Incidence and prevalence of systemic lupus erythematosus among the native Arab population in UAE.

Background and objectives There is a paucity of information about the epidemiology of systemic lupus erythematosus (SLE) amongst Arabs. The objective of this study was to determine the incidence and prevalence of SLE among the native Arab population of United Arab Emirates (UAE). Methods Patients with SLE were identified from three sources: medical records of two local tertiary hospitals (four years; 2009 to 2012), laboratory requests for serum double stranded deoxyribonucleic acid and serum anti-nuclear antibody and confirmed histopathologic diagnosis of SLE (skin and kidney biopsy specimens). All the patients identified with SLE met the criteria of the American College of Rheumatology. Incidence and prevalence were calculated using the state records of the UAE native population as the denominator. The age-adjusted incidence was calculated by direct standardization using the World Health Organization world standard population 2000-2025. Results Sixteen new cases (13 females and three males) fulfilled the American College of Rheumatology SLE criteria. The mean (±SD) age at time of diagnosis was 28.6 ± 12.4 years. The crude incidence ratio (per 100,000 population) was 3.5, 1.1, 2.1 and 2.1 in years 2009, 2010, 2011, 2012, respectively. The age-standardized incidence per 100,000 population for the four years was 8.6 (95% confidence interval 4.2-15.9). The age-standardized prevalence of SLE among the native population according to the 2012 population consensus was 103/100,000 population (95% confidence interval 84.5-124.4). Conclusion The age-adjusted incidence and prevalence among UAE Arabs is higher than has been reported among most other Caucasian populations. Furthermore, the prevalence of SLE in UAE seems much higher than other similar Arab countries in the Gulf region.

Why so much oestriol? A comparison of the aromatisation of androstenedione and 16 alpha-hydroxyandrostenedione when incubated alone or together with human placental microsomes.

Estimates of the relative abundance of 16 alpha-hydroxy- and 16-deoxyoestrogens in late pregnancy urine lie between 13:1 and 5:1, yet the ratio of the concentrations of the major precursors 16 alpha-hydroxydehydroepiandrosterone sulphate and dehydroepiandrosterone sulphate in cord blood is about 2.5:1. This discrepancy might imply that 16 alpha-hydroxy-C19 steroids are used more efficiently for placental oestrogen biosynthesis than are the 16 alpha-deoxy-C19 steroids. On testing this hypothesis by incubation of placental microsomes with 16 alpha-hydroxy- and 16-deoxy- precursors together (concentration ratios 128:1 to 1:1), initial rates of oestrogen formation were highest from the 16-deoxy-C19 steroid. Additionally, whilst each substrate appeared to inhibit the aromatisation of the other, the 16-deoxy-C19 steroid was the more potent inhibitor. These findings were supported by an analogous experiment with placental slices. When each precursor was examined separately with microsomes from 4 placentae, aromatisation of the 16 alpha-hydroxy-C19 steroid (Michaelis constant, (Km) 0.75-1.24 mumol/l, maximum reaction velocity (Vmax) 28-69 pmol product/min/mg protein) was less efficient than that of the 16-deoxy-C19 steroid (Km 0.10-0.15 mumol/l, Vmax 71-145 pmol product/min/mg protein). To reconcile the disparity between the measured utilisation of precursors in vitro and expectations drawn from precursor availability and urinary excretion rates, sources of urinary 16 alpha-hydroxyoestrogens additional to placental aromatisation need to be considered. Hydroxylation of 16-deoxyoestrogens (the phenolic pathway) appears limited but aromatisation in fetal liver of 16 alpha-hydroxyandrostenedione not utilised by the placenta appears to be worth attention.