Prevention of phenytoin associated gingival enlargement--a 15-month longitudinal study.
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Biomedical subjects
Publications and source records attributed to Q T Smith.
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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.
Polyacrylamide gel electrophoresis was used to analyze the effect of Streptococcus sanguis on the anionic proteins in human parotid gland saliva. Cell-free culture supernatants and washed-cell preparations from 23 strains of S. sanguis caused marked modification of various salivary proteins. Control studies showed that the alterations in protein profiles by the bacteria were not due to attachment of protein to the cells. Protease inhibitors were used to confirm that proteolysis by distinct enzymatic activities was responsible for most of the modifications. There was no discernible relationship between the degradation patterns and the various immunologic or genetic groups of S. sanguis. Proteins which contained high concentrations of proline were extensively degraded by S. sanguis. This effect could be blocked with the protease inhibitor phenylmethyl-sulphonyl fluoride.
Cellular glycosaminoglycans were isolated from lymphocytes from patients with cystic fibrosis and controls. The isolated glycosaminoglycans were fractionated by cellulose acetate electrophoresis, analyzed for glucosamine and galactosamine content, and subjected to hydrolysis with bovine testicular hyaluronidase. The total glycosaminoglycan content, the per cent glucosamine and galactosamine, and the distribution of cellular glycosaminoglycans in circulating lymphocytes in cystic fibrosis were no different from controls.
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Parotid salivary proteins from monozygotic twins, dizygotic twins, nontwin sibs, and unrelated male and female subjects of the same age range as the twins were separated by polyacrylamide gel slab electrophoresis at pH 9.0. Variability of the stained protein patterns increased in the order: monozygotic twins; dizygotic twins and nontwin sibs; unrelated subjects. It is concluded that genetic factors are the major contributors to variability of parotid salivary proteins among subjects.
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Serum glutathione reductase (NADPH-GSSG oxidoreductase, EC. 1.6.4.2 (GR)) has been examined in cystic fibrosis subjects (CF), obligate CF heterozygotes, and control subjects. Serum protein concentration was similar in the three groups. Regardless of the units used to express activity (milligrams of protein or milliters of serum) or whether or not samples were dialyzed against water or phosphate buffer, mean serum GR in CF was greater than in control subjects (P less than or equal to 0.002) in all series over several years. Under the above assay conditions no difference in serum GR between control subjects and carriers was detected. Calculated and assayed values of combined control and CF sera agreed as did expected and observed 50% activity in 1:2 sera dilutions in CF, control subjects, and carriers. Addition of FAD to incubation media did not effect enzyme activity in the three groups. Differences between CF and control subjects persisted after dialysis in membranes permitting passage of molecules of approximately 12,000 mol wt or less. These findings would tend to exclude the effect of extraneous serum factors in explaining the diffferences between CF and control subjects. The percentage of initial GR activity after four days storage (0-4 degrees) was significantly greater in CF than in control subjects (P less than 0.025). The effect of heparin on serum GR was recorded as the percentage of activity after incubation with heparin vs. activity in the standard assay for individual subjects. The effect of incubation with 5 mug/ml heparin on serum GR activity was greater in control subjects than in carriers (P less than 0.0005) and CF (P less than 0.0005). Mean serum GR activity in CF and carriers was unaffected by heparin, whereas mean activity in control subjects was decreased. In no control was the percentage of initial activity with heparin greater than the mean of CF and carrier groups. Only 3 of 20 CF and 4 of 20 carrier individuals had percentages lower than the control mean. The CF and carrier distributions were clearly different from the control distribution. Serum GR was determined in seven non-CF individuals with chronic obstructive pulmonary disease (COPD). Activity in the COPD was different from CF and no different from control subjects. In none of these controls or COPD was serum GR as great as the CF mean. Serum GR in no CF was as low as the mean of control subjects or COPD. It is concluded that serum GR activity is greater in CF than in control subjects, carriers, and non-CF COPD subjects; that the difference in activity is not attributable to an extraneous serum factor, that the activity difference is not secondary to chronic respiratory disease; that in comparison with control subjects, GR from CF serum behaves differently after storage; and that serum GR from CF and carriers behaves differently from control GR in the presence of heparin.
Insulin and its vehicle without insulin were administered separately by iontophoresis to patients with cystic fibrosis (CF), obligate heterozygotes, and healthy controls. The resultant sweat chloride concentration after treatment with both preparations was compared in each individual. No difference after the two treatments was found in the control sample. A decrease in sweat chloride concentration after insulin iontophoresis in comparison with the vehicle was observed in both the CF (P smaller than 0.005) and heterozygote (P smaller than 0.01) samples. These observations suggest an involvement of insulin in CF and a possible role of insulin in sweat gland function.
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