scholarly journals A case with a combination of Conn’s syndrome and diffuse toxic goiter

1994 ◽  
Vol 40 (4) ◽  
pp. 38-39 ◽  
Author(s):  
V. A. Yakovlev ◽  
S. B. Shustov ◽  
Yu. Sh. Khalimov

The combination of pathology of the adrenal glands and thyroid gland is very rare and, as a rule, is characterized by adrenal insufficiency and hypothyroidism / Schmidt syndrome), which develop in type II autoimmune polyglandular syndrome. There is a single description of low-krenin aldosteronism due to thyroid cancer. In the available literature, we have not found information about the combination of primary hyperaldosteronism and diffuse toxic goiter.

2020 ◽  
Vol 23 (2) ◽  
pp. 143-147
Author(s):  
V. Yu. Mykhaylichenko ◽  
N. E. Karakursakov ◽  
O. F. Bezrukov ◽  
E. Ya. Kerimov ◽  
S. A. Samarin

The authors analyzed the literature data and their own experience in treating patients with compression syndrome. The aim of our study is to study the presence of compression syndrome in patients with thyroid disease. Methods. Our study included an analysis of 131 patients in the hospital of the Clinical Medical Multidisciplinary Center of St. Luke from 2019 to 2020. We examined the clinical picture of patients with diffuse toxic goiter; benign nodular formations of the thyroid gland with their cervical-retrosternal location; thyroid cancer; lymphomas of the thyroid gland, which performed decompression operations, the remaining patients with this pathology were sent for chemotherapy + monoclonal antibodies. Results. Thus, we observed unilateral paresis of the vocal cord in 27.5%, bilateral - 6.1%, dysphagia - 17.6%, superior vena cava syndrome - 20.6%, and respiratory dysfunction - 58.8%. Conclusions. Compression syndrome was observed in all cases of thyroid lymphoma, and complex with compression of several organs. Complex compression syndrome was observed in 193% of patients with benign nodular formations of the thyroid gland, 90% of diffuse toxic goiter, 113% of thyroid cancer and 317% of thyroid lymphoma.


Author(s):  
Rania Alsayed Murad ◽  
Ashraf Alakkad ◽  
Anwar Adwan ◽  
Mikdam Al Ramahi

A 60-year-old male patient, weighing 40 kg, having a BMI of 13, who was also a known case of Diabetes Mellitus Type II was shifted to the Orthopaedic Ward last month due to a fall, which led him to develop an intertrochanteric fracture in the femur. While the treatment of the patient was in an ongoing status for his fracture, his Diabetes was seen to be poorly controlled, with his blood glucose levels being constantly evaluated to be in a state of severe hypoglycaemia to slightly increased levels of blood glucose. On examination, the patient showed clear signs of being malnourished. He was in a bad and dishevelled state, he had creases on the palmar aspects of his hands and hyperpigmentation on his buccal mucosa. Furthermore, his lab reports revealed abnormalities in nearly every lab test ordered. Not only did he have elevated ACTH levels, but there was also a failure of Cortisol stimulation. His DEXA Scan showed that he was predisposed to develop severe osteoporosis and his malnourished condition was supportive of promoting that condition even more. The patient was diagnosed to be suffering from Autoimmune Polyglandular Syndrome, Type II. This is a rare condition of one of its kind where there is a pre-existence of autoimmune adrenal insufficiency along with either autoimmune thyroid disease or autoimmune diabetes mellitus. Since this condition is rare, it tends to often get overlooked upon diagnosis, leading to misdiagnosis because almost all of the presenting features or the symptoms of the prevalent endocrinological disorders present in this condition mimic either hypothyroidism, or diabetes, or adrenal insufficiency alone, and thus lead to further consequences when the condition does not resolve despite persistent treatment, such as the case in this patient. This paper reviews the background of the patient and the causes that possibly could have made him reach this advanced stage of the disease. The paper also reflects upon the disease, Autoimmune Polyglandular Syndrome Type II, as a whole and elaborates on the symptoms and signs which the patient tens to confuse with other endocrinological diseases. Lastly, this paper shall also review the appropriate management plan for the patient to ease his symptoms and accelerate his recovery process.


2004 ◽  
Vol 10 ◽  
pp. 7-8
Author(s):  
Francisco Puentes ◽  
Carlos Isales ◽  
Thomas Jackson

2021 ◽  
Vol 80 (3) ◽  
pp. 567-578 ◽  
Author(s):  
Rosaria Sciarrillo ◽  
Mariana Di Lorenzo ◽  
Salvatore Valiante ◽  
Luigi Rosati ◽  
Maria De Falco

Abstract Different environmental contaminants disturb the thyroid system at many levels. AlkylPhenols (APs), by-products of microbial degradation of AlkylPhenol Polyethoxylates (APEOs), constitute an important class of Endocrine Disrupting Chemicals (EDCs), the two most often used environmental APs being 4-nonylphenol (4-NP) and 4-tert-octylphenol (4-t-OP). The purpose of the present study was to investigate the effects on the thyroid gland of the bioindicator Podarcis siculus of OP alone and in combination with NP. We used radioimmunoassay to determine their effects on plasma 3,3′,5-triiodo-L-thyronine (T3), 3,3′,5,5′-L-thyroxine (T4), thyroid-stimulating hormone (TSH), and thyrotropin-releasing hormone (TRH) levels in adult male lizards. We also investigated the impacts of AP treatments on hepatic 5′ORD (type II) deiodinase and hepatic content of T3 and T4. After OP and OP + NP administration, TRH levels increased, whereas TSH, T3, and T4 levels decreased. Lizards treated with OP and OP + NP had a higher concentration of T3 in the liver and 5′ORD (type II) activity, whereas T4 concentrations were lower than that observed in the control group. Moreover, histological examination showed that the volume of the thyroid follicles became smaller in treated lizards suggesting that that thyroid follicular epithelial cells were not functionally active following treatment. This data collectively suggest a severe interference with hypothalamus–pituitary–thyroid axis and a systemic imbalance of thyroid hormones. Graphic Abstract


2019 ◽  
Vol 6 ◽  
pp. 2333794X1984507 ◽  
Author(s):  
Ryan Kenneth Smith ◽  
Peter M. Gerrits

Adrenal insufficiency is a rare, potentially life-threatening condition whose diagnosis requires a high index of suspicion. Adrenal insufficiency may be primary, secondary, or tertiary with varied etiologies. Primary insufficiency may be part of a cluster of autoimmune diseases, referred to as autoimmune polyglandular syndrome(s) (APS). We describe a case of a 15-year-old male who presents to a local emergency department complaining of fatigue, fever, abdominal pain, nausea, and vomiting for a few days with a preceding viral illness. The patient was hyponatremic and hyperkalemic with skin hyperpigmentation, raising concern for adrenal insufficiency. Laboratory workup confirmed autoimmune primary adrenal insufficiency, with subsequent laboratory studies revealing autoimmune thyroiditis and celiac disease. Concomitant Addison’s and Hashimoto’s diseases led to a diagnosis of APS type 2. The patient was started on steroid replacement with rapid clinical improvement.


2004 ◽  
Vol 199 (9) ◽  
pp. 1285-1291 ◽  
Author(s):  
Martin A. Kriegel ◽  
Tobias Lohmann ◽  
Christoph Gabler ◽  
Norbert Blank ◽  
Joachim R. Kalden ◽  
...  

In autoimmune polyglandular syndromes (APS), several organ-specific autoimmune diseases are clustered. Although APS type I is caused by loss of central tolerance, the etiology of APS type II (APS-II) is currently unknown. However, in several murine models, depletion of CD4+ CD25+ regulatory T cells (Tregs) causes a syndrome resembling human APS-II with multiple endocrinopathies. Therefore, we hypothesized that loss of active suppression in the periphery could be a hallmark of this syndrome. Tregs from peripheral blood of APS-II, control patients with single autoimmune endocrinopathies, and normal healthy donors showed no differences in quantity (except for patients with isolated autoimmune diseases), in functionally important surface markers, or in apoptosis induced by growth factor withdrawal. Strikingly, APS-II Tregs were defective in their suppressive capacity. The defect was persistent and not due to responder cell resistance. These data provide novel insights into the pathogenesis of APS-II and possibly human autoimmunity in general.


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