Successful off-pump coronary artery bypass graft surgery in a patient with hereditary angioedema

Lehmann, Andreas; Lang, Johannes; Boldt, Joachim; Saggau, W

doi:10.1053/jcan.2002.125132

Cited by 18 publications

(8 citation statements)

References 25 publications

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“…Because antifibrinolytics are less effective in long-term HAE prophylaxis, preoperative treatment focuses on attenuated androgens and C1-INH concentrate. In patients with known HAE caused by C1-INH deficiency, preoperative prophylaxis with attenuated androgens, either danazol or stanozolol, has been shown to be effective in many patients, 359,[364][365][366] although some patients nonetheless developed swelling. 358,367 For short-term prophylaxis, attenuated androgens may be administered from 5 days before to 3 days after the event, danazol at a dose of 10 mg/kg/d, maximum 600 mg per day, or stanozolol at a dose of 6 mg per day.…”

Section: Treatmentmentioning

confidence: 99%

“…According to Dodin et al, 411 the lumbar bone mass slightly increased by the end of the third and sixth months. 366 The current investigation measured the degree to which the minimum effective dose of danazol for HAE control influenced bone turnover. All patients cared for at the Hungarian HAE Center were involved in this study.…”

Section: Treatment-associated Conditionsmentioning

confidence: 99%

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Hereditary and acquired angioedema: Problems and progress: Proceedings of the third C1 esterase inhibitor deficiency workshop and beyond

Agostoni¹,

Aygören‐Pürsün²,

Binkley³

et al. 2004

Journal of Allergy and Clinical Immunology

593

658

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Hereditary angioedema (HAE), a rare but life-threatening condition, manifests as acute attacks of facial, laryngeal, genital, or peripheral swelling or abdominal pain secondary to intra-abdominal edema. Resulting from mutations affecting C1 esterase inhibitor (C1-INH), inhibitor of the first complement system component, attacks are not histamine-mediated and do not respond to antihistamines or corticosteroids. Low awareness and resemblance to other disorders often delay diagnosis; despite availability of C1-INH replacement in some countries, no approved, safe acute attack therapy exists in the United States. The biennial C1 Esterase Inhibitor Deficiency Workshops resulted from a European initiative for better knowledge and treatment of HAE and related diseases. This supplement contains work presented at the third workshop and expanded content toward a definitive picture of angioedema in the absence of allergy. Most notably, it includes cumulative genetic investigations; multinational laboratory diagnosis recommendations; current pathogenesis hypotheses; suggested prophylaxis and acute attack treatment, including home treatment; future treatment options; and analysis of patient subpopulations, including pediatric patients and patients whose angioedema worsened during pregnancy or hormone administration. Causes and management of acquired angioedema and a new type of angioedema with normal C1-INH are also discussed. Collaborative patient and physician efforts, crucial in rare diseases, are emphasized. This supplement seeks to raise awareness and aid diagnosis of HAE, optimize treatment for all patients, and provide a platform for further research in this rare, partially understood disorder.

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Section: Treatmentmentioning

confidence: 99%

Section: Treatment-associated Conditionsmentioning

confidence: 99%

Hereditary and acquired angioedema: Problems and progress: Proceedings of the third C1 esterase inhibitor deficiency workshop and beyond

Agostoni¹,

Aygören‐Pürsün²,

Binkley³

et al. 2004

Journal of Allergy and Clinical Immunology

593

658

View full text Add to dashboard Cite

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“…C1-INH concentrate at a dose of 500 or 1000 U has been used as preoperative prophylaxis in only a few patients. (74,75) The risk of developing angioedema attacks secondary to dental surgery or other oral manipulations cannot be completely avoided by preoperative prophylaxis. It is therefore important to inform patients that an angioedema attack might occur, describe the clinical symptoms of laryngeal edema, and tell them what to do if laryngeal edema occurs.…”

Section: Controlling Triggering Conditionsmentioning

confidence: 99%

Therapeutic options for patients with angioedema due to C1-inhibitor deficiencies: from pathophysiology to the clinic

Castelli¹,

Zanichelli²,

Cugno³

2012

Immunopharmacology and Immunotoxicology

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Deficiencies in the inhibitor of the first component of human complement (C1-INH) are clinically associated with both hereditary angioedema (HAE) and acquired angioedema (AAE). The reduction in C1-INH function leads to the activation of the classical complement pathway and consequent complement consumption, as well as to the activation of the contact system and the generation of bradykinin, the vasoactive peptide that increases vascular permeability and causes angioedema. The clinical features of C1-INH deficiencies are the same in both forms of angioedema, and include subcutaneous non-pruritic swelling, the involvement of the upper respiratory tract, and abdominal pain due to partial obstruction of the gastrointestinal tract; however, AAE patients have no family history of angioedema and are characterised by the late onset of symptoms. The aim of therapy is to prevent or reverse angioedema. Advances in our understanding of the complex effects of C1-INH deficiency at molecular level have led to new targeted approaches to the treatment of HAE and AAE. Three new treatments have recently become available: a kallikrein inhibitor that prevents bradykinin release, an antagonist of bradykinin receptors that blocks bradykinin action, and a recombinant human C1-INH molecule produced in transgenic rabbits that replaces the deficient protein. These new drugs have expanded the armamentarium of treatments for angioedema due to C1-INH deficiency, which was previously limited to attenuated androgen, antifibrinolytic drugs, and C1-INH plasma concentrate.

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“…Furthermore, C1INH concentrates appear to be equal efficacy for all types of HAE attacks - including laryngeal attacks where it can be life-saving [31]. C1 inhibitor concentrates have also been successfully used for both short-term [34-37] and long-term prophylactic treatment of HAE [38-40]. C1INH concentrate became the preferred modality of treatment for acute attacks of HAE in some countries where it is available.…”

Section: Introductionmentioning

confidence: 99%

HAE therapies: past present and future

Zuraw

2010

All Asth Clin Immun

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Successful off-pump coronary artery bypass graft surgery in a patient with hereditary angioedema

Cited by 18 publications

References 25 publications

Hereditary and acquired angioedema: Problems and progress: Proceedings of the third C1 esterase inhibitor deficiency workshop and beyond

Hereditary and acquired angioedema: Problems and progress: Proceedings of the third C1 esterase inhibitor deficiency workshop and beyond

Therapeutic options for patients with angioedema due to C1-inhibitor deficiencies: from pathophysiology to the clinic

HAE therapies: past present and future

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