Smith Q T, Hamilton M J, Biros M H, Pihlstrom B L
Epilepsia. 1979 Feb;20(1):17-23. doi: 10.1111/j.1528-1157.1979.tb04772.x.
Immunoglobulin A, phenytoin, and protein were determined in plasma, unstimulated and stimulated whole saliva and stimulated and unstimulated parotid saliva from seizure subjects, aged 18 or more, who had ingested phenytoin for 1 year or more from controls. Patient subgroups with low plasma IgA and with gingival overgrowth were evaluated separately. Plasma and salivary phenytoin and ratios of salivary to plasma phenytoin concentrations corresponded to published reports. Plasma IgA was significantly decreased in the total patient group. However, salivary IgA expressed as the concentration or as the proportion of salivary protein, with one exception, was not significantly decreased in any type of saliva from the total patient group or subgroups. Significant phenytoin induced increases in salivary IgA were noted. IgA secretion rate by the parotid gland was significantly increased in the total patient group. This investigation does not indicate a deficiency of oral IgA from chronic phenytoin ingestion. Thus, it appears unlikely that decreased oral IgA with a consequent enhanced susceptibility to inflammation contributes to phenytoin associated gingival overgrowth.
