Metabolic Profile of Vasculitis and Arterial Hypertension

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Lipid Metabolism".

Deadline for manuscript submissions: closed (20 March 2024) | Viewed by 1867

Special Issue Editor


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Guest Editor
Unit of Internal Medicine “G. Baccelli” and Unit of Arterial Hypertension “A. Pirrelli”, AUOC Policlinico di Bari University Hospital, Aldo Moro University of Bari, 70121 Bari, Italy
Interests: cardiovascular disease; vasculitis; immune pathways; arterial hypertension; echocardiography

Special Issue Information

Dear Colleagues,

This Special Issue of Metabolites, entitled “Metabolic Profile of Vasculitis and Arterial Hypertension”, will include a selection of articles (both original and review) focusing on the role of metabolism in vascular disease.

Vascular damage is a highly prevalent in the general population. The metabolic pathway is worthy of interest for vascular disease. Changes in lipid profile may influence the inflammatory system, enhancing its role in vascular damage. Associated metabolic, inflammatory, coagulation, and blood pressure disturbances are often described in vasculitis, but also in arterial hypertension. Vasculitis is the paradigm of vascular inflammation. However, recent evidence also showed the role of inflammation and immune-mediated cytokine release in arterial hypertension. Shear stress, high blood pressure variability, vascular resistances, and vascular stiffness are all part of the same world where lipids and inflammation are the main actors in vascular damage. Increasing evidence is questioning the role of inflammation “per se as a risk factor for atherosclerotic cardiovascular disease, suggesting its crucial role in influencing the different associated clinical consequences. Therefore, the study of the metabolic profile in both these diseases may help in understanding the cross talk between these systems.

We are seeking basic, clinical, and multi-disciplinary research that will aid the knowledge base of this topic and helpfully characterize the mechanisms underlying the relationship between metabolic profile, inflammation or atherosclerosis processes in vasculitis and arterial hypertension.

Dr. Sebastiano Cicco
Guest Editor

Manuscript Submission Information

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Keywords

  • metabolic profile
  • arterial hypertension
  • vasculitis
  • metabolic syndrome
  • metabolic dysfunction
  • immune pathways
  • immune cells
  • cardiovascular disease

Published Papers (1 paper)

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Research

13 pages, 1488 KiB  
Article
Changes in Lipids in Granulomatosis with Polyangiitis Relates to Glucocorticoids and History of Hypertension
by Marialuisa Sveva Marozzi, Antonio Vacca, Vanessa Desantis, Teresa Panebianco, Cristiana Catena, Gabriele Brosolo, Silvia Noviello, Anna Cirulli, Antonio Giovanni Solimando, Leonardo Alberto Sechi, Sebastiano Cicco and Roberto Ria
Metabolites 2023, 13(10), 1053; https://doi.org/10.3390/metabo13101053 - 06 Oct 2023
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Abstract
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue Metabolic Profile of Vasculitis and Arterial Hypertension)
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