Psoriasis After Exposure to Angiotensin-Converting Enzyme Inhibitors: French Pharmacovigilance Data and Review of the Literature

Azzouz, Brahim; Morel, Aurore; Kanagaratnam, Lukshe; Herlem, Emmanuelle; Trenque, Thierry

doi:10.1007/s40264-019-00865-8

Cited by 13 publications

(5 citation statements)

References 29 publications

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“…We recently highlighted a significant association between RAAS inhibitor exposure (ACEIs and ARBs) and the risk of psoriasis using the FPVD data. 30,31 Patients concomitantly taking BB and a RAAS inhibitor could be at higher risk of psoriasis. However, our data show that these categories of patients are at lower risk of psoriasis compared to those treated with BB alone.…”

Section: Discussionmentioning

confidence: 99%

“…BBs exert renin angiotensin aldosterone system (RAAS) inhibitory potency through β1‐AR blockade. We recently highlighted a significant association between RAAS inhibitor exposure (ACEIs and ARBs) and the risk of psoriasis using the FPVD data 30,31 . Patients concomitantly taking BB and a RAAS inhibitor could be at higher risk of psoriasis.…”

Section: Discussionmentioning

confidence: 99%

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Psoriasis risk after beta‐blocker exposure: Description of a pharmacovigilance signal

Azzouz

Guizelin

Lambert

et al. 2022

Brit J Clinical Pharma

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Aim We aimed to investigate French pharmacovigilance data. The objective was to characterize psoriatic conditions that occurred after beta‐blocker (BB) exposure and bring to light a possible pharmacovigilance signal. Methods Spontaneous reports of psoriatic conditions recorded in the French National Pharmacovigilance Database (FPVD) between 1985 and 2019 were extracted. We performed a retrospective, descriptive analysis of reports linked to BB exposure. Association between psoriasis risk and BB exposure was assessed using a case/noncase study. Results Two hundred and twenty‐five reports of psoriatic conditions after BB exposure were recorded in the FPVD during the study period. Both cardioselective and noncardioselective, topical and systemic BBs are involved. Therapeutic indication of BB was mainly hypertension. Mean time to onset was 5 months and outcome was favourable in 68% after BB discontinuation. These features were concordant with those of literature reports. The reporting odds ratio (ROR) was 8.95 (95% confidence interval 7.75‐10.33). Conclusion We highlighted a statistically significant disproportionality which constitutes a pharmacovigilance signal. Psoriasis risk with BBs is a class effect. Increasing surveillance during the first year of BB exposure is needed.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Psoriasis risk after beta‐blocker exposure: Description of a pharmacovigilance signal

Azzouz

Guizelin

Lambert

et al. 2022

Brit J Clinical Pharma

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“…Among antihypertensive drugs, ACE inhibitors have been well-studied in the case of PsD progression, and are defined as extensively used medications for the treatment of hypertension (HTN), congestive HF, diabetes, and even the prevention of kidney diseases 65 . According to the data analysis using the French Pharmacovigilance Database (FPVD), though psoriasis is considered one of the serious adverse events in patients receiving ACE inhibitors 66 , the mechanism of ACE-inhibitors induced/aggravated PsD is not fully deciphered. However, it has been thought that ACE inhibitors beyond the modulation of angiotensin II (Ag II) production can also regulate the catabolism of kinins 67 .…”

Section: Possible Causesmentioning

confidence: 99%

Causes of Autoimmune Psoriasis and Associated Cardiovascular Disease: Roles of Human Endogenous Retroviruses and Antihypertensive Drugs—A Systematic Review and Meta-analysis

Rezabakhsh,

Manjili,

Hosseinifard

et al. 2023

Preprint

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Current treatments are ineffective to cure or prevent occurrences of autoimmune psoriasis and psoriatic cardiovascular disease/CVD. Psoriasis is associated with deregulated expressions of human endogenous retroviruses (ERVs) variants. ERV transcripts and proteins are detected in lesioned biopsies—without assembled viral particles—in addition to antibody and T-cell responses against ERV-K dUTPase. In persons living with HIV-1, manifestations of psoriasis are exacerbated variably. These may depend on multiple factors, differences in ERVs expressions, subtypes of HIV-1, and/or epigenetics. This article represents a quantitative risk assessment and meta-analysis approach with an attempt to assess causality. We surmise that mutated ERVs trigger aberrant proliferation and differentiation of keratinocytes, which in turn induce proinflammatory polarization. Independent risk factors and/or covariates with a range of relative risk/RR ratios appear to significantly impact the development of autoimmune psoriasis or immune intolerance, plausibly through ERVs genes activity. Given the antihypertensive drug’s potential in psoriasis development, a probable role in promising either ERVs activation or perturbations in epigenetic factors is questionable. Although the correlational nature of the data based on RR ratios prevents making robust conclusions, we reckon that the likelihood of attributable risk factors for certain antihypertensive drugs may stem from their pleiotropic effects or potentials for inducing ERV-mediated dysregulation of keratinocytes and/or endothelial cells. These findings expand our knowledge regarding ERV activations and HIV-1, antihypertensive drugs use, and incidents of psoriatic disease, and call for exploring cell-specific therapies aimed at blocking or reversing mutated ERVs gene activity toward attaining stable remissions in psoriasis and associated CVD.

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“…11 Other studies have found a probable association between psoriasis aggravation and long-term systemic use of ARBs. 12,13 despite the fact that this effect was not stated in the product's features.…”

Section: Introductionmentioning

confidence: 99%

Anti-inflammatory Effects of Topically Applied Azilsartan in a Mouse Model of Imiquimod-induced Psoriasis

Mohammed¹,

Kadhim²,

AL-Sudani³

et al. 2022

IJDDT

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Background: Many studies showed a possible exacerbation of psoriasis after exposure to angiotensin receptor antagonists. Azilsartan is a competitive angiotensin II receptor antagonist and has anti-inflammatory effects in various inflammatory disorders. Objective: Investigate dose-dependent effects of topical Azilsartan on Imiquimod-induced psoriasis in mice. Methods: Forty-eight mice are allocated into six groups (8 mice per group). They all received Imiquimod for the induction of psoriasis (except Group I, a negative control group). Group II (Induction group) received petroleum gel for six days after induction with Imiquimod. The other groups (III, IV, V, and VI) were given Clobetasol propionate 0.05, 1% Azilsartan, 3% Azilsartan, and a combination of 3% Azilsartan and 0.05% Clobetasol propionate ointments, respectively once daily for six days after induction. Results: Azilsartan decreased psoriasis area severity index (PASI) score and attenuated the histological manifestations after induction. It significantly decreased the serum and tissue levels of the inflammatory biomarkers (TNF-α, IL-17, IL-23, and NF-Kβ), especially when used as an add-on therapy to Clobetasol. Conclusion: Topically-applied Azilsartan shows anti-psoriatic effects in Imiquimod-induced psoriasis in mice via anti-inflammatory and anti-proliferative activities.

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Psoriasis After Exposure to Angiotensin-Converting Enzyme Inhibitors: French Pharmacovigilance Data and Review of the Literature

Cited by 13 publications

References 29 publications

Psoriasis risk after beta‐blocker exposure: Description of a pharmacovigilance signal

Psoriasis risk after beta‐blocker exposure: Description of a pharmacovigilance signal

Causes of Autoimmune Psoriasis and Associated Cardiovascular Disease: Roles of Human Endogenous Retroviruses and Antihypertensive Drugs—A Systematic Review and Meta-analysis

Anti-inflammatory Effects of Topically Applied Azilsartan in a Mouse Model of Imiquimod-induced Psoriasis

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