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Angioedema, a Life-Threatening Adverse Reaction to ACE-Inhibitors

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Angioedema, a Life-Threatening Adverse Reaction to ACE-Inhibitors DOI: 10.2478/rjr-2019-0023 Romanian Journal of Rhinology, Volume 9, No. 36, October - December 2019 LITERATURE REVIEW Angioedema, a life-threatening adverse reaction to ACE-inhibitors Ramona Ungureanu1, Elena Madalan2 1ENT Department, “Dr. Victor Babes” Diagnostic and Treatment Center, Bucharest, Romania 2Allergology Department, “Dr. Victor Babes” Diagnostic and Treatment Center, Romania ABSTRACT Angioedema with life-threatening site is one of the most impressive and serious reasons for presenting to the ENT doctor. Among different causes (tumors, local infections, allergy reactions), an important cause is the side-effect of the angiotensin converting enzyme (ACE) inhibitors drugs. ACE-inhibitors-induced angioedema is described to be the most frequent form of bradykinin- mediated angioedema presented in emergency and also one of the most encountered drug-induced angioedema. The edema can involve one or more areas of the head and neck region, the most affected being the face, the lips, the tongue, followed by the larynx, when it may determine respiratory distress and even death. There are no specific diagnosis tests available and the positive diagnosis of ACE-inhibitors-induced angioedema is an exclusion diagnosis. The authors performed a review of the most important characteristics of the angioedema caused by ACE-inhibitors and present their experience emphasizing the diagnostic algorithm. KEYWORDS: angioedema, ACE-inhibitors, hereditary angioedema, bradykinin, histamine. INTRODUCTION with secondary local extravasation of plasma and tissue swelling5,6. Angioedema (AE) is a life-threatening condition Based on this pathomechanism, the classification presented as an asymmetric, localised, well-demar- of angioedema comprises three major types: 1). cated swelling1, located in the mucosal and submu- bradykinin-mediated – with either complement C1 cosal layers of the upper respiratory airways. The esterase inhibitor (C1INH) deficiency or normal edema can involve one or more areas of the head (or near-normal) antigenic and functional levels, and neck region, the most affected being the face, 2). mast cell-mediated - with normal C1INH divided the lips, the tongue, followed by the larynx, when into IgE-mediated (the determinant factor being a it may cause respiratory distress and even death2. previous sensitisation to an allergen) and non-IgE- Less frequently, it can be located in the hands, feet mediated and 3). idiopathic with normal C1INH7. or abdominal viscera. The bradykinin-mediated AE can be either a he- In the literature, the first case of angioedema reditary (HAE) autosomal dominant disorder – a was presented by Milton in 18763. Six years later, in rare presentation in the emergency unit, due to a 1882, it was described by Quincke4 as angioneu- mutation in the gene encoding C1 esterase inhibi- rotic edema. tor (C1-INH) that affects between 1:10,000 and The physiopathological mechanism of angi- 1:150,000 people in the general population or ac- oedema is explained by a systemic or local release quired (AAE)7,8. The latest, AAE, is presented with of reactive mediators, such as bradykinin, hista- C1INH deficiency frequently associated with lym- mine and other mast cell mediators, which deter- phoproliferative diseases and/or autoantibodies mine an increased permeability of the vessels’ walls against C1INH that may be responsible for C1INH Corresponding author: Ramona Ungureanu, MD, PhD Address: ENT Department, “Dr. Victor Babes” Diagnostic and Treatment Center, 281 Mihai Bravu Street, District 3, 030303, Bucharest, Romania e-mail: [email protected] Received for publication: July 16, 2019 / Accepted: August 30, 2019 178 Romanian Journal of Rhinology, Volume 9, No. 36, October - December 2019 consumption. Another form of AAE associated reaction, and preformed IgE has not been observed. with normal C1INH – drug-induced AE7,9 is the The physiopathological mechanism of ACEI-AE most frequent form of bradykinin-mediated angi- includes the reduction of the bradykinin metabo- oedema presented in emergency, the angiotensin- lism by preventing the conversion of angiotensin I converting enzyme inhibitor-induced angioedema in angiotensin II, in this way increasing the risk of (ACEI-AE) being the leader in this category7,10,11. angioedema. Angiotensin I, produced in the kid- ney by angiotensinogen conversion, is metabolised into angiotensin II in the lungs by the enzyme ACE-INHIBITORS-INDUCED ANGIOEDEMA ACE. Angiotensin II acts as a vasoconstrictor me- (ACEI-AE) diator by activating angiotensin I and angiotensin II receptors and bradykinin inactivation. The ACE Angiotensin-converting enzyme inhibitors rep- is involved in the degradation mechanism of brad- resent an important cause of drug-induced angi- ykinin16,17. Bradykinin acts as a vasodilator. oedema due to their very frequent use in the ACE inhibitors are responsible for the decrease arterial hypertension treatment. The prevalence of of angiotensin II levels and the increase of brady- ACE-inhibitors-induced angioedema in these pa- kinin concentration. This results in high levels of tients was reported to be between 0.1% up to bradykinin with important vasodilation and in- 2.5%10, and it is up to five times greater in people creased vascular permeability with secondary fluid of African descent12,13, with higher risk in smokers extravasation into the subcutaneous tissue and angi- and women; diabetes has been associated with oedema16-19. But, the exclusive role of bradykinin in lower risk7. The involvement of ACE inhibitors producing angioedema is less likely, other possible represents 20 – 40% of the angioedema cases pre- mechanisms being an alteration of the immune re- sented in the emergency unit5,10,14. sponses, enhancement of substance P formation (a The first case of ACEI-AE was described in 1980 vasoactive peptide that increases vascular permea- and it was due to captopril15. Even if at the begin- bility by its action on neurokinin receptor 1) and ning it was considered a rare adverse reaction, later bradykinin-induced histamine release20. on, its incidence increased due to the large pre- Angiotensin-converting enzyme inhibitors-asso- scription of this antihypertensive drug class and due ciated angioedema is located frequently in the to the rise of life expectancy. It is not an allergic head and neck area, involving mostly the face, the Figure 1. Angioedema associated with ACE-inhibitors involving the lips and the left side of the face. Ungureanu et al Angioedema, a life-threatening adverse reaction to ACE-inhibitors 179 lips, the tongue and the upper aerodigestive tract21 TREATMENT OF ACEI-AE (Figure 1). In specific cases visceral angioedema can also be present22,23. The first step in the management of an angi- This type of angioedema is characterised by oedema is to secure the patency of the upper res- asymmetric, non-pruritic, erythematous swelling piratory tract and to establish medication depending with an insidious onset, lasting up to 24 – 72 hours on the severity of the signs and symptoms. and sometimes it may present spontaneous remis- In case of the angioedema caused by ACE inhibi- sion24. It is usually diagnosed in patients over 40 tors, as in any other drug-induced angioedema, the years of age due to the increased prevalence of car- immediate discontinuation of the drugs is mandatory. diovascular pathology in this age decade25. Most It is important to keep in mind that in this type reactions appear in the first week or month of ini- of angioedema the standard treatment for allergic tial therapy and no correlation with a specific ACE- reactions (e.g. antihistamines, corticosteroids, epi- inhibitor or dose was found. Lately, the studies nephrine) may not have the expected effects7,29 revealed a higher frequency of ACEI-AE developed and there can be recurrent episodes of angioedema after multiple years of treatment5,26 rather than at in the first few months after treatment cessation. the initiation of the treatment. Giving the multiple faces of the pathomechanism, other therapies were experienced, but without any proven efficacy, including: tranexamic acid, ecal- DIAGNOSIS OF ACEI-INDUCED lantide (recombinant protein inhibits the conver- ANGIOEDEMA sion of high-molecular-weight kininogen to bradykinin by inhibiting plasma kallikrein), puri- Considering that it is a potential life-threatening fied C1 inhibitor concentrate, fresh frozen plasma condition, it is essential to identify the causes of and Icatibant (a synthetic bradykinin B2-receptor the angioedema. Unfortunately, there are no spe- antagonist that is approved for the acute treatment cific diagnosis tests available and the positive diag- of HAE attacks)7. nosis of ACEI-AE is an exclusion diagnosis. A detailed and carefully guided history of the patient is mandatory in order to establish the po- OUR EXPERIENCE tential allergic or non-allergic type of angioedema, considering the fact that there are patients who, at From January 2017 to October 2018, four pa- the initial evaluation, only present the history of tients (two males and two females), over the age of angioedema and have no signs or symptoms. 50, who experienced multiple episodes of facial, Laboratory testing can give important informa- pharyngeal, laryngeal or tongue edema presented tion about the cause in a patient presented only to our clinic. All 4 patients were undergoing ACEI with a history of angioedema. Deficiency in C4 and drugs treatment for arterial hypertension or other C1 esterase inhibitor are known to relate to HAE cardiac disorders
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