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Spontaneous Chromosome Damage (Micronuclei) in Systemic Sclerosis and Raynaud's Phenomenon
GIOVANNI PORCIELLO, ROBERTO SCARPATO, CLODOVEO FERRI, FRANCA STORINO, FRANCESCA CAGETTI, GABRIELLA MOROZZI, FRANCESCA BELLISAI, LUCIA MIGLIORE, ROBERTO MARCOLONGO, and MAURO GALEAZZI
ABSTRACT. Objective. To evaluate the prevalence of spontaneous chromosome damage in cultured peripheral lymphocytes of patients with systemic sclerosis (SSc), idiopathic Raynaud's phenomenon (RP), and suspected secondary RP, by means of molecular cytogenetic analysis. Methods. We studied 43 patients with SSc, 13 with idiopathic RP, and 16 with suspected secondary RP and 25 healthy controls. As a marker of chromosome alteration we used the micronucleus (MN) assay. All subjects were also classified for antinuclear antibodies, anticentromere antibodies (ACA), or Scl70. To identify the mechanism of MN formation, we also performed MN fluorescence in situ hybridization (FISH) analysis using a pancentromeric DNA probe. Results. Patients with SSc and subjects with RP showed significantly higher MN frequencies than controls (25.9 ± 1.7 and 19.1 ± 2.15, respectively, vs 9.4 ± 2.2; p < 0.001). Subjects with suspected secondary RP displayed MN frequency (23.5 ± 2.7) comparable to that of SSc patients, while spontaneous MN level in idiopathic RP subjects (13.6 ± 3.0) did not differ significantly from controls (9.4 ± 2.2). ACA positive subjects showed the highest MN frequencies (32.8 ± 1.7) compared to subjects with a different antibody pattern (18.3 ± 1.6). Conclusion. Our results show the presence of higher levels of micronuclei in circulating lymphocytes of patients with SSc and subjects with suspected secondary RP. They also suggest a possible role of ACA in determining cytogenetic anomalies. FISH analysis indicated that both aneuploidogenic and clastogenic events contributed to the formation of MN observed in SSc patients and subjects with suspected secondary RP. (J Rheumatol 2003;30:1244-7) Key Indexing Terms:
SYSTEMIC SCLEROSIS From the Istituto di Reumatologia, University of Siena, Siena; Istituto di Reumatologia, University of Pisa; and Dipartimento di Scienze dell'Uomo e dell'Ambiente, University of Pisa, Pisa, Italy. G. Porciello, MD; G. Morozzi, PhD; F. Bellisai, MD, Istituto di Reumatologia; R. Marcolongo, MD, Professor of Rheumatology; M. Galeazzi, MD, Associate Professor of Rheumatology, University of Siena; R. Scarpato, PhD; F. Cagetti, PhD; L. Migliore, MD, Associate Professor, Dipartimento Scienze dell'Uomo e dell'Ambiente, University of Pisa; C. Ferri, MD, Associate Professor of Rheumatogy; F. Storino, MD, Istituto di Reumatologia, University of Pisa. Address reprint requests to Dr. G. Porciello, Istituto di Reumatologia – Policlinico Le Scotte Viale Bracci, 53100 Siena, Italy. E-mail: g.porciello@katamail.com Submitted May 21, 2002; revision accepted November 20, 2002. |