ArticleHeliyon2024
Valsartan/Sacubitril induced isolated angioedema of uvula: A case report.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Losartan-induced Angioedema: A Case Report and Review of Literature.Journal of community hospital internal medicine perspectives · 2026Article
- Article
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Authors and funding
4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Objective: To report a case of drug-induced isolated angioedema secondary to the use of Entresto (Valsartan/Sacubitril). Case summary: A 75-year-old White man presented with swelling of the uvula with a normal tongue shape and gradual onset of speech difficulty, shortness of breath, and difficulty swallowing after taking his chronic medication Entresto (sacubitril/valsartan). The main possibility considered was uvular angioedema, other potential causes were not identified. The angioedema subsequently resided after discontinuation of the medication and observation. The patient was diagnosed with Quincke's disease, specifically isolated angioedema of the uvula, which was attributed to the use of Entresto (specifically, the valsartan component). Discussion: Angiotensin-converting enzyme inhibitors (ACEI) are frequently linked to drug-induced angioedema, which is likely attributable to their effects on bradykinin levels. If elevated bradykinin levels are the primary reason behind angioedema owing to ACE inhibitor use, ARBs are thought to cause very few, if any, occurrences of the condition. There have been numerous cases of angioedema that may have been reported by ARBs. The precise mechanism by which each of these classes of medications causes angioedema is uncertain. The expression and activation of AT2 receptors may be induced by rising angiotensin II levels. ARBs have been demonstrated to elevate bradykinin levels in animal models, an effect that is assumed to be attributable to elevated AT2 receptor stimulation. By inhibiting AT1 receptors and elevating angiotensin II levels, ARBs may exacerbate angioedema. Conclusion: This is one of the first case reports in Palestine of Valsartan/Sacubitril-induced angioedema. This case and the relevant scientific literature are consistent with the hypothesis that ARB causes angioedema. Practitioners should be aware of this potential adverse effect of valsartan although the underlying cause is still not known.
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