Systemic lupus erythematosus (SLE) is an autoimmune disease, non-specific to any organ, characterised by the production of a high variety of autoantibodies, some of which have a direct pathogenic role [1] [2] . Hormonal factors, environmental and genetics factors intervened in the physiopathology [3] . Clinically, SLE is characterised by its polymorphism. We have more and more data on SLE in sub-Saharan Africa [4] - [7] on black subject more specifically particular [3] . Many workers from English or French speaking black Africa have reported the frequency of different clinical and biological manifestations of lupus [3] - [7] .

In Ivory Coast, the study realised by Daboiko [4] in 2004 had mostly described epidemio-clinical aspects of SLE on black subject; our work is coming in addition to complete. It aims to describe autoantibodies profile in SLE on black African subject in Abidjan.

It was a descriptive and retrospective study, carried out on a retrospective setup over 27 years from 1987 to December 2014 the rheumatology department’s record. The following criteria were considered for the patients: should have consulted or have been hospitalized in the rheumatology department during the study period; the SLE diagnostic have been retained in front of at list 4 criteria of ACR. The patient’s age at the diagnostic period matches to the age where the patient respond to ACR criteria’s. For each patient, a form was design, which included clinical manifestations of the disease, blood numeration formula, sedimentation rate, C-reactive protein, and the 24 hours proteinuria.

Immunological investigations had anti-nuclear autoantibodies factors in all the cases; anti-DNA autoantibodies research and anti ENA (anti-Sm, anti-URN-P, anti SSA, anti SSB, Anti Scl 70); and anticardiolipins, rheumatoid factors, and anti-CCP. Immunological samples (ANA, Anti ENA, Anti CCP, Antiphospholipid) were all routed in France (Cerba laboratory) for analysis.

Antinuclear autoantibodies (AAN) were researched using indirect immunofluorescence technic. Anti-DNA native autoantibodies (anti-Sm, anti-SS-A, anti-SS-B and anti-RNP); and antiphospholipids autoantibodies (anticardiolipine: acL) have been researched by ELISA technic.

This investigation was approved by the local Ethics Committee.

The review of literature series only acted as a reference. Clinical signs have not been reported in the same conditions in all the series, the prevalence of a clinical manifestation changes according to whether it was considered at the moment of the diagnosis only; or during the patients monitoring, and the immunological tests have not been realised in the same conditions and with the same technics. In our case, the cost and accessibility of immunological tests (ANA, Anti ENA, Anti CCP, Antiphospholipid) constituted a barrier to diagnosis, immunological samples were all routed in France (Cerba laboratory) for analysis. All these factors may influence the prevalence of various signs and their variability from one series to another.

As Daboiko reported [4] in his sample of 49 lupic in Abidjan, the average age and the population reported in our study, did not have particularities. The clinical predominance is classic [1] - [3] , in fact the SLE is a young woman pathology [1] - [4] . The average age of onset was 35.76 years old. This predominance is less pronounced at the bounding ages, this confirms the hypothesis of endocrine factors implication in the disease ethiopathogeny [1] .

Our study confirms the clinical polymorphism of SLE in Abidjan and its high similitude with other regions of Africa (Table 3).

Clinical manifestations generally associated cutaneo-articular damages, kidneys, cardiovascular, pleuropulmonary and neurologic damages, with some differences according to the country studied (Table 3).

Ig aCL^*: Ig anticardiolipin.

In our study, articular manifestations were at the first considered, followed by general manifestations and cutaneous damages common for Cameroonian series [7] , Moroccan [8] and Tunisian [9] , however for Senegalese series [6] and Gabonese [5] , cutaneous damages were most frequently followed by articular damages.

Articular damages inaugurate the disease in 50% of cases [1] [2] . Arthralgia are frequent (53% in our series), they are often coming with myalgia. Arthritis realise habitually a bilateral and symmetric polyarthritis.

Cutaneous damage’s prevalence varies between 32% and 72% [10] [11] . Butterfly rash, SLE characteristic has been noticed on 43.59% of cases in our series.

Kidney damages are the second causes mortality of SLE. Its frequency varies depending on the series between 13% and 73% [1] [2] [9] [12] [13] . In our study it was 40.17%. It was consistenly less elevated in Gabonese series (16.2%) and Cameroonian (17.9%). Glomerular damage is the characteristic lesion, it manifest by a frank proteinuria [2] .

Neurological damages constitute the third cause of SLE mortality after infectious complications and kidney damage [2] .

Neuropsychiatric manifestations have a variable frequency of 30% to 60% according to series [14] [15] . It was of 36.75% in our study.

Cardiac manifestations interest the tree heart tunics with a predilection for pericardia [2] . Pericarditis has been reported on 22.22% of the cases in our study.

Pleurisy, reported on 11.97% of cases in our series is the most common pulmonary manifestation during SLE [1] [2] . Its frequency varies in literature from 10% up to 52% [2] [9] [13] [16] .

In our countries with high tuberculosis endemicity, it is more often considered like tuberculosis and cured like it. In ours ample, interstitial pneumopathy was the most frequent of pulmonary damages.

The biological anomalies found in our sample are similar to literature data [5] - [7] .

An anaemia is habitual, and most often inflammatory [1] - [3] [5] - [7] [9] . It reveals sometimes the SLE. Its frequency varies in literature from 8% up to 67% [2] [10] [17] . It was the haematological perturbation most frequently seen in our study (86.32%). This high frequency of anaemia also constitutes one of the black subject particularities [3] . Indeed, during compared studies of SLE realised by Petri [17] between black and white Americans subjects, it has been proved a high anaemia frequency on the black American subject.

On the other hand, haemolytic anaemia, SLE characteristic is rare [9] [12] [16] .

Leukopenia frequency varies according to series from 18% up to 83% [1] [2] [16] - [18] . It was slightly elevated (15.38%) in our study. Our frequency was sensibly equal to that of Senegal one [6] , however it was most highest (56%) in Douala’s study in Cameroon [7] . The leukopenia is frequent on the black subject [3] - [20] .

Thrombocytopenia’s frequency varies from 10% up to 26% in the literature [9] [12] [20] , it is 13.67% in our sample. Idem for Senegal [6] and Cameroon [7] , it can be associated to haemolytic anaemia (Evans’ syndrome).

In unanimous way, ANA are quasi-constant in SLE, in fact, antinuclear autoantibodies are positives in most in 90% of the time in African studies: 92% in Tunisia [9] , 95% in Morocco [8] , 100% at Gabon [5] ; 97.8% in Senegal [6] , 94.2% in our study.

Cameroon alone had a rate below 90% (86.1%). These high rates are the same found in American and European studies (99% on North-American [21] ; 96% in European study [12] and Brazilian [22] .

Detection of anti DNA native autoantibodies in our study was 73.53%. This frequency was similar to the one observed in Africa (Tunisia [9] , Morocco [8] , Cameroon [7] ) and North America [21] and in Europe [12] but it was clearly far high than Gabonese study [5] or Senegalese [6] where Anti-DNA natives, haven’t been positives on respectively 63.8% and 45.7% of cases. This can be explained by the variable sensitivity of the different research technics indeed the anti-DNA natives frequency vary from 35% up to 98% depending on series and technics used [1] [2] [10] [13] [23] - [25] .

Elevated rates of anti-DNA native’s autoantibodies are specific from SLE. The anti-DNA native’s autoantibodies rate is correlated to a serious kidney damage existence, and to the Systemic Lupus Erythematous evolution [26] .

Extractable nuclear anti-antigens autoantibodies frequency during SLE, also varies depending on the sensibility of the methods used, depending on series and sometimes depending on ethnic origin [2] .

Anti-Sm autoantibodies are exclusively present on lupic patients.

Their incidence varies from 12% up to 52% [2] [13] [23] [24] [27] [28] . The anti-Sm’s sensibility is particularly elevated on black subjects, in order of 50% [3] - [9] [19] [20] , compared to the Caucasian population, where anti-Sm are found on only 10% to 20% of SLE cases [12] . This has been confirmed in the Senegalese series [7] and in ours, where the anti-SM frequency was elevated respectively in 65.2% and 75% of cases respectively. However, it was clearly lower in the Gabonese series (33.33%) [5] . This low frequency could be explained by the realisation technics. ELISA technic is actually the reference method [2] .

Anti-RNP was present in all our patients (100%) versus 66% in the Tunisian series [9] and 78.3% at Senegal [6] . Anti-ribonucléoproteins autoantibodies (anti-RNP) can been observed on 20% to 30% of lupus, but are not specific to Systemic lupus erythematous [29] . However, it has been showed a more high frequency of anti- RNP on the black African [3] . Indeed, during compared studies of clinical and biological manifestations between black Africans and Caucasians living in Europe [30] or in South Africa [31] , it has been found on black Africans higher frequency of anti-RNP, in addition to myalgia, seritis and kidney insufficiency.

Anti-SS-A autoantibodies have a high predictive value for SLE diagnosis among the patients tested positive on AAN, but negatives on anti-DNA native autoantibodies or Anti Sm [1] [2] . Indeed, in Simmons O’Brien et al.’s study [32] , he found that 47% of patients with kidney damage had anti-SS-A autoantibodies but not anti- DNA native autoantibodies. Patients with anti-SS-A autoantibodies have to be regularly followed to detect the onset of systemic manifestations [32] . Anti-SSA frequency varies during SLE from 20% to 60% according to series [2] [9] [12] [13] , in our study, the frequency was high (75%).

Anti-SSB autoantibodies, are particularly frequent in primitive Sjogren’ syndrome (60% to 80%) while their frequency in SLE is variable according to series, to 5% up to 35% [1] [12] [13] [33] . Their frequency was slightly higher (56.25%) in our study. The elevated frequency of anti SSA and SSB could also be a SLE particularity in black subjects [3] .

Antiphospholipids frequencies during SLE varies according to series from 17% up to 87% [1] [2] [9] [12] [13] . It was 37.50% in our study. It was higher in Tunisian [9] , Senegalese [6] and Cameroonian [7] studies respectively 45% and 50% of cases.

This study shows an increase in SLE in Ivory Coast and a better knowledge of the clinical and immunological profile by the amelioration of the technical expertise and the growing augmentation of rheumatologists.

Our study confirms the SLE clinical polymorphism on one hand, and on the other hand reveals that the lupic serology of black subjects is rich with the existence of multiple types of antinuclear autoantibodies simultaneously (Anti-DNA, Anti-Sm, Anti-RNP, Anti-SSA, Anti-SSB).

Authors have no conflicts of interest to declare.