Coexistence of pernicious anemia and prostate cancer - 'an experiment of nature' involving vitamin B12 modulation of prostate cancer growth and metabolism: a case report

<p>Abstract</p> <p>Introduction</p> <p>This report presents the clinical and laboratory course of a patient with prostate cancer and severe vitamin B₁₂deficiency undergoing watchful waiting for prostate cancer. The possible interaction between therapy for B₁₂deficiency and the natural course of prostate cancer is presented.</p> <p>Case presentation</p> <p>We present the case of a 75-year-old Chinese man with prostate cancer and pernicious anemia. His serum vitamin B₁₂level 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 B₁₂were 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 B₁₂therapy.</p> <p>Conclusion</p> <p>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' B₁₂. Replacement of B₁₂was 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 B₁₂metabolism 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 B₁₂replacement. To our knowledge, this is the first report of a possible cellular kinetic interaction between an epithelial malignancy and vitamin B₁₂metabolism.</p

Control of prostate cancer associated with withdrawal of a supplement containing folic acid, L-methyltetrahydrofolate and vitamin B12: a case report

<p>Abstract</p> <p>Introduction</p> <p>This is the first report of possible direct stimulation of hormone-resistant prostate cancer or interference of docetaxel cytotoxicity of prostate cancer in a patient with biochemical relapse of prostatic-specific antigen. This observation is of clinical and metabolic importance, especially at a time when more than 80 countries have fortified food supplies with folic acid and some contemplate further fortification with vitamin B₁₂.</p> <p>Case presentation</p> <p>Our patient is a 71-year-old Caucasian man who had been diagnosed in 1997 with prostate cancer, stage T1c, and Gleason score 3+4 = 7. His primary treatment included intermittent androgen deprivation therapy including leuprolide + bicalutamide + deutasteride, ketoconazole + hydrocortisone, nilandrone and flutamide to resistance defined as biochemical relapse of PSA. While undergoing docetaxel therapy to treat a continually increasing prostate-specific antigen level, withdrawal of 10 daily doses of a supplement containing 500 μg of vitamin B₁₂as cyanocobalamin, as well as 400 μg of folic acid as pteroylglutamic acid and 400 μg of L-5-methyltetrahydrofolate for a combined total of 800 μg of mixed folates, was associated with a return to a normal serum prostatic-specific antigen level.</p> <p>Conclusion</p> <p>This case report illustrates the importance of the effects of supplements containing large amounts of folic acid, L-5-methyltetrahydrofolate, and cyanocobalamin on the metabolism of prostate cancer cells directly and/or B vitamin interference with docetaxel efficacy. Physicians caring for patients with prostate cancer undergoing watchful waiting, hormone therapy, and/or chemotherapy should consider the possible acceleration of tumor growth and/or metastasis and the development of drug resistance associated with supplement ingestion. We describe several pathways of metabolic and epigenetic interactions that could affect the observed changes in serum levels of prostate-specific antigen.</p