Revue medicale de Bruxelles · 2016
[Non-identified antinuclear antibodies in systemic sclerosis].
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Margot A, Smet J, Soyfoo S
Аннотация
INTRODUCTION: Systemic sclerosis is a rare auto immune disease characterized by a local or diffuse skin condition and a variable visceral impairment. Anti nuclear antibodies (ANA) can be found in 95 % of patients. The most frequent are the anti topoisomerase 1 or anti Scl 70 and the anti-centromeres. Other antibodies have been reported but they are not conventionally sought in clinical practice. They are referred to as " non identified " ANA.
OBJECTIVE: To seek the " non identified " antibodies in patients with scleroderma at Erasme Hospital, to assess their prevalence in this cohort and to correlate their presence with the clinical characteristics.
METHODS: 89 patients out of the cohort of Erasme hospital patients with scleroderma have been looked at. Their clinical and biological data have been identified and a detection of antibodies have been performed by first an immonudot technique and second an EliA technique.
RESULTS: 17 out of the 89 patients of our cohort had " non identified " ANA. Among them, antibodies in 11 patients have been identified by the immunodot, among which 7 anti-PmScl 75 and/or 100,3 RNA polymerase III and 1 antifibrillarin. The EliA technique identif ied antibodies in 10 patients among which 5 anti- PmScl, 2 anti RNA polymerase, 2 anti-fibrillarin and 1 anti-centromere.
CONCLUSION: Auto antibodies other than the antitopoisomerase and anti-centromere have been found in patients with scleroderma in our cohort. Certain links exist between the presence of a given antibody and clinical features. We still have to define whether there exist other auto antibodies of which we still are unaware since in some patient no antibodies were detected.
OBJECTIVE: To seek the " non identified " antibodies in patients with scleroderma at Erasme Hospital, to assess their prevalence in this cohort and to correlate their presence with the clinical characteristics.
METHODS: 89 patients out of the cohort of Erasme hospital patients with scleroderma have been looked at. Their clinical and biological data have been identified and a detection of antibodies have been performed by first an immonudot technique and second an EliA technique.
RESULTS: 17 out of the 89 patients of our cohort had " non identified " ANA. Among them, antibodies in 11 patients have been identified by the immunodot, among which 7 anti-PmScl 75 and/or 100,3 RNA polymerase III and 1 antifibrillarin. The EliA technique identif ied antibodies in 10 patients among which 5 anti- PmScl, 2 anti RNA polymerase, 2 anti-fibrillarin and 1 anti-centromere.
CONCLUSION: Auto antibodies other than the antitopoisomerase and anti-centromere have been found in patients with scleroderma in our cohort. Certain links exist between the presence of a given antibody and clinical features. We still have to define whether there exist other auto antibodies of which we still are unaware since in some patient no antibodies were detected.