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Biomedical subjects

R Rajatanavin

Publications and source records attributed to R Rajatanavin.

87 records · Page 5Linked to original sources
PubMed1985

Radiation-associated recurrent parathyroid adenoma.

Recurrent parathyroid adenoma occurred in a patient who had received radiation treatments to the lateral aspect of the pharynx for lymphoid hyperplasia at the age of 10 years. The interval between the development of the first and second adenomas was 20 years. Although an association between head and neck irradiation and primary hyperparathyroidism is known, we believe this to be the first report of recurrent hyperparathyroidism in an irradiated patient.

Adenoma↗
PubMed1984

Five patients with iodine-induced hyperthyroidism.

Iodine-induced hyperthyroidism has been frequently described when iodine is introduced into an iodine-deficient area. However, it may also occur in patients with and without previous thyroid disease residing in iodine-sufficient areas. Five patients with iodine-induced hyperthyroidism seen in a 12-month period are described. All were exposed to iodine in the form of commonly used drugs (Betadine, Iodo-Niacin, amiodarone, and radiographic contrast dyes). The cause of iodine-induced hyperthyroidism is unclear, but it is probably more common in patients with goiters containing previously existing areas of autonomous function or iodine-poor thyroglobulin. Iodine-induced hyperthyroidism usually abates after iodine withdrawal in patients with multinodular goiters or normal thyroid glands. The hyperthyroidism is usually treated with beta-blockers and antithyroid thionamide drugs, although reinstitution of iodine to block thyroid hormone release or corticosteroids occasionally may be necessary. Iodine-containing drugs should be given with caution to patients with underlying thyroid disease.

Adult↗
PubMed1984

Low serum thyroxine and high serum triiodothyronine in nephrotic rats: etiology and implications for bioavailability of protein-bound hormone.

Traditionally, it has been thought that the bioavailable fraction of circulating serum hormones, i.e. that which is available for cellular uptake and is physiologically active, is limited to the free (nonprotein bound) hormone. However, recent evidence, based on acute organ uptake of labeled hormone, suggests that the amount of hormone which is bioavailable in vivo may exceed that which is calculated to be free in vitro. To explore the bioavailability of circulating protein-bound thyroid hormones under steady state conditions in vivo, we altered serum thyroid hormone-binding proteins in rats by inducing nephrotic syndrome with puromycin aminonucleoside. Nephrotic rats (serum albumin, 1.1 g/dl) were found to have a marked reduction in serum T4 [2.1 +/- 0.2 (SEM) vs. 6.5 +/- 0.3 microgram/dl; P less than 0.01] and an elevation of serum T3 [141 +/- 8 vs. 51 +/- 2 ng/dl; P less than 0.01]. Estimated T4 production rate was normal in nephrotic rats, and the 3- to 4-fold increase in T4 MCR appeared to account for the marked reduction in serum T4. By contrast, increased serum T3 levels in nephrotic rats reflected both a reduction (55%) in T3 MCR and an increased rate of peripheral conversion of T4 to T3. A circulating inhibitor of T4 binding to serum proteins appeared to be present in nephrotic rats. The changes in the various serum components of thyroid hormone [T4-binding prealbumin (TBPA)-bound, albumin-bound, free] produced by nephrotic syndrome were compared with the corresponding changes in indices of thyroid hormone bioavailability (MCR, urinary excretion, hepatic content, TSH suppression, single pass extraction by liver). These comparisons suggested that nephrotic syndrome results in increased bioavailability of circulating T4 and decreased bioavailability of circulating T3. The bioavailable fraction of circulating T3 in vivo seemed to include both free T3 and that which is albumin bound in vitro. The bioavailable fraction of circulating T4 resembled free T4 more than non-TBPA-bound T4 (= albumin bound + free), although a nephrosis-induced increase in bioavailability of TBPA-bound T4 was also possible. We conclude that nephrotic rats have low serum T4, which is related to accelerated T4 clearance, and high serum T3, which is related both to decreased T3 clearance and increased peripheral conversion of T4 to T3. Under steady state conditions in vivo, bioavailable circulating T3 appears to include both free T3 and the T3 that is bound to albumin in vitro.

Animals↗
PubMed1984

Effect of chloride on serum thyroxine binding in familial dysalbuminemic hyperthyroxinemia.

Chloride ion is known to inhibit the T4-albumin interaction in normal serum. To determine the extent of this effect on T4 binding to albumin in patients with familial dysalbuminemic hyperthyroxinemia (FDH), the serum percent free T4 (FT4) was measured by equilibrium dialysis in 0.1 M phosphate buffer, pH 7.4, and in phosphate buffer with 0.14 M NaCl (phosphate-saline buffer) in patients with FDH, normal subjects, and women in the third trimester of pregnancy, who served as a population with high serum T4-binding globulin concentrations. The FT4 was calculated as the product of the percent FT4 and total T4 concentration. The mean values of serum FT4 were similar among the three groups when equilibrium dialysis was performed in phosphate buffer. When the assay was carried out in phosphate-saline buffer, the mean percent FT4 in each group was higher than that obtained in phosphate buffer, resulting in higher mean serum FT4 concentrations. However, the mean serum FT4 in normal subjects and pregnant women remained similar. The increase in percent FT4 in phosphate-saline buffer was proportionally greater in the patients with FDH, and therefore the mean serum FT4 in these patients was significantly higher than that of normal subjects when phosphate-saline buffer was used (2.67 +/- 0.07 (SE) vs. 1.80 +/- 0.09 ng/dl, P less than 0.001), and all FT4 values were above the normal range. It is concluded that chloride ion inhibits serum T4 binding in patients with FDH more than it does in normal subjects, perhaps due to the fact that albumin plays a much greater role in overall T4 binding in these patients.

Chlorides↗
PubMed1984

Environmental iodine intake and thyroid dysfunction during chronic amiodarone therapy.

Amiodarone, an iodine-containing drug used frequently in the treatment of cardiac arrhythmias and angina pectoris, has many effects on thyroid hormone metabolism, including decreasing the production of triiodothyronine (T3) and decreasing the clearance of thyroxine and reverse T3. These effects result in elevated serum thyroxine and reverse T3 concentrations and decreased serum T3 concentrations. In addition, iodine-induced hyperthyroidism or hypothyroidism may occur in patients chronically treated with amiodarone. This study is a retrospective analysis of the incidence of thyroid dysfunction in Lucca and Pisa, West Tuscany, Italy, and in Worcester, Massachusetts. Hyperthyroidism was a more frequent (9.6%) complication of amiodarone therapy in West Tuscany, where iodine intake is moderately low; hypothyroidism was more frequent (22%) in Worcester, where iodine intake is sufficient. In patients receiving chronic amiodarone therapy, clinically suspected hyperthyroidism is best confirmed by showing elevations in serum T3 or free T3 concentrations; hypothyroidism is best diagnosed by showing an elevated serum thyrotrophin concentration. Thyroid function should be carefully monitored in patients receiving amiodarone chronically, especially if they have goiter or Hashimoto's thyroiditis.

Adult↗
PubMed1983

Age affects the generation of serum thyronine-binding protein by rats fed a low protein-high carbohydrate diet.

The feeding of a low protein-high carbohydrate (PM) diet to young (8-week-old) rats induces the production of serum thyronine-binding globulin. The effect of age on this process was studied in older (5-month-old) rats. In contrast to the findings in 8-week-old rats, no significant differences in the serum concentrations of T3 and free T3 and the percentage of free T3 (equilibrium dialysis) were observed between the 5-month-old rats fed the control diet and those fed the PM diet. There were also no significant differences between the two diet groups in the distribution of tracer [125I]T4 and [125I]T3 among the serum proteins as assessed by gel electrophoresis. The changes in thyronine-binding globulin and subsequent alterations in T3 binding previously observed in young rats fed a PM diet do not occur in older rats, suggesting that the age and perhaps the weight of rats must be considered in studies related to diet-induced effects on thyroid hormone economy.

Age Factors↗
PubMed1982

Familial dysalbuminemic hyperthyroxinemia: a syndrome that can be confused with thyrotoxicosis.

We investigated 15 euthyroid patients from eight families with a recently recognized syndrome, familial dysalbuminemic hyperthyroxinemia (FDH), that could be mistaken for thyrotoxicosis. The syndrome is characterized by elevations in serum thyroxine and the free-thyroxine index (FT4l), which are due to an abnormal serum albumin that preferentially binds thyroxine. This albumin has an abnormal binding site with a much greater affinity for thyroxine (relative to its affinity for triiodothyronine) than that of the hormone-binding site on thyroxine-binding globulin. Results of thyrotropin-releasing hormone and thyroid-suppression tests, as well as direct measurements of the free-thyroxine concentration by equilibrium dialysis, are normal in these patients, although the serum triiodothyronine concentration may be slightly elevated. Although its prevalence is uncertain, FDH may be more common than suspected; we have seen 26 cases within the past year.

Adolescent↗
PubMed1982

Low protein-high carbohydrate diet induces alterations in the serum thyronine-binding proteins in the rat.

The serum T3 concentration was increased in 8-week-old lean Zucker rats fed a low protein-high carbohydrate diet for 2 weeks. This increase was secondary to the generation of a binding protein migrating in the postalbumin zone in polyacrylamide gel electrophoresis employing 125I-labeled T3 and is termed rat thyronine-binding globulin. The presence of this T3-binding protein in serum resulted in a marked decrease in the percent free T3 assessed by equilibrium dialysis and a normal free T3 concentration. An increase in the binding of T4 in the postalbumin zone was also observed, but no changes in the dialyzable fraction of T4 or the total and free T4 concentrations occurred. In contrast to these findings in lean Zucker rats fed the low protein-high carbohydrate diet, no change in the pattern of 125I-labeled T3 and T4 binding, the dialyzable fraction of T3 or T4, or total and free T3 or T4 concentrations were observed in the obese Zucker rats fed this diet. The present findings suggest that diet-induced alterations in thyroid hormone-binding proteins must be considered in the interpretation of data which involve alterations in total thyroid hormone concentrations in serum and their role in affecting tissue metabolism.

Animals↗