Abstract
Circulating angiotensin-II protects the circulation against sudden falls in blood pressure and is generated by the enzymatic action of angiotensin converting enzyme (ACE) on angiotensin-I. The ACE genes have 2 allelic forms, “I” and “D.” The “D” genotype has both highest angiotensin-II generation and serum ACE levels compared to “I”. 120 patients with IgE-anaphylaxis, 119 healthy controls, and 49 atopics had serum ACE levels, ACE genotype, and renin levels determined. Plasma renin levels were identical for all groups. Serum ACE levels and genotypes were similar for healthy controls (HC) and atopics, but lower in anaphylaxis (P = 0.012), with ACE genotypes also showing increased “I” genes (P = 0.009). This effect was more pronounced in subjects manifesting airway angioedema and cardiovascular collapse (AACVS) than mild cutaneous and respiratory (CRA) symptoms. AACVS was significantly associated with the presence of “I” genes. For “ID” genotype OR is 5.6, 95% CI 1.8 to 17.4, and for “II” genotype OR is 44, 95% CI 5 to 1891 within the anaphylaxis group = 0.001. The results show a difference in the genotype frequency between control and anaphylaxis, suggesting a role for the renin angiotensin system in anaphylaxis manifesting with airway angioedema and cardiovascular collapse.
Highlights
IgE mediated anaphylactic reaction can result in clinical symptoms ranging from mild cutaneous effects (Grade I) to cardiac arrest from profound hypotension and circulatory collapse (Grade 4) Terr classification [1]
Within the cutaneous and respiratory (CRA) and angioedema and cardiovascular collapse (AACVS) subgroups, both remained statistically lower than healthy controls (HC) and atopics
This confirmed serum angiotensin converting enzyme (ACE) levels were significantly lower in the anaphylaxis group and AACVS subdivision compared with HC and atopics
Summary
IgE mediated anaphylactic reaction can result in clinical symptoms ranging from mild cutaneous effects (Grade I) to cardiac arrest from profound hypotension and circulatory collapse (Grade 4) Terr classification [1]. The effects of released histamine are central to this and produce falls in systolic blood pressure with angioedema from histamine effects on the microcirculation [2, 3]. There are unanswered questions as to which host factors may be influencing the effects of the released histamine [5,6,7]. Angiotensin-II (AII) is the most potent vasoconstrictor that is rapidly generated in response to hypotension and protects against profound falls in systemic blood pressure such as those that occur in haemorrhage or shock [8,9,10]
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