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Background/Aims: Homocysteine and possibly also folate and vitamin B₁₂ are involved in the pathogenesis of cardiovascular disease. We investigated the prevalence of hyperhomocysteinemia in patients with coronary heart disease (CHD), as well as folate and vitamin B₁₂, the main nutritional factors determining the level of homocysteine. Methods: Patients with angiographically documented CHD were prospectively investigated (n = 315, 70% male, mean age 61 [range 36–81] years). Fasting total serum homocysteine was determined by high-performance liquid chromatography and fluorescence detection. Folic acid and vitamin B₁₂ were measured with AxSYM® Systems. Results: Median homocysteine concentrations for homocysteine, folate and vitamin B₁₂ were 12.8 µmol/l, 6.8 ng/ml and 345 pg/ml, respectively. Homocysteine levels >10 µmol/l were found in 82% of men and 73% of women. In 19% of the patients serum folate was <3 ng/ml and 22% of the patients had serum vitamin B₁₂ values <250 pg/ml. In a multivariate linear regression model, folate and vitamin B₁₂ showed significant negative correlations to homocysteine, explaining 5 and 3% of its variability. Age and creatinine were the most important determinants for serum homocysteine, contributing 12 and 7%, respectively. Discussion: The main determinants of total homocysteine in patients with CHD are higher age and increased creatinine. The association of lower levels of folate and vitamin B₁₂ with higher levels of homocysteine may indicate poor dietary habits in these patients.

Reactive arthritis (ReA) occurs after a urogenital infection usually with Chlamydia trachomatis or an enteritis due to Yersinia, Salmonella, Campylobacter or Shigella, Shigella, except during epidemics, is not considered to be a frequent cause of enteric reactive arthritis. However this might be due to the lack of a reliable antibody test, which makes diagnosis difficult. We compared synovial and peripheral blood lymphocyte proliferation to various bacterial antigens in 19 consecutive patients with ReA or undifferentiated oligoarthritis. In five patients Shigella was identified as the causative microbe by a specific synovial lymphocyte proliferation. All five patients had a history of symptomatic diarrhoea and had negative stool cultures by the time arthritis developed. Four of the five were HLA B27 positive. We conclude that Shigella may be underestimated as a cause of non-epidemic ReA.