FURTHER STUDIES ON THE RATE OF DISAPPEARANCE OF LABELLED THYROXINE FROM THE INTRAVASCULAR COMPARTMENT OF MAN, WITH REFERENCE TO THE ROLE OF THYROXINE BINDING PROTEINS

1967 ◽  
Vol 55 (3) ◽  
pp. 497-521 ◽  
Author(s):  
Brian R. Webster ◽  
Amy Britton ◽  
Robert Volpé ◽  
Calvin Ezrin

ABSTRACT The disappearance of an intravenously injected tracer dose of 131I-labelled L-thyroxine from the circulation has been followed for 70 minutes. We have confirmed that the most significant separation between euthyroid subjects and patients with hyperthyroidism or myxoedema is given by the single exponential slope of the regression of blood radioactivity occurring between 20 and 50 minutes after T4* injection. This slope is referred to as the acute T4* half-time. When there is no alteration in total TBG the acute T4* half-time is closely related to the plasma BEI concentration. Increase in the latter due to Graves' disease, toxic nodular goitre, or exogenous administration of thyroxine or desiccated thyroid, results in a comparable acceleration in the acute T4* half-time compared to the value in euthyroid control subjects. Conversely patients with a low BEI due to primary or radioactive iodine induced myxoedema all have a significantly slow acute T4* half-time compared to normal subjects. There was no specific abnormality in the handling of thyroxine by patients with Graves' disease in contrast to the earlier findings of Lennon et al. (1961). Hypermetabolism per se does not affect the acute T4* half-time. The administration of pharmacological doses of triiodothyronine, unlike similar doses of thyroxine, failed to affect the acute T4* half-time. The acute T4* half-time is consistently related in an inverse manner to the concentration of unsaturated thyroxine-binding sites in association with TBG. These data show no such correlation between TBPA binding and the acute T4 half-time. Synthetic oestrogen, by increasing the unsaturated thyroxine-binding capacity of TBG, produces a profound slowing of the acute T4* halftime.

2011 ◽  
Vol 14 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Franciszek Rogowski ◽  
Saeid Abdelrazek ◽  
Piotr Szumowski ◽  
Anna Zonenberg ◽  
Adam Parfienczyk ◽  
...  

1969 ◽  
Vol 62 (2) ◽  
pp. 199-209 ◽  
Author(s):  
B.-A. Lamberg ◽  
A. Gordin ◽  
M. Viherkoski ◽  
G. Kvist

ABSTRACT The long-acting thyroid stimulator (LATS) was determined by means of the McKenzie assay in 68 patients with hyperthyroidism. The patients were classified into the following groups: Group 1. Graves' disease (diffuse goitre with hyperthyroidism with or without exophthalmos). Of the 35 patients tested 25 (71 %) were LATS-positive. Group 2. Graves' disease with nodular goitre (nodular goitre with hyperthyroidism and with exophthalmos). The present series includes only 4 such patients, although this combination is by no means uncommon in Finland. Two of the patients were LATS-positive. It has been suggested that these patients represent Graves' disease superimposed upon endemic nodular goitre. Group 3. Toxic nodular goitre. The present series comprises 23 patients with toxic multinodular goitre, of whom 10 (44%) were LATS-positive. In view of the findings on thyroid palpation, on thyroid scintigraphy, the presence or absence of LATS in the blood and some other criteria, these patients can be divided into two categories, (a) one with Graves' disease superimposed upon nodular goitre of endemic origin (see group 2) and (b) the other with classical multinodular goitre. Analysis of the scintigrams showed that in some patients (with either exophthalmos or LATS in the blood and nodular goitre = Graves' disease + nodular goitre) it was not the nodules that were activated but the paranodular tissue, a finding which gave a scintigram typical of patients with classical Graves' disease. In some LATS-positive cases, however, some nodules were also activated to the same extent. The difference between these scintigrams and those typical of classical multinodular goitre is particularly stressed since in Finland »toxic nodular goitre« is the prevailing type of hyperthyroidism. Group 4. Single toxic adenoma. Two patients out of 6 were LATS-positive. This is in contrast to the findings of other authors according to which LATS has never been found in patients with toxic adenoma. A hypothesis is put forward that in these patients subclinical Graves' disease (LATS in the blood) coincided with a primarily autonomous, hyperactive but not necessarily toxic single thyroid adenoma, which was more susceptible to the stimulating activity of LATS than the surrounding tissue.


1984 ◽  
Vol 105 (4) ◽  
pp. 500-504 ◽  
Author(s):  
Andrzej Gardas ◽  
Barbara Czarnocka ◽  
Janusz Nauman

Abstract. The presence of antithyroid plasma membrane antibodies (ATMA) has been detected in 97% of patients with untreated hyperthyroid Graves' disease, 85% of methimazole treated hyperthyroid Graves' disease, 25% of Hashimoto's thyroiditis and 6.9% of patients with toxic nodular goitre. The ATMA index was negative in all healthy blood donors, in patients with non-toxic nodular goitre, with the thyrocardiac syndrome and with simple obesity. Studies of patients with non-thyroid autoimmune diseases revealed that ATMA is positive in 11% of patients with scleroderma, 17.6% of systemic lupus erythematosus and 16% of rheumatoid arthritis. The amount of immunoglobulin bound to thyroid plasma membranes after pre-incubation with serum from patients with Graves' disease varied from 4.2 to 25.2 pmoles per mg of membrane protein; these values are several times higher than the maximal binding capacity for thyrotrophin which is 1.28 pmole/mg protein. In the majority of the cases studied TSH did not significantly inhibit IgG bound from thyroid plasma membranes. Significant amounts of IgG were displaced by an excess of TSH only in three cases with untreated hyperthyroid Graves' disease.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Andrew L Frelinger ◽  
Youfu Li ◽  
Matthew D Linden ◽  
Inge Tarnow ◽  
Marc R Barnard ◽  
...  

Background: Aspirin “resistance” (i.e. hyporesponsiveness to aspirin in a platelet function test) has been widely reported, but the underlying mechanism is unclear. We examined the role of pre-existent platelet hyperreactivity in aspirin “resistance”. We also determined the correlation between aspirin resistance defined by serum thromboxane (TX) B 2 (the most specific test of aspirin’s effect) and other assays of platelet function. Methods: Platelet function measured before and after aspirin 81 mg daily for 7 days was analyzed by Spearman’s rank correlation. Normal subjects (n=165) were studied because virtually all clinically relevant patients are already taking aspirin. An additional advantage of the use of normal subjects is that the platelet response to stimuli is not influenced (with resultant increased scatter of the data) by an underlying disease, e.g. coronary artery disease, which causes platelet hyperreactivity. Results: The proportion of the post-aspirin platelet function predicted by the pre-aspirin platelet function was 28.3 ± 7.5% (mean ± asymptotic standard error) for serum TXB 2 , 39.3 ± 6.8% for urinary 11-dehydro TXB 2 , 4.4 ± 7.7% for arachidonic acid-induced platelet aggregation, 40.4 ± 7.1% for ADP-induced platelet aggregation, 26.3 ± 9.2% for the VerifyNow Aspirin Assay®, and 45.0 ± 10.9% for the TEG® PlateletMapping ™ System with arachidonic acid. Spearman rank order correlations were highly significant for comparisons between assays when both pre-aspirin and post-aspirin results were included in the analysis. However, residual serum TXB 2 levels post-aspirin treatment were not significantly associated with post-treatment results of any of the other assays. Platelet count correlated with pre-aspirin serum TXB 2 and VerifyNow Aspirin Assay, but not with any post-aspirin platelet function test. Conclusions: Aspirin “resistance” (i.e. hyporesponsiveness to aspirin in a laboratory test) is in part unrelated to aspirin but is the result of underlying platelet hyperreactivity prior to the institution of aspirin therapy. Individuals identified as aspirin “resistant” defined by serum TXB 2 are not the same individuals identified by the other tests.


2001 ◽  
Vol 28 (9) ◽  
pp. 1360-1364 ◽  
Author(s):  
C. Körber ◽  
P. Schneider ◽  
N. Körber-Hafner ◽  
H. Hänscheid ◽  
C. Reiners

1994 ◽  
Vol 40 (6) ◽  
pp. 803-806 ◽  
Author(s):  
Luca Chiovato ◽  
Ferruccio Santini ◽  
Paolo Vitti ◽  
Giovanna Bendinelli ◽  
Aldo Pinchera

2019 ◽  
Author(s):  
Jennifer Nill ◽  
Tina Jeoh

AbstractInterfacial enzyme reactions require formation of an enzyme-substrate complex at the surface of a heterogeneous substrate, but often multiple modes of enzyme binding and types of binding sites complicate analysis of their kinetics. Excess of heterogeneous substrate is often used as a justification to model the substrate as unchanging; but using the study of the enzymatic hydrolysis of insoluble cellulose as an example, we argue that reaction rates are dependent on evolving substrate interfacial properties. We hypothesize that the relative abundance of binding sites on cellulose where hydrolysis can occur (productive binding sites) and binding sites where hydrolysis cannot be initiated or is inhibited (non-productive binding sites) contribute to rate limitations. We show that the initial total number of productive binding sites (the productive binding capacity) determines the magnitude of the initial burst phase of cellulose hydrolysis, while productive binding site depletion explains overall hydrolysis kinetics. Furthermore, we show that irreversibly bound surface enzymes contribute to the depletion of productive binding sites. Our model shows that increasing the ratio of productive- to non-productive binding sites promotes hydrolysis, while maintaining an elevated productive binding capacity throughout conversion is key to preventing hydrolysis slowdown.


2008 ◽  
Vol 158 (6) ◽  
pp. 823-827 ◽  
Author(s):  
Mirna Abraham-Nordling ◽  
Ove Törring ◽  
Mikael Lantz ◽  
Bengt Hallengren ◽  
Hans Ohrling ◽  
...  

ObjectivesTo investigate the incidence of hyperthyroidism in Stockholm County, in those patients who were diagnosed with hyperthyroidism for the first time during the years 2003–2005.DesignAll new cases of hyperthyroidism ≥18 years of age were prospectively registered to calculate the total incidence of hyperthyroidism, as well as the incidence of the subgroups: Graves' disease (GD), toxic multinodular goitre and solitary toxic adenoma (STA). Eight specialized units/hospitals in Stockholm County participated in the registration. The participating physicians were all specialists in medical endocrinology, oncology, nuclear medicine or surgery.ResultsDuring a 3-year period, 1431 new patients of hyperthyroidism were diagnosed in a well-defined adult population (>18 years of age) of in average 1 457 036 inhabitants. This corresponds to a mean annual incidence of hyperthyroidism of 32.7/100 000. The incidence of GD was 24.5/100 000 per year, toxic nodular goitre was 3.3/100 000 per year and STA was 4.9/100 000 per year.ConclusionsThe total incidence of hyperthyroidism in Stockholm County was found to be 32.7/100 000 per year, of which 75% had GD. There were a higher percentage of smokers among the patients with hyperthyroidism compared with the overall population in Stockholm, but no difference in the frequency of smoking between patients with GD and toxic nodular goitre.


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