The functional state of the parathyroid glands among patients with autoimmune thyroiditis with the presence of calcifications in the thyroid glands

2020 ◽  
Author(s):  
Emma Badalyan ◽  
Maria Badalyan
1994 ◽  
Vol 141 (2) ◽  
pp. 309-315 ◽  
Author(s):  
R Paschke ◽  
F Schuppert ◽  
M Taton ◽  
T Velu

Abstract Cytokines are thought to mediate the initiation and perpetuation of autoimmune thyroiditis. However, this concept is mainly based on in vitro findings and to date only interleukin (IL)-6 and interferon-γ (IFN-γ) have been detected in Graves' disease in vivo. The cytokine pattern produced by T-helper (Th) cells has important regulatory effects on the nature of the immune response. We therefore determined these cytokine mRNAs in Graves' disease and Hashimoto's thyroiditis. RNA was extracted by cesium chloride gradient centrifugation from the thyroid tissue of 12 patients undergoing thyroid resection for Graves' disease and from two patients being treated for Hashimoto's thyroiditis. Two patients with parathyroid adenomas and one patient with a goiter were used as controls. RNA was also extracted from normal human thyroid epithelial cells in primary culture. The cDNAs were prepared by reverse transcription and amplified for IL-2, -4, -5, -6 and -10 and IFN-γ by polymerase chain reaction. All the cytokine mRNAs were detected in the Hashimoto's thyroid glands in large quantities. Six of the 12 Graves' disease thyroid glands showed, when compared with controls, an increased accumulation of transcripts for: IFN-γ, IL-2, -4 and -10 or IL-2, -4 and IFN-γ or IL-2 and IFN-γ or IFN-γ alone, each in one case or IL-2 alone in two cases. These cytokine profiles were not representative of a Th1 or Th2 phenotype. Increased amounts of cytokine mRNA in thyroid glands from Graves' disease patients were mostly associated with high microsomal antibody titres and/or prominent intrathyroidal lymphocytic infiltration. IL-6 and/or IL-10 mRNAs were detectable in all Graves' disease thyroid glands and in control thyroid tissue. IL-10 mRNA was not detectable in normal human thyroid epithelial cells in primary culture. Graves' disease and Hashimoto's thyroiditis clearly differ with respect to the number of positive intrathyroidal cytokine mRNAs and their levels. The different cytokine patterns in Graves' disease and in Hashimoto's thyroiditis could reflect the clinical spectrum of autoimmune thyroiditis which is characterized by thyroid tissue destruction and/or thyroid autoantibody production. These data suggest that the course of autoimmune thyroiditis is regulated by the interplay of several cytokines. Journal of Endocrinology (1994) 141, 309–315


2021 ◽  
Vol 22 (1) ◽  
pp. 85-96
Author(s):  
K.K. Kadhim ◽  
N.S. Al-Samarrae ◽  
J.Y. Al-Fayas

 The thyroid gland of Moorhen has two separated lobes. These lobes were located in the throracic inlet and receive blood supply from the cranial, middle and caudal thyroid arteries. The histological organization of the thyroid gland in Moorhen is surrounded by a distinct connective tissue capsule and the parenchymal cells were arranged into colloid filled follicles enmeshed in the highly vascular interstitial connective tissue. The bilaterally paired, round to oval, parathyroid glands in Moorhen were located intrathoracically near or close to the caudal pole of the thyroid glands. They receive blood by short branches from caudal thyroid artery and small branch from the common carotid artery. The parathyroid glands in Moorhen have a thin connective tissue capsule. Its parenchymal cells were arranged into an irregular, anastomosing cords of chief cells. No oxyphil cells were found in the parathyroid glands of Moorhen.


1916 ◽  
Vol 24 (5) ◽  
pp. 547-559 ◽  
Author(s):  
Andreas Tanberg

The following conclusions may be drawn from the experiments presented in this article. 1. Excessive meat diet develops hypertrophy of the thyroid gland. A definite hypertrophy of the parathyroid gland under the same conditions has not been established. A meat diet does not develop hypertrophy of the thyroid gland when insufficiency of the parathyroid gland exists at the same time, even if no clinical symptoms are present. Where a pronounced hypertrophy caused by a meat diet has already developed, the hypertrophy disappears and the gland assumes its ordinary appearance after extirpation of a sufficiently large number of parathyroid glands. 2. After parathyroidectomy no hypertrophy of the thyroid gland takes place. In chronic tetany the thyroid gland seems, on the contrary, to atrophy in spite of a meat diet. 3. After complete extirpation of the thyroid gland, the parathyroid gland does not change its structure, even in cases where the cachexia lasts for several years. Small remaining parts of the thyroid gland may through hypertrophy develop into compact tissue and thereby seemingly present some points of resemblance to the parathyroid gland. 4. When the parathyroid gland hypertrophies, as in some forms of chronic tetany, this hypertrophy is characterized by the development of large, transparent, sharply defined cells, with large nuclei rich in chromatin. 5. The parathyroid and thyroid glands are independent organs, each having specific functions. This, however, does not exclude the occurrence of a direct or indirect interaction in the functions of the two systems. 6. There is reason to believe that an insufficiency of the parathyroid gland checks to some extent the function of the thyroid gland. No proof of the existence of a vicarious cooperation between the two glands has been established.


2013 ◽  
Vol 03 (02) ◽  
pp. 257-261
Author(s):  
Ospan Mynbaev ◽  
Marina Eliseeva ◽  
Artem Chernov ◽  
Ioannis Kosmas ◽  
Andrea Tinelli ◽  
...  

1991 ◽  
Vol 128 (2) ◽  
pp. 239-NP ◽  
Author(s):  
R. S. Sundick ◽  
D. Herdegen ◽  
T. R. Brown ◽  
A. Dhar ◽  
N. Bagchi

ABSTRACT Several studies have shown that iodine plays a role in spontaneous autoimmune thyroiditis in man and other animals. In addition, abnormalities of iodine metabolism have been found in patients with Hashimoto's thyroiditis and in chickens of the obese strain (OS), an animal model of spontaneous autoimmune thyroiditis. We have examined several parameters of iodine metabolism before immune damage in this model and in the related Cornell strain (CS), a strain which develops a late-onset mild thyroiditis, to discover a possible causal relationship between altered iodine metabolism and the initiation of autoimmunity. Thyroglobulin was purified from individual chicken thyroid glands and analysed for iodine by the ceric sulphate method. Analogous to the thyroglobulin of Hashimoto's patients, the iodine content of OS thyroglobulin (27 atoms/molecule) was lower than that of normal-strain thyroglobulin (46 atoms/molecule) when the chickens were provided with a normal diet. Also, under conditions of TSH suppression, the iodine content of OS thyroglobulin (18 atoms/molecule) was lower than that of CS thyroglobulin (36 atoms/molecule) and of normal-strain thyroglobulin (32 atoms/molecule). In contrast with Hashimoto's patients, however, the OS and CS chickens had practically no inorganic iodide in their thyroid glands; electrophoretic analysis of thyroid homogenates revealed that essentially all (> 99·62%) 125I was organified by 16 h in all strains of birds tested. Despite the relatively poor iodination of thyroglobulin exhibited by OS chickens, they did not iodinate additional 'unique' proteins, when examined by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) of thyroid proteins labelled with 125I in vivo. The release of 125I in vivo under conditions of TSH suppression was examined in chicks receiving thyroxine and propylthiouracil. After 14 days both OS and CS chicks showed poorly suppressible release of 85% and 92% respectively, while the normal strain released 33 %. To determine whether the autonomous function of OS and CS thyroid glands was present in a restricted number of follicles or cells or whether it occurred in a majority of cells, autoradiograms of thyroid glands labelled in vivo from TSH-suppressed chickens were examined. Silver grains were present in all cells, indicating that autonomous function was a characteristic of all cells. These thyroid gland abnormalities are compared with those found in Hashimoto's patients and discussed in the context of their aetiological significance. Journal of Endocrinology (1991) 128, 239–244


1980 ◽  
Vol 152 (4) ◽  
pp. 1115-1120 ◽  
Author(s):  
R Maron ◽  
I R Cohen

Autoimmune thyroiditis (EAT) can be induced by immunizing mice against mouse thyroglobulin. A gene critical to the phenotypical expression of EAT was mapped to the H-2K locus by studying B6 mice and its mutant strain B6.H-2ba. To identify organs in which expression of the gene was decisive for the EAT phenotype, we transplanted thyroid or irradiated thymus glands into various strains of normal mice or thymusless nude mice. We found that the pathophysiology of EAT was controlled by the expression of specific H-2 genes in both the target thyroid gland and the thymus gland.


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