Thyroid stimulating immunoglobulins in Graves' disease with goitre growth, low thyroxine and increasing triiodothyronine during PTU treatment

1984 ◽  
Vol 107 (4) ◽  
pp. 482-488 ◽  
Author(s):  
Laszlo Hegedüs ◽  
Jens M. Hansen ◽  
Karine Bech ◽  
Jens P. Kampmann ◽  
Keld Jensen ◽  
...  

Abstract. In 50 consecutive patients with Graves' disease treated with PTU, 7 (group 1) developed increasing goitre in spite of unmeasurable TSH. Thyroid variables were compared with those from 10 controls with an ordinary response to PTU (group 2). Serum T4 decreased in group 1 from 246 ± 47 nmol/l (mean ± sd) to 40 ± 9 nmol/l after 6 weeks of PTU treatment and continued to be below the normal range during the next 4 months. In group 2 serum T4 decreased from 190 ± 35 to 88 ± 47 nmol/l and stayed in the normal range. Serum T3 was normalized in both groups after 6 weeks but increased to values above the normal range in group 1 after that time. In spite of unmeasurable TSH during the 6 months of treatment in group 1, thyroid volume, determined ultrasonically, increased significantly from 60 ± 29 to 93 ± 68 ml (P < 0.05), but was unaltered in group 2 about 25 ml. Thyroid stimulating antibodies (TSAb) measured by adenylate cyclase activation (normal below 109%) decreased in group 2 from 117 ± 23 to 90 ± 17% (P <0.01) (6 months of therapy), but increased significantly in group 1, from 201 ± 47% to a maximum value of 234 ± 69% (P < 0.05). TSH binding inhibitory immunoglobulins (TBII) (given as per cent inhibition, normal below 26%) decreased in group 2 from 43 ± 29 to 29 ± 27% (P < 0.05) but were unaltered high in group 1,66 ± 25% before therapy and 57 ± 26% after 6 months of therapy. A positive correlation was found between thyroid volume and TSAb and TBII levels (P < 0.05, P < 0.05) before treatment as well as during the treatment period of 6 months. In 5 of 7 patients of group 1 either 131I therapy or subtotal thyroidectomy were necessary to control the disease. It is proposed that TSAb and TBII remaining abnormal in this subgroup of patients with Graves' disease, might in part explain the unusual response to PTU-treatment.

2000 ◽  
Vol 39 (05) ◽  
pp. 133-138 ◽  
Author(s):  
W. Dembowski ◽  
H.-J. Schroth ◽  
K. Klinger ◽  
Th. Rink

Summary Aim of this study is to evaluate new and controversially discussed indications for determining the thyroglobulin (Tg) level in different thyroid diseases to support routine diagnostics. Methods: The following groups were included: 250 healthy subjects without goiter, 50 persons with diffuse goiter, 161 patients with multinodular goiter devoid of functional disorder (108 of them underwent surgery, in 17 cases carcinomas were detected), 60 hyperthyroid patients with autonomously functioning nodular goiter, 150 patients with Hashimoto’s thyroiditis and 30 hyperthyroid patients with Graves’ disease. Results: The upper limit of the normal range of the Tg level was calculated as 30 ng Tg/ml. The evaluation of the collective with diffuse goiter showed that the figure of the Tg level can be expected in a similar magnitude as the thyroid volume in milliliters. Nodular tissue led to far higher Tg values then presumed when considering the respective thyroid volume, with a rather high variance. A formula for a rough prediction of the Tg levels in nodular goiters is described. In ten out of 17 cases with thyroid carcinoma, the Tg was lower than estimated with thyroid and nodular volumes, but two patients showed a Tg exceeding 1000 ng/ml. The collective with functional autonomy had a significantly higher average Tg level than a matched euthyroid group being under suppressive levothyroxine substitution. However, due to the high variance of the Tg values, the autonomy could not consistently be predicted with the Tg level in individual cases. The patients with Hashimoto’s thyroiditis showed slightly decreased Tg levels. In Graves’ disease, a significantly higher average Tg level was observed compared with a matched group with diffuse goiter, but 47% of all Tg values were still in the normal range (< 30 ng/ml). Conclusion: Elevated Tg levels indicate a high probability of thyroid diseases, such as malignancy, autonomy or Graves’ disease. However, as low Tg concentrations cannot exclude the respective disorder, a routine Tg determination seems not to be justified in benign thyroid diseases.


Author(s):  
Gamze Akkuş ◽  
Yeliz Sökmen ◽  
Mehmet Yılmaz ◽  
Özkan Bekler ◽  
Oğuz Akkuş

Background: We aimed prospectively investigate the laboratory and electrocardiographic parameters (hearth rate, QRS, QT, QTc, Tpe, Tpe/QTc, arrhythmia prevalance) in patients with graves disease before and after antithyroid therapy. Methods: 71 patients (48 female, 23 male), age between 18-50 (mean±SD: 36.48±12.20 ) with GD were included into the study. Patients treated with antithyroid therapy (thionamids and/or surgical therapy) to maintain euthyroid status. Patients were examined in terms of electrocardiographic parameters before and after the treatment. Results: Mean TSH, free thyroxin (fT4) and tri-iodothyrionine (fT3) levels of all patients were 0.005±0.21, 3.27± 1.81, 11.42±7.44, respectively. While 9 patients (group 2) underwent surgical therapy, had suspicious of malignant nodule or large goiter and unresponsiveness to medical treatment; the other patients (n=62, group 1) were treated with medical therapy. Patients with surgical therapy had more increased serum fT4 (p=0.045), anti-thyroglobulin value (p=0.018) and more severe graves orbitopathy (n=0.051) before treatment when compared to medical therapy group. Baseline Tpe duration and baseline Tpe/QTc ratio and frequency of supraventricular ectopic beats were found to be significantly higher in group 2 when compared to group 1 (p=0.00, p=0.005). Otherwise baseline mean heart rate, QRS duration, QTc values of both groups were similar. Although the patients became their euthyroid status, group 2 patients had still suffered from more sustained supraventricular ectopics beats than group 1. Conclusion: Distinct from medical treatment group, surgical treatment group with euthyroidism at least 3 months had still suffered from an arrhythmia (Tpe, Tpe/QTc, supraventricular and ventricular ectopic beats).


1980 ◽  
Vol 93 (1) ◽  
pp. 13-19 ◽  
Author(s):  
Reiko Demura ◽  
Hajime Yamaguchi ◽  
Ichiji Wakabayashi ◽  
Hiroshi Demura ◽  
Kazuo Shizume

Abstract. The effect of growth hormone (hGH) on the hypothalamic-pituitary-thyroid function was studied in patients with pituitary dwarfism. Twenty-six patients were given KABI hGH, 0.5 U/kg/week, for a period of 4—18 months. Three groups of patients were identified according to their T4 levels before and during the treatment. Group 1: T4 levels were initially normal and stayed in the normal range throughout a course of treatment. Group 2: T4 levels were initially normal but dropped to the subnormal range after hGH. Group 3: T4 levels were initially subnormal and decreased further after hGH. Changes in T4 levels after hGH in groups 2 and 3 were accompanied by a decrease in plasma T3RSU without concomitant decrease in plasma T3. Clinically, most of them lacked symptoms and signs of hypothyroidism and exhibited a good growth response to hGH. Plasma TSH response to TRH in these patients revealed a sustained delayed pattern, which was suggestive of hypothalamic hypothyroidism. This pattern of TSH response to TRH became further exaggerated after hGH therapy. In contrast, TSH response to TRH among patients in group 1 was normal and was not influenced by hGH. Administration of 4.0 U of KABI hGH daily for 21 consecutive days to 3 patients resulted in a shortened half-life of T4 and inversely prolonged that of T3. These results suggest that various degrees of TRH deficiency exist among patients with idiopathic pituitary dwarfism. Therapy with hGH discloses a mild TRH deficiency by accelerating the half-life of T4. This also causes a further drop in the T4 levels in those with marked TRH deficiency. The development of clinical hypothyroidism is not so obvious in these patients because of inverse delay in half-life of T3 by hGH.


1981 ◽  
Vol 240 (4) ◽  
pp. F269-F275 ◽  
Author(s):  
M. M. Popovtzer ◽  
H. Wald

The effect of 25(OH)vitamin D3 [25(OH)D3] on the phosphaturic action of glucagon was studied using clearance techniques in the following groups of rats: group 1, parathyroidectomized (PTX) glucagon-infused rats receiving intravenous 25(OH)D3; group 2, PTX 25(OH)D3-pretreated rats receiving intravenous glucagon; and group 3, the thyroparathyroidectomized glucagon-infused rats receiving intravenous 25(OH)D3. The effect of 25(OH)D3 on glucagon-induced increase of cAMP in kidney slices and glucagon-activated adenylate cyclase (AC) in kidney membrane fractions was studied in vitro. In group 1, 25(OH)D3 suppressed the glucagon-induced phosphaturia by reducing fractional excretion of phosphorus (CP/CIn) from 0.175 +/- 0.02 (mean +/- SE) to 0.112 +/- 0.12 (P less than 0.05); this was associated with a reduction of urinary cAMP from 1,830 +/- 230 to 660 +/- 120 pmol/min (P less than 0.01). In group 2, pretreatment with 25(OH)D3 reduced CP/CIn from 0.221 +/- 0.025 to 0.108 +/- 0.012 (P less than 0.005). In group 3, 25(OH)D3 reduced CP/CIn from 0.165 +/- 0.012 to 0.075 +/- 0.011 (P less than 0.005). In vitro, 25(OH)D3 blunted the glucagon-induced activation of the AC/cAMP system by reducing AC from 570 +/- 30 to 325 +/- 28 pmol cAMP.mg protein-1.h-1 (P less than 0.01) and the cAMP level from 11.2 +/- 0.9 to 8.5 +/- 0.7 pmol cAMP/g wet tissue (P less than 0.05). These results show that 25(OH)D3 blunts the phosphaturic action of glucagon and suggest that this response may be mediated through suppression of the AC/cAMP system.


2019 ◽  
Vol 03 (03) ◽  
pp. E96-E101
Author(s):  
Antina Schulze ◽  
Martin Busse

AbstractDental occlusion may affect static and dynamic balance. The effects of a mouthguard on pinpoint accuracy in volleyball were investigated in 28 players who completed a volleyball specific test. Also, masticatory electromyographic tests were performed. The mean pinpoint accuracy was significantly higher with a mouthguard (68.6±9.3 vs. 64.0±7.0 points from 100; p< 0.006). However, differential mouthguard effects were seen, and three subgroups were classified: Group 1 (markedly improved pinpoint accuracy), Group 2 (improved pinpoint accuracy), and Group 3 (reduced pinpoint accuracy). Group 1 had a high masseter resting tone, the masseter activity was low in MVC (maximum voluntary clench) and increased in BOC (maximum bite on cotton rolls; p< 0.04). This indicates a masseter weakness, which would be compensated by a mouthguard. In Group 2, the masseter activity in MVC was high-normal with an imbalance which was improved in BOC (p< 0.01), indicating a possible mouthguard benefit. In Group 3, MVC and BOC were in a high-normal range and showed no relevant deficits. In these subjects the mouthguard had adverse effects. Overall, subjects with masticatory deficits had a benefit from the mouthguard in pinpoint accuracy. Positive or negative mouthguard responders may be detectible from electromyographic tests.


2011 ◽  
Vol 57 (3) ◽  
pp. 17-20
Author(s):  
M S Sheremeta ◽  
N Iu Sviridenko ◽  
I M Belovalova ◽  
P I Garbuzov

The primary objective of the present work was to study the clinical course of endocrine ophthalmopathy (EOP) following radioiodine therapy (RIT) of Graves' disease (GD) and depending on its effect (development of post-radiation hypothyroidism). The secondary objective was to determine risk factors of EOP progression after radioiodine therapy. This prospective study included 38 patients (76 eyes) allocated to two groups. The patients of group 1 (n=19/38 eyes) presented with thyrotoxicosis at each visit and continued to use thyrostatic agents; those in group 2 (n=19/38 eyes) had hypothyroidism at its early stages (3 and 6 months) and were given substitution therapy with levothyroxin. The development of post-radiation hypothyroidism was shown to strongly influence the clinical course of EOP. In the patients of group 1, EOP remained active throughout the entire observation period (12 months) in the absence of appreciable variations of its integral severity index. In group 2, the same index decreased significantly, but active forms of EOP could be detected by the time of onset of hypothyroidism (6 months) (p=0.0000). After 12 months, the level of anti-TSH receptor antibodies in the patients of group 1 was significantly higher than in those of group 2 (10.8±8.3 and 2.9±2.0 respectively, p=0.0003). The regression rate of EOP symptoms following radioiodine therapy (RIT) of Graves' disease was a function of the efficacy of thyroid 131I radioablation. It is concluded that persistence of anti-TSH receptor antibodies was responsible for the deterioration of the clinical picture of endocrine ophthalmopathy after radioiodine therapy.


1998 ◽  
Vol 83 (4) ◽  
pp. 1222-1225
Author(s):  
A. De Bellis ◽  
S. Di Martino ◽  
F. Fiordelisi ◽  
V. I. Muccitelli ◽  
A. A. Sinisi ◽  
...  

It is commonly recognized that a few patients with Graves’ disease (GD) develop an overt ophthalmopathy, although most of them show subclinical extraocular muscle enlargement by appropriate imaging techniques. At present, it is not possible to identify the subgroup of GD patients with subclinical retroorbital connective involvement. Recently, it has been shown that increase of soluble intercellular adhesion molecule-1 (sICAM-1) serum levels is correlated to clinical activity score in active Graves’ ophthalmopathy (GO) patients with or without hyperthyroidism, suggesting that sICAM-1 serum values could reflect the degree of ocular inflammatory activity. The aim of this longitudinal study was to evaluate sICAM-1 serum levels in GD patients without clinical ophthalmopathy and to assess their possible relationship with occurrence of GO. We measured sICAM-1 serum levels in 103 initially hyperthyroid GD patients without clinical ophthalmopathy and in 100 healthy subjects. All patients were treated with methimazole for 2 yr. Sera were collected from all patients before treatment and then monthly for the first 6 months of therapy, every 2 months in the following 6 months, and finally at the end of the follow-up study. Patients developing GO were excluded from the follow-up at the onset of ophthalmopathy. During the follow-up 17 GD patients (16.5%, group 1) developed overt eye involvement (14 as active inflammatory ophthalmopathy and 3 as ophthalmopathy without clinical retroorbital connective inflammation) and 86 (83.5%, group 2) did not. At start of the study, the mean of sICAM-1 serum concentrations did not differ significantly between the 2 groups, but it was significantly higher than in controls in both groups. No significant correlation between serum sICAM-1 concentrations and free thyroid hormone levels was found in the 2 groups of patients. During the follow-up study, a further increase of sICAM-1 serum levels was observed in 12 of the 14 patients (85.7%) of group 1 who developed active inflammatory ophthalmopathy not only at the onset but also before clinical GO appearance. On the contrary, the 3 patients of group 1 that developed ophthalmopathy without clinical retroorbital inflammation did not show any further increase of sICAM-1 levels at every time of follow-up in comparison with the starting values, even if their sICAM-1 levels were always higher than in normal controls. Finally, group 2 patients showed significantly decreased sICAM-1 levels throughout the follow-up period when compared with the starting values, although they were still significantly higher than in controls. These results indicate that a further increase of sICAM-1 serum levels before the onset of clinical ophthalmopathy may be a marker of subclinical retroorbital connective inflammation in GD patients. Therefore, our study suggests that serial determinations of sICAM-1 serum levels could help to identify and trace at the right time those GD patients prone to developing active inflammatory ophthalmopathy.


Author(s):  
Naoki Hattori ◽  
Kohzo Aisaka ◽  
Akira Shimatsu

AbstractMacroprolactinaemia is a major cause of hyperprolactinaemia. The detectability of macroprolactin varies widely among different immunoassay systems, but the causes are not fully known. This study aimed to identify the factors influencing the detectability of macroprolactin by immunoassay systems.The study included 1544 patients who visited an obstetric and gynaecological hospital. Macroprolactinaemia was screened using the polyethylene glycol (PEG) method and confirmed using gel filtration chromatography and the protein G method. The prolactin (PRL) values determined by enzyme immunoassay (EIA) were compared with those of a chemiluminescence immunoassay system (Centaur) that is known to cross-react the least with macroprolactin.Macroprolactinaemia was found in 62 of 1544 patients (4.02%) who visited an obstetric and gynaecological hospital. The ratio of EIA-determined total PRL to free PRL in the supernatant after PEG precipitation was significantly elevated in all 62 serum samples with macroprolactin compared to those in 1482 serum samples without macroprolactin. In contrast, the ratio of Centaur-determined total PRL to free PRL was significantly elevated in 32 serum samples (group 1) and was within the normal range in 30 (group 2) of 62 serum samples with macroprolactin. The prevalence of non-IgG-type macroprolactin was significantly higher in group 1 than in group 2. Centaur diagnosed hyperprolactinaemia less frequently than EIA (n=2 vs. 16) in 62 patients with macroprolactinaemia. Those two hyperprolactinaemic patients diagnosed by Centaur had non-IgG-type macroprolactin.Macroprolactinaemia was present in 4% of patients visiting an obstetric and gynaecological hospital. The nature of macroprolactin (IgG-type or non-IgG-type) may partly explain why macroprolactin detectability varies among different immunoassay systems.


2005 ◽  
Vol 153 (1) ◽  
pp. 15-21 ◽  
Author(s):  
Berit E Jensen ◽  
Steen J Bonnema ◽  
Laszlo Hegedüs

Objective: We evaluated, in a retrospective study, whether glucocorticoids given in order to avoid initiation or aggravation of ophthalmopathy during radioiodine (131I) therapy have an inadvertent effect on the final thyroid function. Methods: Consecutive patients with Graves’ disease (median age 50 years, range 21–82 years) treated with 131I therapy for the first time were included. Ninety-six patients (group 1) were given prednisolone (25 mg daily for 30 days beginning 2 days before 131I therapy) because of present or previous mild ophthalmopathy or the presence of risk factors (tobacco smoking and high concentrations of TSH-receptor antibodies) for developing this complication. One hundred and eleven patients received 131I therapy without prednisolone prophylaxis (group 2). Results: The patients in group 1 were younger than those in group 2 (44.6±12.0 years versus 51.3±15.1 years; P = 0.001). At 1 year post therapy the patients were classified as hypothyroid, euthyroid or hyperthyroid. In group 1, the numbers of patients were 23, 35 and 38, respectively, while the corresponding numbers in group 2 were 26, 40 and 45, respectively (P = 0.99 between groups). The cure rate (attainment of euthyroidism or hypothyroidism) was 60% in group 1 and 59% in group 2 (P = 0.97). No significant between-group difference was found, neither in the median time-interval until development of hypothyroidism nor until recurrence of the hyperthyroid-ism. Using logistic regression the cure rate correlated negatively with age (P = 0.041) and the size of the thyroid gland (P = 0.010) and positively with serum TSH at treatment (P = 0.034), whereas no significant impact was found for the use of prednisolone, gender, smoking, presence of anti-thyroid peroxidase antibodies, use of anti-thyroid drugs or the presence of eye symptoms. Conclusions: Although glucocorticoids in some contexts seem to attenuate the radiation-induced oxidative stress this had no impact on the final outcome following 131I therapy of patients with Graves’ disease.


1977 ◽  
Vol 232 (5) ◽  
pp. E515
Author(s):  
M M Popovtzer ◽  
M S Blum ◽  
R S Flis

The present study evaluated the effect of 25(OH)vitamin D3[25(OH)vit D3] on the phosphaturic action of calcitonin in anesthetized parathyroidectomized rats. In group 1, calcitonin was given intravenously over six clearance periods. In group 2, after three periods of calcitonin given intravenously, 25(OH)vit D3 was added and given together with calcitonin for three additional periods. During calcitonin infusion, Cp/CIn 0.18 +/- 0.02 (mean +/- SE) in group 1 was not different from the corresponding Cp/CIn 0.18 +/- 0.03 in group 2; but when 25(OH)vit D3 was added, Cp/CIn 0.12 +/- 0.01 in group 2 was lower (P less than 0.001) than the corresponding Cp/CIn 0.26 +/- 0.02 in group 1. With intravenous calcitonin the urinary excretion of cycle AMP (UcAMP) 97 +/- 29 in group 1 did not differ from the corresponding UcAMP 86 +/- 27 pmol/min in group 2, but when 25(OH)vit D3 was added UcAMP 41 +/- 12 in group 2 was lower (P less than 0.001) than the corresponding UcAMP 131 +/- 14 pmol/min in group 1. This study demonstrated that 25(OH)vit D3 blocks the phosphaturic action of calcitonin. The associated fall in Uctamp suggests that25 (OV)vit D3 acts possibly by inhibiting the calcitonin-induced activation of adenylate cyclase in the kidney. However, other alternative mechanisms of action have not been excluded.


Sign in / Sign up

Export Citation Format

Share Document