When local treatments for prostate cancer have failed, and prostate-specific antigen (PSA) rises in the absence of symptoms, there is little consensus as to the best management strategy. Calcitriol has been shown to prolong the doubling time of PSA in this context, but near-toxic doses are required. We investigated the effect of the nutrient vitamin D (cholecalciferol), a biochemical precursor of calcitriol, on PSA levels and the rate of rise of PSA in these patients. Fifteen patients were given 2,000 IU (50 microg) of cholecalciferol daily and monitored prospectively every 2-3 mo. In 9 patients, PSA levels decreased or remained unchanged after the commencement of cholecalciferol. This was sustained for as long as 21 mo. Also, there was a statistically significant decrease in the rate of PSA rise after administration of cholecalciferol (P = 0.005) compared with that before cholecalciferol. The median PSA doubling time increased from 14.3 mo prior to commencing cholecalciferol to 25 mo after commencing cholecalciferol. Fourteen of 15 patients had a prolongation of PSA doubling time after commencing cholecalciferol. There were no side effects reported by any patient. Further study is needed to confirm this finding and to explore the potential therapeutic benefit of nutrient vitamin D in prostate cancer.

Sitagliptin is a dipeptidyl peptidase-4 (DPP IV, CD26) inhibitor indicated for treatment of Type II diabetes as a second line therapy after metformin. We report fifteen sitagliptin intolerant patients who developed anterior and posterior rhinorrhea, cough, dyspnea, and fatigue. Symptoms typically developed within 1 to 8 weeks of starting, and resolved within 1 week of stopping the drug. Peak expiratory flow rates increased 34% in 8 patients who stopped sitagliptin. Similar changes were found in 4 out of 5 persons who had confirmatory readministration. Chart review identified 17 patients who tolerated sitagliptin and had no symptomatic changes. The sitagliptin intolerant group had higher rates of clinically diagnosed allergic rhinitis (15/15 vs. 6/18; p = 0.00005), Fisher's Exact test) and angiotensin converting enzyme inhibitor - induced cough (6/13 vs. 1/18; p = 0.012). Nasal and inhaled glucocorticoids may control the underlying allergic inflammation and abrogate this new sitagliptin - induced pharmacological syndrome. Potential mucosal and central nervous system mechanisms include disruption of neuropeptides and/or cytokines that rely on DPP IV for activation or inactivation, and T cell dysfunction.

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