María José Soto-Cárdenas1, Myriam Gandía1, Pilar Brito-Zerón1, Maria Teresa Arias1, Noelia Armiger1, Albert Bové1, Xavier Bosch1, Soledad Retamozo1, Miriam Akasbi1, Marta Pérez-De-Lis1, Hoda Gueitasi1, Belchin Kostov1, Roberto Pérez-Alvarez1, Antoni Siso-Almirall1, Francisco Lozano1, Manuel Ramos-Casals2. 1. From the Sjögren Syndrome Research Group (AGAUR), Laboratory of Autoimmune Diseases Josep Font, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS); Department of Autoimmune Diseases, Department of Internal Medicine, Instituto Clínic de Medicina y Dermatología, Immunology Department, Hospital Clínic; Primary Care Research Group, Centre d'Assistència Primària ABS Les Corts, GESCLINIC; Department of Cell Biology, Immunology and Neurosciences, School of Medicine, University of Barcelona, Barcelona; Group of Immunoreceptors, Department of Internal Medicine, Hospital Infanta Leonor, Madrid; Department of Internal Medicine, Hospital do Meixoeiro, Vigo; Department of Internal Medicine, University of Cadiz, Hospital Puerta del Mar, Cádiz, Spain.M.J. Soto-Cárdenas, MD, PhD; M. Gandía, MD, PhD, AGAUR, Laboratory of Autoimmune Diseases Josep Font, IDIBAPS, Department of Autoimmune Diseases, and the Department of Internal Medicine, University of Cadiz, Hospital Puerta del Mar; P. Brito-Zerón, MD, PhD; A. Bové, MD, PhD; S. Retamozo, MD; H. Gueitasi, MD; M. Ramos-Casals, MD, PhD, AGAUR, Laboratory of Autoimmune Diseases Josep Font, IDIBAPS, Department of Autoimmune Diseases; M.T. Arias, BSc, Immunology Department, Hospital Clínic; N. Armiger, BSc, Group of Immunoreceptors, IDIBAPS; X. Bosch, MD, PhD, Department of Internal Medicine, Instituto Clínic de Medicina y Dermatología; M. Akasbi, MD, PhD, Department of Internal Medicine, Hospital Infanta Leonor; M. Pérez-De-Lis, MD, PhD; R. Pérez-Alvarez, MD, PhD, Department of Internal Medicine, Hospital do Meixoeiro; B. Kostov, MSC; A. Siso-Almirall, MD, PhD, Primary Care Research Group, IDIBAPS, Centre d'Assistència Primària ABS Les Corts, GESCLINIC; F. Lozano, MD, PhD, Immunology Department, Hospital Clínic, Barcelona, and the Group of Immunoreceptors, IDIBAPS, and the Department of Cell Biology, Immunology and Neurosciences, School of Medicine, University of Barcelona. 2. From the Sjögren Syndrome Research Group (AGAUR), Laboratory of Autoimmune Diseases Josep Font, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS); Department of Autoimmune Diseases, Department of Internal Medicine, Instituto Clínic de Medicina y Dermatología, Immunology Department, Hospital Clínic; Primary Care Research Group, Centre d'Assistència Primària ABS Les Corts, GESCLINIC; Department of Cell Biology, Immunology and Neurosciences, School of Medicine, University of Barcelona, Barcelona; Group of Immunoreceptors, Department of Internal Medicine, Hospital Infanta Leonor, Madrid; Department of Internal Medicine, Hospital do Meixoeiro, Vigo; Department of Internal Medicine, University of Cadiz, Hospital Puerta del Mar, Cádiz, Spain.M.J. Soto-Cárdenas, MD, PhD; M. Gandía, MD, PhD, AGAUR, Laboratory of Autoimmune Diseases Josep Font, IDIBAPS, Department of Autoimmune Diseases, and the Department of Internal Medicine, University of Cadiz, Hospital Puerta del Mar; P. Brito-Zerón, MD, PhD; A. Bové, MD, PhD; S. Retamozo, MD; H. Gueitasi, MD; M. Ramos-Casals, MD, PhD, AGAUR, Laboratory of Autoimmune Diseases Josep Font, IDIBAPS, Department of Autoimmune Diseases; M.T. Arias, BSc, Immunology Department, Hospital Clínic; N. Armiger, BSc, Group of Immunoreceptors, IDIBAPS; X. Bosch, MD, PhD, Department of Internal Medicine, Instituto Clínic de Medicina y Dermatología; M. Akasbi, MD, PhD, Department of Internal Medicine, Hospital Infanta Leonor; M. Pérez-De-Lis, MD, PhD; R. Pérez-Alvarez, MD, PhD, Department of Internal Medicine, Hospital do Meixoeiro; B. Kostov, MSC; A. Siso-Almirall, MD, PhD, Primary Care Research Group, IDIBAPS, Centre d'Assistència Primària ABS Les Corts, GESCLINIC; F. Lozano, MD, PhD, Immunology Department, Hospital Clínic, Barcelona, and the Group of Immunoreceptors, IDIBAPS, and the Department of Cell Biology, Immunology and Neurosciences, School of Medicine, University of Barcelona. mramos@clinic.ub.es.
Abstract
OBJECTIVE: To analyze the etiopathogenic role of genetic polymorphisms and serum levels of surfactant protein-D (SP-D) in primary Sjögren syndrome (pSS). METHODS: We analyzed 210 consecutive patients with pSS. SFTPD genotyping (M11T polymorphism rs721917) was analyzed by sequence-based typing and serum SP-D by ELISA. RESULTS: Thirty-two patients (15%) had the Thr11/Thr11 genotype, 80 (38%) the Met11/Met11 genotype, and 96 (46%) the Met11/Thr11 genotype; 2 patients could not be genotyped. Patients carrying the Thr11/Thr11 genotype had a higher prevalence of renal involvement (13% vs 1% and 4% in comparison with patients carrying the other genotypes, p = 0.014). Serum SP-D levels were analyzed in 119 patients (mean 733.94 ± 49.88 ng/ml). No significant association was found between serum SP-D levels and the SP-D genotypes. Higher mean values of serum SP-D were observed in patients with severe scintigraphic involvement (851.10 ± 685.69 vs 636.07 ± 315.93 ng/ml, p = 0.038), interstitial pulmonary disease (1053.60 ± 852.03 vs 700.36 ± 479.33 ng/ml, p = 0.029), renal involvement (1880.64 ± 1842.79 vs 716.42 ± 488.01 ng/ml, p = 0.002), leukopenia (899.83 ± 661.71 vs 673.13 ± 465.88 ng/ml, p = 0.038), positive anti-Ro/SS-A (927.26 ± 731.29 vs 642.75 ± 377.23 ng/ml, p = 0.006), and positive anti-La/SS-B (933.28 ± 689.63 vs 650.41 ± 428.14 ng/ml, p = 0.007), while lower mean values of serum SP-D were observed in patients with bronchiectasis (489.49 vs 788.81 ng/ml, p = 0.019). CONCLUSION: In pSS, high SP-D levels were found in patients with severe glandular involvement, hypergammaglobulinemia, leukopenia, extraglandular manifestations, and positive anti-Ro/La antibodies. The specific association between SP-D levels and pulmonary and renal involvements may have pathophysiological implications.
OBJECTIVE: To analyze the etiopathogenic role of genetic polymorphisms and serum levels of surfactant protein-D (SP-D) in primary Sjögren syndrome (pSS). METHODS: We analyzed 210 consecutive patients with pSS. SFTPD genotyping (M11T polymorphism rs721917) was analyzed by sequence-based typing and serum SP-D by ELISA. RESULTS: Thirty-two patients (15%) had the Thr11/Thr11 genotype, 80 (38%) the Met11/Met11 genotype, and 96 (46%) the Met11/Thr11 genotype; 2 patients could not be genotyped. Patients carrying the Thr11/Thr11 genotype had a higher prevalence of renal involvement (13% vs 1% and 4% in comparison with patients carrying the other genotypes, p = 0.014). Serum SP-D levels were analyzed in 119 patients (mean 733.94 ± 49.88 ng/ml). No significant association was found between serum SP-D levels and the SP-D genotypes. Higher mean values of serum SP-D were observed in patients with severe scintigraphic involvement (851.10 ± 685.69 vs 636.07 ± 315.93 ng/ml, p = 0.038), interstitial pulmonary disease (1053.60 ± 852.03 vs 700.36 ± 479.33 ng/ml, p = 0.029), renal involvement (1880.64 ± 1842.79 vs 716.42 ± 488.01 ng/ml, p = 0.002), leukopenia (899.83 ± 661.71 vs 673.13 ± 465.88 ng/ml, p = 0.038), positive anti-Ro/SS-A (927.26 ± 731.29 vs 642.75 ± 377.23 ng/ml, p = 0.006), and positive anti-La/SS-B (933.28 ± 689.63 vs 650.41 ± 428.14 ng/ml, p = 0.007), while lower mean values of serum SP-D were observed in patients with bronchiectasis (489.49 vs 788.81 ng/ml, p = 0.019). CONCLUSION: In pSS, high SP-D levels were found in patients with severe glandular involvement, hypergammaglobulinemia, leukopenia, extraglandular manifestations, and positive anti-Ro/La antibodies. The specific association between SP-D levels and pulmonary and renal involvements may have pathophysiological implications.
Authors: Sergi Casadó-Llombart; Hoda Gheitasi; Silvia Ariño; Marta Consuegra-Fernández; Noelia Armiger-Borràs; Belchin Kostov; Manuel Ramos-Casals; Pilar Brito-Zerón; Francisco Lozano Journal: Front Med (Lausanne) Date: 2022-03-18