Nazzal Maisa A, Iter Abbas, Dawabsheh Ameed Q, Bsharat Majd A
Department of Infection Control and Prevention, Ibn Sina Specialized Hospital, Jenin, P200, Palestine.
Department of Internal Medicine, Ibn Sina Specialized Hospital, Jenin, P200, Palestine.
Heliyon. 2024 Oct 16;10(21):e39423. doi: 10.1016/j.heliyon.2024.e39423. eCollection 2024 Nov 15.
To report a case of drug-induced isolated angioedema secondary to the use of Entresto (Valsartan/Sacubitril).
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).
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.
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.
报告一例因使用恩格列净(缬沙坦/沙库巴曲)继发药物性孤立性血管性水肿的病例。
一名75岁白人男性,在服用慢性药物恩格列净(沙库巴曲/缬沙坦)后出现悬雍垂肿胀,舌形正常,并逐渐出现言语困难、呼吸急促和吞咽困难。主要考虑的可能性是悬雍垂血管性水肿,未发现其他潜在病因。停药并观察后,血管性水肿随后消退。该患者被诊断为昆克氏病,具体为孤立性悬雍垂血管性水肿,归因于使用恩格列净(具体而言,缬沙坦成分)。
血管紧张素转换酶抑制剂(ACEI)常与药物性血管性水肿相关,这可能归因于它们对缓激肽水平的影响。如果缓激肽水平升高是ACE抑制剂所致血管性水肿的主要原因,那么血管紧张素受体阻滞剂(ARB)被认为极少引发这种情况(如果有引发的话)。已有大量血管性水肿病例可能是由ARB报告的。这些药物类别中每种导致血管性水肿的确切机制尚不确定。血管紧张素II水平升高可能诱导AT2受体的表达和激活。在动物模型中,ARB已被证明可升高缓激肽水平,这种作用被认为归因于AT2受体刺激增强。通过抑制AT1受体并升高血管紧张素II水平,ARB可能会加重血管性水肿。
这是巴勒斯坦首例关于缬沙坦/沙库巴曲诱发血管性水肿的病例报告之一。该病例及相关科学文献与ARB导致血管性水肿的假说一致。尽管潜在原因仍不清楚,但从业者应意识到缬沙坦的这种潜在不良反应。