Failure of pneumococcal vaccine in children with sickle-cell disease.
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Anemia, Sickle Cell↗
Biomedical subjects
S M Fikrig
Publications and source records attributed to S M Fikrig.
Antibody response to capsular polysaccharide vaccine of Streptococcus pneumoniae in patients with nephrotic syndrome.
Twenty-three normal subjects and 19 patients with nephrotic syndrome were vaccinated with tridecavalent pneumococcal capsular polysaccharide vaccine of Streptococcus pneumoniae. The antibody response of the nephrotic patients to pneumococcal capsular antigens was equal to that of the control subjects. These findings indicate that patients with nephrotic syndrome, despite hypogammaglobulinemia, can mount an adequate antibody response to pneumococcal polysaccharides and that there is no evidence of suppressor thymus-derived (T) cells of dysfunctioning bone marrow-derived (B) cells in these patients.
Adolescent↗
Monoclonal IgG anticoagulants delaying fibrin aggregation in two patients with systemic lupus erythematosus (SLE).
There is paucity of information regarding the prolonged plasma thrombin time known to occur in some patients with systemic lupus erythematosus. Detailed investigations of plasma from two such patients disclosed that IgG accounted for this defect in each case. IgG isolated from plasma of either patient possessed the property of delaying fibrin aggregation and prolonging the clotting times of fibrinogen. Preincubation of IgG from either patient with anti-IgG or anti-Fab (rabbit) serum abolished this anticoagulant property. Moreover, the anticoagulant IgG from the first patient was neutralized with anit-k chain and anti-IgG3, that from the second patient with anti-lambda chain and anti-IgG1 serum. These anticoagulants were also dissimilar with respect to their interactions with fibrin(ogen). IgG from the first patient had no anticoagulant activity against fibrin(ogen) species lacking intact Aalpha chains. IgG from the second patient displayed undiminished anticoagulant effect on such fibrin(ogen) species. We conclude that each anticoagulant interacted with a distinct region(s) on the fibrinogen molecule and that these interactions affect or involve sites that participate in the fibrin self-assembly process.
Adolescent↗
Neutrophil chemotaxis in patients with burns.
In a group of 22 patients with second and third degree burns, seven were found to have impaired chemotaxis. The chemotactic defect was present from two to 68 days and eventually became normal. The impairment was found to be due to a primary transient defect in polymorphonuclear leukocytes and not to an inhibitor or inactivator in the serum.
Adolescent↗
Diabetes and neutrophil chemotaxis.
The chemotaxis of PMN cells from adult and juvenile diabetics and proper control subjects was found to be comparable. Similarly, chemotactic activity generated from diabetic sera was not different from the activity generated from the normal sera.
Chemotaxis, Leukocyte↗