The Diagnostic Value of Alpha-1-Antitrypsin Phenotype in Patients with Granulomatosis with Polyangiitis
The deficiency of alpha-1 protease inhibitor, or alpha-1-antitrypsin (A1AT), predisposes to chronic lung diseases and extrapulmonary pathology. Besides classical manifestations, such as pulmonary emphysema and liver disease, alpha-1-antitrypsin deficiency (A1ATD) is also known to be associated with...
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| Veröffentlicht in: | International Journal of Rheumatology 2016-01, Vol.2016 (2016), p.75-79 |
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| creator | Surkova, E. A. Blinova, T. V. Belyaeva, I. B. Mazurov, V. I. Lapin, Sergey V. Titova, O. N. Emanuel, V. L. Pervakova, M. Y. Chudinov, A. L. |
| description | The deficiency of alpha-1 protease inhibitor, or alpha-1-antitrypsin (A1AT), predisposes to chronic lung diseases and extrapulmonary pathology. Besides classical manifestations, such as pulmonary emphysema and liver disease, alpha-1-antitrypsin deficiency (A1ATD) is also known to be associated with granulomatosis with polyangiitis (GPA or Wegener’s granulomatosis). The aim of our study was to evaluate the frequency of allelic isoforms of A1AT and their clinical significance among GPA patients. Detailed clinical information, including Birmingham Vasculitis Activity Score (BVAS), incidence of lung involvement, anti-proteinase 3 (PR3) antibodies concentrations, and other laboratory data were collected in 38 GPA patients. We also studied serum samples obtained from 46 healthy donors. In all collected samples A1AT phenotyping by isoelectrofocusing (IEF) and turbidimetric A1AT measurement were performed. Abnormal A1AT variants were found in 18.4% (7/38) of cases: 1 ZZ, 4 MZ, 2 MF, and only 1 MZ in control group (2%). The mean A1AT concentration in samples with atypical A1AT phenotypes was significantly lower (P=0.0038) than in normal A1AT phenotype. We found that patients with abnormal A1AT phenotypes had significantly higher vasculitis activity (BVAS) as well as anti-PR3 antibodies concentration. We conclude that A1AT deficiency should be considered in all patients with GPA. |
| doi_str_mv | 10.1155/2016/7831410 |
| format | Article |
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A. ; Blinova, T. V. ; Belyaeva, I. B. ; Mazurov, V. I. ; Lapin, Sergey V. ; Titova, O. N. ; Emanuel, V. L. ; Pervakova, M. Y. ; Chudinov, A. L.</creator><contributor>Burgos-Vargas, Ruben</contributor><creatorcontrib>Surkova, E. A. ; Blinova, T. V. ; Belyaeva, I. B. ; Mazurov, V. I. ; Lapin, Sergey V. ; Titova, O. N. ; Emanuel, V. L. ; Pervakova, M. Y. ; Chudinov, A. L. ; Burgos-Vargas, Ruben</creatorcontrib><description>The deficiency of alpha-1 protease inhibitor, or alpha-1-antitrypsin (A1AT), predisposes to chronic lung diseases and extrapulmonary pathology. Besides classical manifestations, such as pulmonary emphysema and liver disease, alpha-1-antitrypsin deficiency (A1ATD) is also known to be associated with granulomatosis with polyangiitis (GPA or Wegener’s granulomatosis). The aim of our study was to evaluate the frequency of allelic isoforms of A1AT and their clinical significance among GPA patients. Detailed clinical information, including Birmingham Vasculitis Activity Score (BVAS), incidence of lung involvement, anti-proteinase 3 (PR3) antibodies concentrations, and other laboratory data were collected in 38 GPA patients. We also studied serum samples obtained from 46 healthy donors. In all collected samples A1AT phenotyping by isoelectrofocusing (IEF) and turbidimetric A1AT measurement were performed. Abnormal A1AT variants were found in 18.4% (7/38) of cases: 1 ZZ, 4 MZ, 2 MF, and only 1 MZ in control group (2%). The mean A1AT concentration in samples with atypical A1AT phenotypes was significantly lower (P=0.0038) than in normal A1AT phenotype. We found that patients with abnormal A1AT phenotypes had significantly higher vasculitis activity (BVAS) as well as anti-PR3 antibodies concentration. We conclude that A1AT deficiency should be considered in all patients with GPA.</description><identifier>ISSN: 1687-9260</identifier><identifier>EISSN: 1687-9279</identifier><identifier>DOI: 10.1155/2016/7831410</identifier><identifier>PMID: 27127514</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Limiteds</publisher><subject>Alpha 1-antitrypsin ; Care and treatment ; Diagnosis ; Disease ; Genetic aspects ; Genotype & phenotype ; Immunoglobulins ; Inflammation ; Laboratories ; Lung diseases ; Neutrophils ; Patients ; Phenotype ; Wegener's granulomatosis</subject><ispartof>International Journal of Rheumatology, 2016-01, Vol.2016 (2016), p.75-79</ispartof><rights>Copyright © 2016 M. Y. Pervakova et al.</rights><rights>COPYRIGHT 2016 John Wiley & Sons, Inc.</rights><rights>Copyright © 2016 M. Y. Pervakova et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2016 M. Y. Pervakova et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-a636t-1be3d24e248b2085f3a46207a8e7ae5724035f2da0b224885df488f27087281d3</citedby><cites>FETCH-LOGICAL-a636t-1be3d24e248b2085f3a46207a8e7ae5724035f2da0b224885df488f27087281d3</cites><orcidid>0000-0002-4998-3699 ; 0000-0001-8367-3144 ; 0000-0003-4678-3904 ; 0000-0002-7675-5683 ; 0000-0003-4896-3319 ; 0000-0002-7981-6349 ; 0000-0001-5191-0221 ; 0000-0001-9630-257X ; 0000-0002-2079-0439</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4835640/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4835640/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27127514$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Burgos-Vargas, Ruben</contributor><creatorcontrib>Surkova, E. A.</creatorcontrib><creatorcontrib>Blinova, T. V.</creatorcontrib><creatorcontrib>Belyaeva, I. B.</creatorcontrib><creatorcontrib>Mazurov, V. I.</creatorcontrib><creatorcontrib>Lapin, Sergey V.</creatorcontrib><creatorcontrib>Titova, O. N.</creatorcontrib><creatorcontrib>Emanuel, V. L.</creatorcontrib><creatorcontrib>Pervakova, M. Y.</creatorcontrib><creatorcontrib>Chudinov, A. L.</creatorcontrib><title>The Diagnostic Value of Alpha-1-Antitrypsin Phenotype in Patients with Granulomatosis with Polyangiitis</title><title>International Journal of Rheumatology</title><addtitle>Int J Rheumatol</addtitle><description>The deficiency of alpha-1 protease inhibitor, or alpha-1-antitrypsin (A1AT), predisposes to chronic lung diseases and extrapulmonary pathology. Besides classical manifestations, such as pulmonary emphysema and liver disease, alpha-1-antitrypsin deficiency (A1ATD) is also known to be associated with granulomatosis with polyangiitis (GPA or Wegener’s granulomatosis). The aim of our study was to evaluate the frequency of allelic isoforms of A1AT and their clinical significance among GPA patients. Detailed clinical information, including Birmingham Vasculitis Activity Score (BVAS), incidence of lung involvement, anti-proteinase 3 (PR3) antibodies concentrations, and other laboratory data were collected in 38 GPA patients. We also studied serum samples obtained from 46 healthy donors. In all collected samples A1AT phenotyping by isoelectrofocusing (IEF) and turbidimetric A1AT measurement were performed. Abnormal A1AT variants were found in 18.4% (7/38) of cases: 1 ZZ, 4 MZ, 2 MF, and only 1 MZ in control group (2%). The mean A1AT concentration in samples with atypical A1AT phenotypes was significantly lower (P=0.0038) than in normal A1AT phenotype. We found that patients with abnormal A1AT phenotypes had significantly higher vasculitis activity (BVAS) as well as anti-PR3 antibodies concentration. We conclude that A1AT deficiency should be considered in all patients with GPA.</description><subject>Alpha 1-antitrypsin</subject><subject>Care and treatment</subject><subject>Diagnosis</subject><subject>Disease</subject><subject>Genetic aspects</subject><subject>Genotype & phenotype</subject><subject>Immunoglobulins</subject><subject>Inflammation</subject><subject>Laboratories</subject><subject>Lung diseases</subject><subject>Neutrophils</subject><subject>Patients</subject><subject>Phenotype</subject><subject>Wegener's granulomatosis</subject><issn>1687-9260</issn><issn>1687-9279</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkkFv0zAUgCMEYlPZjTOKhISQIJvtxLFzQarGGKBJ9DC4Wq-Jk3hy7RI7TP33e6GlXREHEimO7c-f7fdekryk5JxSzi8YoeWFkDktKHmSnNJSiqxionq6_y_JSXIWwh3Bh0kuC_I8OWGCMsFpcZp0t71OPxronA_R1OkPsKNOfZvO7bqHjGZzF00cNutgXLrotfNxs9bp1IFotIshvTexT68HcKP1K4g-mN3YwtsNuM6YaMKL5FkLNuizXTtLvn-6ur38nN18u_5yOb_JoMzLmNGlzhtWaFbIJSOStzkUJSMCpBaguWAFyXnLGiBLhozkTYvflgkiBZO0yWfJh613PS5XuqnxhANYtR7MCoaN8mDU8Ywzver8L1XInJdonyVvd4LB_xx1iGplQq2tBaf9GBQVkotCMsYRff0XeufHweH1JoqikVX5gerAamVc63HfepKqOcekCFqJCqnzf1D4Nnplau90a3D8aMGbRwt6DTb2wdsxGu_CMfh-C9aDD2HQ7T4YlKipiNRURGpXRIi_ehzAPfynZBB4twV64xq4N_-p08joFg40JWX1W_d1C4AZsFAOIVygh1PMMkHx5KRsagQRmG3CquOO4Arv-gDA4enT</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Surkova, E. 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A.</au><au>Blinova, T. V.</au><au>Belyaeva, I. B.</au><au>Mazurov, V. I.</au><au>Lapin, Sergey V.</au><au>Titova, O. N.</au><au>Emanuel, V. L.</au><au>Pervakova, M. Y.</au><au>Chudinov, A. L.</au><au>Burgos-Vargas, Ruben</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Diagnostic Value of Alpha-1-Antitrypsin Phenotype in Patients with Granulomatosis with Polyangiitis</atitle><jtitle>International Journal of Rheumatology</jtitle><addtitle>Int J Rheumatol</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>2016</volume><issue>2016</issue><spage>75</spage><epage>79</epage><pages>75-79</pages><issn>1687-9260</issn><eissn>1687-9279</eissn><abstract>The deficiency of alpha-1 protease inhibitor, or alpha-1-antitrypsin (A1AT), predisposes to chronic lung diseases and extrapulmonary pathology. Besides classical manifestations, such as pulmonary emphysema and liver disease, alpha-1-antitrypsin deficiency (A1ATD) is also known to be associated with granulomatosis with polyangiitis (GPA or Wegener’s granulomatosis). The aim of our study was to evaluate the frequency of allelic isoforms of A1AT and their clinical significance among GPA patients. Detailed clinical information, including Birmingham Vasculitis Activity Score (BVAS), incidence of lung involvement, anti-proteinase 3 (PR3) antibodies concentrations, and other laboratory data were collected in 38 GPA patients. We also studied serum samples obtained from 46 healthy donors. In all collected samples A1AT phenotyping by isoelectrofocusing (IEF) and turbidimetric A1AT measurement were performed. Abnormal A1AT variants were found in 18.4% (7/38) of cases: 1 ZZ, 4 MZ, 2 MF, and only 1 MZ in control group (2%). The mean A1AT concentration in samples with atypical A1AT phenotypes was significantly lower (P=0.0038) than in normal A1AT phenotype. We found that patients with abnormal A1AT phenotypes had significantly higher vasculitis activity (BVAS) as well as anti-PR3 antibodies concentration. 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| subjects | Alpha 1-antitrypsin Care and treatment Diagnosis Disease Genetic aspects Genotype & phenotype Immunoglobulins Inflammation Laboratories Lung diseases Neutrophils Patients Phenotype Wegener's granulomatosis |
| title | The Diagnostic Value of Alpha-1-Antitrypsin Phenotype in Patients with Granulomatosis with Polyangiitis |
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