STIMULATION WITH THYROTROPHIN-RELEASING HORMONE (TRH) DURING ANTITHYROID TREATMENT

1975 ◽  
Vol 78 (3) ◽  
pp. 461-467 ◽  
Author(s):  
Ulrik Birk Lauridsen ◽  
Carsten Kirkegaard ◽  
Thorkild Friis ◽  
Kaj Siersbæk-Nielsen

ABSTRACT During antithyroid treatment a total of 88 TRH tests was performed in 56 clinical euthyroid patients. 56 % had negative response to TRH (i. e. Δ TSH < 2 μU/ml) after being treated in average 12.6 months and no relation between the duration of treatment and the outcome of the TRH test was found. In the group with positive TRH tests (i. e. Δ TSH > 2 μU/ml) the mean T4 value was slightly decreased (5.8 ± sd 2.5 μg/100 ml) while the mean T3 value was normal (121 ± sd 32 ng/100 ml). The group with negative TRH tests had quite normal serum T4 values (9.3 ± sd 3.1μg/100 ml) but in general high normal or elevated serum T3 values (175 ± sd 31 ng/100 ml). Our results seem to indicate that serum T3 is of greater importance than serum T4 with regard to the outcome of the TRH test. The majority of the cases with negative TRH tests, however, had serum T3 and T4 values within normal range. In almost all patients with a negative TRH test a negative T3 suppression of 131I uptake in the thyroid gland was found while a positive TRH test was not correlated with suppressibility of 131I uptake.

1974 ◽  
Vol 75 (2) ◽  
pp. 274-285 ◽  
Author(s):  
A. Gordin ◽  
P. Saarinen ◽  
R. Pelkonen ◽  
B.-A. Lamberg

ABSTRACT Serum thyrotrophin (TSH) was determined by the double-antibody radioimmunoassay in 58 patients with primary hypothyroidism and was found to be elevated in all but 2 patients, one of whom had overt and one clinically borderline hypothyroidism. Six (29%) out of 21 subjects with symptomless autoimmune thyroiditis (SAT) had an elevated serum TSH level. There was little correlation between the severity of the disease and the serum TSH values in individual cases. However, the mean serum TSH value in overt hypothyroidism (93.4 μU/ml) was significantly higher than the mean value both in clinically borderline hypothyroidism (34.4 μU/ml) and in SAT (8.8 μU/ml). The response to the thyrotrophin-releasing hormone (TRH) was increased in all 39 patients with overt or borderline hypothyroidism and in 9 (43 %) of the 21 subjects with SAT. The individual TRH response in these two groups showed a marked overlap, but the mean response was significantly higher in overt (149.5 μU/ml) or clinically borderline hypothyroidism (99.9 μU/ml) than in SAT (35.3 μU/ml). Thus a normal basal TSH level in connection with a normal response to TRH excludes primary hypothyroidism, but nevertheless not all patients with elevated TSH values or increased responses to TRH are clinically hypothyroid.


1968 ◽  
Vol 14 (2) ◽  
pp. 172-178 ◽  
Author(s):  
R B Payne ◽  
M J Levell

Abstract The serum sodium concentrations of three groups of patients selected from laboratory records and of one group of outpatients selected for a prospective study were examined. The mean serum sodium concentration of inpatients with normal serum urea concentrations was 8.5 mEq./ L. lower than that of a group of healthy normal subjects. Part of this difference (2.6 mEq./L.) could be attributed to a nonspecific effect of illness. It was not possible to demonstrate any effect due to the hospital environment, but the results do not exclude the possibility of such an effect. It was concluded that all or most of the remaining difference was due to weighting of the inpatient data by low values of pathologic significance; the proportion of these low values was too great to allow a normal range to be extracted from the data by statistical methods. The concept of the normal range is discussed. It is suggested that two ranges are required for serum sodium, a normal range (137-147 mEq./L. in this laboratory) to make assertions about alterations in specific diseases, and a range derived from patients likely to have no manifest disturbances of salt and water metabolism (135-144 mEq./ L.) to detect such disturbances.


1979 ◽  
Vol 91 (4) ◽  
pp. 674-679 ◽  
Author(s):  
Jens Faber ◽  
Dorte Cohn ◽  
Carsten Kirkegaard ◽  
Morten Christy ◽  
Kaj Siersbæk-Nielsen ◽  
...  

ABSTRACT Fourteen patients with Idiopatic Addison's disease (IAD) were studied in order to detect a possible subclinical hypothyroid state. All were clinically euthyroid with normal serum thyroxine (T4) and serum 3,5′,3′-triiodothyronine (T3). Eleven had circulating thyroid microsomal antibodies in blood. The mean basal serum TSH was significantly higher than that of the control group but only three patients had values above the upper normal range. The mean value of serum T4 was decreased as compared to that of the normal persons, while serum 3,3′,5′-triiodothyronine was elevated. 7.5 mU bovine thyrotrophin per kilogram body weight injected intravenously caused a rise in serum T3 not different from the response in normals. However, as well increasing serum TSH as increasing microsomal antibody titer correlated significantly to decreasing thyroidal release of T3. Our results suggest that clinically euthyroid patients suffering from IAD might have a beginning thyroidal insufficiency because of a progressive immunological damage of the thyroid.


The purpose of this study is to determine the activity of serum adenosine deaminase (ADA) in healthy people, in connection with significant differences in published reference ranges from different authors. In our study, we examined 160 healthy subjects aged 18 to 84, of whom 64 were men and 96 women. We have determined serum adenosine deaminase levels using a method based on the ability of the enzyme adenosine deaminase to catalyze the deamination of adenosine to inosine and ammonia. The catalytic concentration is determined spectrophotometrically by the rate of reduction of NADH measured at 340 nm. We found that normal serum ADA values among our healthy subjects are higher than the recommended reference range for the method we use, namely below 18 U/l. Using the percentile method, we worked out the following reference ranges: for women 14.53 - 25.73 U/l and for men 18.46 – 27.50 U/l. For women, the mean value is 21.07 U/l, and for men 21.30 U/l. At 95% CI, the serum ADA values of almost all subjects included in the study are within the recommended and other authors range of 11.50 - 25.00 U/l.


Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1400-1400
Author(s):  
Zeina G Elamil ◽  
Hande H. Tuncer ◽  
Roy Tara ◽  
Samer A. Al Homsi

Abstract Abstract 1400 Introduction: Hemostatic abnormalities are frequently encountered during initial presentation of acute myeloid leukemia (AML) as well as during induction treatment. Patients often present with decreased platelet counts and sometimes with abnormalities of the coagulation parameters with or without bleeding manifestations. In the absence of overt disseminated intravascular coagulopathy (DIC), transfusion practices during treatment are essentially based on the platelet count. Fibrinogen is an important element of the clotting mechanisms, constituting a template for both thrombin binding and the fibrinolytic system. We sought to determine the prevalence of altered serum fibrinogen levels during induction treatment in AML and its clinical significance. Methods: We prospectively measured serum fibrinogen on a daily basis in patients with newly diagnosed AML treated with induction anti-tumor chemotherapy at our institution from February 2007 to July 2010. Inclusion criteria included the diagnosis of AML and no overt DIC. Results: The study population included 17 patients (47% females) with mean age of 55.3 years (range 18 –80 years). At presentation, the mean platelet count was 62 × 109/L (range 3 – 252 × 109/L), the mean prothrombin time was 11.4 seconds (range 9.6–13.4 secs, normal range 10—13.7 secs), the mean international normalized ratio was 1.1 (range 0.9–1.3; normal range 0.9–1.1) and the mean activated partial thromboplastin time was 26.56 seconds (range 20.1–41 secs, normal range 22.3–34.0 secs). All patients had normal serum fibrinogen levels at presentation (mean 380.6 mg/dl; range 258–567 mg/dl; normal range 200–400 mg/dl). Thirteen patients were treated with idarubicin and cytarabine, 3 patients received a FLAG (fludarabine, cytarabine and G-CSF) regimen and one patient had amonafide and cytarabine. Serum fibrinogen levels were recorded on all patients on a daily basis (Figure 1). Nine (53%) developed hypofibrinogenemia on the fourth day of induction, 2 (12%) on day 5, 3 (17%) on day 6, 2 (12%) on day 7, and one (6%) on day 8 of the induction. Eight patients (47%) received prophylactic cryoprecipitate when the serum fibrinogen levels fell below 150 mg/dl. We did not observe a significant trend difference in serum fibrinogen levels between patients who received cryoprecipitate and those who did not. Serum fibrinogen levels were back to normal without transfusion support by day 6 for one patient (5.88 %), day 7 for 2 patients (11.76 %), day 8 for 3 patients (17.65 %), day 9 for one patient (5.88 %), day 10 for one patient (5.88 %), day 11 for 3 patients (17.65 %), day 12 for 6 patients (35.3 %). Conclusion: Patients with acute myeloid leukemia receiving induction chemotherapy may frequently develop isolated hypofibrinogenemia without evidence of disseminated intravascular coagulation. This finding is usually self-limited and disappears shortly after the completion of antitumor chemotherapy, usually by day 12. The mechanism of this under-recognized phenomenon is unclear. Its common occurrence raises questions about the appropriateness of transfusion practices in AML based solely on the platelet count and argues in favor of the need of more global tests such as thromboelastography. Disclosures: No relevant conflicts of interest to declare.


1980 ◽  
Vol 93 (4) ◽  
pp. 396-401 ◽  
Author(s):  
S. Grasso ◽  
S. Filetti ◽  
D. Mazzone ◽  
V. Pezzino ◽  
R. Vigo ◽  
...  

Abstract. The function of the thyroid pituitary axis was investigated in 8 anencephalic infants with no hypothalamus. Thyrotrophin (TSH), thyroxine (T4), 3,5,3′-triiodothyronine (T3) and 3,3,′5′-triiodothyronine (reverse T3, rT3) were measured in the cord blood in 5 cases and during the first 4 h of life in 3 cases, TSH response to synthetic thyrotrophin-releasing hormone (TRH) (200 μg iv) was carried out in two cases and thyroid hormone response to bovine TSH (5 IU iv) was evaluated in 3 cases. The following results were obtained: 1) The pituitary gland was found in all infants and the thyroid was normal both grossly and by microscopic sections. 2) TSH levels at birth were normal but there was no spontaneous post-delivery surge. 3) T4 and T3 values at delivery were within normal range, but no T3 increase was present after birth. rT3 levels at birth were higher than normal in 3 cases. 4) Administration of TRH caused a marked and rapid TSH release. 5) Thyroid hormone response to TSH was normal. The present findings suggest that in the anencephalic foetus both pituitary TSH-secreting cells and the thyroid gland do develop despite the absence of the hypothalamus and are able to function if adequately stimulated.


1974 ◽  
Vol 20 (3) ◽  
pp. 317-319 ◽  
Author(s):  
Richard J L Bondar ◽  
Gerald A Moss

Abstract Free glutamate increases the apparent serum γ-glutamyltranspeptidase (γ-GTP) activity in the normal range by 100%, and in the 10-fold normal range by 20%. This increase is greatest, and is the same, at two very different concentrations, 60 and 1000 µmol of glutamate per liter of the final reaction mixture. Glutamate concentrations greater than 10 mmol/liter inhibit serum γ-GTP. Elevated serum glutamate concentrations or glutamate released by substrate breakdown will therefore give false and possibly variable results. To minimize variations in activity, the assay should be run in the presence of 1.0 mmol of glutamate per liter. This concentration, which is 100 times greater than that which normal serum would contribute (with respect to free glutamate) to the assay system, thus masks any effect of extraneous glutamate.


1971 ◽  
Vol 134 (3) ◽  
pp. 259-275 ◽  
Author(s):  
Shaun Ruddy ◽  
Lloyd K. Everson ◽  
Peter H. Schur ◽  
K. Frank Austen

An effective molecule titration for the ninth component of complement in the biologic fluids of man was developed using EAC1-8 cells produced by treating EAC14 cells with a chromatographic fraction of human serum containing C2, C3, C5, C6, C7, and C8. Kinetic studies of the interaction of EAC1-8 with C9 indicated that this component was depleted from the fluid phase, and that the lytic reaction proceeded most rapidly at ionic strength 0.145, and at a temperature of 37°C. The mean value for C9 in normal serum was 52,000 ±12,000 units/ml. The mean serum C9 for patients with DJD, rheumatoid arthritis, or SLE without active renal disease was approximately twice the mean for normal individuals. Patients with SLE and active renal disease had a mean C9 value which fell within the normal range, but was significantly lower than in patients with SLE who did not have active renal disease. Two instances of absolutely subnormal C9 levels were observed in patients during attacks of florid SLE, including nephritis. Since the usual change in serum C9 in rheumatic diseases is a marked elevation, the occurrence of a subnormal value reflects circumstances in which depletion due to activation of the sequence exceeds the increases associated with the inflammatory response.


1978 ◽  
Vol 87 (4) ◽  
pp. 728-733 ◽  
Author(s):  
Toshio Matsumoto ◽  
Etsuro Ogata ◽  
Michiko Yamamoto ◽  
Yuji Aiyoshi ◽  
Shigenobu Nagataki

ABSTRACT Several steps of thyroid hormogenesis were studied on a subhyoid ectopic thyroid tissue in a case of compensated hypothyroidism with simultaneous sublingual and subhyoid ectopic thyroid. The patient, a 19-year-old girl, had normal values for serum T4, T3U and T3, and an elevated serum TSH level. The thyroidal 131I uptake was elevated both at 3 h and 24 h after oral 131I intake. No significant discharge of radioiodine was observed after perchlorate load. On the thyroid biopsy specimen, peroxidase activity was shown to be normal by both assays of guaiacol oxidizing and iodinating activity. Thyroglobulin was 19S and was normally iodinated in vitro with peroxidase. Iodine content of thyroglobulin was within the normal range. The mean percentage distribution of 131I administered 7 days prior to the biopsy showed no significant difference from the normal pattern. From these studies, no specific defects in thyroid hormogenesis could be detected in this case. It is suggested that abnormalities in thyroid function in this case are mainly due to insufficient functioning mass in the ectopic thyroid.


Endocrinology ◽  
2014 ◽  
Vol 155 (1) ◽  
pp. 315-325 ◽  
Author(s):  
Julia Müller ◽  
Steffen Mayerl ◽  
Theo J. Visser ◽  
Veerle M. Darras ◽  
Anita Boelen ◽  
...  

The monocarboxylate transporter Mct10 (Slc16a10; T-type amino acid transporter) facilitates the cellular transport of thyroid hormone (TH) and shows an overlapping expression with the well-established TH transporter Mct8. Because Mct8 deficiency is associated with distinct tissue-specific alterations in TH transport and metabolism, we speculated that Mct10 inactivation may compromise the tissue-specific TH homeostasis as well. However, analysis of Mct10 knockout (ko) mice revealed normal serum TH levels and tissue TH content in contrast to Mct8 ko mice that are characterized by high serum T3, low serum T4, decreased brain TH content, and increased tissue TH concentrations in the liver, kidneys, and thyroid gland. Surprisingly, mice deficient in both TH transporters (Mct10/Mct8 double knockout [dko] mice) showed normal serum T4 levels in the presence of elevated serum T3, indicating that the additional inactivation of Mct10 partially rescues the phenotype of Mct8 ko mice. As a consequence of the normal serum T4, brain T4 content and hypothalamic TRH expression were found to be normalized in the Mct10/Mct8 dko mice. In contrast, the hyperthyroid situation in liver, kidneys, and thyroid gland of Mct8 ko mice was even more severe in Mct10/Mct8 dko animals, suggesting that in these organs, both transporters contribute to the TH efflux. In summary, our data indicate that Mct10 indeed participates in tissue-specific TH transport and also contributes to the generation of the unusual serum TH profile characteristic for Mct8 deficiency.


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