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Research Article Open Access
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.
Vitamin D deficiency, Inflammation, Acute pancreatitis, Sarcoidosis, Negative-Phasereactant, Hypercalcemia, IgG4 related disease, Pancreas, Imaging, Autoimmune pancreatitis, Inflammatory