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To compare the rates of cure of septic abortion and pelvic inflammatory disease using a daily dose of clindamycin with gentamicin versus divided doses, we conducted a retrospective cohort study, where the electronic records of 661 patients who used clindamycin 1 × , 3 × or 4 ×/day (groups 1, 3 and 4, respectively) between September 2002 and August 2010 were analysed. Major outcomes included rates of cure and failure according to the clinical records. Secondary endpoints were percentage of adverse effects related to medication regimen and the prevalence of positive VDRL and HIV. Similar conditions were observed in all groups - septic abortion: 167/116/123; pelvic inflammatory disease: 73/95/87 (groups 1, 3 and 4, respectively). No significant difference was found among groups for age or for rate of cure. Rates of cure (cure/total [rate (95%CI)]) in groups 1, 3 and 4 were 236/240 [0.983 (0.957-0.993)], 205/211 [0.971 (0.939-0.986)], 203/210 [0.966 (0.932-0.983)], respectively. Days of use of clindamycin was significantly reduced in group 1, compared to groups 3 and 4 (2.6 ± 1.3 vs. 3.5 ± 2.5 vs. 3.3 ± 1.9-mean ± SD; p < 0.0001 - ANOVA), but this may be due to differences in how length of therapy was measured and not the effect on clinical cure.

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Background Vitamin D has pleiotropic actions on many chronic diseases. Multiple studies have confirmed vitamin D deficiency in patients with systemic lupus erythematosus (SLE). Genetic polymorphisms located in VDR gene and low levels of 25-hydroxyvitamin D (25OHD) may increase the risk of cardiovascular event. The relationship of vitamin D with cardiovascular risk factors in SLE patients have been described, but more studies are needed to further clarification. Objectives To study the influence of vitamin D on cardiovascular disease in SLE patients. Methods One hundred eighty-one SLE patients previously studied to investigate the influence of BsmI and FokI VDR gene polymorphisms and serum levels of 25OHD were evaluated for the presence of cardiovascular disease (CVD) defined as stroke,transient ischemic attack (TIA), angina pectoris (AP), myocardial infarction (MI) and arterial thrombosis (AT). Results The mean age and disease duration were 42.0±13.5 and 9.6±7.6 years, respectively. One hundred and seventy (93.9%) patients was female and 134 (74%) was classified as Euro-derived. Eighteen (9.9%) patients had CVD (10 stroke,1 TIA, 3 AP, 3 MI, 1 AT). There was nostatistically significant difference in genotypic and allelic frequencies of BsmI and FokI polymorphisms among patients with CVD and patients without CVD (18.8% vs.13.5% BB, 50% vs. 51.8% Bb, 32.2% vs. 34.7% bb, p=0.618 and 58.8% vs. 47.2% FF, 29.4% vs. 43.7% Ff, 11.8% vs. 9.2% ff, p=0.591, respectively). The mean serum levels of 25OHD were 25.5±11.4 ng/ml. Patients with CVD had 25OHDlevels similar to patients without CVD (24.3±11.6 ng/ml vs. 25.7±11.4 ng/ml, p=0.638). After adjustment for phototype, ethnicity, age, gender, SLEDAI, antiphospholipid syndrome, smoking status, dyslipidemia, hypertension, body mass index, hydroxychloroquine use, current corticosteroids use and vitamin D supplementation, the 25OHD levels remained similar in both groups. Conclusions Neither the BsmI and FokI polymorphisms nor the levels of vitamin D were associated with presence of CVD in our SLE patients, even after adjusting for possible confounding factors. Additional studies are needed to corroborate our findings. References Valdivielso J.M., Fernandez E. Vitamin D receptor polymorphisms and diseases. Clin Chim Acta. 2006 Sep; 371(1-2):1-12. Wang T.J., et al. Vitamin D deficiency and risk of cardiovascular disease. Circulation. 2008 Jan 29; 117(4):503-11. Wu P.W., et al. 25-hydroxyvitamin D and cardiovascular risk factors in women with systemic lupus erythematosus. Arthritis Rheum. 2009 Oct 15; 61(10):1387-95. Kamen D.L. Vitamin D in lupus - new kid on the block? Bull NYU Hosp Jt Dis. 2010; 68(3):218-22. Monticielo O.A., et al. The role of BsmI and FokI vitamin D receptor gene polymorphisms and serum 25-hydroxyvitamin D in Brazilian patients with systemic lupus erythematosus. Lupus 2012 Jan; 21(1):43-52. Disclosure of Interest None Declared