[Elevated thyroid hormone levels in the absence of hyperactivity].

Elevated blood levels of thyroid hormones may be due to causes other than glandular hyperactivity. We have seen transient increases in total thyroxine (TT4), free thyroxine index (FTI), free thyroxine (FT4), and total triiodothyronine (TT3) in 12 women and 3 men with subacute thyroiditis and 2 women with painless (silent) postpartum thyroiditis. Elevated TT4, FTI, and FT4 were found in 11 of 85 patients treated with amiodarone. High TT4, but not FTI or FT4, was seen in 4 women using contraceptives, in 2 pregnant women and in 2 men with liver dysfunction. All hormones, except TSH, were elevated in a patient in whom thyrotoxicosis factitia was later proved. High FTI, TT4 or FT4 but not TT3 were detected in 11 of 20 patients treated with l-throxine after surgical thyroidectomy and in 10 of 68 treated for hypothyroidism. To avoid treating when thyroxicosis is not present and to avoid reducing or stopping vital drug treatment, familiarity with these states which alter blood hormone levels is important.

PIP: Elevation of the thyroid hormone levels might be induced by causes not reflecting overexpressivity of the gland. According to the authors' experience in Israel, mistakes have been encountered frequently in the averaging of the results, which on occasion brought about withdrawal of therapy without any justified reason, or therapy administration without need. 15 patients diagnoses with subcutaneous thyroiditis were treated with aspirin, prednisone, and propranolol, and reached normal levels of hormones in 6-8 weeks of time. In postpartum thyroiditis, normal levels of thyroid hormone were reached in 3-4 months without pharmacological intervention. Extrinsic overdose of iodine (aniodaron administration) was completed in all patients without any sign of thyroid overactivity. Alleged high levels of TT4 (total thyroxin) were diagnoses in women taking oral contraceptives and in men with cirrhotic liver disease but with normal levels of free thyroxin index and TT3. Overactivity of the thyroid gland was suspected in a patient receiving up to 100 mcg dose of eltroxin who tried to lose weight according to this method. Patients who used L-thyroxine after complete/partial thyroidectomy had high levels of TT4 but in all the TT3 and thyroid stimulating hormone levels were normal. The need for recognition of these cases is emphasized in order to avoid any over treatment which is harmful and depressive or from lowering the dose and halting the use of valuable drugs without obvious reason.

Effects of glibenclamide on serum lipids, lipoproteins, thromboxane, beta-thromboglobulin, and prostacyclin in non-insulin-dependent diabetes mellitus.

A study was conducted to determine the effects of glibenclamide on serum lipoproteins, apolipoproteins, thromboxane (TXA2), prostacyclin (PGI2), and beta-thromboglobulin (B-TGL) in patients with newly diagnosed non-insulin-dependent diabetes mellitus (NIDDM). In 20 NIDDM patients, aged 34 to 67 (mean, 53.6) years, without clinical signs of atherosclerotic disease and whose blood sugar level was over 140 mg/dl after four weeks of dietary treatment, fasting blood samples were taken before the beginning of the trial, after four weeks of dietary treatment, and after four and eight weeks of combined dietary and glibenclamide treatment. Pretrial levels of total serum cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) in the diabetic patients did not differ from those in nondiabetic controls, whereas high-density lipoprotein cholesterol (HDL-C) levels and the percentage of TC bound to HDL (HDL-C%) were significantly lower in the patients than in controls. After combined dietary and glibenclamide treatment and the normalization of blood sugar, both HDL-C (mg/dl) levels and HDL-C% levels increased significantly. TC, TG, and LDL-C levels decreased. Levels of apolipoproteins A1 and A2 rose and apolipoprotein B fell, but differences were not significant. TXB2 and 6-keto-PGF1-alpha (the inert metabolites of TXA2 and PGI2) and B-TGL were determined by radioimmunoassay. TXB2 and B-TGL levels decreased significantly after glibenclamide administration, indicating attenuation of platelet aggregation. No changes in PGI2 were observed. The results demonstrate the favorable effect of glibenclamide on lipoproteins and apolipoproteins in NIDDM patients, especially in increasing HDL-C levels and HDL-C%, and in attenuating platelet aggregation as indicated by reduction of TXB2 and B-TGL.

Thromboxane, prostacyclin, beta-thromboglobin, and diabetes mellitus.

Plasma levels of beta-thromboglobin (beta-TH) and of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1-alpha, the stable metabolites of thromboxane A2 and prostacyclin, were determined by radioimmunoassay methods in eight patients with noninsulin-dependent diabetes before and after dietary treatment and after administration of the sulfonylurea drug glibenclamide. Blood examinations were performed when hyperglycemia was detected for the first time, four weeks after a dietary regimen was started, and four and eight weeks after glibenclamide treatment was begun. Drug treatment was instituted because, despite a suitable diet, patients' postprandial blood sugar was higher than 8 mmol/L (145 mg/dl). At the initial examination, elevated TXB2 and beta-TH levels indicating platelet hyperactivity and hyperglycemia were found. TXB2 and beta-TH levels decreased significantly after glibenclamide treatment was started, as did the blood glucose level. There was no change in 6-keto-PGF1-alpha. We interpret these results to indicate that diabetes is associated with hyperactivity of platelet aggregation and that control of blood glucose is important because a lower blood glucose level attenuates platelet hyperactivity. Whether the decrease in platelet hyperactivity is a direct result of the lowered blood sugar or reflects the influence of the drug treatment requires clarification.