Clinical implication of chronic paranasal sinusitis for the classification of microscopic polyangiitis.
Journal
International journal of clinical practice
ISSN: 1742-1241
Titre abrégé: Int J Clin Pract
Pays: India
ID NLM: 9712381
Informations de publication
Date de publication:
Jan 2020
Jan 2020
Historique:
received:
23
07
2019
revised:
22
09
2019
accepted:
28
09
2019
pubmed:
2
10
2019
medline:
26
8
2020
entrez:
2
10
2019
Statut:
ppublish
Résumé
Chronic paranasal sinusitis (CPS) has been known as a surrogate marker for granulomatosis with polyangiitis (GPA). We investigated whether CPS at diagnosis may have an influence on the classification and outcomes of microscopic polyangiitis (MPA). We retrospectively reviewed the medical records of 106 immunosuppressive drug-naïve patients with MPA. We compared variables at diagnosis of MPA patients with CPS with either MPA patients without CPS or 29 GPA patients with CPS. We applied the algorithm for antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) proposed by the European Medicine Agency to 22 MPA patients with CPS and reclassify them. Death, relapse and end-stage renal disease were assessed as the poor outcomes. Except for ENT manifestations, only pulmonary manifestation was more frequently observed in MPA patients with CPS than those without (77.3% vs 47.6%). No proteinase 3-ANCA was detected in all MPA patients with CPS. Meanwhile, general (63.6% vs 27.6%) and renal manifestations (81.8% vs 44.8%) more often developed in MPA patients with CPS than GPA patients with CPS. Of 22 MPA patients with CPS, 21 patients underwent biopsies. When CPS was not considered as a surrogate marker for GPA, all patients with CPS were reclassified as MPA. Ground glass opacity and reticulation on high-resolution computed tomography and renal vasculitis were helpful clues supporting the classification of MPA in patients with CPS. CPS at diagnosis was not associated with the outcomes of MPA. CPS might not be a sufficient surrogate marker for GPA in the classification of AAV.
Sections du résumé
BACKGROUND
BACKGROUND
Chronic paranasal sinusitis (CPS) has been known as a surrogate marker for granulomatosis with polyangiitis (GPA). We investigated whether CPS at diagnosis may have an influence on the classification and outcomes of microscopic polyangiitis (MPA).
METHODS
METHODS
We retrospectively reviewed the medical records of 106 immunosuppressive drug-naïve patients with MPA. We compared variables at diagnosis of MPA patients with CPS with either MPA patients without CPS or 29 GPA patients with CPS. We applied the algorithm for antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) proposed by the European Medicine Agency to 22 MPA patients with CPS and reclassify them. Death, relapse and end-stage renal disease were assessed as the poor outcomes.
RESULTS
RESULTS
Except for ENT manifestations, only pulmonary manifestation was more frequently observed in MPA patients with CPS than those without (77.3% vs 47.6%). No proteinase 3-ANCA was detected in all MPA patients with CPS. Meanwhile, general (63.6% vs 27.6%) and renal manifestations (81.8% vs 44.8%) more often developed in MPA patients with CPS than GPA patients with CPS. Of 22 MPA patients with CPS, 21 patients underwent biopsies. When CPS was not considered as a surrogate marker for GPA, all patients with CPS were reclassified as MPA. Ground glass opacity and reticulation on high-resolution computed tomography and renal vasculitis were helpful clues supporting the classification of MPA in patients with CPS. CPS at diagnosis was not associated with the outcomes of MPA.
CONCLUSION
CONCLUSIONS
CPS might not be a sufficient surrogate marker for GPA in the classification of AAV.
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e13431Subventions
Organisme : National Research Foundation of Korea
ID : 2017R1D1A1B03029050
Organisme : Korea Health Industry Development Institute
ID : HI14C1324
Pays : Republic of Korea
Informations de copyright
© 2019 John Wiley & Sons Ltd.
Références
Jennette JC, Falk RJ, Bacon PA, et al. 2012 revised international chapel hill consensus conference nomenclature of vasculitides. Arthritis Rheum. 2013;65:1-11.
Millet A, Pederzoli-Ribeil M, Guillevin L, Witko-Sarsat V, Mouthon L. Antineutrophil cytoplasmic antibody-associated vasculitides: is it time to split up the group? Ann Rheum Dis. 2013;72:1273-1279.
Furuta S, Chaudhry AN, Hamano Y, et al. Comparison of phenotype and outcome in microscopic polyangiitis between Europe and Japan. J Rheumatol. 2014;41:325-333.
Nagata T, Hara K, Oka T, et al. Microscopic polyangiitis associated with sinobronchial syndrome. Intern Med. 2001;40:544-547.
Kadowaki T, Yano S, Yamadori I, et al. A case of sinobronchial syndrome complicated with myeloperoxidase antineutrophil cytoplasmic antibody associated vasculitis: review of the literature. Intern Med. 2012;51:763-767.
Watts R, Lane S, Hanslik T, et al. Development and validation of a consensus methodology for the classification of the ANCA-associated vasculitides and polyarteritis nodosa for epidemiological studies. Ann Rheum Dis. 2007;66:222-227.
Mukhtyar C, Lee R, Brown D, et al. Modification and validation of the Birmingham Vasculitis Activity Score (version 3). Ann Rheum Dis. 2009;68:1827-1832.
Stone JH, Hoffman GS, Merkel PA, et al. A disease-specific activity index for Wegener's granulomatosis: modification of the Birmingham Vasculitis Activity Score. International Network for the Study of the Systemic Vasculitides (INSSYS). Arthritis Rheum. 2001;44:912-920.
Guillevin L, Pagnoux C, Seror R, Mahr A, Mouthon L, Toumelin PL. The Five-Factor Score revisited: assessment of prognoses of systemic necrotizing vasculitides based on the French Vasculitis Study Group (FVSG) cohort. Medicine. 2011;90:19-27.
Mukhtyar C, Hellmich B, Jayne D, Flossmann O, Luqmani R. Remission in antineutrophil cytoplasmic antibody-associated systemic vasculitis. Clin Exp Rheumatol. 2006;24:S-93-98.
Isa H, Luthert P, Rose G, et al. Tissue interleukin-17 and interleukin-23 as biomarkers for orbital granulomatosis with polyangiitis. Ophthalmology. 2015;122:2140-2142.
Wawrzecka A, Szymańska A, Jeleniewicz R, Szymański M. Granulomatosis with polyangiitis with bilateral facial palsy and severe mixed hearing loss. Case Rep Otolaryngol. 2016;2016:5206170.
Terrier B, Dechartres A, Girard C, et al. Granulomatosis with polyangiitis: endoscopic management of tracheobronchial stenosis: results from a multicentre experience. Rheumatology (Oxford). 2015;54:1852-1857.
Ezzat WH, Compton RA, Basa KC, Levi J. Reconstructive techniques for the saddle nose deformity in granulomatosis with polyangiitis: a systematic review. JAMA Otolaryngol Head Neck Surg. 2017;143:507-512.
Berden AE, Ferrario F, Hagen EC, et al. Histopathologic classification of ANCA-associated glomerulonephritis. J Am Soc Nephrol. 2010;21:1628-1636.
Yoo J, Ahn SS, Jung SM, Song JJ, Park YB, Lee SW. Should nasal biopsy inevitably be performed for classifying granulomatosis with polyangiitis in patients with rhinosinusitis? a retrospective chart review study. Rheumatol Int. 2019;39:885-892.
Suzuki A, Sakamoto S, Kurosaki A, et al. Chest high-resolution CT findings of microscopic polyangiitis: a Japanese first nationwide prospective cohort study. AJR Am J Roentgenol. 2019 [Epub ahead of print].
Yoo J, Kim HJ, Ahn SS, et al. The utility of the ACR/EULAR 2017 provisional classification criteria for granulomatosis with polyangiitis in Korean patients with antineutrophil cytoplasmic antibody-associated vasculitis. Clin Exp Rheumatol. 2018;36(Suppl 111):85-87.
Cornec D, Cornec-Le Gall E, Fervenza FC, Specks U. ANCA-associated vasculitis - clinical utility of using ANCA specificity to classify patients. Nat Rev Rheumatol. 2016;12:570-579.
Devaney KO, Travis WD, Hoffman G, Leavitt R, Lebovics R, Fauci AS. Interpretation of head and neck biopsies in Wegener's granulomatosis. A pathologic study of 126 biopsies in 70 patients. Am J Surg Pathol. 1990;14:555-564.
de Souza A, van Timmeren M, Sanders J-S, et al. M2 macrophage is the predominant phenotype in airways inflammatory lesions in patients with granulomatosis with polyangiitis. Arthritis Res Ther. 2017;19:100.