Hyperhomocysteinemia is an established risk factor for thrombosis. In patients with myeloproliferative disorders, thrombotic events are common. Our aim was to investigate whether the increased burden of proliferating cells present in these patients implies a risk of homocysteine (HCY) accumulation secondary to depletion of folate and/or cobalamin. Fifty patients (PV, 25; ET, 10; IMF, 15) and 163 healthy volunteers (HV) participated in the study. The prevalence of hyperhomocysteinemia was 56.0% in PV, 70.0% in ET, 60.0% in IMF, and 34.9% in HV. The mean P-homocysteine (P-HCY) was 13.88 ± 4.24 μmol/L in PV, 12.78 ± 3.70 in ET, 11.34 ± 4.22 in IMF, and 9.71 ± 2.76 in HV. In PV and ET, but not in IMF, the mean P-HCY was significantly higher than in the HV group (P < 0.001, P = 0.028, and P = 0.163, respectively). Thirty-three percent of the patients with hyperhomocysteinemia displayed metabolic changes compatible with cobalamin deficiency (P-HCY and P-methylmalonic acid both elevated), while 67% were folate deficient (P-HCY elevated, P-methylmalonic acid normal). Supplementation therapy with the relevant vitamin was implemented in 11 vitamin-deficient patients and led to normalization of metabolite levels in all cases. No correlation between hyperhomocysteinemia and thrombosis was found. Our data indicate that patients with PV, ET, and IMF frequently develop hyperhomocysteinemia due to discrete depletion of cobalamin or folate. Vitamin therapy leads to normalization of P-HCY and should be considered, even though hyperhomocysteinemia does not seem to be of crucial importance for the thrombotic tendency in the myeloproliferative disorders. (C) 2000 Wiley-Liss, Inc.
|Tidsskrift||American Journal of Hematology|
|Status||Udgivet - 5 okt. 2000|