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Changes in Lipids in Granulomatosis with Polyangiitis Relates to Glucocorticoids and History of Hypertension

Granulomatosis with polyangiitis (GPA) is an ANCA-associated small-vessel vasculitis. Vessel wall inflammation induces multiple vascular damages, leading to accelerated atherosclerosis. Metabolic profile and cardiovascular risk are somewhat understood in GPA patients. Cardiovascular atherosclerotic...

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Autores principales: Marozzi, Marialuisa Sveva, Vacca, Antonio, Desantis, Vanessa, Panebianco, Teresa, Catena, Cristiana, Brosolo, Gabriele, Noviello, Silvia, Cirulli, Anna, Solimando, Antonio Giovanni, Sechi, Leonardo Alberto, Cicco, Sebastiano, Ria, Roberto
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10608943/
https://www.ncbi.nlm.nih.gov/pubmed/37887378
http://dx.doi.org/10.3390/metabo13101053
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author Marozzi, Marialuisa Sveva
Vacca, Antonio
Desantis, Vanessa
Panebianco, Teresa
Catena, Cristiana
Brosolo, Gabriele
Noviello, Silvia
Cirulli, Anna
Solimando, Antonio Giovanni
Sechi, Leonardo Alberto
Cicco, Sebastiano
Ria, Roberto
author_facet Marozzi, Marialuisa Sveva
Vacca, Antonio
Desantis, Vanessa
Panebianco, Teresa
Catena, Cristiana
Brosolo, Gabriele
Noviello, Silvia
Cirulli, Anna
Solimando, Antonio Giovanni
Sechi, Leonardo Alberto
Cicco, Sebastiano
Ria, Roberto
author_sort Marozzi, Marialuisa Sveva
collection PubMed
description Granulomatosis with polyangiitis (GPA) is an ANCA-associated small-vessel vasculitis. Vessel wall inflammation induces multiple vascular damages, leading to accelerated atherosclerosis. Metabolic profile and cardiovascular risk are somewhat understood in GPA patients. Cardiovascular atherosclerotic disease (ASCVD) may represent a risk for outcomes. Our purpose is to evaluate ASCVD risk in GPA patients. Thirty-six patients received GPA diagnosis (T0) and were evaluated after 1 (T1) and 2 (T2) years follow-up. All patients were treated with high-dose glucocorticoid, one-year tapered, along with immunosuppressants. Total cholesterol significantly increased in T1 vs. T0 and T2. LDL exhibited the same trend, while triglycerides increased in both T1 and T2 vs. T0. No difference was found in HDL. A significant hsCRP decrease was detected at T1 and T2 vs. T0, but not between T2 and T1. Moreover, we found a significant reduction in ESR at T2 compared with T1 and T0 and at T1 compared to T0. Hypertensive patients presented a pronounced increase in lipids, while inflammation reduced slowly compared to normotensives. Our data suggest that the increase in cholesterol and LDL in T1 is a consequence of glucocorticoids. These data can be useful in the evaluation of both CV diseases and lipid metabolism, which are closely related to vessel inflammation.
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spelling pubmed-106089432023-10-28 Changes in Lipids in Granulomatosis with Polyangiitis Relates to Glucocorticoids and History of Hypertension Marozzi, Marialuisa Sveva Vacca, Antonio Desantis, Vanessa Panebianco, Teresa Catena, Cristiana Brosolo, Gabriele Noviello, Silvia Cirulli, Anna Solimando, Antonio Giovanni Sechi, Leonardo Alberto Cicco, Sebastiano Ria, Roberto Metabolites Article Granulomatosis with polyangiitis (GPA) is an ANCA-associated small-vessel vasculitis. Vessel wall inflammation induces multiple vascular damages, leading to accelerated atherosclerosis. Metabolic profile and cardiovascular risk are somewhat understood in GPA patients. Cardiovascular atherosclerotic disease (ASCVD) may represent a risk for outcomes. Our purpose is to evaluate ASCVD risk in GPA patients. Thirty-six patients received GPA diagnosis (T0) and were evaluated after 1 (T1) and 2 (T2) years follow-up. All patients were treated with high-dose glucocorticoid, one-year tapered, along with immunosuppressants. Total cholesterol significantly increased in T1 vs. T0 and T2. LDL exhibited the same trend, while triglycerides increased in both T1 and T2 vs. T0. No difference was found in HDL. A significant hsCRP decrease was detected at T1 and T2 vs. T0, but not between T2 and T1. Moreover, we found a significant reduction in ESR at T2 compared with T1 and T0 and at T1 compared to T0. Hypertensive patients presented a pronounced increase in lipids, while inflammation reduced slowly compared to normotensives. Our data suggest that the increase in cholesterol and LDL in T1 is a consequence of glucocorticoids. These data can be useful in the evaluation of both CV diseases and lipid metabolism, which are closely related to vessel inflammation. MDPI 2023-10-06 /pmc/articles/PMC10608943/ /pubmed/37887378 http://dx.doi.org/10.3390/metabo13101053 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Marozzi, Marialuisa Sveva
Vacca, Antonio
Desantis, Vanessa
Panebianco, Teresa
Catena, Cristiana
Brosolo, Gabriele
Noviello, Silvia
Cirulli, Anna
Solimando, Antonio Giovanni
Sechi, Leonardo Alberto
Cicco, Sebastiano
Ria, Roberto
Changes in Lipids in Granulomatosis with Polyangiitis Relates to Glucocorticoids and History of Hypertension
title Changes in Lipids in Granulomatosis with Polyangiitis Relates to Glucocorticoids and History of Hypertension
title_full Changes in Lipids in Granulomatosis with Polyangiitis Relates to Glucocorticoids and History of Hypertension
title_fullStr Changes in Lipids in Granulomatosis with Polyangiitis Relates to Glucocorticoids and History of Hypertension
title_full_unstemmed Changes in Lipids in Granulomatosis with Polyangiitis Relates to Glucocorticoids and History of Hypertension
title_short Changes in Lipids in Granulomatosis with Polyangiitis Relates to Glucocorticoids and History of Hypertension
title_sort changes in lipids in granulomatosis with polyangiitis relates to glucocorticoids and history of hypertension
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10608943/
https://www.ncbi.nlm.nih.gov/pubmed/37887378
http://dx.doi.org/10.3390/metabo13101053
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