Biomedical subjects

H Bürgi

Publications and source records attributed to H Bürgi.

At least 73 records · Page 4Linked to original sources

PubMed1976

Changes of circulating thyroxine, triiodothyronine and reverse triiodothyronine after radiographic contrast agents.

Thyroid function was studied for 42 days in 58 patients, 28 of whome had euthyroid goiter, after urography (diatrizoic acid), cholangiography (ioglycamic acid), and cholecystography (Naiopanoate). After urography and cholangiography short-lived increases of the serum thyroxine occurred in a few patients, but the mean thyroxine and triiodothyronine concentration did not change. By contrast, 7 days after oral cholecystography serum thyroxine had risen consistently by 22% with a concomittant rise of the free thyroxine, while triiodothyronine declined by 15%. The thyroxine metabolite 3,3',5'-triiodo-1-thyronine (reverse T3) rose by 50% and serum thyrotropin concentration doubled. After 42 days thryoxine and triiodothyronine had returned to baseline, and none of the 58 patients developed clinical hyperthyroidism. In patients with severe myxoedema kept on a constant replacement dose with 1-thyroxine NA-iopanoate produced similar changes with the exception of the rise of the serum thyroxine. The primary event after Na-iopanoate seems to be a fall of the serum triiodothyronine, which in turn augments thyrotropin and indirectly thyroxine secretion. the marked and sometimes sustained rose of serum thyroxine after cholecystography may lead to the erroneous diagnosis of hyperthyroidism.

Adult↗

PubMed1976

Inhibition of thyroglobulin biosynthesis and degradation by excess iodide. Synergism with lithium.

Lithium and excess iodide inhibit the release of thyroid hormone from preformed stores. We thus tested the hypothesis that this was due to an inhibition of thyroglobulin breakdown. Rats were pre-treated with propyl-thiouracil (PTU) for 3 weeks in order to deplete their thyroids of thyroglobulin. While the PTU was continued, lithium chloride (0.25 mEq./100 g weight) or potassium iodide (3 mg per rat) were injected every 12 h for d days. Thereafter the thyroglobulin content in thyroid gland homogenates was measured. PTU pre-treatment lowered the thyroglobulin content from 4.21 to 0.22 mg/100 mg gland. Lithium caused a marked re-accumulation of thyroglobulin to 0.60 mg/100 mg within 3 days. While iodide alone had only a borderline effect, it markedly potentiated the action of lithium and a combination of the two drugs increased the thyroglobulin content to 1.04 mg/100 mg. Thyroxine was injected into similarly pre-treated animals to suppress secretion of thyrotrophic hormone. This markedly inhibited the proteolysis of thyroglobulin and 1.3 mg/100 mg gland accumulated after 3 days. Excess iodide, given in addition to thyroxine, decreased the amount of thyroglobulin accumulated to 0.75 mg/100 mg gland. To study whether this could be explained by an inhibitory action of iodide on thyroglobulin biosynthesis, thyroid glands from animals treated with excess iodide were incubated in vitro in the presence of 0.2 mM iodide for 3 h. Iodide decreased the incorporation of radioactive leucine into total thyroidal protein and into thyroglobulin by 25 and 35% respectively. Iodide did not inhibit protein synthesis in the kidney, liver or muscle tissue. Thus, large doses of iodide selectively inhibit thyroglobulin biosynthesis.

Animals↗

PubMed1976

A transient rise of hormone secretion: a response of the stimulated rat thyroid gland to small increments of iodide supply.

Small doses of iodide (2 times 3.2 mug at 12 h interval), below those capable of inducing Wolff-Chaikoff effect, were injected into rats kept on a moderately low iodine diet. By means of a 125I equilibration technique as well as by direct measurement of cold T4, it was demonstrated that the level of circulating PB125I (representing iodothyronines as confirmed by column chromatography) increased by a mean of 40% within 24 h following the first iodide injection. The serum TSH concentration (measured by radioimmunoassay) was simultaneously depressed. Thus, in stimulated thyroid glands, a biologically significant fraction of an iodide load escapes autoregulatory control of iodothyronine synthesis. A small, transient increase of hormone release is likely to represent the physiological response of a normal gland to a sudden supplement of iodide supply. The ensuing depression of TSH secretion may be necessary for final adjustment of thyroid function. It is considered to be the last step in a cascade of mechanisms whose interaction keeps the thyroidal hormone output within narrow limits in the face of a fluctuating iodide supply. Failure of one or several of these mechanisms in the goitrous human gland could conceivable explain the phenomenon of "Jod Basedow".

Animals↗

PubMed1975

[Endocrine ophthalmology. An overview of pathology, classification, and therapy].

A new uniform nomenclature will allow more accurate clinical study of endocrine ophthalmopathy, a disease that remains an enigma. Clinical eye disease develops in 30-60% of patients with Graves' disease, but the severe malignant form occurs in a maximum of 5%, and most of these latter patients have been rendered euthyroid or hypothyroid by treatment of the hyperthyroidism. Despite claims to the contrary, there is no convincing evidence that the mode of treatment (antithyroid drugs, surgery or radioiodine) has a bearing on the development of ophthalmopathy. Circulating fragments of the TSH-molecule, which produce swelling of retroorbital tissue, and as autoimmune processes of the delayed type are currently under consideration as causative factors. Medical treatment of endocrine ophthalmopathy has only a limited effect. In cases of rapid progression with deterioration of vision it is recommended that operative decompression, preferably into the maxillary and ethmoidal sinus, be performed without delay. Retroorbital administration of 2000 rad by a highly collimated megavoltage beam appears to be a valuable alternative to surgery.

Adult↗

PubMed1975

[When is a radioisotope diagnosis indicated in thyroid diseases and when is it superfluous?].

In response to the question when radioactive isotopes (radionuclides) are necessary or superfluous in the diagnostic workup of thyroid disease, the following observations can be made: 1. Radionuclides are almost ubiquitously used for the specific and relevant in-vitro tests for measuring the circulating thyroid hormones (T4 und T3, etc.) and necessitate a very small quantity of serum. They lead in approximately 90% of cases of the correct diagnosis, especially when supported by careful clinical workup. 2. The use of radionuclides is of unquestionable value for scanning the thyroid gland and thus permitting the localization of normal vs. ectopic thyroid tissue, and the recognition of active ("warm" or "hot") vs. inactive ("cold") areas, especially in nodular goiter. 3. As the best screening tests for hypo- or hyperthyroidism are those related to the level of circulating thyroid hormones (see above), thyroid radionuclide uptake tests have lost much of their diagnostic value. However, the measurement of thyroidal radionuclide uptake remains valuable whenever radioiodine treatment is considered and in detailed thyroid function studies, and its also useful in the follow-up of drug-treated hyperthyroid patients. Thyroid uptake measurements may be of particular interest in so-called dynamic tests (e.g. TSH-stimulation, T3-suppression). 4. Finally, attention is drawn to the fact that, according to AITCHISON et al. (1), our capacity to interpret multidimensional information properly is limited. Thus, experience and precise knowledge help to economize the use of radionuclides and permit minimal application with maximal output.

Binding Sites↗

PubMed1975

Autoradiographic localization of slow turnover iodocompounds within the follicular cells of the rat thyroid gland.

In addition to thyroglobulin, several low molecular wt iodinated glycopeptides are present in the thyroid gland. Some of these compounds are considered to be slowly metabolized remnants of intracellular lysis of engulfed colloid droplets. In this paper we present autoradiographic evidence obtained by light microscopy, suggesting that breakdown products of thyroglobulin digestion can indeed be located within the thyroid cells. The thyroid glands of rats were labeled with 125I to approach isotopic equilibrium. The tracer was then withdrawn from the otherwise unchanged high-iodine diet, and thyroidal radioactivity was washed out for 80 days. Autoradiographs of glands containing 10% or less of the tracer present at equilibrium showed the bulk of 125I within the follicular cells while the colloid was only slightly labeled. An additional finding was the presence of dense radioactive inclusions in the lumina of many follicles. They are assumed to represent clusters of thyroglobulin molecules not readily available to pinocytosis. In addition to autoradiographic evidence, the identity of intracellularly located radioactivity with slow-turnover enzyme-resistant iodocompounds is supported by double labeling experiments, using 125I as the "old" tracer, accumulating within the cells, and 131I as the "new" label representing intraluminal 19 S thyroglobulin. Experimental manipulations which tended to deplete the thyroid of thyroglobulin, increased the 125I/131I ratio in the gland as predicted by the working hypothesis. Thus, this paper describes a new kind of autoradiographic ring reaction due to a hitherto barely considered intracellular organic iodine pool.

Animals↗

PubMed1975

[Decompression of the orbit in malignant exophthalmos (author's transl)].

Transantral decompression of the orbit for malignant exophthalmos can be recommended on the experiences of Walsh and Ogura, and Gorman et al. The case of a 70 year old man with exophthalmos and marked deterioration of bilateral visual acuity that recovered postoperatively is reported. The exophthalmos disappeared completely.

Aged↗

PubMed1975