Prevalence of Fat Soluble Vitamin Deficiency in Chronic Pancreatitis: A Comparison by Dominant Etiological Risk Factor (TIGAR-O)

Abstract

Introduction: An increased risk of fat-soluble vitamin (FSV) deficiency has nearly become a defining characteristic of chronic pancreatitis (CP), despite the evidence base for this contention having been extrapolated from observational studies in pediatric cystic fibrosis (CF) patients and the conspicuous absence of fulminant FSV deficiency in patients with non-CF CP1,2. In a cohort of patients with Mannheim ‘definite'3 CP, we attempted to detect any difference in the prevalence of FSV deficiency between patients with different dominant risk factors for having acquired CP4.Figure 1Methods: Our electronic medical record (EMR) was queried for patients between 18-90 years of age, carrying any ICD-9 code related to CP. Inclusion criteria: blood 25-OH vitamin D level & met criteria for the diagnosis of ‘definite' CP3. Patients were grouped by their dominant risk factor for CP by the TIGAR-O classification4. Serum levels of vitamins A, 25-OH D, E, and K, were recorded. Patients were categorized qualitatively as deficient or not deficient. Statistical analysis dictated that we combine those with idiopathic, autoimmune, recurrent & severe acute pancreatitis and obstruction mediated disease. χ2 analysis was used to compare the combined group with the toxin and genetically mediated CP groups. Results: The overall prevalence of vitamin A, 25-OH vitamin D, vitamin E & vitamin K were 17.4% (23/132), 80.1% (118/146), 20.3% (24/118) and 27.4% (37/135). The prevalence of any FSV deficiency in this cohort was 81.5% (119/146). There was no difference in the prevalence of any FSV deficiency between the three groups (See Figure 2). In a secondary analysis, those with 25-OH vitamin D deficiency and those without 25-OH vitamin D deficiency were compared. Vitamin A, E or K deficiency was nearly non-existent in patients without 25-OH vitamin D deficiency (χ2 = 11.61, p=.001). Conclusion: This is the first study to investigate FSV deficiency in a Mannheim ‘definite' cohort of CP patients and to compare the prevalence of FSV deficiency by TIGAR-O classification. Despite the different mechanisms of pancreatic injury and resulting histopathology between these groups, we found no statistical difference in the prevalence of FSV deficiency between them. Surprisingly, we found that of the 19.2% (28/146) patients not deficient in 25-OH vitamin D, only a single patient, 3.5% (1/28), was deficient in vitamin K and none of these patients were deficient in vitamin A or E.