Biomedical subjects
Publications and source records attributed to C Kirkegaard.
Thyrotropin response to thyrotropin-releasing hormone is impaired during endogenous depression and normalized between the depressive periods. Changes in the thyrotropin response to thyrotropin-releasing hormone were shown to be of predictive value and might be useful in the control of continuation therapy with antidepressants in patients with endogenous depression.
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The combination of electroconvulsive treatment (ECT) and i.v. L-tryptophan (T) was compared with ECT and saline in double-blind study comprising 20 patients with endogenous depression. No significant difference was found with regard to the number of ECT given nor in the rate of reduction of depressive symptoms. Except for a slight decrease of plasma total tryptophan in the palcepo group, no difference were found in plasma total and free tryptophan nor in the concentration of total tryptophan in the cerebrospinal fluid.
The concentrations of insulin and thyroid hormones, tryptophan, electrolytes, urea, plasma proteins in the cerebrospinal fluid, and glucose in blood and cerebrospinal fluid in manic-melancholic patients were studied. As control groups served patients suffering from other psychiatric disorders as well as neurological and orthopedic patients. Apart from the blood values of thyroid hormones, the results showed no differences between the various diagnostic groups, neither in the abnormal states nor when recovered. For blood thyroxine and free thyroxine index, a statistically significant differences was seen in unipolar (melancholic) patients, namely a decrease concomitant with the clinical improvement. A tendency in the opposite direction of the thyroxine values was found in bipolar (melancholic) patients. In the manic group a marked decrease in the thyroxine values was obtained in the lithium-treated patients.
Kinetic studies of T4 and T3 using a noncompartmental approach were performed in seven patients with pretreatment severe hypothyroidism maintained on L-T4 replacement. Each subject received a combined tracer dose of labeled T4 and T3 as an iv bolus before and during peroral treatment with propranolol. Serum T4 was unchanged, while a significant decrease of 13% was found in serum T3. The disposal rates (DR) of T4 and T3 decreased significantly, and the ratio between the DR off T3 and the DR of T4, the conversion rate, was significantly reduced during propranolol treatment. The decrease in the DR of T4 suggests a reduction in the bioavailability of L-T4 during propranolol, possibly due to a decrease in intestinal absorption. The decrease in the conversion rate indicates a reduced extrathyroidal conversion of T4 to T3 during propranolol treatment.
A possible extrathyroidal effect of propylthiouracil (PTU) and carbimazole on serum levels of thyroxine (T4), triiodothyronine (T3), 3,3',5'-triiodothyronine (reverse T3) and on thyrotrophin-releasing hormone (TRH) induced thyrotrophin (TSH) release was estimated in 19 patients with severe hypothyroidism treated with T4. During PTU medication a significant decrease in serum T3 from 90 +/- 16 (SD) to 79 +/- 23 ng/100 ml (P less than 0.01) and a reciprocal increase in serum reverse T3 from 51 +/- 14 (SD) to 58 +/- 20 ng/100 ml (P less than 0.025) were found. No significant changes in serum T4, basal serum TSH or response to TRH could be demonstrated. Carbimazole did not change any of the parameters studied.
A simple radioimmunoassay for serum reverse triiodothyronine on small reusable Sephadex G 25 fine columns has been developed. The assay was unaffected by serum volumes of up to 100 microliter. The recovery of reverse T3 added to serum was in the mean 98.3 +/- SEM 3.2% and the coefficient of variation within and between assay determinations 5.4% and 7.5%, respectively. The detection limit was 2.2 pg reverse T3/column. Serum reverse T3 in 58 euthyroid controls was in mean 48 +/- SD 9 ng/100 ml, and was positively correlated to age (P less than 0.001). No overlap was found between the control group, and the hypo- and hyperthyroid group respectively. Three patients with T3-toxicosis had a normal serum rT3.
The urinary excretion and serum levels of thyroxine (T4), triiodothyronine (T3) and 3,3',5'-triiodothyronine (reverse T3) was estimated in a longitudinal study of human newborns. The maternal and cord blood was also studied. Neonatal renal function was evaluated using endogenous creatinine clearance. In cord blood serum T3 was found to be lower than in maternal blood, but reverse T3 highly elevated. During the first 5 days of life serum T4 and T3 increased with maximum at 48 and 24 h in contrast to reverse T3 which remained high and then declined rapidly after 4 days. Creatinine clearance during the first 3 days of life increased from 5.3 to 21.9 ml/min/1.73 m2. In the same period the urinary T4 excretion increased from 79 to 281 ng/24 h, urinary T3 excretion from 16 to 44 ng/24 h and urinary reverse T3 from 4 to 15 ng/24 h. The renal excretion of thyroid hormones, corrected for body surface, was decreased compared to adult controls, corresponding to an immature renal function. The lack of ability to excrete thyroid hormones involved primary T3 and reverse T3 suggesting particular immaturity of tubular secretion of these hormones during the neonatal period.
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The relation between clinical status and serial determinations of serum T3, serum T4 and serum TSH has been evaluated in the early phase of medical antithyroid treatment in 12 unselected hyperthyroid patients, and in 19 patients who later during treatment accidentally developed low serum T4 values. Determination of both serum T3 and serum T4 was found necessary to avoid undertreatment. Two patients with signs of hypothyroidism in the early phase developed low serum T4, while serum T3 and serum TSH remained normal. In all of the 19 patients selected with low serum T4, serum T3 was normal. Serum TSH was elevated in 5 patients without hypothroid symptoms, while 2 developed hypothyroid symptoms in spite of normal serum TSH values. Our results suggest that serum T4 is a more sensitive parameter than both serum TSH and serum T3 in avoiding overtreatment during medical antithyroid treatment.
Seventy-seven patients with Graves' disease, with an average of 56 years of age were treated with carbimazole in the period 1968-1975. The duration of therapy was on an average, 17.9 months and the follow-up on an average, 28.5 months. Remission was found only in 32% of the patients. Data on the urinary iodine excretion from a total of 127 euthyroid controls and 15 patients with Graves' disease living in the same area were collected during the periods: 1962-1964, 1965-1968, 1971-1973 and 1972-1974. No significant difference was found in the urinary iodine excretion in the period 1962-1973 and no significant difference was found in the urinary iodine excretion between the patients with Graves' disease and the euthyroid controls. Our data demonstrate a high relapse rate following long-term treatment with anti-thyroid drugs in an area with relative low iodine intake.
Thyrotrophin releasing hormone (TRH) stimulation test with 200 microng 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 microng 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.
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