Diphenylhydantoin half-life was determined in 5 patients before and during treatment with carbamazepine. It caused a significant decrease in the diphenylhydantoin half-life from 10.6 hours to 6.4 hours. Seven patients who for a period had been given diphenylhydantoin were also started on carbamazepine. This resulted in a fall in serum diphenylhydantoin levels in 3 of the patients. Alterations in warfarin half-life, serum warfarin, and plasma prothrombinproconvertin concentration during carbamazepine treatment were compatible with a stimulation of warfarin metabolism. The effect of carbamazepine on diphenylhydantoin and warfarin metabolism is probably explained by an induction of the drug-metabolizing enzyme system in the liver.
The IgG subclass distribution of autoantibodies to thyroglobulin and thyroid microsomal antigen was studied in 21 patients with Graves' disease during fluctuations in total IgG class autoantibody levels induced by various forms of therapy. In addition, changes in autoantibody subclass distributions were investigated during the natural course of Hashimoto's disease in seven patients taking thyroxine. The autoantibodies were principally of subclasses IgG1 and/or IgG4 in Graves' patients although IgG2 contributed significantly to thyroglobulin antibodies in 5/7 Hashimoto sera. In Graves' disease the distribution of microsomal and thyroglobulin antibodies among the IgG subclasses remained essentially unchanged over periods of 6 months-2 years whether autoantibody levels decreased during carbimazole therapy or increased transiently following 131Iodine treatment or subtotal thyroidectomy. Similar observations were made for thyroglobulin antibodies in Hashimoto patients studied over 2 1/2-4 years; furthermore, the IgG subclass distribution of microsomal antibodies was usually different from that of thyroglobulin antibodies in the same patient. These observations suggest that the microsomal and/or thyroglobulin antibody subclass distribution is characteristic for a particular individual and may be regarded as the 'fingerprint' of an individual's response to these thyroid autoantigens.
The half-life (T /2) of penicillin in blood was determined in 61 patients. An inverse relationship of penicillin T/2 and endogenous creatinine clearance was found. In a group of elderly patients with normal serum creatinine, penicillin T/2 was prolonged due to age-dependent decrease in renal function. The effect of several drugs on the active renal tubular transport mechanism of penicillin was studied. Probenecid increased penicillin T/2 from an average of 40.4 to 104.3 minutes. Penicillin T/2 in the younger patients using probenecid was of the same order as penicillin T/2 in elderly individuals not using probenecid. Phenylbutazone increased penicillin T/2 almost as much as did probenecid. Sulfinpyrazone, acetylsalicylic acid, indomethacin, and sulfaphenazole in therapeutic doses increased penicillin T /2 to a smaller degree. There was no significant change in penicillin T /2 after therapeutic doses of chlorothiazide, sulfamethizole, and sulfamethoxypyridazine.Recently a relationship between penicillin half-life ( T /2), glomerular filtration rate, and para-aminohippuric acid ( PAH) clearance was demonstrated. 12 Many acidic drugs are secreted by the same proximal tubular active transport mechanism as penicillin, but only probenecid and the phenylbutazones have been shown to reduce the rate of renal excretion of penicillin in man. 2 • 3 • 9 Lengthening the penicillin halflife might enhance the therapeutic effect, but it might also increase certain risksY This investigation was undertaken to study the relationship between penicillin T /2 in blood and age-dependent changes in renal
Thyrotrophin releasing hormone (TRH) stimulation test with 200 \g=m\g iv was performed in 35 patients with atoxic sporadic goitre. In 23 patients with diffuse goitre 7 showed a lack of increase in serum thyrotrophin (TSH) at a significantly increased frequency compared to controls (P = 0.0028). In 4 patients with solitary nodules 2 showed no significant response to TRH (negative), while 3 of the 8 patients with multinodular goitres had negative TRH test. Only 6 of the 12 TRH negative patients also had non-suppressible 131I uptake following T3. No significant difference in age and thyroid parameters was found between the TRH negative and TRH positive patients. In 7 TRH negative patients the test was repeated with 400 \g=m\g TRH but all remained negative. Five of these patients were given TRH perorally 80 mg daily for 2 weeks resulting in a significant increase in serum T4 and T3. No detectable increase in TSH was found. The response to iv bovine TSH in 4 TRH negative patients was found to be normal, suggesting that there was normal thyroid sensitivity to TSH. Our findings suggest that patients with TRH negative atoxic goitre can release biological active TSH following prolonged TRH stimulation. The high frequency of a negative standard TRH test in atoxic goitre seems to diminish the diagnostic value of the standard TRH test.Several studies on the thyrotrophin (TSH) response to intravenous doses of thyrotrophin releasing hormone (TRH) in clinical euthyroid patients with sporadic atoxic goitre have demonstrated a lack of response in a varying percentage of the patients studied (Pickardt et al. 1973;Ridgway et al. 1973; Dige-Petersen 8c Hummer 1974).
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