QUANTITATIVE STUDIES OF IODINE METABOLISM IN SPORADIC, NON-TOXIC GOITRE

1974 ◽  
Vol 76 (1) ◽  
pp. 67-73 ◽  
Author(s):  
H. Agerbæk ◽  
S. E. Jensen

ABSTRACT In 129 patients with non-toxic goitre and 27 normal controls, thyroid dynamic patterns were estimated in an attempt to elucidate pathogenesis. The clinically euthyroid state was confirmed by measurement of PBI, T3-sephadex uptake and BMR. Thyroid clearance (th. cl.), plasma iodide (PII), and absolute iodine uptake (AIU) were determined and a perchlorate discharge test performed. Twenty patients (16%) had a high AIU and were thus suspected of having dyshormonogenesis; nine were thoroughly investigated and in six dyshormonogenesis was found. Both normals and non-toxic goitre patients had a low PII, but in the goitrous patients values were lowest. The thyroid clearance of iodide was significantly higher in the goitre patients, suggesting iodine deficiency to be a major aetiologic factor for goitre formation. AIU was higher in the goitre patients than in normals, suggesting a larger iodine leakage from the thyroid in these patients.

1965 ◽  
Vol 48 (1) ◽  
pp. 14-22 ◽  
Author(s):  
S. A. Aboul-Khair ◽  
J. Crooks

ABSTRACT Studies of iodine metabolism have been carried out in 15 pregnant women, 33 cases with sporadic goitre and 11 with thyrotoxicosis. A low plasma inorganic iodine was common to the three groups. In pregnancy and sporadic goitre the thyroid clearance of iodine was elevated and the absolute iodine uptake normal. A high thyroid clearance of iodine in thyrotoxicosis was associated with a high absolute iodine uptake. The results suggest that both pregnancy and sporadic goitre are physiological responses to an iodine deficiency state while the iodine deficiency state of thyrotoxicosis is secondary to increased thyroid activity.


1964 ◽  
Vol 04 (01) ◽  
pp. 45-55
Author(s):  
B. Malamos ◽  
D. A Koutras ◽  
J. Sfontouris ◽  
G. Rigopoulos

SummaryIn the last two years, three families with an inborn error in iodine metabolism (thyroid dyshormonogenesis) have been detected and studied at the Department of Clinical Therapeutics of Athens University, and this shows that such defects, although rare, are not absent from Greece.From the first family three siblings were studied. A boy of 18 and a girl of 10 years were typical goitrous cretins, and a perchlorate discharge test showed impaired organic binding of the iodine trapped by the thyroid gland. The third sibling, a girl of 15, was euthyroid but had a diffuse goitre and a slightly increased uptake of radioiodine by the thyroid. The perchlorate discharge test, performed twice, was consistently negative. If the goitre in this last case represents a minor degree of the same metabolic abnormality as in the two other siblings with goitrous cretinism, it may be concluded that minor degree of impaired organic binding of iodide may not be detectable by the perchlorate test.The second family was affected with Pendred’s syndrome, i.e. goitre with deaf-mutism and positive perchlorate discharge. The father of the proposita (a woman of 29) and two maternal uncles and a maternal aunt were similarly affected. The occurrence of the syndrome in more than one generation is rare, since it is transmitted by a recessive gene. A sister of the proposita had a goitre without deaf-mutism, and this suggests that partial forms of the syndrome may perhaps occur in relatives of typical cases.The third family consisted of two brothers, who developed a large goitre soon after puberty. Thyroidectomy was followed by hypothyroidism. Biochemical investigations revealed the presence of a butanol-insoluble iodinated compound in the serum.The search for thyroid auto-antibodies by the tanned-redcell agglutination and the complement-fixation technique gave negative results in all the cases.


1966 ◽  
Vol 53 (2) ◽  
pp. 264-270 ◽  
Author(s):  
G. M. Bax

ABSTRACT Pendred's syndrome is a condition which, in its complete form, is characterized by congenital deaf-mutism, goitre, and defective organic binding of iodide in the thyroid. However, there are less typical cases, e. g. without a goitre, with only limited hearing loss, or a normal perchlorate discharge test. A family was studied in which Pendred's syndrome was found in two generations. The complete form was present in two members; two other members were considered to show less typical forms of the same disorder. All were euthyroid. Three out of five sons were deaf-mute and goitrous. Perchlorate caused a discharge of radioiodine from the thyroid in two of them, and also in the father who had no goitre and a slight loss of hearing only detectable by audiometry. Peripheral deiodination of radioactive diiodotyrosine was normal in all patients, but had been abnormal in one son while he was hypothyroid.


1964 ◽  
Vol 46 (4) ◽  
pp. 679-683 ◽  
Author(s):  
W. D. Alexander ◽  
Th. Veiger Gudmundsson ◽  
M. M. Bluhm ◽  
R. McG. Harden

ABSTRACT The relation between plasma inorganic iodine level, thyroid clearance and absolute iodine uptake of the thyroid gland has been studied in Iceland and compared with results obtained in Glasgow using identical methods. In Iceland the plasma inorganic iodine (PII) is higher than in Glasgow due to the high iodine content of the diet and the thyroid clearance lower. This adjustment is, however, incomplete, relatively high PII levels being associated with a low thyroid clearance and a raised absolute uptake by the thyroid. There was no evidence of increased hormone production as reflected in the serum PBI.


1978 ◽  
Vol 89 (4) ◽  
pp. 673-678 ◽  
Author(s):  
Karine Bech ◽  
Lis Skovsted ◽  
Kaj Siersbæk-Nielsen ◽  
Jens Mølholm Hansen

ABSTRACT Iodine metabolism and thyroid hormones in blood were studied in 19 men and 11 women who had been treated with thiazides for arterial hypertension from 1 month to 15 years. The results were compared with the findings from age-matched normal controls. No differences were found regarding 24-h 131I-thyroid uptake, thyroid iodide clearance, renal iodide clearance, plasma inorganic iodide, absolute iodine uptake (AIU), serum thyroxine (T4 (D)), resin T3 test (T3U) and TSH after TRH. Twenty-four-hour urinary iodine was higher in the patients treated with diuretics which could be explained by increased iodine intake. The findings of increased serum triiodothyronine (T3 (RIA)) and reverse T3 (rT3) might be due to changes in distribution volume in the thiazide-treated patients. Long-term treatment with thiazides in man do not lead to iodine depletion.


1972 ◽  
Vol 34 (3) ◽  
pp. 594-597 ◽  
Author(s):  
HENRY W. GRAY ◽  
LESLIE A. HOOPER ◽  
WILLIAM R. GREIG ◽  
IAIN R. MCDOUGALL

2005 ◽  
Vol 152 (3) ◽  
pp. 347-353 ◽  
Author(s):  
Toshiki Nagasaki ◽  
Masaaki Inaba ◽  
Shuichi Jono ◽  
Yoshikazu Hiura ◽  
Hideki Tahara ◽  
...  

Hypothyroidism is associated with increased morbidity from cardiovascular disease, and an increase in serum osteoprotegerin (OPG) has recently been reported to be associated with the severity of coronary heart disease and cardiovascular mortality. The present study was designed to examine whether hypothyroidism causes an increase in serum OPG, and to determine whether levothyroxine (L-T4) replacement therapy might suppress serum OPG levels in hypothyroid patients. Fifty-three hypothyroid patients with chronic thyroiditis and age- and sex-matched normal control subjects were examined for the levels of serum OPG and plasma von Willebrand factor (vWF), a vascular injury marker. Thirty-seven of the hypothyroid patients were further monitored for changes in these markers during 1 year in a euthyroid state induced by L-T4 replacement therapy. Baseline OPG was significantly higher in hypothyroid patients than in normal controls (4.51 ± 0.50 vs 3.72 ± 0.23 pmol/l (mean ± S.E.); P = 0.0182). In multivariate analysis, baseline OPG was significantly associated with baseline levels of TSH (r = 0.280, P = 0.0162) and vWF (r = 0.626, P < 0.0001). During one year of L-T4 replacement therapy, hypothyroid patients showed a significant decrease in OPG levels from 4.35 ± 0.51 to 3.48 ± 0.26 pmol/l (P = 0.0166), a level comparable to normal controls. The change in serum OPG levels during L-T4 replacement therapy was significantly and independently associated in a negative fashion with baseline vWF (r = −0.503, P = 0.0014). This study suggested that the severity of hypothyroidism and vascular injury might have important independent roles in increasing the serum OPG level in hypothyroid patients. Furthermore, it was demonstrated that a sustained euthyroid state might have the potential to decrease the serum OPG level in hypothyroid patients and that the degree of vascular injury in the hypothyroid state is independently associated with a decrease in serum OPG during a 1-year normalization of thyroid function.


1999 ◽  
Vol 84 (8) ◽  
pp. 2736-2738 ◽  
Author(s):  
Bijayeswar Vaidya ◽  
Rebecca Coffey ◽  
Beth Coyle ◽  
Richard Trembath ◽  
Camille San Lazaro ◽  
...  

Pendred syndrome is the autosomal recessively transmitted association of familial goiter and congenital deafness. There is no specific biochemical marker of this disease, and the diagnosis depends upon the demonstration of the triad of congenital sensorineural hearing loss, goiter, and abnormal perchlorate discharge test. Pendred syndrome is caused by mutations within the putative ion transporter gene (PDS gene), located on chromosome 7q. A wide variation in the clinical presentation of this condition, and its well documented phenotypic overlap with other thyroid disorders (such as Hashimoto’s thyroiditis), can lead to diagnostic difficulties. The potential for misdiagnosis increases when these disorders occur coincidentally in the same family. We describe a kindred in which Pendred syndrome, autoimmune thyroiditis, and simple goiter coexisted, to highlight these diagnostic pitfalls and to illustrate the use of mutational analysis in resolving diagnostic confusion.


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