vitamin-b-12 and Arthritis--Psoriatic

Although anemia is frequent in inflammatory rheumatic diseases, data regarding vitamin B12 status is scarce. The purpose of this study was to analyze the incidence and nature of B12 and folic acid (FA) deficiencies in a cohort of rheumatic patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), and systemic lupus erythematosus (SLE).. Levels of B12, FA, and parameters of anemia were recovered or examined in 276 outpatients. In those with recent findings of low serum B12 levels, further studies of serum homocysteine (Hcy) and urine methylmalonic acid (MMA) levels were performed.. The incidence of anemia was high: 49%, 46%, and 35%, in RA, SLE, and PsA, respectively. Low levels of serum B12 were also frequent (24%), with almost similar occurrence in the three disease groups. Deficiency in FA was rare (<5%). Mean levels of both vitamins did not differ significantly among the three groups. No correlation between serum B12 levels and anemia was found. In the 15 patients with recently detected low B12 levels, Hcy and MMA were evaluated before and following B12 therapy. In ten of them, baseline Hcy levels were high, while MMA was increased in one patient only. Response to B12 administration, i.e., a decrease in Hcy and/or MMA levels, was noticed in four patients only, suggesting that only 26% of the low-serum-B12 patients had true B12 deficiency.. The incidences of anemia and decreased serum B12 levels were high in these three groups of rheumatic patients. However, true tissue deficiency seems to be much rarer.

Topics: Adult; Aged; Aged, 80 and over; Anemia; Arthritis, Psoriatic; Arthritis, Rheumatoid; Cohort Studies; Female; Folic Acid Deficiency; Homocysteine; Humans; Incidence; Israel; Lupus Erythematosus, Systemic; Male; Methylmalonic Acid; Middle Aged; Retrospective Studies; Treatment Outcome; Vitamin B 12; Vitamin B 12 Deficiency

This study investigated whether methotrexate, by interrupting the methyl transfer function of folate, can induce genomic DNA hypomethylation in patients with inflammatory arthritis. Consecutive subjects with inflammatory arthritis (rheumatoid or psoriatic), who were taking methotrexate (n = 7) or other medications (n = 6), and control subjects, either healthy or with osteoarthritis and taking nonsteroidal anti-inflammatory agents only (n = 9) were recruited. The methylation status of genomic DNA from peripheral blood mononuclear cells was determined. Plasma levels of folate, B12, and pyridoxal-5'-phosphate (PLP), all of which are involved in biologic methylation, were also examined. The extent of genomic DNA methylation was lowest in subjects with inflammatory arthritis who were not taking methotrexate, highest in subjects with inflammatory arthritis who were taking methotrexate, and intermediate in control subjects (p < 0.05). Plasma levels of folate and B12 were similar among the three groups. The mean plasma PLP level in subjects with inflammatory arthritis was 33% lower than that in control subjects (p = 0.04). No significant correlation between genomic DNA methylation and folate, B12, and PLP levels was observed. These data do not support the hypothesis that methotrexate induces genomic DNA hypomethylation. However, these data indicate that inflammatory arthritis is associated with genomic DNA hypomethylation that is reversed with methotrexate. Future studies using a larger number of subjects are warranted to confirm these findings.

Topics: Adult; Antirheumatic Agents; Arthritis, Psoriatic; Arthritis, Rheumatoid; DNA Methylation; Female; Folic Acid; Homocysteine; Humans; Male; Methotrexate; Middle Aged; Vitamin B 12