Angioedema due to acquired C1-esterase inhibitor deficiency in a patient with Helicobacter pylori infection.

The first component of the classical pathway of the complement system, C1 is regulated by a serum protein, the C1-esterase inhibitor (C1-INH). Deficiency of this protein leads to the release of vasoactive mediators (C2 kinin and bradykinin) that increase vascular permeability and can induce edema formation in subcutaneous and submucosal tissues. The genetic variant of C1-INH deficiency is inherited as an autosomal dominant trait and causes hereditary angioneurotic edema.

The efficacy of short-term danazol prophylaxis in hereditary angioedema patients undergoing maxillofacial and dental procedures.

Purpose: This study evaluated the efficacy of short-term danazol prophylaxis in hereditary angioedema patients undergoing maxillofacial or dental procedures.

Patients And Methods: Twelve patients with a history of edema after dental procedures were administered danazol (600 mg/d) 4 days preoperatively and 4 days postoperatively. The serum levels of complement components were determined preoperatively and postoperatively as well as at 6, 12 and 24 hours in six patients.

Coincidence of hereditary angioedema (HAE) with Crohn's disease.

A patient with two diseases, based presumably on different immunopathological mechanisms, hereditary angioedema (HAE) and Crohn's disease, was followed for 8 years. For more than three years of this observation period, detailed laboratory data were also available and could be analyzed. Both diseases had severe courses requiring chronic treatment with danazol and sulfasalazine, respectively.

[Efficacy of short-term danazol treatment in hereditary angioneurotic edema patients undergoing maxillofacial and dental surgical procedures].

The authors evaluated the efficacy of short-term danazol prophylaxis in 12 hereditary angioedema patients undergoing maxillofacial or dental procedures. Hereditary angioedema is an autosomal dominant disorder resulting from the deficiency of the C1 esterase inhibitor. Characteristic clinical manifestations include the formation of subcutaneous and submucosal edema.

[Simultaneous occurrence of hereditary angioneurotic edema and Crohn disease].

Hereditary C1 esterase inhibitor deficiency is often associated with immunpathologic disorders. The authors present a case of the rare coincidence of hereditary angioedema (HAE) and Crohn's disease. The history of the patient is analysed along with the familial occurrence of the disease.

Immunoglobulin levels of tonsillar cells.

Immunoglobulin G, A and M contents of homogenized tonsillar lymphocytes were measured. Higher Ig values were found in adults than in children. Inflammatory processes increased the immunoglobulin levels of tonsillar lymphocytes.

Clinical immunological study of T lymphocytes and EA rosette forming cells in tonsils.

Tonsillar E and EA rosette forming lymphocyte subpopulations were studied in 120 tonsillectomized patients. T cell ratios was usually lower in the tonsils than in the blood. EA binding cells were studied with indicator systems of human or rabbit antibody sensitized red cells, respectively.

Bioplast fibrin implants in nasoseptal perforation.

This study includes 9 cases of nasoseptal perforation following submucous septectomy. Sheets from Bioplast fibrin, an absorbable biomaterial, were implanted to prevent thepersistence of perforations. Postoperative mucosal growth on both implant surfaces ensured closure in 6 of the 9 cases.

[Equilibrium troubles with cervical syndrome and their relation with otorhinolaryngology (author's transl)].

The equilibrium troubles occuring in connection with cervical locomotoric diseases and their otorhino-laryngologic relations have been studied in the ORL Department of National Institute of Rheumatism and Medical Hydrology. It has been found that: a) there is no connection between the seriousness of roentgenologic deformations and equilibrium troubles; b) the damage of the periphery is not characteristic; c) the complaints and symptoms are explained by the hypoxia of vestibular kern-areas as well as by damages of receptors in cervical muscles, bands and joints; d) hypotension and other central vascular damages form an important factor in the development of equilibrium troubles.