Seventy female and three male Omani systemic lupus erythematosus (SLE) patients are described. At disease onset, 45 (62%) were under 20 years of age, and the remainder were between 20 and 44. Of all cases, 48% were familial. Over 5 years, the cumulative frequencies of autoantibodies was: antinuclear antibodies (ANA) 97%, anti-double-stranded DNA (anti-dsDNA) antibodies 92%, extractable nuclear antigen (ENA) antibodies 64%, antineutrophil cytoplasmic antibodies (ANCA) 58%, antiphospholipid (APL) antibodies 80%, and rheumatoid factor (Rf) 22%. Ribonucleoprotein (RNP) antibodies were found in 15/45 younger-onset and 2/28 older-onset patients (chi(2)=6.63, P<0.02). The mean SLE disease activity score (SLEDAI) was 13.5+11.4, and the cumulative frequencies of systemic involvement were: neurological 33.8%, vascular 10.4%, musculoskeletal 53.9%, renal 50.7%, dermal 80.5%, serosal 23.9%, immunological 95%, constitutional 31.3%, and haematological 26.0%. Linear regression analysis showed that high-titre ANA were predictors for pyuria (odds ratio [OR] 9.06, P=0.01). Antiextractable nuclear antigen antibodies were predictors for disease of the neurological (OR 26.3, P=0.008) and serosal (OR 27.7, P=0.005) systems, and anti-Sm antibodies for alopecia (OR 5.93, P=0.088) and hypocomplementaemia (OR 14.6, P= 0.016). Antibodies of known diagnostic utility may also give insights into the pathogenesis of SLE.

sFas is elevated in sera of SLE patient. Since sFas correlates with indices of organ damage but not with disease activity, it may be a marker of organ damage in SLE and may act to protect certain organs from further damage by inhibiting Fas-mediated apoptosis.

The prevalence of symptoms in 34 Omani patients with Behcet's disease (BD) was: recurrent oral ulceration 100%, arthritis/arthralgia and genital ulceration 74% each, folliculitis 64%, neurological lesions 62%, retinal vasculitis 30%, iritis and hypopyon 26%, gastrointestinal lesions 12%, venous thrombosis and cardiovascular lesions 9% each, and pleuropulmonary lesions and epididymitis 6% each. Antiphospholipid (APL) antibodies (both anticardiolipin [ACAs] and anti-beta2 glycoprotein I [abeta2GPIs]) were present in 11/34 (32%) of the BD patients and in 54/73 (74%) of Omani patients with systemic lupus erythematosus (SLE) (chi2 = 21.2, P<0.001). In patients possessing APL antibodies, there was no significant difference in mean antibody levels between BD and SLE patients. IgM isotype antibodies, in the absence of IgG, were more prevalent in BD (5/11) than in SLE (10/54) patients (chi2 =3.8, P = 0.05). The frequency of organ involvement was similar in patients with and without APL antibodies (chi2 = 1.226, P > 0.05). This study fails to demonstrate a pathognomonic role for APL antibodies in BD.

Tribal differences are demonstrated in the presentation of lupus in Omani Gulf Arabs (OGA) and Omani Arabs of Persian descent (OAP), both groups resident in and indigenous to the Sultanate of Oman. The OAP have a lower risk of joint complications, skin rash, and dsDNA antibodies than OGA (beta coefficient and 95% confidence interval [CI], -35.6, -16.4, and -2.31 and -38.05 to -33.06, -19.49 to -13.3, and -4.1 to -0.6, respectively). The OGA have higher levels of IgG isotype APL antibodies than OAP, both anticardiolipin (ACA) (t= 1.75, P= 1.04) and anti-beta2glycoprotein I (infinitybeta2GPI) (t=3.64, P=0.004) antibodies, while OAP have higher levels of ACAs, IgM isotype (t=2.86, P=0.0024), than OGA. Antiphospholipid (APL) antibodies associate differently with clinical symptoms, both within OAP and between OAP and OGA. Patients from Dakiliyah have a higher risk of joint disease than those from Muscat (relative risk ratio 5.0, 95% CI 1.3-18.3). Differences in symptomatology suggest variations in genetic linkages to human systemic lupus erythematosus.