Vitamin D status and per-oral vitamin D supplementation in patients suffering from chronic pancreatitis and pancreatic cancer disease.

UNLABELLED: Exocrine pancreatic insufficiency due to chronic pancreatitis may result--depending on the degree of insufficiency--, in a decrease in serum 25-hydroxyvitamin D (25(OH)D) level. However, the data in the literature concerning the rate and extent of vitamin D deficiency in pancreatic cancer with or without previous pancreas resection, are very rare, in particular regarding the question how to supplement these patients with vitamin D. In recent years, vitamin D is increasingly being discussed as one factor involved not only in musculo-skeletal diseases but also in cardiovascular and autoimmune diseases, cancer development, diabetes mellitus and overall mortality.

PATIENTS AND METHODS: In all, 248 ambulatory patients (n=140 patients suffering from exocrine pancreatic insufficiency due to chronic pancreatitis, pancreatic cancer with/without previous resections of the pancreas n=108 patients without pancreatic disease), we measured the serum 25(OH)D concentrations by the chemoluminescence method. In addition, in 91 of these patients (n=65 pancreatic patients, n=26 controls), we started supplementation with oral vitamin D in combination with dietary advice and adequate substitution with pancreatic enzyme preparations, followed by subsequent serum 25(OH)D determinations. The oral vitamin D doses varied from 1000 IU per day over 1× 20,000 IU per week, or 2-3 times 20,000 IU per week up to 20,000 IU per day in single patients, depending on the underlying disease and the estimated degree of maldigestion/malassimilation. In addition, in a pilot trial vitamins A and E were measured in the serum from 121 and 105 of these patients respectively (resp.) (HPLC method).

RESULTS: Serum 25(OH)D concentrations were <30 ng/ml in 93% of the patients with pancreatic diseases,<20 ng/ml in 77.9%, <10 ng/ml in 32.1% and <4 ng/ml in 9.3%. The results were comparable to those in patients suffering from chronic pancreatitis and those with pancreatic tumor disease, with or without a previous tumor resection (n=51 Whipple procedure, n=11 left resection, n=9 total duodeno-pancreatectomy). Similar data were also found in the controls, only slightly higher. In contrast to the vitamin D data, however, determination of vitamins A and E in the serum resulted in values within the normal range for the majority of the patients of both groups, suggesting a diminished vitamin D uptake as being at least one reason to explain the low serum vitamin D concentrations in the patients with pancreatic diseases. Individual supplementation with oral vitamin D in all patients studied (n=91) resulted in an increase of the serum 25(OH)D concentrations into the normal range (14.2±5.8 up to 42.3±12 in controls, 11.9±7.4 up to 46.6±15.7 in patients with pancreatic diseases). The data of a subgroup of patients with continuous long-term supplementation, however, suggest that some patients with pancreatic diseases may need a significantly higher vitamin D supplementation, up to 20000 IU per day in single patients, compared to the controls.

CONCLUSION: The results demonstrate that vitamin D deficiency is a common problem in patients suffering from exocrine pancreatic insufficiency from various reasons as well as in our controls. Apart from insufficient sun exposure, exocrine pancreatic insufficiency, as well as a too low vitamin D uptake with food seem to represent the main causes of low serum 25(OH)D. In nearly all patients, the serum 25(OH)D concentrations could be normalized by oral supplementation of vitamin D in the case of individual therapy based on routine serum controls.