI score were calculated. Results: We analyzed 150 patients. Thirteen were excluded because of vitamin supplementation, gastric/small bowel resection, or hematologic malignancies, as these have been related to abnormal vitamin B12 levels.
Of the 137 included patients, 70 (51%) were male, and the mean age was 57 +/- 12 years. Seventyseven (56%) were Hispanic and 116 (85%) white. The mean vitamin B12 level was 953 pg/mL +/- 380 in the cirrhotic population compared to 652 pg/mL +/- 346 in those who were not (p=0.001) (Table 1).
To determine the accuracy of vitamin B12 level as a diagnostic test for cirrhosis, different cutoffs were analyzed. Table 1: Non-invasive Serologic Markers for Advanced Liver Fibrosis
Conclusion: Serum vitamin B12 level, a routine, widely available test, appears to be a useful non-invasive marker that can predict cirrhosis in patients with chronic liver disease. Larger prospective studies in the future using vitamin B12 levels alone or in combination with other non-invasive tests are need to validate our finding.
Introduction:
Liver diseases are known to correlate with low vitamin levels such as vitamin D, A, or E. Vitamin B12 deficiency and liver disease are often comorbid conditions given the high rate of dietary deficiency or malabsorption in this patient population, especially among those who have alcohol related liver disease. Some studies have shown those with non-alcoholic fatty liver disease (NAFLD) to have lower vitamin B12 levels. However, there is still little evidence on the correlation between NAFLD and B12 deficiency as well as any association with the degree of liver injury.