Medical Literature - 1982

Acute upper airway obstruction in the adult. 1. Causative disease processes.

Boster SR, Martinez SA. 12/1982 Postgrad.Med.

1982 55-7; Dec;72(6):50-52

Infectious processes that can cause acute upper airway obstruction in adults include Ludwig’s angina, retropharyngeal infection, acute epiglottis, diphtheria, tetanus, and peritonsillar abscess. They are uncommon but potentially lethal. Ludwig’s angina in particular quickly progresses to airway obstruction. In most cases, the mainstays of management are antibiotics, surgical drainage, and if necessary, airway maintenance by tracheostomy, cricothyrotomy, or nasotracheal or endotracheal intubation. Hereditary angioneurotic edema causes episodes of laryngeal edema that may lead to suffocation. In an acute episode the airway must be maintained by endotracheal intubation.

Not available online.

Hereditary angioedema: an appraisal of 104 cases

Cicardi M, Bergamaschini L, Marasini B, Boccassini G, Tucci A, Agostoni A. 7/1982 American Journal of the Medical Sciences


One hundred and four patients affected by hereditary angioedema belonging to 31 families have been studied. Twenty-two percent had the variant form related to the deficiency of the functional activity of serum C1 esterase inhibitor. The remaining 78% of patients had the predominant form, characterized by low antigenic levels and low functional activity of serum C1 esterase inhibitor. Attacks of swelling affected the subcutaneous tissue in 86% of patients; the upper airways in 76% of patients, and the bowel mucose in 75% of patients. Before treatment was available the mortality rate was 56%. One or more attacks a month were present in 46% of cases. The infusion of C1 inhibitor concentrate promptly reversed 14 severe attacks without any side effect. Twenty-nine patients were given long term prophylactic treatment with androgen derivatives with full success. Tranexamic acid reduced the frequency of swelling of 70% of the patients.

Available online at: (small fee)

Effect of treatment with 17 alpha-alkylated androgens on C4 conversion products in hereditary angioedema studied by crossed immunoelectrophoresis

Bergamaschini L, Cicardi M, Tucci A, Agostoni A. 7/1982 Journal of Clinical Pathology


During agarose electrophoresis C4 in the normal human serum is converted into cleavage products of Beta 1 and Beta 2 mobility. By contrast in the serum of untreated patients with hereditary angiodema C4 gives only one Beta 2 peak on crossed immunoelectrophoresis. The normal C4 electrophoretic pattern is restored in serum of patients treated with stanazolol but not with danazol despite the same C1-esterase inhibitor (C1 INH) activities and C4 serum concentration. We suggest that stanazolol besides having specific effect on C1 INH activity can interfere with other protease inhibitors affecting C1 activation.

Available online at:

Hereditary angioneurotic edema and HLA types in two Danish families

Eggert J, Zachariae H, Svejgaard E, Svejgaard A, Kissmeyer-Nielsen F. 7/1982 Archives of Dermatological Research


HLA types were determined in 19 patients and 9 healthy members of 2 Danish families with hereditary angioneurotic edema. The study revealed no connections between hereditary angioneurotic edema and the HLA system.

Available online at: (small fee)

The C1 esterase inhibitor and hereditary angioedema

Frank MM. 4/1982 Journal of Clinical Immunology


Available online at: (small fee)

Funding for Canadian Hereditary Angioedema Network has been generously provided by unrestricted grants from:


CSL Behring


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