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Y Frobert

Publications and source records attributed to Y Frobert.

23 records · Page 2Linked to original sources

[Immunity in cystic fibrosis. A comparative study of chronic bronchorrhea of different etiology].

Various aspects of immunity in cystic fibrosis were studied in 24 children and compared with the results in 13 children with other types of chronic bronchial infection. The complement was not significantly altered: number of lymphocytes, delayed hypersensitivity skin reactions, number of T (an B) cells, phytohaemagglutinin lymphocyte stimulation were virtually normal. Only the phagocytic activities (chemotaxis, phagocytosis, bacteridal activity) were altered in 20 out of 24 patients with cystic fibrosis and in a comparable percentage of patients with other types of chronic bronchial infection. No serum inhibitory factor was found and leukocyte enzyme activities were normal. This deficiency of phagocytic functions seems to be, at least in part, secondary to infection.

Bronchial Diseases

[Non specific immunity of children with selective IgA deficiency. Aggravating role of abnormal phenotype of alpha-1-antitrypsin (author's transl)].

Among 998 children with recurrent respiratory diseases 26 children with selective IgA deficiency were found. Three groups were considered according to IgA level in serum: group I with IgA under 0.05 g per litre; group II with IgA between 0.05 and 0.3 g per litre; group III with IgA above 0.3 and under 1 g per litre. Non specific immunity was studied in these patients including immunoglobulin levels, alpha-1-antitrypsin (A.A.T.) phenotypes, phagocytosis of staphylococcus aureus by PMN, lysozyme level, complement system. Cellular immunity was evaluated by IDR tests and rosette forming cells (RE). Only non specific immune systems were disturbed in some patients and appeared as aggravating factors in IgA deficient patients. We found: Abnormal phenotypes of ATT in 11 cases; deficiencies of engulfment in 6 cases, of bactericidal activities of PMN in 7 cases out of 16 studied; decrease of lysozyme level in 4 cases out of 17 studied; increase of IgE level in 9 cases with atopic symptoms in 7 patients. In our experience the chief aggravating factor in IgA deficient patients is abnormal phenotype of AAT.

Adolescent