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Journal articles on the topic 'Angioedema'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

Šiupšinskienė, Nora, Žygimantas Tverskis, and Sigutė Norkienė. "ANGIOTENZINĄ KONVERTUOJANČIO FERMENTO INHIBITORIAUS SUKELTOS ANGIOEDEMOS GYDYMAS." Health Sciences 30, no. 7 (2021): 35–38. http://dx.doi.org/10.35988/sm-hs.2020.173.

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Angiotenziną konvertuojančio fermento (AKF) inhibitorių sukelta angioedema yra pavojinga gyvybei būklė, kuri pasireiškia maždaug 0,5 proc. pacientų, vartojančių AKF inhbitorius. Nors AKF inhibitorių sukeltos angioedemos patofiziologija susijusi su padidėjusiu bradikinino kiekiu kraujo plazmoje, standartinis gydymas paprastai apima kortikosteroidus ir antihistamininius medikamentus. Apžvalgos tikslas yra apibendrinti įrodymus, pagrindžiančius farmakoterapiją, gydant AKF inhibitorių sukeltą angioedemą.

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2

Fikri, C., Y. Zarouali, M. Aboudourib, O. Hocar, and S. Amal. "Histaminic Angioedema in Children: A Rare Entity Not to be ignored." Scholars Journal of Medical Case Reports 11, no. 11 (2023): 2061–63. http://dx.doi.org/10.36347/sjmcr.2023.v11i11.036.

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Angioedema is a common symptom to different etiologies, the diagnostic orientation is based on the associated signs. The most common are histamine, non IgE-mediated, benign and often associated with urticaria. Angioedema by anaphylaxis and bradykinin angioedemas are rare but potentially severe by upper airway involvement. We report the case of a 14 years old patient with a history of bilateral orbital swelling associated with deep urticaria, and a brother followed for angioedema. Presenting bilateral palpebral and jugal edema, associated with uticarian tasks in the trunk and back. The diagnosi

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3

Zuraw, Bruce L., and Sandra C. Christiansen. "Pathophysiology of Hereditary Angioedema." American Journal of Rhinology & Allergy 25, no. 6 (2011): 373–78. http://dx.doi.org/10.2500/ajra.2011.25.3661.

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Background Laryngeal angioedema may be associated with significant morbidity and even mortality. Because of the potential severity of attacks, both allergists and otolaryngologists must be knowledgeable about the recognition and treatment of laryngeal angioedema. This study describes the clinical characteristics and pathophysiology of bradykinin-mediated angioedema. Methods A literature review was conducted concerning the clinical characteristics and pathophysiology of types I and II hereditary angioedema (HAE), type III HAE, acquired C1 inhibitor (C1INH) deficiency, and angiotensin-converting

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4

Ertürk, Nihal, Şadan Soyyiğit, Gülhan Kurtoğlu Çelik, and Edip Varan. "Assessment of emergency physicians’ awareness and knowledge of hereditary angioedema." Intercontinental Journal of Emergency Medicine 2, no. 3 (2024): 50–55. http://dx.doi.org/10.51271/icjem-0038.

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Aims: Hereditary angioedema can occur with life-threatening attacks of severe laryngeal edema, and epinephrine is insufficient in the treatment of attacks. We sought an answer to the question, 'Do emergency physicians, who frequently encounter angioedema cases that are so important for the emergency department, have sufficient awareness about this issue?' Methods: In this study, the online questionnaire was conducted among physicians working in adult emergency departments between April and August 2022. The questionnaire form consisted of two parts. The first part contained three questions abou

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5

Cosme, Joana, Amélia Spínola, Manuel Branco Ferreira, and Manuel Pereira Barbosa. "Hospitalizations due to Angioedema without Urticaria in a Portuguese Center: Five Year Retrospective Study." Acta Médica Portuguesa 32, no. 11 (2019): 714. http://dx.doi.org/10.20344/amp.11893.

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Introduction: Hospitalizations due to angioedema are important especially in debilitating or life-threatening situations. The aim of this study was to evaluate the frequency and etiology of angioedema without urticaria in hospital admissions.Material and Methods: The admissions between 2009 and 2013 in Centro Hospitalar Lisboa Norte with a diagnosis grouped under the ICD9 codes of angioedema were retrospectively analysed. The episodes of angioedema with urticaria were excluded. The admissions were categorized into 2 groups: A — hospitalizations motivated by the angioedema; B — hospitalizations

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6

Haydon, Richard. "Urticaria-angioedema and nonurticarial angioedema." Current Opinion in Otolaryngology & Head and Neck Surgery 8, no. 3 (2000): 239–44. http://dx.doi.org/10.1097/00020840-200006000-00021.

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7

Young, Marielle C., and Aleena Banerji. "Angioedema without urticaria: Diagnosis and management." Allergy and Asthma Proceedings 46, no. 3 (2025): 185–91. https://doi.org/10.2500/aap.2025.46.250013.

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Angioedema is nonpitting swelling that involves the deeper subcutaneous and submucosal layers of tissue. Angioedema can be classified as histaminergic, bradykinin mediated, or idiopathic in etiology. Bradykinin-mediated angioedema presents without urticaria, whereas histaminergic angioedema is usually associated with urticaria (i.e., chronic spontaneous urticaria and angioedema) but manifests with isolated angioedema in ∼20% of patients and clinically overlaps with idiopathic angioedema. Bradykinin-mediated angioedema most commonly occurs in hereditary angioedema (HAE) with or without C1-ester

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8

Kulthanan, Kanokvalai, Sukhum Jiamton, Kanonrat Boochangkool, and Kowit Jongjarearnprasert. "Angioedema: Clinical and Etiological Aspects." Clinical and Developmental Immunology 2007 (2007): 1–6. http://dx.doi.org/10.1155/2007/26438.

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Angioedema is an abrupt swelling of the skin, mucous membrane, or both including respiratory and gastrointestinal tracts. This study aimed to report an experience of angioedema in a university hospital with respect to etiologies, clinical features, treatment, and outcome. One hundred and five patients were enrolled. About half had angioedema without urticaria. The common sites of involvement were periorbital area and lips. Forty five patients (49%) had systemic symptoms. The most common cause of angioedema was allergic angioedema. Nonsteroidal anti-inflammatory drug-induced angioedema and idio

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9

Holguín-Gómez, Luisa María, Luz Adriana Vásquez-Ochoa, and Ricardo Cardona. "Angioedema." Revista Alergia México 63, no. 4 (2016): 373. http://dx.doi.org/10.29262/ram.v63i4.220.

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El angioedema se define como el edema de piel o mucosas, incluidas las de los tractos respiratorio y gastrointestinal, de carácter autolimitado, que en la mayoría de los casos se resuelve en forma completa en menos de 72 horas. Ocurre por aumento de la permeabilidad de los capilares mucosos, submucosos y vénulas poscapilares, con la consiguiente extravasación del plasma. Existen diferentes tipos de angioedema: el histaminérgico (que puede ser mediado o no por inmunoglobulina E), el hereditario, por déficit de C1 inhibidor adquirido, por inhibidores de la enzima convertidora de la angiotensina,

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10

Southward, Jessica, Elizabeth Irvine, and Marina Rabinovich. "Probable Amlodipine-Induced Angioedema." Annals of Pharmacotherapy 43, no. 4 (2009): 772–76. http://dx.doi.org/10.1345/aph.1l527.

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Objective: To report a case of angioedema likely associated with amlodipine administration in a patient with a right thalamic hemorrhagic stroke. Case Summary: A 50-year-old female experienced angioedema during hospitalization for s right thalamic hemorrhagic stroke. She had no past history of angioedema and all of her medications were assessed for risk of angioedema. After careful evaluation, case reports linking calcium channel blockers (CCBs) and angioedema led to further examination of amlodipine as a cause. Amlodipine therapy had been initiated 24 hours prior to the development of angioed

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11

Wong, Sansan, and Ira Lawrence. "Angioedema." Allergy and Asthma Proceedings 11, no. 4 (1990): 163–64. http://dx.doi.org/10.2500/108854190778880033.

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12

Seth, Divya, and Deepak Kamat. "Angioedema." Pediatric Annals 48, no. 12 (2019): e473-e478. http://dx.doi.org/10.3928/19382359-20191118-01.

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13

LoVerde, Daniel, Daniel Clark Files, and Guha Krishnaswamy. "Angioedema." Critical Care Medicine 45, no. 4 (2017): 725–35. http://dx.doi.org/10.1097/ccm.0000000000002281.

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14

Chawla, Sanjay, and Mark Riederer. "Angioedema." Clinical Pediatrics 46, no. 8 (2007): 748–51. http://dx.doi.org/10.1177/0009922806297161.

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15

Collins-Yoder, Angela Smith. "Angioedema." Dimensions of Critical Care Nursing 35, no. 4 (2016): 181–89. http://dx.doi.org/10.1097/dcc.0000000000000188.

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16

Kaplan, Allen P. "Angioedema." World Allergy Organization Journal 1, no. 6 (2008): 103–13. http://dx.doi.org/10.1097/wox.0b013e31817aecbe.

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17

Megerian, Cliff A., James E. Arnold, and Melvin Berger. "Angioedema." Laryngoscope 102, no. 3 (1992): 256???260. http://dx.doi.org/10.1288/00005537-199203000-00005.

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18

Bramante, Robert Matthew, and Masha Rand. "Angioedema." New England Journal of Medicine 365, no. 2 (2011): e4. http://dx.doi.org/10.1056/nejmicm1014034.

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19

Riedl, Marc A. "Angioedema." Immunology and Allergy Clinics of North America 37, no. 3 (2017): i. http://dx.doi.org/10.1016/s0889-8561(17)30054-1.

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20

Farnam, Jafar, and J. Andrew Grant. "Angioedema." Dermatologic Clinics 3, no. 1 (1985): 85–95. http://dx.doi.org/10.1016/s0733-8635(18)30920-3.

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21

Chillón Arce, Roberto, Paula Núñez Gaviño, Inés López Fernández, Beatriz Folgar Leiro, and Carmen Marcos Bravo. "Angioedema." FMC - Formación Médica Continuada en Atención Primaria 24, no. 7 (2017): 390–94. http://dx.doi.org/10.1016/j.fmc.2016.12.004.

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22

Kaplan, Allen P., and Malcolm W. Greaves. "Angioedema." Journal of the American Academy of Dermatology 53, no. 3 (2005): 373–88. http://dx.doi.org/10.1016/j.jaad.2004.09.032.

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23

Frigas, Evangelo, and Ugochukwu C. Nzeako. "Angioedema." Clinical Reviews in Allergy & Immunology 23, no. 2 (2002): 217–32. http://dx.doi.org/10.1385/criai:23:2:217.

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24

Luyasu, Samuel, Delphine Charignon, Denise Ponard, Christian Drouet, and Arije Ghannam. "Angioedema." Annals of Allergy, Asthma & Immunology 121, no. 2 (2018): 248–49. http://dx.doi.org/10.1016/j.anai.2018.04.026.

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25

Tarbox, James A., Arpana Bansal, and Alan N. Peiris. "Angioedema." JAMA 319, no. 19 (2018): 2054. http://dx.doi.org/10.1001/jama.2018.4860.

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26

Bork, Konrad. "Angioedema." Immunology and Allergy Clinics of North America 34, no. 1 (2014): 23–31. http://dx.doi.org/10.1016/j.iac.2013.09.004.

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27

Schauberger, E., and J. Bernstein. "P169 When angioedema is not angioedema." Annals of Allergy, Asthma & Immunology 119, no. 5 (2017): S44. http://dx.doi.org/10.1016/j.anai.2017.08.156.

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28

Oka Sari Utari, I. Gusti Ayu, Sudiasa Sudiasa, and R. Yully Prapyatiningsih. "DIAGNOSIS DAN PENATALAKSANAAN ANGIOEDEMA DI BIDANG THT-KL." JURNAL KEDOKTERAN 4, no. 2 (2019): 30. http://dx.doi.org/10.36679/kedokteran.v4i2.103.

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Angioedema adalah edema yang melibatkan lapisan yang lebih dalam dari kulit yaitu dermis, jaringan subkutan, mukosa dan submukosa karena terjadinya peningkatan permeabilitas kapiler akibat mediator inflamasi. Angioedema pertama kali disebarluaskan oleh Heinrich Quincke pada tahun 1882 sehingga angioedema sering juga disebut dengan Quincke edema. Pada angioedema, edema yang timbul adalah non-pitting, berbatas tegas, pucat dan tidak gatal namun angioedema dapat juga timbul bersamaan dengan urtikaria sehingga bisa disertai gatal-gatal dan kemerahan. Angioedema dapat terjadi pada daerah wajah teru

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29

Manto, Irina A., Elena A. Latysheva, Elena A. Bliznetz, et al. "Hereditary Angioedema (HAE) with a mutation in the plasminogen gene: a retrospective study of a cohort of 14 patients from Russia." Russian Journal of Allergy 18, no. 2 (2021): 5–19. http://dx.doi.org/10.36691/rja1446.

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BACKGROUND: In 2018, a new form of hereditary angioedema without C1-inhibitor deficiency hereditary angioedema with a mutation in the plasminogen gene was identified. The world scientific literature describes a small number of patients with this form of the disease and, therefore, new research is relevant. AIMS: To identify the sociodemographic and clinical features of patients with hereditary angioedema with plasminogen gene mutation; to evaluate the treatment efficacy; to conduct a comparative analysis in a group of patients with hereditary angioedema type I/II. MATERIAL AND METH

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30

Borisova, T. V., and S. I. Sokurenko. "CLASSIFICATION, DIAGNOSIS, AND APPROACH TO TREATMENT FOR ANGIOEDEMA." Journal of Clinical Practice 5, no. 3 (2014): 71–82. http://dx.doi.org/10.17816/clinpract5371-82.

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Angioedema is defined as localized and self-limiting edema of the subcutaneous and submucosal tissue, due to a temporary increase in vascular permeability caused by the release of vasoactive mediators. When angioedema recurs without significant wheals, the patient should be diagnosed to have angioedema as distinct disease. In the absence of the accepted classification, different types of angioedema are not uniquely identified. Four types of accuired and three types of hereditary angioedema were identified as separate forms from the analysis of literature. Here, we summarize the data and the re

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Kısakürek, Zeynep Büşra, Sadi Can Sönmez, Emre Osmanbaşoğlu, Erman Öztürk, and Ayşe Bilge Öztürk. "Larynx Angioedema as a Signal in Chronic Lymphocytic Leukemia: A Case-based Guide for Acquired Angioedema in the Setting of Lymphoproliferative Disorders." Asthma Allergy Immunology 19, no. 2 (2021): 110–13. http://dx.doi.org/10.21911/aai.614.

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ABSTRACT Patients with angioedema can present to the internal medicine, emergency medicine, dermatology, or ear nose throat clinics. Physicians may need to assess the patients whose angioedema is unresponsive to antihistamines systematically in collaboration with other subspecialties including hematology, rheumatology, allergy, and immunology. We aimed to provide a concise review of the diagnosis and multi-disciplinary management of acquired angioedema through a case presentation. A 61-year-old woman presented with recurrent angioedema of 4 episodes within one year. She was evaluated by variou

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32

Perman, Bryton, Shraddha Narechania, and Mark Malesker. "Geriatric Pharmacotherapy Case Series: Recurrent Angioedema Following Discontinuation of ACE Inhibitor Therapy." Senior Care Pharmacist 38, no. 1 (2023): 16–20. http://dx.doi.org/10.4140/tcp.n.2023.16.

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Introduction Angiotensin-converting enzyme inhibitors (ACEIs) are first-line pharmaceutical agents in common chronic conditions such as hypertension and heart failure with reduced ejection fraction. When angioedema occurs, if secondary to ACEIs, discontinuation of the ACEI is necessary to mitigate the risk of recurrent angioedema. While angioedema is a well-known adverse effect of ACEIs, it is not well-known that angioedema may recur even after ACEI discontinuation. Additionally, only few reports in the literature describe this phenomenon. This case describes an older man with a history of chr

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33

Weng, Ping-Kun, Hsing-Won Wang, John K. Lin, and Wen-Yang Su. "Late-Onset Life-Threatening Angioedema and Upper Airway Obstruction Caused by Angiotensin-Converting Enzyme Inhibitor: Report of a Case." Ear, Nose & Throat Journal 76, no. 6 (1997): 404–7. http://dx.doi.org/10.1177/014556139707600611.

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Angioedema is a rare but potentially lethal adverse effect when associated with upper airway obstruction. Sporadic cases of angioedema secondary to angiotensin converting enzyme inhibitors (ACEI) have been reported in the literature. The overall incidence is around 0.1% to 0.2%, and the time of onset is usually during the first week of ACEI therapy. Late-onset angioedema secondary to treatment with ACEIs is much more frequent than appreciated, and is largely unrecognized because of the absence of temporal correlation between ACEI therapy and the development of angioedema. Since angioedema may

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34

Dortas Junior, Sergio Duarte, Solange Oliveira Rodrigues Valle, Soloni Afra Pires Levy, et al. "Prevalence of autoantibodies in a group of hereditary angioedema patients." Anais Brasileiros de Dermatologia 87, no. 2 (2012): 332–34. http://dx.doi.org/10.1590/s0365-05962012000200030.

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Hereditary Angioedema is a dominantly inherited disease. Routine screening of autoantibodies (AAB) is not recommended for individuals with Hereditary Angioedema; however, prevalence of these antibodies in Hereditary Angioedema patients is not well documented. We aim to determine the prevalence of AAB so that individuals at risk of developing autoimmune diseases can be identified. Fifteen patients with Hereditary Angioedema attended at Clementino Fraga Filho University Hospital accepted to participate in this study. Prevalence of AAB was 40%. Our data indicate high prevalence of AAB in patients

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35

Krause, Amanda Jayne, Naiya Balubhai Patel, and Jennifer Morgan. "An unusual presentation of ACE inhibitor-induced visceral angioedema." BMJ Case Reports 12, no. 9 (2019): e230865. http://dx.doi.org/10.1136/bcr-2019-230865.

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ACE inhibitors (ACEi) are common anti-hypertensive drugs that can cause angioedema. Though classic, or facial angioedema is rare, visceral angioedema is even less common. When angioedema occurs, it typically presents early, within 30 days of initiating therapy. Visceral angioedema most commonly presents with nausea, emesis, abdominal pain and diarrhoea, and thus is often mistaken for an episode of gastroenteritis. When a CT scan is obtained, it typically shows characteristic findings, including ascetic fluid, mild mesenteric oedema and thickening of the small bowel. In this case report, we pre

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36

Jasti, Vivek Vardhan, Jay Anderson, and Ifa Abdujelil. "Angioedema without urticaria after recent initiation of celecoxib." BMJ Case Reports 16, no. 9 (2023): e255446. http://dx.doi.org/10.1136/bcr-2023-255446.

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Angioedema is potentially life-threating swelling of integument and mucosa that has multiple potential aetiologies with varying mechanisms. Drug-induced angioedema is often easily correlated with the offending agent and can be prevented with discontinuation of the medication. Many medications have now been implicated in drug-induced angioedema but the two most common are ACE inhibitors and non-steroidal anti-inflammatory drugs (NSAIDs). This case highlights severe angioedema secondary to celecoxib and reviews varying aetiologies of angioedema and NSAID hypersensitivity reactions.

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Sczepanski, Matthew, and Paul Bozyk. "Institutional Incidence of Severe tPA-Induced Angioedema in Ischemic Cerebral Vascular Accidents." Critical Care Research and Practice 2018 (September 27, 2018): 1–6. http://dx.doi.org/10.1155/2018/9360918.

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Introduction. Tissue plasminogen activator (tPA) is commonly used in ischemic cerebral vascular accidents (CVAs). tPA is generally well tolerated; however, orolingual angioedema is a well-documented adverse effect. Angioedema is generally mild, transient, and unilateral but can manifest as severe, life-threatening upper airway obstruction requiring intubation. Reported incidence for all severities ranges from one to five percent, whereas reported incidence of severe cases ranges from 0.18 to 1 percent of patients receiving tPA for ischemic CVA. Angiotensin-converting enzyme (ACE) inhibitors an

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Bal, Christina, Ruth Baumgartner, Daniela Gompelmann, and Marco Idzko. "Angioedema as a predominant symptom of Bordetella pertussis infection." BMJ Case Reports 14, no. 3 (2021): e239243. http://dx.doi.org/10.1136/bcr-2020-239243.

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A 41-year-old woman was referred to our hospital with a 6-week history of severe angioedema, dyspnoea and coughing. Initial investigations focused on common causes of angioedema. Clinical presentation and resistance to treatment with antihistamines and steroids made histamine-mediated angioedema unlikely. Bradykinin-mediated angioedema, such as hereditary or drug-induced angioedema, was excluded by a thorough history investigation and laboratory testing for C1-esterase and C4.In rare cases, exogen pathogens cause angioedema. After profound testing for respiratory pathogens, Bordetella pertussi

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Barzaga, P. A., B. Ryhal, and P. Carroll. "Angioedema—Not! Eosinophilic fasciitis presenting as angioedema." Journal of Allergy and Clinical Immunology 111, no. 2 (2003): S323. http://dx.doi.org/10.1016/s0091-6749(03)81176-4.

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40

Feldman, Matthew F., David A. Khan, E. Sherwood Brown, and Jonathan A. Bernstein. "Factitious angioedema: a mimic of refractory “angioedema”." Journal of Allergy and Clinical Immunology: In Practice 2, no. 6 (2014): 795–97. http://dx.doi.org/10.1016/j.jaip.2014.08.010.

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41

Shercliffe, R., and K. Dass. "ANGIOEDEMA AFTER SILDENAF/ ANGIOEDEMA AFTER SILDENAFIL EXPOSURE." Annals of Allergy, Asthma & Immunology 121, no. 5 (2018): S78. http://dx.doi.org/10.1016/j.anai.2018.09.257.

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42

Andrási, Noémi, Nóra Veszeli, Kinga Viktória Kőhalmi, et al. "Idiopathic Nonhistaminergic Acquired Angioedema Versus Hereditary Angioedema." Journal of Allergy and Clinical Immunology: In Practice 6, no. 4 (2018): 1205–8. http://dx.doi.org/10.1016/j.jaip.2018.04.018.

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43

Wada, Akane, Yu Sawada, Hitomi Sugino, and Motonobu Nakamura. "Angioedema and Fatty Acids." International Journal of Molecular Sciences 22, no. 16 (2021): 9000. http://dx.doi.org/10.3390/ijms22169000.

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Angioedema is a life-threatening emergency event that is associated with bradykinin and histamine-mediated cascades. Although bradykinin-mediated angioedema currently has specific therapeutic options, angioedema is sometimes intractable with current treatments, especially histamine-mediated angioedema, suggesting that some other mediators might contribute to the development of angioedema. Fatty acids are an essential fuel and cell component, and act as a mediator in physiological and pathological human diseases. Recent updates of studies revealed that these fatty acids are involved in vascular

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44

Moldovan, Dumitru, Noémi Bara, Valentin Nădășan, Gabriella Gábos, and Enikő Mihály. "Consequences of Misdiagnosed and Mismanaged Hereditary Angioedema Laryngeal Attacks: An Overview of Cases from the Romanian Registry." Case Reports in Emergency Medicine 2018 (October 22, 2018): 1–6. http://dx.doi.org/10.1155/2018/6363787.

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Emergency department (ED) physicians frequently encounter patients presenting with angioedema. Most of these involve histamine-mediated angioedema; however, less common forms of angioedema (bradykinin-mediated) also occur. It is vital physicians correctly recognize and treat this; particularly since bradykinin-mediated angioedema does not respond to antihistamines, corticosteroids or epinephrine and hereditary angioedema (HAE) laryngeal attacks can be fatal. Here we present four case reports illustrating how failures in recognizing, managing, and treating laryngeal edema due to HAE led to asph

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Chinju, Mahesh P A, and Shilpa Palaksha. "Ketorolac induced non allergic angioedema: A case report." International Journal of Research in Pharmaceutical Sciences 11, no. 3 (2020): 4342–46. http://dx.doi.org/10.26452/ijrps.v11i3.2650.

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Non- Steroidal anti-inflammatory drugs (NSAIDs) are among the most commonly prescribed category of drugs. NSAIDs are the main cause of allergic reactions both in adults and children. Hypersensitivity reactions due to NSAIDs involve 0.3% to 0.5% of the overall population. Among the different types of NSAIDs induced hypersensitivity reactions, urticaria and angioedema are the most common. Angioedema can be of two types, allergic(IgE) & Nonallergic( Non IgE) mediated. Allergic angioedema is immune mediated but non allergic angioedema mimic immune mediated allergic reaction without underlying

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46

Irons, Brian K., and Ashwani Kumar. "Valsartan-Induced Angioedema." Annals of Pharmacotherapy 37, no. 7-8 (2003): 1024–27. http://dx.doi.org/10.1345/aph.1c520.

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OBJECTIVE: To report a case of dose-dependent angioedema secondary to the use of the angiotensin-receptor blocker (ARB) valsartan. CASE SUMMARY: A 64-year-old Hispanic woman presented with swelling of the lips shortly after an increase in her valsartan dose for uncontrolled hypertension. Other potential causes were not identified. The angioedema subsequently resided after a dosage reduction and observation. Use of the Naranjo probability scale indicated a probable relationship between the angioedema and valsartan therapy in this patient. DISCUSSION: Drug-induced angioedema is often associated

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Kedarisetty, Suraj, Evan Jones, Derrick Tint, and Ahmed M. S. Soliman. "Air Pollution and Angioedema." Otolaryngology–Head and Neck Surgery 161, no. 3 (2019): 431–38. http://dx.doi.org/10.1177/0194599819846446.

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Objective To identify environmental factors that may precipitate angioedema. Study Design Case series with chart review. Setting An urban tertiary care medical center. Subjects and Methods After institutional review board approval was obtained, a chart review of all patients who presented to Temple University Hospital with angioedema from January 2012 to December 2014 was performed. Patient demographics and hospital course were gathered. Environmental data on the dates of presentation, including precipitation, humidity, and air pollution, were obtained from regional Environmental Protection Ag

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Bliznetz, Elena A., Ekaterina A. Viktorova, Elena A. Vishneva, et al. "Hereditary angioedema. Clinical guidelines. (D84.1)." Russian Journal of Allergy 18, no. 2 (2021): 77–114. http://dx.doi.org/10.36691/rja1447.

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Hereditary angioedema is a rare, potentially life-threatening genetic disease that manifests with skin and mucous/submucosal swelling that occurs under the influence of bradykinin. The clinical guidelines for hereditary angioedema (code for the International Statistical Classification of Diseases and Related Health Problems D84.1) were developed in December 2020 by the Russian Association of Allergology and Clinical Immunology, Association of Medical Geneticists, National Association of Experts in the Field of Primary Immunodeficiencies, Union of Pediatricians of Russia. In December 2020, the

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Kucharczyk, Aleksandra, Grzegorz Porębski, Michał Rząd, et al. "Lanadelumab demonstrates high efficacy in reducing the frequency of angioedema attacks in patients with severe HAE in real-life settings." Pediatria i Medycyna Rodzinna 19, no. 4 (2023): 334–42. http://dx.doi.org/10.15557/pimr.2023.0054.

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Introduction and objective: Evaluation of lanadelumab efficacy in preventing angioedema attacks in patients with severe hereditary angioedema due to C1-inhibitor deficiency in Poland and descriptive analysis of this group of patients. Materials and methods: Retrospective analysis of patients treated with lanadelumab in Poland. Data were acquired from the electronic database of the National Health Fund, compiled from 15 hereditary angioedema centres. Only patients with severe hereditary angioedema course (at least 12 severe – abdominal, pharyngeal or laryngeal – hereditary angioedema attacks pe

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Longhurst, Hilary J., and Konrad Bork. "Hereditary angioedema: an update on causes, manifestations and treatment." British Journal of Hospital Medicine 80, no. 7 (2019): 391–98. http://dx.doi.org/10.12968/hmed.2019.80.7.391.

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Hereditary angioedema is a rare genetic disorder caused by deficiency of C1 esterase inhibitor (C1-INH) and characterized by recurrent episodes of severe swelling that affect the limbs, face, intestinal tract and airway. Since laryngeal oedema can be life-threatening as a result of asphyxiation, correct diagnosis and management of hereditary angioedema is vital. Hereditary angioedema attacks are mediated by bradykinin, the production of which is regulated by C1-INH. Hereditary angioedema therapy relies on treatment of acute attacks, and short- and long-term prophylaxis. Acute treatment options

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