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Biomedical subjects

J J Staub

Publications and source records attributed to J J Staub.

At least 109 records · Page 6Linked to original sources
PubMed1976

[The systolic time intervals in functional disorders of the thyroid: a simple and fast screening test].

The systolic time intervals (LVET, PEP, and ratio LVET/PEP) were determined in 53 patients presenting with signs or symptoms of thyroid dysfunction. Patients with clinical evidence of congestive heart failure, with arterial hypertension or old myocardial infarction, and patients receiving cardioactive drugs, were excluded from the study. Thyroid function was evaluated by means of T3-RIA, serum thyroxin and TRH stimulation test.

Adult↗
PubMed1976

[Development of a simple oral short test with the TSH releasing hormone (TRH) and its use in thyroid diagnosis].

A simple test with 40 mg of oral TRH after overnight fasting was developed and can be characterized as follows: This short oral TRH test has been found to be a most valuable thyroid function test for detection of hyper- and hypothyroidism. It is as reliable as the intravenous TRH test. Oral TRH produces much stronger and more prolonged TSH stimulation similar to that of a depot preparation. Therefore, the incidence of euthyroid controls with absent or subnormal TSH response to TRH is definitely lower than after intravenous TRH. In patients with low TSH response after i.v. TRH the oral TRH test is of particular diagnostic value in distinguishing euthyroid function from TSH suppression or pituitary failure. 40 mg or oral TRH produces reliable stimulation of T3 in most euthyroid subjects. In patients with hyper- and hypothyroidism no increase of T3 is obserable. Oral TRH allows simultaneous assessment of pituitary TSH and thyroid reserve in a single test. The practical advantages (side effects in only 2% [for i.v. TRH 60%], only 1 or 2 blood samples, fewer sampling errors and no i.v. injection) outweigh the disadvantages (longer duration of the test, dependence on food intake and gastrointestinal absorption).

Administration, Oral↗
PubMed1976

[The hypophyseal TSH reserve in surgical patients with bland goiter and recurrent goiter].

Serum-T4, -T3, FTI, basal TSH and TRH-induced TSH response were measured in 80 patients with simple nontoxic goiter and in 24 patients with nontoxic recurrent goiter in a surgical unit. 55 of the 80 patients with simple goiter and 11 patients with recurrent goiter had normal individual TSH values. Mean FTI and serum T3 were not statistically different from age and sex related normal values, except serum-T3, which was above normal in elderly goiter patients. The incidence of elevated TSH reserve (preclinical hypothyroidism) was significantly higher (p less than 0.0005) in recurrent than in simple goiter (10 of 24 vs. 8 of 80 patients). Simple goiter aptients with preclinical hypothyroidism had a lower-than-normal mean serum T4 level, whereas mean serum T4 and T3 concentrations were higher than normal in preclinically hypothyroid recurrent goiter patients. In these subjects raised TSH values and goitrogenesis possibly may be related to lower sensitivity of the pituitary to thyroid hormones. 17 simple goiter patients and 3 recurrent goiter patients with normal circulating serum T4 and T3 levels showed no response to TSH to TRH. This suprising finding is related to preclinical hyperthyroidism on the basis of autonomously functioning thyroid compartments. In 12 tested patients TRH responsiveness recovered following goiter resection. The mean T3 response to TRH in goiter patients with normal or elevated TSH reserve was subnormal. This indicates that thyroid reserve is potentially decreased even in goiter patients whose thyroid function was, on the evidence of normal TSH values, actually appropriate.

Adult↗
PubMed1976

Thyroid cancer: a study of 573 thyroid tumors and 161 autopsy cases observed over a thirty-year period.

Five hundred and seventy-three thyroid tumors from surgical material and 161 autopsy cases were studied as to incidence, types, and precursor changes using the new WHO-classification. In the surgical material 225 tumors were follicular, 145 papillary, 147 anaplastic, 23 squamous cell, and 10 medullary. Twenty-three sarcomas were found. tthe percentage of follicular carcinoma had decreased, whereas that of papillary carcinoma increased and that of anaplastic carcinoma remained constant. In over 50% of anaplastic carcinomas neoplastic follicular structures have been identified. As a rule the more sections are prepared, the more papillary carcinomas and the less sarcomas are diagnosed. Thyroid tumors leading to death were found in 0.33% of 53,134 consecutive autopsies. Anaplastic (52.3%) and follicular (33.5%) carcinoma were most frequently encountered. Metastases of follicular and anaplastic carcinoma were most often found in the lung, pleura, and bones, whereas lymph nodes of the neck, lung, and bones were predominantly involved in cases of the papillary type. Therapy of thyroid carcinoma is total thyroidectomy. The transition of follicular carcinoma to the anaplastic type has to be avoided whenever possible.

Adenocarcinoma↗
PubMed1976

Preclinical hyperthyroidism in multinodular goiter.

The thyrotropin (TSH) response to thyrotropin-releasing hormone(TRH) (200 mug iv) was determined in 80 surgical patients with nontoxic multinodular goiter. The TSH reserve was normal in multinodular goiter. The TSH reserve was normal in 55 and elavated in 8 patients. No TSH response to TRH (deltaTSH less than or equal to 1 muU/ml) was detectable in 17 patients (21%). Individual and mean serum T4, FT4I and serum T3 values did not differ from normal in 13 of the TRH unresponsive patients; in 4 patients FT4I or serum T3 was marginally elevated. No statistical differences were noted for I131-uptake, PBI131 and conversion rate between controls and TRH unresponsive patients. All patients who failed to respond to TRH were euthyroid on clinical evaluation. Goiters were large multinodular and long-standing in most instances. In 12 tested subjects TRH responsiveness recovered following partial thyroidectomy. In 3 of 7 TRH unresponsive euthyroid patients tested 9-12 days post surgery a transient lack of TSH to respond to TRH was observed. Recovery of TRH responsiveness was accompanied by a significant (P IS LESS THAN 0, 02) decrease in serum T4and FT4I in the euthyroid range, whereas no change in serum T3 occurred. It is suggested that TRH unresponsiveness represents a state of preclinical hyperthyroidism maintained by autonomously functioning goiter compartments.

Adult↗
PubMed1975

Effect of oral thyrotrophin-releasing hormone on serum thyroxine in growth hormone deficient and normal children.

Oral administration of synthetic TRH in a dose of 80 mg/1-73 m-2 at 0 and 12 h to normal and constitutionally small children caused a significant increase of total serum thyroxine (T4) within 6-24 h. The mean maximal T4 increment was +3-7 plus or minus 1-1 and +3-8 plus or minus 1-2 mug/dl (mean plus or minus 1 SD) respectively in the two groups. Of seventeen euthyroid GH deficient children, fifteen showed a normal and two patients a slightly subnormal response. Of fifteen hypothyroid GH deficient children nine had a prompt and normal increase of serum T4 indicating primary TRH deficiency. Two had a delayed T4 response and four had no response, even after prolonged stimulation. The localization of the primary defect in these latter subjects with severe hypothyroidism can not be made by measuring T4 only, since the thyroid gland may become unresponsive to TSH after longstanding TSH deficiency. TSH measurements are necessary in these circumstances for a clear localization of the primary defect. One GH deficient patient with hypothalamic TRH deficiency was treated with high oral TRH doses for 7 months and showed no side effects.

Administration, Oral↗
PubMed1973

Comparison of corticotrophin and corticosteroid response to lysine vasopressin, insulin, and pyrogen in man.

Plasma corticotrophin (ACTH) and corticosteroid levels in response to lysine vasopressin (LVP), insulin hypoglycaemia, and pyrogen have been compared in seven subjects with normal pituitary adrenal function. Intramuscular vasopressin was a weak stimulus to corticotrophin release, peak values lying within the range 49 to 141 pg/ml. Insulin hypoglycaemia consistently caused a more noticeable increase, with peak levels between 114 and 364 pg/ml, while pyrogen was the most powerful, corticotrophin levels rising to between 209 and 1,725 pg/ml. Peak plasma corticosteroid levels showed less pronounced differences between the three tests, and correlated poorly with peak ACTH levels. Thus, relatively small acute changes in corticotrophin levels produce near-maximal adrenal stimulation. Under these conditions, plasma corticosteroid measurements do not accurately reflect circulating corticotrophin levels. These findings help to explain the physiological basis of several observations on the corticosteroid responses to these clinical test procedures.

11-Hydroxycorticosteroids↗