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Biomedical subjects

C Kirkegaard

Publications and source records attributed to C Kirkegaard.

At least 37 records · Page 2Linked to original sources
PubMed1988

Metabolic clearance and production of diiodotyrosine in healthy man.

Metabolic clearance rate (MCR) and daily production rate (PR) of diiodotyrosine (DIT) were estimated using a constant infusion technique of trace amounts of [125-I]-DIT followed by chromatographical isolation of tracer. Median DIT MCR was in eight healthy subjects estimated to 162 l/day x 70 kg (range 135-242), whereas PR was 52 nmol/day x 70 kg (range 25-126). The median serum DIT concentration was 0.27 nmol/l (range 0.16-0.62). In five L-thyroxine substituted subjects without endogenous thyroxine (T4) production, serum DIT concentrations were below 0.02 nmol/l, suggesting that more than 94% of daily produced DIT is secreted by the thyroid gland.

Adult↗
PubMed1987

Thyroid stimulating antibodies in rheumatoid arthritis: an in vitro phenomenon.

The purpose of the study was to evaluate the frequency of thyroid stimulating immunoglobulins and their possible effect in vivo in patients with rheumatoid arthritis. Thyroid stimulating antibodies (TSAb) were present in 17 (68%) of 25 patients with rheumatoid arthritis, whereas only 2 (8%) had thyrotropin binding inhibiting immunoglobulins (TBII). The groups with and without TSAb were comparable with regard to sex, age, anti-inflammatory drugs, serum thyroglobulin levels, antithyroglobulin and antimicrosomal antibodies, rheumatoid factor, as well as to the serum levels of thyroxine and 3, 5, 3'-triiodothyronine. A possible stimulating effect of TSAb in vivo was evaluated by an ultrasensitive immunoradiometric assay for TSH. Both groups had normal serum TSH levels, and no significant difference was found between the two groups suggesting that the demonstration of TSAb in vitro is not always associated with a stimulation of the thyroid gland in vivo.

Adult↗
PubMed1987

Discordance between the cortisol response to insulin-hypoglycemia and 30-minute ACTH stimulation test in chronic alcoholic men.

An insulin hypoglycemia test and a 30-min ACTH stimulation test was performed in 10 chronic alcoholic men, who had been abstinent from alcohol for at least one month. Attenuated serum cortisol responses were found in six of the patients despite a normal ACTH test. Four patients showed normal responses to both the insulin hypoglycemia test and the short ACTH test. No correlation was demonstrated between the cortisol response and the severity of alcoholism, cerebral atrophy, and peripheral neuropathy. It is concluded that in chronic alcoholism the short ACTH test may fail in disclosing hypofunction of the integrated hypothalamic-pituitary-adrenocortical (HPA) axis as assessed with the insulin hypoglycemia test.

Adrenocorticotropic Hormone↗
PubMed1987

The thyrotropin response to thyrotropin-releasing hormone as a biological marker of suicidal risk in depressive patients.

In order to evaluate a possible predictive value for committing suicide of a reduced thyrotropin-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH) stimulation we studied 306 depressed patients. The patients were followed for a mean of 5.8 (SD 2.9) years. During this period, 18 patients committed suicide. The TSH response to TRH stimulation in these 18 patients who committed suicide was lower than in the patients who did not commit suicide. The difference is not statistically significant. It is concluded that the TSH response to TRH cannot be said to identify the patients who later commit suicide.

Adjustment Disorders↗
PubMed1987

Relationships between serum thyrotropin, serum free thyroxine (T4), and 3,5,3'-triiodothyronine (T3) and the daily T4 and T3 production rates in euthyroid patients with multinodular goiter.

Serum TSH, as measured by a sensitive assay, and serum free T4 and T3, as measured by an ultrafiltration technique, were compared in 14 euthyroid patients with multinodular goiter and 14 normal subjects. T4 and T3 turnover studies also were performed, using the single injection, noncompartmental approach. The goitrous patients had serum free T3 levels within the normal range, but their median serum T3 level was increased compared to that in the normal subjects [goitrous patients, 5.48 pmol/L (range, 4.41-9.03); normal subjects, 4.12 pmol/L (range, 2.58-5.78); P less than 0.01]. The T3 production rate (PR) also was elevated in the patients (median, 39.4 nmol/day X 70 kg; range, 28.7-70.5) compared to that in the normal subjects 31.1 nmol/day X 70 kg; range, 24.4-45.2); P less than 0.05). No differences were found between the two groups with regard to serum free T4 levels or T4 PRs. Serum TSH levels in the patients were reduced (median, 0.20 mU/L; range, less than 0.05-1.6) compared to those in normal subjects (1.8 mU/L; range, 0.36-5.1; P less than 0.01). A significant inverse correlation was found between serum TSH levels and free T3 levels (r = 0.70; P less than 0.001), whereas serum TSH did not correlate with serum free T4 or the PR of T4 or T3. Our data suggest that clinically and biochemically euthyroid patients with multinodular goiter have slight T3 hyperproduction, and TSH secretion in the patients studied was more closely related to serum free T3 levels than to serum free T4 levels or the T3 or T4 PR.

Adult↗
PubMed1987

Pituitary-thyroid axis in critical illness.

Severe nonthyroidal illness has been claimed to cause secondary hypothyroidism. We reevaluated this concept measuring serum free T4 and free T3 by an ultrafiltration method and serum TSH by an ultrasensitive technique (detection limit, and serum TSH by an ultrasensitive technique (detection limit, 0.05 mU/L). Forty-five critically ill patients suffering from hepatic coma (n = 10), terminal cancer (n = 9), stroke (n = 8), and respiratory insufficiency not treated (n = 7) and treated (n = 11) with dopamine were studied. The mortality rate was 80%. No patients received glucocorticoids, and only patients in the last group received dopamine. Serum total as well as free thyroid hormone index values were grossly reduced in the majority of the patients. The 34 patients not receiving dopamine in general had normal values of serum free T4 (32 of 34) and free T3 (31 of 34), measurable TSH (33 of 34), and detectable TSH responses to iv TRH (33 of 34). In contrast, the dopamine-treated patients had reduced serum free T4 and TSH levels compared to normal subjects (P less than 0.05), as well as reduced TSH responses to TRH (P less than 0.01). Serum free T4 and free T3 were below the normal range in 3 patients and 1 patient, respectively, and serum TSH was below the detection limit in 2 patients. We conclude that critically ill patients with nonthyroidal illness not receiving dopamine have normal pituitary-thyroid function, whereas dopamine induces some degree of secondary hypothyroidism.

Adult↗
PubMed1987

Renal handling of thyroxine, 3,5,3'- and 3,3',5'-triiodothyronine, 3,3'- and 3',5'-diiodothyronine in man.

The 24-h urinary excretion and renal clearance of thyroxine (T4), 3,5,3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), 3,3'-diiodothyronine (3,3'-T2), and 3',5'-diiodothyronine (3',5'-T2) were measured in 17 healthy subjects. The median urinary excretion was (pmol/24h) T4: 1242, T3: 828, rT3: 12.9, 3,3'-T2: 331, and 3',5'-T2: 5.8. The corresponding renal clearances were in median (ml/min) T4: 31, T3: 133, rT3: 15, 3,3'-T2: 683, and 3',5'-T2: 4.5. The clearances differed mutually (P less than 0.01) as well as from the creatinine clearance (P less than 0.01) which was in median 87 ml/min. Thus, all iodothyronines studied were subject to tubular transport mechanisms besides glomerular filtration. The 3 iodothyronines with 2 iodine atoms in the phenolic ring of the thyronine molecule, T4, rT3 and 3',5'-T2, were mainly tubularly reabsorbed, whereas those with only one iodine atom in the phenolic ring, T3 and 3,3'-T2, were mainly tubularly secreted. It might be hypothesized that the number of iodine atoms in the phenolic ring determines the direction of the tubular transport (presence of 2 iodine atoms is associated with tubular reabsorption, and of one iodine atom with secretion), whereas the rate of tubular transport decreases with decreasing number of iodine atoms in the tyrosylic ring.

Adult↗
PubMed1987

The influence of free fatty acids on the free fraction of thyroid hormones in serum as estimated by ultrafiltration.

Thyroid hormones are displaced from their binding proteins in serum during nonthyroidal somatic illness, and FFA have been claimed to contribute. It seems mandatory to evaluate this effect using techniques for the measurements of serum free thyroid hormones in which serum remains undiluted. We measured the effect of 7 common human FFA on the free fraction of T4, T3 and rT3 in serum from healthy subjects using an ultrafiltration technique by which serum is diluted only minimally. In addition we measured the effect of oleic acid on the free fractions of the iodothyronines in pooled serum from healthy subjects and in pooled serum from patients with nonthyroidal illness. All FFA tested were able to displace both T4, T3 and rT3, but to a varying degree, arachidonic and linoleic acid being the most potent ones. A 20% increase in the free fractions of T4, T3 and rT3, respectively, was obtained by adding between 1.7-3.3 mmol/l, 1.3-4.6 mmol/l and 1.0-2.4 mmol/l of the different FFA. A serum pool obtained from patients with nonthyroidal somatic illness was more sensitive to oleic acid than a serum pool obtained from healthy subjects, since 2-3 times less oleic acid was necessary to induce a 20% increase in the free fractions of thyroid hormones. It is concluded that FFA are able to displace both T4, T3 and rT3 from their serum binding proteins in healthy subjects as well as in patients with nonthyroidal illness. However, serum from patients with nonthyroidal illness was more sensitive to the displacing activity of oleic acid than serum from healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebrovascular Disorders↗
PubMed1986

Influence of free thyroid hormone levels on the TSH response to TRH in endogenous depression.

The TSH response to TRH (delta max TSH) and the serum concentrations of free thyroxine (FT4), 3,5,3'-, and 3,3',5'-triiodothyronine (FT3 and FrT3) were studied in two groups of patients with endogenous depression before and after clinical recovery following electroconvulsive treatment (ECT). Before ECT, the patients from group 1 (n = 17) had a reduced delta max TSH (p less than 0.01), which after ECT rose to values not different from those found in controls. FT4 levels were elevated before ECT (p less than 0.01), and they decreased after ECT (p less than 0.05) to levels similar to those found in controls. FT3 and FrT3 levels were not different from the control values, but FrT3 decreased during ECT (p less than 0.01). In group 2 (n = 19), delta max TSH was reduced both before (p less than 0.02) and after (p less than 0.01) ECT. FT4 levels were increased both before and after ECT (p less than 0.02). Both parameters were unaffected by ECT. The data are compatible with the assumption that the decreased TSH response to TRH found in patients with endogenous depression is secondary to an increase in circulating FT4.

Aged↗
PubMed1985

Effect of amitriptyline on the thyrotropin response to thyrotropin-releasing hormone in endogenous depression.

Patients with endogenous depression whose depressive episodes were clinically resolved after electroconvulsive therapy were divided into two groups: one in which patients remained well (n = 16) and another in which patients relapsed within 6 months (n = 11). Treatment with amitriptyline for 3 weeks did not affect the median thyrotropin (thyroid-stimulating hormone; TSH) response to thyrotropin-releasing hormone (TRH) in recovered patients, whereas that in relapsed patients was significantly enhanced. The data suggest that amitriptyline affects the TSH response to TRH differently in stably recovered and relapsed patients. If this effect is maintained beyond the 3-week period studied, treatment with amitriptyline will invalidate the predictive value of the TRH test.

Aged↗
PubMed1985

Urinary excretion of unconjugated and conjugated 3,5-diiodothyronine.

A radioimmunoassay for the estimation of 3,5-diiodothyronine (3,5-T2) in human urine has been established. The urinary excretion of both glucuronide and sulfate conjugates of 3,5-T2 were estimated after enzymatic deconjugation. In 19 healthy controls the median excretion of unconjugated 3,5-T2 was 276 pmol/d, whereas the median excretion of glucuronidated and sulfated 3,5-T2 in 7 healthy subjects was 448 and 451 pmol/d, respectively. The median excretion of 154 pmol/d in 9 hypothyroid patients did not differ from that found in controls. In contrast 12 patients with hyperthyroidism had an enhanced excretion, 1312 pmol/d (P less than 0.01). Compared with previous data on the daily degradation of 3,5-T2, it is concluded that approximately one-sixth of degradated 3,5-T2 is excreted in the urine.

Adult↗
PubMed1985

Dexamethasone suppression test, TRH test and Newcastle II depression rating in the diagnosis of depressive disorders.

The dexamethasone suppression test (DST), the thyrotropin releasing hormone (TRH) test and the Newcastle II depression rating (NII) were compared with the clinical diagnosis and evaluated in 61 patients fulfilling the criteria of an affective disorder according to the DSM-III classification. A statistically significant correlation between clinical diagnosis and DST as well as NII, but not between clinical diagnosis and TRH test, was found. There was no correlation between DST and the severity of depression according to the Hamilton depression rating. The nosographic and the diagnostic specificities and sensitivities for the DST, TRH test and NII and DST and NII, a nosographic sensitivity of 50% and a nosographic specificity of 84% were found. Correspondingly, the diagnostic sensitivity was 43% and the diagnostic specificity was 88%. The DST and the TRH test were found of no value in the prediction of the response to antidepressive treatment. Mainly because of a low diagnostic sensitivity the NII, the DST and the TRH test are of limited value in the diagnosis of depressive disorders.

Adult↗
PubMed1985

The effects of phenytoin (diphenylhydantoin) on the extrathyroidal turnover of thyroxine, 3,5,3'-triiodothyronine, 3,3',5'-triiodothyronine, and 3',5'-diiodothyronine in man.

The extrathyroidal metabolism of T4, T3, rT3, and 3',5'-diiodothyronine (3',5'-T2) was studied before and after treatment with 350 mg phenytoin (DPH) daily for 14 days in six hypothyroid patients receiving constant L-T4 replacement. The total and free serum concentrations of the four iodothyronines were reduced by approximately 30% during DPH treatment, whereas the free fractions in serum were unaltered. Concomitantly, serum TSH increased 137% (P less than 0.02). The production rate (PR) of T4 decreased 16% (P less than 0.005), indicating decreased intestinal absorption (bioavailability) of oral L-T4 during DPH treatment. The fractional rate of 5'-deiodination of T4 to T3 increased from 27% to 31% (P less than 0.05), whereas the rate of 5-deiodination of T4 to rT3 decreased from 45% to 25% (P less than 0.05). The urinary excretion of free and conjugated T4 was 2.3% of the T4 PR and was unaffected by DPH. Thus, the amount of T4 metabolized through nondeiodinative pathways apart from urinary excretion increased from 25% to 44% (P less than 0.05). The apparent distribution volume (Vd) of T4 increased (P less than 0.05), whereas the pool size was unchanged. The PR of T3 did not change during DPH treatment, nor did the mean transit time or the cellular clearance. The rT3 PR was reduced by 54% (P less than 0.02) during DPH treatment. Concomitantly, the transit time increased 10-fold (P less than 0.05), whereas Vd and pool size increased 5-fold (P less than 0.01 and P less than 0.05, respectively). The turnover of 3',5'-T2, in contrast to that of the other iodothyronines, did not change significantly during DPH treatment. T3 formation from T4 was measured in liver microsomal fractions from rats treated for 8 days with DPH and was almost identical to that in untreated animals. The data demonstrate that DPH in therapeutic concentrations did not affect serum protein binding of the iodothyronines. DPH reduced the intestinal absorption of T4 and increased the nondeiodinative metabolism of T4. The resulting decrease in total and free serum T4 and T3 was associated with an increase in serum TSH, demonstrating reduced negative feedback on the pituitary. Our data do not support the assumption that DPH induces increased hepatic deiodinating enzyme activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1985

The bioavailability of thyroxine and 3,5,3'-triiodothyronine in normal subjects and in hyper- and hypothyroid patients.

A new method for the estimation of the bioavailability of thyroxine (T4) and 3,5,3'-triiodothyronine (T3) is described based on gel separation followed by antibody extraction of labelled T4 and T3 from serum, and using the area under the curve of disappearance of the tracer (AUC) for the calculations. The peak serum concentrations of radioactive labelled T4 and T3 were reached approximately 90 min after oral administration of both tracers. The relative difference of duplicate estimations was below 10% (n = 3). The bioavailability of T4 in 6 euthyroid controls was in median 65% (range 64-75%), and it was significantly increased both in hyperthyroidism (88% (75-99%), n = 6, P less than 0.01) and hypothyroidism (84% (67-100%), n = 6, P less than 0.02). The bioavailability of T3 in 6 euthyroid controls was in median 78% (69-99%) and significantly greater than that of T4 (P less than 0.02). The bioavailability was unaffected by hyperthyroidism (79% (61-98%), n = 9) and hypothyroidism (77% (66-97%), n = 7). No significant difference between T4 and T3 bioavailabilities was found in hyper- or hypothyroidism. The clinical implication of the present study is that the bioavailability of T4 and T3 is almost identical and approximately 80% in patients with severe hypothyroidism.

Adult↗
PubMed1984

Thyroid stimulating immunoglobulins in patients in long-term remission after Graves' disease.

Thyroid stimulating antibodies (TSAb) and thyrotropin binding inhibiting immunoglobulins (TBII) were measured in 32 patients with Graves' disease who had been in remission for at least two years after treatment was been stopped. Seventeen patients had been treated with antithyroid drugs, and 15 patients with 131Iodine. In the first group 3 of 17 patients had TSAb and one TBII, whereas in the second group 4 of 15 patients had TSAb and two TBII. One patient from each group had inhibiting TSAb. During the follow-up one patient from each group relapsed, whereas 5 patients from the second group developed myxoedema. No relationship between the clinical outcome and TSAb and TBII was found.

Adult↗
PubMed1984

Prediction of relapse with the TRH test and prophylactic amitriptyline in 39 patients with endogenous depression.

The authors conducted a double-blind prospective study of 39 patients with unipolar endogenous depression who recovered after ECT. Thyrotropin (TSH)-releasing hormone (TRH) tests were performed before and after ECT. Patients were divided into three groups on the basis of their altered TSH response: Persistent remission was predicted for patients in group 1 (N = 15) and relapse was predicted for groups 2A (N = 13) and 2B (N = 11). Patients in groups 1 and 2A received placebo and those in group 2B received amitriptyline for 6 months. Fewer relapses occurred in groups 1 and 2B than in group 2A (p less than .05), showing that relapse can be predicted by the TRH test and prevented by amitriptyline.

Adult↗