Conditions Of Iodine Deficiency Research Articles

The role of triiodothyronine (T3) in the maintenance of euthyroidism in endemic goitre.

SUMMARYSerum concentrations of triiodothyronine (T3), thyroxine (T4) and thyroid stimulating hormone (TSH) have been measured in subjects from an endemic goitrous area of New Guinea. An increase in TSH concentration and a decrease in T4 concentration was found in both goitrous and non‐goitrous subjects, both abnormalities being more frequent in the goitrous group. In the majority of subjects (93%) the T3 level fell within the normal range. Euthyroidism appears to be preserved in the iodine deficient state by the continued production of normal amounts of T3, the intrinsic metabolic activity of T4 being relatively unimportant.

Iodoamino acid distribution in the thyroid of rats on different iodine intakes and with normal plasma protein bound iodine.

ABSTRACT Groups of rats were fed a low iodine diet, or the same diet supplemented with known amounts of iodine. About 2–3 weeks later radioiodine (*I) was injected and the rats were killed on the next day or at different daily intervals after »blocking« with KClO4 and withdrawal of I supplements. Most of the animals had normal thyroid weights and plasma PBI. A few groups of rats were in a mildly iodine deficient state. The patterns of *I and 127I distribution among thyroidal iodine containing compounds was determined. It was found that these patterns were not the same in all thyroids with normal weights. Thus the pattern changed slightly but gradually concomitantly with the iodine intake and/or the thyroidal iodine content: The M*IT/D*IT2)3), MIT/DIT and T3*/T4* ratios decreased as the iodine intake and/or thyroidal iodine content increased. A decrease in the thyroidal I stores after pre-labelling of the thyroidal I-containing compounds also resulted in the same changes in the *I distribution pattern. Normal thyroids containing the same amount of iodine have similar iodoamino acid composition. The present data show that the iodoamino acid composition of the normal thyroid is affected by the availability of iodine, though to a lesser degree than that of I-deficient glands.

SUBSTANTIATION OF NEW APPROACH TO PREVENTING IODINE DEFICIENCY AND METABOLISM CORRECTION

The article presents the material devoted to one of the global, vital problems of mankind iodine deficiency. Taking into account the fact that in conditions of constant iodine deficiency it is very problematic to ensure the health of highly productive animals, the issues of prevention of iodine deficiency are economically important for industrial livestock. On the pages of this article for the first time in veterinary medicine the prospects of application in non-infectious and infectious pathology of a new iodometabolic preparation on the basis of well-known in veterinary medicine and medicine preparation Iodinol and succinic acid. Comparative testing of the complex preparation and Pharmacopoeia Iodinol on cows with clinically expressed iodine deficiency state indicates that the modified Iodinol with intramuscular administration provides high efficiency of correction of pathobiochemical processes and normalization of hormonal function of the thyroid gland. New qualities of the modified Iodinol open new prospects of its application in infectious and non-infectious pathology.

Endemic goiter in the Cauca Valley. I. Results and limitations of twelve years of iodine prophylaxis.

The effects of iodine prophylaxis on the endemic goiter of the Cauca Valley, Colombia, S. A., were investigated by a longitudinal epidemiologic study carried out in school and general populations during an 8-yr period. The results obtained were compared with observations made prior to iodine prophylaxis, which was begun in 1955. Before the iodization program was started, statistically significant differences existed in the prevalence rates of goiter in towns near one another. Once iodine prophylaxis was established, we found: 1) a marked decrease in the percentage frequency of goiter in the towns with high rates, but no change in those with low rates; 2) constant and fixed prevalence rates of goiter of around 30% in school and adult populations of Candelaria in the Cauca Valley during the past 8 yr while on an adequate and uniform iodine supplementation as documented by consistently high urinary iodine excretions, low normal thyroidal 131I uptakes and sufficient iodine content of the salt; 3) an incidence or attack rate of goiter in school children of 12.8% for an 8-month period; 4) the absence of goiter during the first 5 yr of age and its subsequent appearance while taking iodine; 5) the development of goiter in children born while there was an appropriate maternal iodine intake; and 6) a statistically significant difference in the percentage frequency of goiter between school children of similar age distribution, socioeconomic status and urinaiy iodine excretions but living 20 miles apart. These facts provide evidence to support the thesis that the goiter endemia that is still present in Candelaria in the Cauca Valley is not responsive to an adequate iodine supplementation and therefore must be caused by factors other than a state of iodine deficiency. The conditioning influence of iodine on the over-all magnitude of the problem and of age and sex in the development, relative frequencies and persistence of goiter is discussed and the possibility of “goitrogenic” substances as causative factor(s) of the Cauca Valley endemia is postulated.

Effect of iodine deficiency on iodine-containing compounds of rat tissues.

The distribution and quantitation of endogenously labeled iodine-containing compounds in normal and iodine-deficient rats were determined under steady state conditions. An isotope equilibrium method based on chronic feeding of 125I-labeled diet of known specific activity containing 0.06 μg 127I/g (experimental) and 0.22 fig 127I/g (control) was employed. Iodine deficiency was associated with the usually described rise in thyroid weight and MIT/DIT and T3/T4 ratios, even though there was a significant absolute decrease in all iodine compounds. Despite the iodine deficiency state the absolute concentration of T4 exceeded that of T3. Quantities found per g thyroid were 5.3 μg DIT, 5.7 μg MIT, 2.6 μg T4 and 1.7 μg T3. The T3/T4 ratio in plasma and tissues also rose, but for different reasons, as there was an absolute rise in T3 in plasma and most tissues and an absolute fall in T4 in plasma and all tissues. Despite these changes the absolute concentration of T4 still exceeded that of T3 in plasma and most tis...

A STUDY OF THE MECHANISMS INVOLVED IN THE PRODUCTION OF IODINE-DEFICIENCY GOITER.

ABSTRACT An extensive study of the temporal sequence of changes in thyroid function after initiation of a low iodine regimen has been made in rats. Variables measured include: thyroid weight, 131I uptake, monoiodotyrosine/diiodotyrosine (MIT/DIT) and triiodothyronine/thyroxine (T3/T4) ratios, iodide clearance, and 127I content. Also measured were protein-bound iodine (PBI), inorganic iodide and thyrotrophin (TSH) levels in the serum. Significant thyroid hypertrophy was produced during the first week and before there was a fall in serum PBI. Temporally related to the appearance of goiter were a rise in 131I uptake, MIT/DIT ratio and iodide clearance and a fall in thyroidal 127I concentration. In contrast, a fall in total thyroidal 127I appeared later and was closely correlated with a decline in serum PBI concentration and a rise in the thyroidal T3/T4 ratio. Manipulations such as hypophysectomy, injections of iodide, thyroxine or TSH, and refeeding a high iodine diet gave results consistent with the view that changes produced by iodine deficiency involve both autonomous and TSH-dependent thyroidal mechanisms. Although elevated serum TSH levels could not be demonstrated until after the first week of the iodine-deficient regimen, the total evidence of these studies permits the conclusion that increased TSH secretion is the most important factor in producing the thyroidal response to iodine deficiency. It is shown that homeostatic mechanisms allow maintenance of a normal level of circulating thyroid hormone in an iodine-deficient state until the body iodine pool becomes too severely depleted to supply adequate iodide substrate to the thyroid. The changes observed closely resemble those found in human iodine-deficient goiters. Although the large goiters produced after several weeks of an iodine-deficient regimen were hyperplastic, they could readily be converted to typical colloid goiters by feeding a high iodine diet for a few days.

A COMPARATIVE STUDY OF IODINE METABOLISM IN PREGNANCY, SPORADIC GOITRE AND THYROTOXICOSIS.

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.

Iodine metabolism in a region of endemic goiter.

SummaryStudies carried out in the Venezuelan Andes show that in this region there is an increase in thyroid clearance of iodine, thyroid uptake, conversion ratios and 24 hour protein-bound I131. Renal clearance of I131 is normal and urinary and salivary I127 low. Urinary I127 is low. It is concluded that in this region there exists a state of iodine deficiency, leading to compensatory thyroid avidity for iodine. There is no compensatory renal conservation of iodine.