Abstract

Objective: 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 marginally known in the GPA patients. Our purpose is to evaluate lipid profile and ASCVD-risk in GPA patients. Design and method: We selected 36 patients who received GPA diagnosis (T0) and evaluated them after 1 (T1) and 2 (T2) years follow-up. All patients were treated with high-dose glucocorticoid, one-year tapered, associated with immunosuppressants. Pathological history and a complete list of drugs at different time points were recorded. Results: The study reveals noteworthy alterations in lipid profiles, with a substantial increase observed in total cholesterol during both T1 and T2 in comparison to T0. A similar trend was noted in LDLand triglycerides. Conversely, no discernible differences were identified in HDL levels. Additionally, a considerable decrease in high-sensitivity C-reactive protein was observed at T1 and T2 in relation to T0, with no significant variance between T2 and T1. Furthermore, a notable reduction in erythrocyte sedimentation rate was noted at T2 as opposed to both T1 and T0, as well as at T1 compared to T0. Moreover, an interesting observation pertains to hypertensive patients who exhibited a marked escalation in lipid levels, juxtaposed with a gradual reduction in inflammation when compared to normotensive individuals. In particular, notable distinctions emerge between the two groups at both T1 and T2 concerning total cholesterol and LDL (p=0.027), despite comparable baseline values at T0. Then, while triglyceride levels start at similar values at T0, a substantial increase is observed at T1 in hypertensive patients and, conversely, at T2, normotensive individuals experience a significant rise in triglyceride levels, accompanied by a noteworthy reduction in hypertensive subjects. Conclusions: The findings indicate that lipid profile alterations, likely influenced by glucocorticoid treatment, may not be directly linked to inflammation. Furthermore, there is a higher relation between hypertension and these alterations. Actual data doesn’t reveal increased mortality in hypertensive GPA patients but further research is required to pinpoint specific patterns characterizing cardiovascular risk and progression in this context.

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