Angioedema - Our Experience Focused On Socio-Demographic, Etiological and Clinical Characteristics of the Condition and Its Management

Authors

  • Svetlan Dermendjiev Division of Occupational Disorders and Toxicology, 2nd Medicine Department, Medical Faculty, Medical University, Plovdiv, Bulgaria
  • Vesela Slavcheva Blagoeva Medical University, Plovdiv, Bulgaria

DOI:

https://doi.org/10.3889/oamjms.2019.040

Keywords:

Angioedema, Triggering factors, Clinical features, Underlying disorders

Abstract

BACKGROUND: Angioedema (AE) is acute oedema of the skin and mucous surfaces, involving the respiratory and gastrointestinal tracts. AE could be a life-threatening medical condition. Regardless of its growing clinical importance, many aspects of its aetiology and pathogenesis remain poorly understood. Its incidence, demographic characteristics, diagnosis and therapy, need further investigation.

AIM: This study reports our experience with angioedema concerning its social and demographic characteristics, aetiology, clinical features, diagnosis and treatment outcomes. Study design: Eighty-eight patients with AE were enrolled. The study is a retrospective analysis of patients treated in our Clinics.

METHODS: All participants were asked on a voluntary basis to fill out a specially designed questionnaire on the day of their discharge. Other important data sources included: patients’ history and notes during the hospital stay, information from previous admissions, etc. Parametric and non-parametric statistical methods were used for data processing. Data analysis was performed using SPSS (SPSS Inc., IBM SPSS Statistica) version 20.0

RESULTS: Based on our results, AE affects more frequently patients over 50 years of age, regardless of their sex. Urban residents prevail, among them - more commonly working women. Non-steroidal anti-inflammatory drugs (NSAIDs), hormones and antibiotics were among the most common triggers – in 8%, 4.5% and 11.4% of the cases respectively. In 9.09% of the patients, food-induced AE was seen, the most common foods reported, were – nuts, eggs and egg products. The common sites of involvement were periorbital area and lips. In only 9.1% of the patients, oedema progressed to spread to the upper respiratory tract. Cardiac conditions were the most frequent underlying disorders – 33%, of the patients, auto-immune thyroiditis was the second most common-14.8%, followed by musculo- skeletal disorders (10.2%) and diabetes (4.5%) Family history of allergy was seen in 8.4% of the patients, the most frequent allergic disorder, reported, was asthma. In patients with HAE, family history was present in 2.9% of the patients.

CONCLUSIONS: All patients received therapy with steroids and antihistamines, resulting in resolution of symptoms and no invasive procedures were necessary. Based on our results, the diagnosis of AE is often difficult and delayed and requires specialist evaluation. If recognised on time and adequately treated, the outcomes are favourable.

Downloads

Download data is not yet available.

Metrics

Metrics Loading ...

Plum Analytics Artifact Widget Block

References

Quincke H. Uber akutes unschriebenes H autodem. [About an acute described skin edrema]. Monatshe Prakt Dermatol. 1882; 1:129–131.

Donati M. De medica historia mirabili. Mantuae, per Fr. Osanam, 1586.

Milton JL. On giant urticaria. Edinburgh Medical Journal. 1876; 22(6):513. DOI: https://doi.org/10.25291/VR/22-VLR-513

Osler W. Landmark publication from The American Journal of the Medical Sciences: Hereditary angio-neurotic oedema. The American journal of the medical sciences. 2010; 339(2):175-8. https://doi.org/10.1097/MAJ.0b013e3181b2803f PMid:20145434 DOI: https://doi.org/10.1097/MAJ.0b013e3181b2803f

Landerman NS. Hereditary angioneurotic edema: I. Case reports and review of the literature. Journal of Allergy. 1962; 33(4):316-29. https://doi.org/10.1016/0021-8707(62)90031-X DOI: https://doi.org/10.1016/0021-8707(62)90031-X

Donaldson VH, Evans RR. A biochemical abnormality in hereditary angioneurotic edema: absence of serum inhibitor of C′ 1-esterase. The American journal of medicine. 1963; 35(1):37-44. https://doi.org/10.1016/0002-9343(63)90162-1 DOI: https://doi.org/10.1016/0002-9343(63)90162-1

Evans TC, Roberge RJ. Quincke's disease of the uvula. Am J Emerg Med. 1987; 5:211-16. https://doi.org/10.1016/0735-6757(87)90323-8 DOI: https://doi.org/10.1016/0735-6757(87)90323-8

Bozkov B, Baleva M, Nikolov et al. Hereditary AE – results from previous studies and perspectives. 3 rd National Congress of Allergy. 1994; 4-6.

Cicardi M, Aberer W, Banerji A, Bas M, Bernstein JA, Bork K, Caballero T, Farkas H, Grumach A, Kaplan AP, Riedl MA. Classification, diagnosis, and approach to treatment for angioedema: consensus report from the H ereditary A ngioedema I nternational W orking G roup. Allergy. 2014; 69(5):602-16. https://doi.org/10.1111/all.12380 PMid:24673465 DOI: https://doi.org/10.1111/all.12380

Cicardi M, Bergamaschini L, Zingale LC, Gioffre D, Agostoni A. Idiopathic nonhistaminergic angioedema. Am J Med. 1999; 106:650–654. https://doi.org/10.1016/S0002-9343(99)00123-0 DOI: https://doi.org/10.1016/S0002-9343(99)00123-0

Chiu AG, Burningham AR, Newkirk KA, Krowiak EJ, Davidson BJ, Deeb ZE. Angiotensin-converting enzyme inhibitor-induced angioedema: a multicenter review and an algorithm for airway management. Annals of Otology, Rhinology & Laryngology. 2001; 110(9):834-40. https://doi.org/10.1177/000348940111000906 PMid:11558759 DOI: https://doi.org/10.1177/000348940111000906

Cebrail AKYÃœZ, Mustafa Suphi ELBÄ°STANLI. Incarceration by Rope: A Rare Cause of Uvula Edema, Tr J Emerg Med. 2013; 13(2):96-97 DOI: https://doi.org/10.5505/1304.7361.2013.72623

Bork K, Staubach P, Eckardt AJ, Hardt J. Symptoms, course, and complications of abdominal attacks in hereditary angioedema due to C1 inhibitor deficiency. Am J Gastroenterol. 2006; 101:619–627. https://doi.org/10.1111/j.1572-0241.2006.00492.x PMid:16464219 DOI: https://doi.org/10.1111/j.1572-0241.2006.00492.x

Bork K, Gul D, Hardt J, Dewald G. Hereditary angioedema with normal C1 inhibitor: clinical symptoms and course. Am J Med. 2007; 120:987–992. https://doi.org/10.1016/j.amjmed.2007.08.021 PMid:17976427 DOI: https://doi.org/10.1016/j.amjmed.2007.08.021

Cohen EG, Soliman AM. Changing trends in angioedema. The Annals of Otology, Rhinology and Laryngology. 2001; 110(8):701–706. https://doi.org/10.1177/000348940111000801 PMid:11510724 DOI: https://doi.org/10.1177/000348940111000801

Rees RS, Bergman J, Ramirez-Alexander R. Angioedema associated with lisinopril. The American journal of emergency medicine. 1992; 10(4):321-2. https://doi.org/10.1016/0735-6757(92)90010-U DOI: https://doi.org/10.1016/0735-6757(92)90010-U

Zotter Z, Csuka D, Szabó E, Czaller I, Nébenführer Z, Temesszentandrási G, Fustˆ G, Varga L, Farkas H. The influence of trigger factors on hereditary angioedema due to C1-inhibitor deficiency. Orphanet journal of rare diseases. 2014; 9(1):1. https://doi.org/10.1186/1750-1172-9-44 PMid:24678771 PMCid:PMC3977696 DOI: https://doi.org/10.1186/1750-1172-9-44

Lewis JH. Idiopathic gastric acid hypersecretion: treatment implications for refractory acid/peptic disorders. Alimentary pharmacology & therapeutics. 1991; 5:15-24. https://doi.org/10.1111/j.1365-2036.1991.tb00745.x DOI: https://doi.org/10.1111/j.1365-2036.1991.tb00745.x

Powell RJ, Du Toit GL, Siddique N, Leech SC, Dixon TA, Clark AT, Mirakian R, Walker SM, Huber PA, Nasser SM. BSACI guidelines for the management of chronic urticaria and angioâ€oedema. Clinical & Experimental Allergy. 2007; 37(5):631-50. https://doi.org/10.1111/j.1365-2222.2007.02678.x PMid:17456211 DOI: https://doi.org/10.1111/j.1365-2222.2007.02678.x

Powell R, Leech SC, Till S, Huber PA, Nasser SM, Clark AT. BSACI guideline for the management of chronic urticaria and angioedema. Clinical & Experimental Allergy. 2015; 45(3):547-65. https://doi.org/10.1111/cea.12494 PMid:25711134 DOI: https://doi.org/10.1111/cea.12494

Zingale L, Beltrami L, Zanichelli A, Maggioni L, Pappalardo E, Cicardi B, Cicardi M. Angioedema without urticaria: a large clinical survey. CMAJ. 2006; 175(9):1065-70. https://doi.org/10.1503/cmaj.060535 PMid:17060655 PMCid:PMC1609157 DOI: https://doi.org/10.1503/cmaj.060535

Zuberbier T, Aberer W, Asero R, Bindslevâ€Jensen C, Brzoza Z, Canonica GW, Church MK, Ensina LF, Giménezâ€Arnau A, Godse K, Gonçalo M. The EAACI/GA 2 LEN/EDF/WAO Guideline for the definition, classification, diagnosis, and management of urticaria: the 2013 revision and update. Allergy. 2014; 69(7):868-87. https://doi.org/10.1111/all.12313 PMid:24785199 DOI: https://doi.org/10.1111/all.12313

Zuberbier T, Balke M, Worm M, Edenharter G, Maurer M. Epidemiology of urticaria: a representative crossâ€sectional population survey. Clinical and Experimental Dermatology: Clinical dermatology. 2010; 35(8):869-73. https://doi.org/10.1111/j.1365-2230.2010.03840.x PMid:20456386 DOI: https://doi.org/10.1111/j.1365-2230.2010.03840.x

Brickman CM, Tsokos GC, Below JE, Lawley TJ, Santaella M, Hammer CH, Frank MM. Immunoregulatory disorders associated with hereditary angioedema: I. Clinical manifestations of autoimmune disease. Journal of allergy and clinical immunology. 1986; 77(5):749-57. https://doi.org/10.1016/0091-6749(86)90424-0 DOI: https://doi.org/10.1016/0091-6749(86)90424-0

Roche O, Blanch A, Caballero T, Sastre N, Callejo D, López-Trascasa M. Hereditary angioedema due to C1 inhibitor deficiency: patient registry and approach to the prevalence in Spain. Annals of Allergy, Asthma & Immunology. 2005; 94(4):498-503. https://doi.org/10.1016/S1081-1206(10)61121-0 DOI: https://doi.org/10.1016/S1081-1206(10)61121-0

Published

2019-01-28

How to Cite

1.
Dermendjiev S, Blagoeva VS. Angioedema - Our Experience Focused On Socio-Demographic, Etiological and Clinical Characteristics of the Condition and Its Management. Open Access Maced J Med Sci [Internet]. 2019 Jan. 28 [cited 2024 Jul. 26];7(3):341-6. Available from: https://oamjms.eu/index.php/mjms/article/view/oamjms.2019.040

Issue

Section

B - Clinical Sciences

Most read articles by the same author(s)