No abstract

No abstract

Treatment with the chemotherapeutic combination of 160 mg. trimethoprim plus 800 mg. sulfamethoxazole twice daily increased the serum creatinine level by an average of 2 mg. per 1. in 21 patients. The effect was clearly reversible. The chemical analysis of creatinine was not affected by the addition of trimethoprim, sulfamethoxazole or their metabolites. In 2 subjects given the drug combination for 12 days renal excretion and 24-hour clearances of creatinine decreased but iothalamate 131I clearance was unchanged. Consequently, the rise in serum creatinine does not indicate any decrease in the glomerular filtration rate. The serum creatinine started to rise within 4 hours after oral administration of a single dose. The rise in serum creatinine could be produced with trimethoprim alone but not with sulfamethoxazole alone. When the plasma creatinine was raised to 100 mg. per l. in healthy subjects (by giving creatinine orally), trimethoprim increased the creatinine levels 10 times as much as at normal plasma levels. The effect was interpreted as a competitive inhibition of the mechanism for tubular secretion of creatinine through the base-secreting pathway.

Quantitative immunoglobulin determinations were performed by a single radial imrmmo‐diffusion method with verified specificity and precision. The identification of sernm‐IgA or secretory‐IgA in gingival fluid was carried out in double diffusion in gel experiments with the use of a specific anti‐serum to “secretory piece”. Gingival fluid was collected with micropipettes by capillarity from subjects with different degrees of gingival inflammation. Blood and mixed saliva were sampled from each individual at the same time. In accordance with previous studies the gingival fluid occured after irritation of the gingival tissue. The amount of the gingival fluid increased with the severity of the inflammation. The contents of the different immumoglobulins in gingival fluid conformed to those, in serum. The possible reason of a slight tendency to lower contents of IgA and IgM in gingival fluid compared to those in serum in subjects with chronically inflamed gingivae is discussed. No “secretory piece” was demonstrated in any samples of gingival fluid tested at different dilutions. The immunoglobulin A in gingival fluid was indicated to be of serum‐IgA‐type. The origin of the immunoglobulins in gingival fluid is discussed.

No abstract