Coexistence of pernicious anemia and prostate cancer - 'an experiment of nature' involving vitamin B(12 )modulation of prostate cancer growth and metabolism: a case report.
J Med Case Reports. 2009;3:9295. Epub 2009 Nov 24. PMID: 20062784
Department of Nutrition and Neoplasia, Whittier Cancer Research Building, Bailey Street, Whittier, CA 90601, USA.
INTRODUCTION: This report presents the clinical and laboratory course of a patient with prostate cancer and severe vitamin B(12 )deficiency undergoing watchful waiting for prostate cancer. The possible interaction between therapy for B(12 )deficiency and the natural course of prostate cancer is presented. CASE PRESENTATION: We present the case of a 75-year-old Chinese man with prostate cancer and pernicious anemia. His serum vitamin B(12 )level was 32 pg/ml (300-900 pg/ml) and holotranscobalamin was 0 pg/ml (>70 pg/ml). There was an unexpected rapid progression of Gleason's score during 10 months of watchful waiting. After the diagnosis of pernicious anemia was made, therapeutic injections of vitamin B(12 )were started. We observed a significant acceleration in prostate-specific antigen and prostatic acid phosphatase and a shortening of prostate-specific antigen doubling time after initiation of B(12 )therapy. CONCLUSION: We propose that the relatively short period of watchful waiting before histological progression of Gleason's score (GS [3+2] = 5 to GS [3+4] = 7 over 10 months) may have been a result of depleted holotranscobalamin 'active' B(12). Replacement of B(12 )was associated with an initial rapid increase in serum prostate-specific antigen and prostatic acid phosphatase followed by stabilization. The patient represents an 'experiment of nature' involving vitamin B(12 )metabolism and raises the question as to whether rapid histological progression of Gleason's score was related to absence of serum holotranscobalamin while prostate-specific antigen and prostatic acid phosphatase, markers of cell growth, were accelerated by vitamin B(12 )replacement. To our knowledge, this is the first report of a possible cellular kinetic interaction between an epithelial malignancy and vitamin B(12 )metabolism.