Vitamin D Deficiency in Patients with Pancreatitis: Is Vitamin D Replacement Required?
Zhiyong Han*, Samantha L Margulies, Divya Kurian and Mark S Elliott
Department of Biochemistry and Molecular Medicine, The George Washington University School of Medicine and Health Sciences, Washington, DC, USA
- Corresponding Author:
- Zhiyong Han
Department of Biochemistry and Molecular Medicine
The George Washington University School of Medicine and Health Sciences
Washington, DC 20037, USA
E-mail: [email protected]
Received Date: March 16, 2016; Accepted Date: March 28, 2016; Published Date: April 04, 2016
Citation: Han Z, Margulies SL, Kurian D, Elliott MS (2016) Vitamin D Deficiency in Patients with Pancreatitis: Is Vitamin D Replacement Required?. Pancreat Disord Ther 6:172. doi:10.4172/2165-7092.1000172
Copyright: © 2016 Han Z, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Clinical findings have shown that approximately 40% of patients with pancreatitis, acute or chronic, have severe vitamin D deficiency; this can reach up to 60% of patients with chronic pancreatitis. These findings raise an important question: Is vitamin D deficiency a cause or a result of pancreatitis? The answer(s) to this question is clinically important given that high oral doses of vitamin D supplementation are widely prescribed for individuals with vitamin D deficiency. Considering that there is active conversion of 25(OH)D3 to 1,25(OH)2D3 by activated macrophages in tissues undergoing inflammation, that elevation of the blood levels of 1,25(OH)2D3 levels can cause hypercalcemia, that hypercalcemia can precipitate pancreatitis, that excessive use of vitamin D supplementation can cause acute pancreatitis and that sarcoidosis causes elevated blood levels of 1,25(OH)2D3, hypercalcemia and acute pancreatitis, it is reasonable to consider both 25(OH)D3 and 1,25(OH)2D3 as negative acute-phase reactants, specifically in the context of the pathogenesis of pancreatitis. Thus, down-regulation of blood levels of 25(OH)D3 and 1,25(OH)2D3 in patients with pancreatitis appears to be a protective mechanism to prevent the development hypercalcemia, which would exacerbate the pancreatitis. Therefore, it is reasonable to consider that vitamin D replacement treatment may produce more harm than benefit for patients with pancreatitis.