Thyroid hormones increased urinary

The major location of calcium in the body is in the skeleton, which contains more than 90% of the body calcium as phosphate and carbonate. Bone resorption and formation keeps this calcium in dynamic equilibrium with ionized and complexed calcium in blood, cellular fluids and membranes. Homeostasis is mainly regulated by the parathyroid hormone and vitamin D which lead to increased blood calcium levels, and by a thyroid hormone, calcitonin, which controls the plasma calcium concentration J5 Increasing the concentration of calcitonin decreases the blood calcium level, hence injections of calcitonin are used to treat severe hyperalcaemia arising from hyperparathyroidism, vitamin D intoxication or the injection of too high a level of parathyroid extract. High levels of calcitonin also decrease resorption of calcium from bone. Hypocalcaemia stimulates parathyroid activity, leading to increased release of calcium from bone, reduction in urinary excretion of calcium and increased absorption of calcium from the intestine. Urinary excretion of phosphate is enhanced. 

In rats equilibrated with radioiodine-labelled T4 or T3 roughly half of the radioactivity appears as I- in the urine and the other half as free iodothyronines in the feces [12]. Treatment of the rats with 6-propyl-2-thiouracil (PTU) results in a marked decrease in urinary radioactivity and a reciprocal increase in fecal clearance [12]. Also, in humans, PTU has been shown to inhibit peripheral iodothyronine deiodination besides its well-known effect on thyroid hormone biosynthesis [13]. Compared with the rat, deiodination is an even more important pathway for the clearance of thyroid hormone in man as evidenced by the greater proportion undergoing urinary clearance [2]. Furthermore, estimation of iodothyronine turnover kinetics in humans has demonstrated that a major fraction of T4 disposal is accounted for by plasma production rates of T3 and rT3 [2,3],... 

Plasma growth hormone concentration may rise by as much as 15 times at the start of a fast but may return to normal after 3 days. Reduced energy expenditure is associated with decreased concentrations of thyroid hormones. Free and total triiodothyronine decrease by up to 50% witliin 3 days of the start of a fast. Free thyroxine concentration is also affected, but to a lesser extent total thyroxine is little changed. Urinary free cortisol is decreased by fasting, and the plasma cortisol concentration (free and total) shows a slight increase together with loss of the normal diurnal variation. 

Disturbances of calcium homeostasis have often been reported in diseases involving abnormal secretion of thyroid hormone. In thyrotoxicosis (G5, K2) the disturbance, if present, usually manifests itself as hypercalcemia of moderate degree, with loss of calcium from the bones and increased urinary output of calcium, thus suggesting a possible deficiency of thyrocalcitonin output in this type of thyroid disease. Most such observations antedate the discovery of thyrocalcitonin, and there is not yet much information on the response of such patients to an... 

Increased pentose excretion has been shown to follow experimental trauma, after craniofacial injuries in man, in response to cold exposure, and following the administration of thyroid hormone or cortisone. Drug-induced pentosuria has been known for a long time, but it has not been well studied. Morphine is the best-known inducer of pentosuria antipyretics have a similar effect. Urinary pentose increases in response to fever and during allergic responses (T4). 

Notes Laboratory parameters of mothers and their neonates in maternal subciinicai hypothyroidism maternai thyroid hormone ieveis were either siightiy increased (TSH and TT3) or near normai (TT4). Both mothers and their neonates had decreased MUi and increased TTvoi. These observations were the consequences of iodine deficiency (MUi median urinary iodine TSH thyroid-stimuiating hormone TT3 serum totai T3 TT4 serum totai T4 TTvoi totai thyroid voiume). 

In KBD subjects, the evolution of thyroid function after correction of iodine was similar in selenium supplemented and nonsupplemented subjects. This finding corroborated previous studies, suggesting only a moderate effect of selenium deficiency on thyroid hormones in human (Calomme et al, 1995 St. Germain and Galton, 1997). In Tibet, the administration of an intramuscular injection of 475-mg of iodine to KBD subjects was sufficient to correct iodine deficiency for 16 months, because at this time serum T3 increased again to pre-iodine levels and mean iodine urinary concentrations had fallen... 

Low urinary iodine excretion is being reflected in clinical measures of changes in thyroid hormone levels and increased thyroid volumes. 

Prolonged treatment with glucocorticoid hormones can cause calciuria. Furthermore, insulin, glucagon, growth hormone, thyroid hormone, catecholamines, and angiotensin have been reported to increase urinary calcium excretion while estrogen causes a decreased urinary calcium excretion. Antidiuretic hormones may cause increased excretion depending on other factors. 

More iodine is present in the urine (five times the normal) and feces of hyperthyroid patients than of normal individuals. Yet, if radioactive iodine is administered to hyperthyroid individuals, the urinary exretion of the hormone is less than in normal persons freshly administered iodine is apparently retained in the body. The reduced excretion of radioactive iodine probably results from greater uptake of radioiodine in the thyroid this increase in thyroidal uptake of radioiodine is consistently observed in patients with hyperthyroidism after oral or intravenous administration of radioiodine. Thyroid slices obtained from hyperthyroid patients clear the iodine from the medium at a much faster rate that slices obtained from normal individuals. 

Consequently, the workshop recommends specific monitoring of iodine intake of mothers and infants in Europe by periodic analysis of urinary iodine levels, and to the extent feasible, of serum TSH and thyroid hormone measures. The daily intake of iodine should be at least 200 pg in pregnant and lactating women and 90-120 pg in young infants. To reach these objectives, the mothers diet should be systematically supplemented with iodine whenever necessary, by vitamins/minerals tablets as prescribed by physicians. Breast milk is the best source of iodine for the infant, and exclusive breast feeding for 4-6 months should be encouraged. However, when circumstances require that infants receive formula, the iodine content of formula milk should be increased fiom the traditional recommendation of S pg/dl milk to 10 pg/dl for full term and 20 pg/dl for premature babies. 

In the most simplistic physiological model, inadequate intake of iodine results in a reduction in thyroid hormone production, which stimulates increased TSH production. TSH acts directly on thyroid cells, and without the ability to increase hormone production, the gland becomes hyperplastic. In addition, iodine trapping becomes more efficient, as demonstrated by increased radioactive iodine uptake in deficient individuals. However, this simplistic model is complicated by complex adaptive mechanisms which vary depending on the age of the individual affected. In adults with mild deficiency, reduced intake causes a decrease in extrathyroidal iodine and reduced clearance, demonstrated by decreased urinary iodine excretion, but iodine concentration in the gland may remain within normal limits. With further reduction in intake, this adaptive mechanism is overwhelmed, and the iodine content of the thyroid decreases with alterations in iodination of thyroglobulin, in the ratio of DIT to MIT, and reduction in efficient thyroid hormone production. The ability to adapt appears to decrease with decreasing age, and in children the iodine pool in the thyroid is smaller, and the dynamics of iodine metabolism and peripheral use more rapid. In neonates, the effects of iodine deficiency are more directly reflected in increased TSH. Diminished thyroid iodine content and increased turnover make neonates the most vulnerable to the effects of iodine deficiency and decreased hormone production, even with mild deficiency. 

Oral contraceptives have their most significant effect on endocrine parameters. Blood cortisol, thyroxine, protein-bound iodine, T3 uptake, and urinary free cortisol are elevated. Urinary 17,21-dihydroxy steroids, 17-ketosteroids, and estrogens are decreased. There is no effect on urinary catecholamines or VMA (Table 10) (LIO). The effect of thyroid functions tests is due to the administered hormone stimulating an increase in the production of thyroid-binding globulin which in turn binds 1-thyroxine. The lowering of free thyroxine stimulates the anterior pituitary to produce thyrotropin, which in turn stimulates the thyroid to produce more thyroxine. Since the additional thyroxine is bound to the extra protein, there is an equilibrium and the patient remains clinically euthyroid, but the protein-bound iodine and the thyroxine are elevated. 

Urinary iodine concentration and palpation of goiter among schoolchildren is the most frequent method used by cross-sectional surveys to measure iodine deficiency. Because iodine is excreted by the kidneys, the urinary concentration of iodine is an indicator of iodine intake. Lower production of thyroxine leads to increased production of the thyroid-stimulating hormone, which results in thyroid hyperplasia known as goiter. The World Health Organization (2001) classifies iodine deficiency into mild, moderate and severe when urinary excretion is, respectively, 50—99, 20 9 and <20 p,g/l of urine. 

In iodine-deficient regions, free tetraiodothyronine (fT4) increases, especially in multinodular goiters, whereas thyroid-stimulating hormone (TSH) levels decrease significantly, especially in multinodular and diffuse goiters (Fassbender et al., 2001). The more contrast agent was used, the more urinary iodine excretion was measured. These observations are probably due to the fact that the thyroid transport mechanism for iodine is not saturated by high-iodine plasma concentrations (Fassbender et al., 2001). The concentration of total T3 remains constant (Fassbender et al., 2001). However, TSH levels decrease in... 

In healthy volunteers with normal thyroid function orally administered two or four kelp capsules (containing 660 or 1320 pg of iodine) daily for 4 weeks, dose-related increases in TSH levels and urinary iodine levels were observed. In the high-dose group, a decrease in triiodothyronine and increase in poststimulation TSH response in the thyrotropin-releasing hormone stimulation test were observed. No... 

In an open label study, patients with a basal thyroid-stimulating hormone (TSH) value less than 1.0 mU/1 and hyperthyroidism-associated symptoms were administered one tablet containing 20 mg of European bugleweed daily for approximately 15 weeks. In treated patients, an increase in urinary thyroxine (T ) excretion was observed, along with a reduction in symptoms related to hyperthyroidism, notably, a reduction in heart rate in the morning. In this study, European bugleweed was generally well tolerated, with only minor adverse events reported in the study. Of these, only one adverse event, subjective "disturbances of the cardiac rhythm," was reported after 7 weeks of treatment (Beer et al. 2008). 

This hormone is secreted by the parathyroid glands, which are four in number and lie on the posterior surface of the thyroid gland. The exact manner in which the hormone exerts its action upon calcium and phosphorus metabolism has not been proved satisfactorily, but the most immediate effect of administration of parathyroid extract which has been generally observed is an increased excretion of phosphorus in the urine, which is accompanied by a lowering of the serum inorganic phosphate. The increase in the urinary phosphate excretion has been ascribed by Harrison and Har-... 

Potassium iodide, given in adequate quantities at the appropriate times, can almost completely block thyroidal uptake of radioiodide. Although the predominant mechanism is (Stemthal, 1980) not well established, several mechanisms have been postulated including isotope dilution, saturation of the iodide transport mechanism, interference with intrathyroidal organification of iodide, and inhibition of hormone release. (Wolff, 1980, Dumont 1990) In addition, KI blockade prevents recirculation of metabolized radioiodine and therefore increases its rate of urinary excretion. 

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