scholarly journals Course of hatch and developmental changes in thyroid hormone concentration in blood of chicken embryo following in ovo riboflavin supplementation

2014 ◽  
Vol 38 ◽  
pp. 230-237 ◽  
Author(s):  
Karolina Barbara TRZECIAK ◽  
Marcin Wojciech LIS ◽  
Andrzej SECHMAN ◽  
Barbara PŁYTYCZ ◽  
Agata RUDOLF ◽  
...  
2002 ◽  
Vol 41 (04) ◽  
pp. 178-183 ◽  
Author(s):  
V. Fidler ◽  
K. Zaletel ◽  
S. Gaberšček ◽  
S. Hojker ◽  
E. Pirnat

Summary Aim: In spite of extensive use of 131I for treatment of hyperthyroidism, the results of early outcome are variable. In our prospective clinical study we tested whether 131I induced necrosis causing clinical aggravation of hyperthyroidism and increasing the free thyroid hormone concentration in the serum of patients with solitary toxic adenoma not pretreated with antithyroid drugs. Patients and methods: 30 consecutive patients were treated with 925 MBq 131I. Serum concentration of thyrotropin (TSH), free thyroxine (fT4), free triiodothyronine (fT3), thyroglobulin (Tg), and interleukin-6 (IL-6) were measured before and after application of 131I. Results: After application of 131I no clinical worsening was observed. FT4 and fT3 concentration did not change significantly within the first five days, whereas both of them significantly decreased after 12 days (p <0.0001). Slight and clinically irrelevant increase in the level of the two thyroid hormones was observed in 9 patients. Furthermore, we observed a prolonged increase in Tg concentration and a transient increase in IL-6 concentration. Conclusion: Neither evidence of any clinical aggravation of hyperthyroidism nor any significant increase in thyroid hormone concentration by 131I induced necrosis of thyroid cells was found. Therefore, the application of 131I may be considered as a safe and effective treatment for patients with hyperthyroidism due to toxic adenoma.


2021 ◽  
Vol 49 (3) ◽  
pp. 030006052199619
Author(s):  
Yusaku Mori ◽  
Munenori Hiromura ◽  
Michishige Terasaki ◽  
Hideki Kushima ◽  
Makoto Ohara ◽  
...  

Background Methimazole (MMI) is used to treat hyperthyroidism in Graves’ disease. It is rare to encounter patients in whom hyperthyroidism cannot be controlled using high doses of MMI. Case presentation: A 21-year-old woman was referred to our hospital because of MMI-resistant Graves’ disease. Although her MMI dose had been increased to 120 mg/day, her serum thyroid hormone concentration was too high to be measured. Additional therapy with lithium carbonate, and then with dexamethasone and inorganic iodine, was initiated. After 14 days, the patient’s serum thyroid hormone concentration normalized, while she was taking 150 mg/day MMI, 800 mg/day lithium carbonate, 6 mg/day dexamethasone and 306 mg/day inorganic iodine, and total thyroidectomy was then performed. The patient was discharged 8 days after the thyroidectomy and experienced no major complications. Conclusions We have presented a rare case of Graves’ disease that was resistant to high-dose MMI. Combination therapy of MMI with lithium carbonate, dexamethasone and inorganic iodine may represent a therapeutic option for the preoperative preparation of patients with MMI-resistant Graves’ disease.


BMC Genomics ◽  
2008 ◽  
Vol 9 (1) ◽  
pp. 78 ◽  
Author(s):  
Robert B Page ◽  
Stephen R Voss ◽  
Amy K Samuels ◽  
Jeramiah J Smith ◽  
Srikrishna Putta ◽  
...  

1983 ◽  
Vol 245 (1) ◽  
pp. E32-E37
Author(s):  
H. Ikeda ◽  
M. A. Greer

Five adenohypophyses from donors of the same strain, age, and sex were transplanted under the renal capsule of young adult female rats. At least 3 wk later, enzymatically dispersed cells from eutopic or heterotopic adenohypophyses from the same rat were perifused in vitro in a small chamber. Thyrotropin (TSH) and prolactin (PRL) secretion per 10(6) cells were significantly less from heterotopic than from eutopic cells under all conditions. In cells from euthyroid animals, TRH induced TSH secretion only in the eutopic cells but induced PRL secretion in both eutopic and heterotopic cells. Hypothyroidism increased TRH-induced TSH secretion and content in the cell lysate in both eutopic and heterotopic cells but increased TRH-induced PRL secretion only in the eutopic cells. The increase in TSH secretion induced by hypothyroidism in the heterotopic cells was of borderline statistical significance. The inability of TRH to induce TSH secretion in heterotopic pituitary cells from euthyroid rats may be due to a lower set point for thyroid hormone inhibition of TSH secretion in the heterotopic thyrotrophs. Heterotopic pituitary TSH secretion is probably suppressed by the normal plasma thyroid hormone concentration maintained by the eutopic pituitary and may be stimulated by TRH only in the presence of a subnormal plasma thyroid hormone concentration.


1992 ◽  
Vol 87 (1) ◽  
pp. 6-13 ◽  
Author(s):  
Begoña Gancedo ◽  
Isabel Corpas ◽  
Angel Luis Alonso-Gómez ◽  
María Jesús Delgado ◽  
Gabriella Morreale de Escobar ◽  
...  

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