Search Results

You are looking at 21 - 30 of 3,834 items for

  • Abstract: goiter x
  • Abstract: Graves x
  • Abstract: hyperthyroidism x
  • Abstract: hypothyroidism x
  • Abstract: levothyroxine x
  • Abstract: T3 x
  • Abstract: T4 x
  • Abstract: thyroglobulin x
  • Abstract: thyroid x
  • Abstract: thyroiditis x
  • Abstract: thyrotoxicosis x
  • Abstract: thyroxine x
  • Refine by Access: All content x
Clear All Modify Search
Restricted access

J. Chakravarty, A. R. Guansing, S. Chakravarty, and C. V. Hughes

ABSTRACT

Systolic time intervals consisting of indices of electromechanical systole (QS2-I), left ventricular ejection time (LVET-I) and pre-ejection period (PEP-I) were calculated serially during therapy in 12 euthyroid, 9 hypothyroid and 9 hyperthyroid individuals. These parameters were analyzed sequentially together with the changes in serum thyroxine (T4), triiodothyronine (T3) and thyrotrophin (TSH) in order to determine the sensitivity of these non-invasive procedures in monitoring peripheral thyroid hormone effect. The results are expreseed in mean ± sem. QS2-I (506.3 ± 8.2 ms) and PEP-I (102.9 ± 4.2) were shortened (P < 0.02 and P < 0.001, respectively) in hyperthyroidism and prolonged (579.3 ± 7.3 and 169.6 ± 3.6 ms) in hypothyroidism (P < 0.01 and P < 0.001, respectively) compared to euthyroid controls (538.1 ± 8.8 and 130.3 ± 5.3 ms), while LVET-I did not change significantly in either condition. Simultaneous determinations of circulating T4, T3 and TSH showed changes appropriate to both hypo- and hyperthyroid states. In 2 patients with T3-thyrotoxicosis, PEP-I was decreased to an average of 103.1 ms, while in 2 patients with compensated hypothyroidism (normal T4 but elevated TSH) this was prolonged to 163.7 ms (average) compared to euthyroid controls. During treatment the hypothyroid group showed significant sequential correlation of TSH and PEP-I. In the hyperthyroid individuals, PEP-I correlated significantly with T4 and T3. PEP-I may be a useful, sensitive, quantitative biologic indicator of thyroid hormone effect on myocardial function.

Restricted access

K. Siersbæk-Nielsen and J. Mølholm Hansen

ABSTRACT

Tyrosine and free thyroxine in the CSF and in serum has been measured in 24 euthyroid patients, in 11 patients with thyrotoxicosis and in 4 patients suffering from myxoedema. The thyrotoxic patients had elevated tyrosine levels in the CSF and in the serum, but rise in tyrosine was greater in the CSF than in the serum and the mean ratio CSF tyrosine/serum tyrosine was significantly elevated as compared to the euthyroid group. In the hypothyroid group, in spite of decreased serum tyrosine values the CSF tyrosine was not decreased. Free thyroxine in the CSF was elevated in the thyrotoxic patients and decreased in the hypothyroid patients. In euthyroid, hyperthyroid and hypothyroid patients an equilibrium was found between free thyroxine in the CSF and in the serum. No correlation was found within the groups between the individual values of tyrosine in the serum and in the CSF or between tyrosine and free thyroxine in the serum and in the CSF.

Restricted access

Daniel Glinoer, Nicole Puttemans, André J. Van Herle, Monique Camus, and André M. Ermans

ABSTRACT

A sequential study of various parameters of thyroid metabolism has been carried out in 2 patients during the weeks following the clinical onset of subacute thyroiditis, the aim being to define the nature and extent of the anomalies of thyroid function. In the early stage, serum thyroxine, protein bound iodine and T3 resin uptake levels were in the thyrotoxic range. In both cases, the serum thyroxine values further decreased with a half-life of 7 days and reached the hypothyroid range at the 6–7th week. Both 131I uptake and TSH plasma levels were found to be low and concomitantly rose at the 6–7th week. In one patient the serum thyroglobulin level was strikingly elevated at the beginning and then fell fairly rapidly; however in both patients, the serum thyroglobulin values remained abnormal. The present study confirmed the concept of a sudden release of preformed hormone stores. Furthermore, the following points were evident: a) marked and transient release of thyroglobulin; b) interruption of the secretory activity during at least 7 weeks; c) adequate functioning of the pituitary-thyroid control mechanism and d) partial recovery of the thyroidal iodine uptake at a time when the hormone secretion was still undetectable.

Restricted access

A. M. Pascual-Leone, E. Besa, F. Hervás, F. Escrivá, and C. Alvarez

Abstract. Rats receiving large doses of thyroxine (30 μg/5 doses) during their first days of life develop an apparently permanent alteration of the hypothalamus-pituitary-thyroid complex. This neonatal thyrotoxicosis has been called neo-T4 syndrome. A state of permanent but not very severe hypothyroidism seems to be induced, accompanied by a decrease in pituitary GH content at least until day 22. In this work, growth hormone content has been measured by a specific radioimmunoassay in the anterior pituitary of 45 and 78 day old neo-T4 and control (saline-injected) rats. GH content of the adult neo-T4 treated animals was significantly lower than that of the adult controls. Administration of different doses of T4 (1.7 μg/100 g body weight/3 doses or 2.5 μg/100 g body weight/8 doses, to 70 day old rats, and 5 μg/100 g body weight/3 doses to 42 day old rats) to adult neo-T4 rats did not alter these decreased pituitary GH levels. This differs from hypothyroid rats, in which T4 administration has been shown to increase pituitary GH content. A third approach was to thyroidectomize neo-T4 and control rats and administer 5 μg T4/100 g body weight, which produced the same increase in pituitary GH in both groups of animals. These results seem to indicate that changes in pituitary GH content of neo-T4 rats are not due to hypothyroidism. Thus, it would appear that treatment with large T4 doses during the early perinatal period not only deranges the hypothalamic-pituitary-thyroid axis but other pituitary functions as well.

Restricted access

Jan H. Solem and Helge Svaar

Abstract. Documented thyrotoxicosis developed in a 12 year old girl with chronic autoimmune thyroiditis. During the following 3 years there was a spontaneous progression from hyperthyroidism to hypothyroidism and vice versa fluctuating from one metabolic state to another. The diagnosis of Hashimoto's thyroiditis was based upon thyroid function tests, elevated titres of antibodies against thyroid constituents, and upon thin-needle biopsy of the enlarged thyroid gland.

Restricted access

H. L. Krüskemper and K. D. Morgner

ABSTRACT

  1. When orally applicated, D-thyroxine (1–4 mg) lead in normal subjects to a dose dependent rise of PB127I, which was accompanied with characteristic changes of 131I-triiodothyronine-resin uptake.

  2. D-thyroxine caused a smaller rise of PB127I of short duration when compared with L-thyroxine.

  3. In patients suffering from thyroid disorders, D-thyroxine is eliminated from serum in analogy with L-thyroxine, i. e. accelerated in hyperthyroidism, delayed in hypothyroidism.

Free access

Anthony J O’Sullivan, Mridula Lewis, and Terrance Diamond

Objective: Amiodarone-induced thyrotoxicosis (AIT) is a challenging management problem, since patients treated with amiodarone invariably have underlying heart disease. Consequently, thyrotoxicosis can significantly contribute to increased morbidity and mortality. The aim of this study was to compare the clinical outcome and hormone profiles of patients with AIT (n = 60) with those with Graves’ thyrotoxicosis (n = 49) and toxic multinodular goitre (MNG, n = 40).

Design: A retrospective study of patients with AIT in a single institution was conducted.

Methods: Data from patients with AIT over 12 years were collected.

Results: Mean TSH levels were significantly suppressed in all three groups. However, there was no intergroup significant difference. Free thyroxine (T4) levels were significantly higher in AIT (45.6 ± 3.5 pmol/l) and Graves’ disease (44.6 ± 4.0 pmol/l) compared with toxic MNG (31.5 ± 5.1 pmol/l, P < 0.05). In contrast, free triiodothyronine (T3) levels were only significantly higher in Graves’ disease (14.7 ± 1.5 pmol/l, P = 0.002) compared with AIT (8.6 ± 0.7 pmol/l) and toxic MNG (7.4 ± 0.5 pmol/l). Six deaths occurred in the patients with AIT (10.0%, P < 0.01) and no deaths occurred in the other groups. Amiodarone treatment (P = 0.002) was the most significant predictor of death, whereas free T4, free T3 and age did not affect outcome. Within the amiodarone-treated group severe left ventricular dysfunction (P = 0.0001) was significantly associated with death.

Conclusions: (i) AIT differs from other forms of thyrotoxicosis, and (ii) severe left ventricular dysfunction is associated with increased mortality in AIT.

Restricted access

C.J. Pearce and R. L. Himsworth

Abstract. Serum concentrations of total thyroxine (T4) and total triiodothyronine (T3) were measured in a group of patients (n = 113) presenting with untreated hyperthyroidism due to Graves' disease and in subjects receiving oral T4 replacement (n = 93) in whom the total T4 concentration was supraphysiological (> 150 nmol/l). The mean total T4 concentration in the hyperthyroid group was 226 nmol/l, sd 59, range 151–420, and the mean total T3 concentration was 6.8 nmol/l, sd 2.73, range 3.1–17.5. For the group receiving T4 the mean total T4 concentration was 175 nmol/l, sd 25, range 150–258, and the mean total T3 concentration was 2.66 nmol/l, sd 0.45, range 1.7–4.2. In the hyperthyroid group a highly significant linear correlation was found between total T4 and total T3, T3 = 0.0354 T4 – 1.21, r = 0.761, P ⪡0.001, while in the patients taking T4 this correlation was less close, T3 = 0.0073 T4 + 1.39, r = 0.398, P⪡0.001. The two groups are readily distinguished by expressing total T4 as a molar ratio of total T3. In the hyperthyroid group the mean T4:T3 ratio was 35.6, sd 7.8, range 19.9–56.1, compared to the patients on T4 where the mean T4:T3 ratio was 67.0, sd 11.7, range 44.3–114 (t = 22.5, P⪡0.0001). An arbitrarily chosen value of 50 for the T4:T3 ratio affords a simple and convenient means of distinguishing the two categories: in only 3 patients with Graves' disease (2.6%) was the ratio above this, and it was below in only 5 patients (5.4%) taking T4. Where there is doubt as to the aetiology of hyperthyroxinaemia this simple operation will differentiate between hyperthyroidism caused by Graves' disease and surreptitious ingestion of T4. In other clinical situations where symptoms of hyperthyroidism are associated with a T4:T3 ratio greater than 50 the combination may suggest subacute thyroiditis or iodide-induced thyroid dysfunction.

Free access

LH Duntas, E Mantzou, and DA Koutras

OBJECTIVE: Selenium (Se) in the form of selenocysteine is an essential component of the family of the detoxifying enzymes glutathione peroxidase (Gpx) and of the iodothyronine selenodeiodinases that catalyse the extrathyroidal production of tri-iodothyronine (T(3)). Thus, Se deficiency may seriously influence the generation of free radicals, the conversion of thyroxine (T(4)) to T(3) and the autoimmune process. Therefore, we performed a randomised, placebo-controlled prospective study to investigate the effects of Se treatment on patients with autoimmune thyroiditis (AIT). DESIGN AND METHODS: Sixty five patients aged 22-61 years (median age 48 years) with AIT were recruited into two groups. Group I (Gr I) (n=34) was treated with selenomethionine (Seme) 200 microg, plus L-thyroxine (LT(4)) to maintain TSH levels between 0.3-2.0 mU/l, whereas group II (Gr II) (n=31) received LT(4) plus placebo over a period of 6 months. Moreover, the pharmacokinetics of Seme were studied in 10 patients and eight volunteers at baseline and 2 h, 4 h, 6 h and 24 h after oral administration of a 200 microg tablet of Seme. Finally, Se levels were measured at the end of the study in some patients of both groups and their results were correlated with thyroid hormone levels. RESULTS: In the pharmacokinetics study, basal serum concentration of Se (75+/-6 microg/l) was within the reference range (70-125 microg/l), it promptly increased at 2 h, peaked at 4 h (147+/-17 microg/l; P<0.0001) and it was abundant in serum at 24 h. In Gr I, antibodies against thyroid peroxidase (anti-TPO) levels showed an overall decrease of 46% at 3 months (from 1875+/-1039 U/l to 1013+/-382 U/l; P<0.0001) and of 55.5% at 6 months. In Gr II the overall decrease of anti-TPO amounted to 21% at 3 months and to 27% at 6 months (from 1758+/-917 U/l to 1284+/-410 U/l; P<0.005). There were no significant changes of antibodies against thyroglobulin levels between the groups. At the end of this study Se levels were found to be statistically significantly increased in Gr I (n = 9/34) compared with Gr II (n=11/31) (97+/-8.4 vs 79+/-8; P<0.01) but no correlation with thyroid hormone was found. CONCLUSIONS: Seme is proven to be rapidly absorbed by the gastrointestinal tract. It appears to be useful as adjunctive therapy with LT(4) in the treatment of AIT. The exact mechanism(s) is not very well determined, it might enhance the activity of detoxifying enzymes and enforce the defense against oxidative stress.

Restricted access

A. Gordin and B.-A. Lamberg

ABSTRACT

Fourteen patients with subacute thyroiditis were studied. In the acute stage 6 were overtly and 2 equivocally hyperthyroid. Total thyroxine (T4) or protein-bound iodine (PBI) was elevated in 10 patients out of 14 and absolute free thyroxine (AFT4) in 10 out of 13 cases. The serum thyrotrophin (TSH) values ranged from 1.3 to 7.9 μU/ml, all but one being below 4.0 μU/ml (normal range 1.6–6.9 μU/ml). There was no response in serum TSH to thyrotrophin releasing hormone (TRH) in 9 subjects tested in the acute stage, irrespective of whether they were clinically hyperthyroid or euthyroid. This indicates that in the acute stage of subacute thyroiditis the thyroid hormone level is increased sufficiently to inhibit TSH release. In 8 patients the TRH stimulation test was carried out serially at 2 to 3 monthly intervals but in 5 only after 2 to 6 months. In a few patients the serum TSH level rose above the normal upper limit. The response to TRH became normal within 2 to 5 months but in one patient only after a period of exaggerated response indicative of temporary subclinical hypothyroidism. In one patient the response was still exaggerated one year after the acute phase, indicating that normalization of the thyroid-pituitary relationship may be a very slow process.