RÉSUMÉ
We studied the bactericidal activity (against P. aeruginosa) and chemotactic ability of polymorphonuclear leukocytes from 26 diabetic patients in three treatment groups (oral hypoglycemic, daily insulin, and continuous insulin infusion). Patients were studied before entry into intensified management protocols, and after intensified management in 11 of the 26 patients. Diabetic serum had a persistent inhibitory effect on both diabetic and normal white cells, but normal serum was unable to fully correct diabetic white cell killing to control values. After intensified management of diabetes, there was an improvement in bactericidal function of diabetic patient white cells, but not in the effect of diabetic serum. Diabetic serum, and to a lesser extent diabetic white blood cells, are defective mediators of killing of P. aeruginosa. Chemotaxis was normal in all patient groups. These findings confirm the earlier work of others showing that some patients with diabetes mellitus have a defect in host defense against infection with bacteria.
Sujet(s)
Chimiotaxie des leucocytes , Diabète de type 1/sang , Diabète de type 2/sang , Granulocytes neutrophiles/physiologie , Adulte , Sujet âgé , Glycémie/analyse , Diabète de type 1/traitement médicamenteux , Hémoglobine glyquée/analyse , Humains , Hypoglycémiants/usage thérapeutique , Insuline/usage thérapeutique , Pompes à insuline , Adulte d'âge moyen , Pseudomonas aeruginosaRÉSUMÉ
A male patient presented with polyostotic fibrous dysplasia, elevated serum gonadotropin levels, primary gonadal failure, and an immunoglobulin M (IgM) monoclonal gammopathy. When the patient's serum was added to radioiodinated human follicle-stimulating hormone (125I-hFSH)-bovine testis membrane-receptor complex solubilized by detergent, followed by the addition of antihuman immunoglobulin G ((anti-hIgG), the preformed complex was precipitated. No such precipitation was seen when normal human or rabbit serum, serum from a patient with polyostotic fibrous dysplasia, or serum from other patients with polyclonal gammopathies were utilized. The patient's serum did not precipitate free 125I-hFSH. Detergent-solubilized testis receptor not complexed to hFSH, as well as highly purified radioiodinated receptor were also precipitated when this serum was added followed by anti-hIgG. Our results indicate that serum from the patient contained antibodies to FSH testis receptor. It is possible that antibodies to gonadal receptors may exist in other patients, although it is not yet possible to assume a causal relationship between the presence of receptor antibodies and gonadal failure.