Response of total and 'free' thyroid hormones and diiodotyrosine to bovine TSH in subclinical hypothyroidism

1986 ◽  
Vol 112 (4) ◽  
pp. 509-516
Author(s):  
G. Benker ◽  
H. Rasche ◽  
Th. Olbricht ◽  
H. Meinhold ◽  
J. Teuber ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Subclinical Hypothyroidism ◽  
Thyroid Autoimmunity ◽  
Addison’S Disease ◽  
Primary Hypothyroidism ◽  
Addison's Disease ◽  
Thyroid Autoantibodies ◽  
Schmidt’S Syndrome ◽  
Normal Controls

Abstract. Thirty-three patients with Addison's disease were studied. Twenty-two had idiopathic Addison's disease; within this group, 14 patients had clinical or subclinical hypothyroidism, and 16 had increased titres of thyroid autoantibodies. Five patients had tuberculous, and eight had unclassifiable Addison's disease; only one patient in the latter group had evidence of thyroid autoimmunity. A stimulation test with 15 mU bTSH/kg was performed in three patients with Schmidt's syndrome (coexisting Addison's disease and manifest primary hypothyroidism), 15 patients with either subclinical hypothyroidism or increased titres of thyroid autoantibodies, 10 patients without thyroid involvement, and 10 normal controls. There was no detectable increase of 'free' and total thyroid hormones in Schmidt's syndrome. The mean increases after 3–4 h of T4, fT4, T3 and fT3 were 22, 35, 63 and 66%, respectively, in patients without thyroid involvement, and 13, 24, 46 and 45% in patients with subclinical hypothyroidism. 'Free' but not total thyroid hormones rose significantly (P <0.01) higher in patients without signs of thyroid involvement than in patients with subclinical hypothyroidism and/or thyroid autoantibodies. Thyroid hormone response to bTSH in Addison's disease with apparently healthy thyroid glands was not different from normal controls. Serum diiodotyrosine rose in all groups except in hypothyroidism; hypothyroid patients had, however, basal levels well within the normal range. Thus, thyroid hormone synthesis appears to be blocked at a point distal to diiodotyrosine formation in this particular situation. These results support the assumption that TSH elevation in idiopathic Addison's disease is due to coexisting thyroid autoimmunity and that it reflects incipient thyroid failure. This can be demonstrated by a diminished response of 'free' T4 and 'free' T3 to exogenous stimulation with bTSH.

High Prevalence of Thyroid Autoimmunity in Idiopathic Addison's Disease

Autoimmunity ◽  
1994 ◽  
Vol 18 (3) ◽  
pp. 213-216 ◽  
Author(s):  
Anna Kasperlik-Zaluska ◽  
Barbara Czarnocka ◽  
Wlodzimierz Czech
Keyword(s):  
Thyroid Autoimmunity ◽  
Addison’S Disease ◽  
Addison's Disease ◽  
High Prevalence

Osmoregulation of arginine-8-vasopressin secretion in primary hypothyroidism and in Addison's disease

1987 ◽  
Vol 114 (3) ◽  
pp. 389-395 ◽  
Author(s):  
F. Laczi ◽  
T. Janáky ◽  
T. Iványi ◽  
J. Julesz ◽  
F. A. László
Keyword(s):  
Healthy Volunteers ◽  
Plasma Osmolality ◽  
Addison’S Disease ◽  
Primary Hypothyroidism ◽  
Addison's Disease ◽  
Water Metabolism ◽  
Positive Correlation ◽  
Vasopressin Secretion ◽  
Impaired Water ◽  
Hypothyroid Patients

Abstract. The osmoregulation of arginine-8-vasopressin (AVP) was investigated in 14 patients with primary hypothyroidism and in 6 with Addison's disease. Plasma AVP was measured by radioimmunoassay. Patients with primary hypothyroidism were classified into subgroups with elevated (6.81 ± 1.12 pmol/l) or normal (3.92 ± 0.96 pmol/l) basal levels of plasma AVP. Following the infusion of 2.5% saline, a positive correlation was established between plasma AVP and plasma osmolality. A decreased osmotic threshold was found in hypothyroid patients with augmented basal AVP levels (pAVP = 0.37 (pOs-265), r = 0.71, P < 0.01) as compared with that in hypothyroid patients with a normal AVP level (pAVP = 0.42 (pOs-280), r = 0.93, P < 0.001). A relationship was demonstrated between the alteration in the AVP osmoregulation and the severity of the thyroid insufficiency. Patients with Addison's disease exhibited an increased basal level of plasma AVP (9.59 ± 1.25 pmol/l) and a decreased osmotic threshold (pAVP = 0.42 (pOs-261), r = 0.63, P < 0.01) contrasted to that of healthy volunteers (pAVP = 0.41 (pOs-280), r = 0.83, P < 0.001). The osmoregulation disturbance of the AVP secretion may play a major role in the impaired water metabolism in primary hypothyroidism and in Addison's disease.

Mineralocorticoid Before Glucocorticoid Deficiency in a Dog with Primary Hypoadrenocorticism and Hypothyroidism

2013 ◽  
Vol 49 (1) ◽  
pp. 54-57 ◽  
Author(s):  
Kathryn M. McGonigle ◽  
John F. Randolph ◽  
Sharon A. Center ◽  
Richard E. Goldstein
Keyword(s):  
Clinical Signs ◽  
Addison’S Disease ◽  
Serum Cortisol ◽  
Primary Hypothyroidism ◽  
Addison's Disease ◽  
Acth Stimulation Test ◽  
Acth Stimulation ◽  
Clinical Illness ◽  
Glucocorticoid Deficiency ◽  
Electrolyte Abnormalities

A dog with an unexpected presentation of primary hypoadrenocorticism was evaluated for clinical signs and electrolyte abnormalities characteristic of Addison’s disease. Although the initial adrenocorticotropic hormone (ACTH) stimulation test documented serum cortisol concentrations within the reference range, subsequent assessments confirmed hypoaldosteronism. Mineralocorticoid replacement promptly normalized electrolytes and transiently improved clinical illness. Six weeks after initial ACTH stimulation testing, the dog became glucocorticoid deficient. Concurrent primary hypothyroidism was also documented. Hypoaldosteronism preceding hypocortisolemia is a unique presentation of canine Addison’s disease.

Addison’s disease with primary hypothyroidism in a case of visceral leishmaniasis and HIV coinfection

2021 ◽  
Vol 14 (3) ◽  
pp. e238488
Author(s):  
Monu Rani ◽  
Rakesh Garg ◽  
Venkatesh Darshan Agraharabachalli Nanjunde ◽  
Rajesh Rajput
Keyword(s):  
Visceral Leishmaniasis ◽  
Addison’S Disease ◽  
Primary Hypothyroidism ◽  
Addison's Disease ◽  
Intermittent Fever ◽  
Hiv Coinfection ◽  
Left Hypochondrium ◽  
Bone Marrow Histopathology ◽  
History Of ◽  
Synacthen Test

A 41-year-old man presented with vomiting and loose stools. He had a history of long-term intermittent fever, generalised skin hyperpigmentation, dragging sensation in the left hypochondrium and unintentional weight loss. He was receiving combination antiretroviral therapy since 2010 for HIV infection. He also received antitubercular therapy for tuberculous spondylitis. During the hospital stay, he was found to have postural hypotension, hypoglycaemia, hyponatraemia, hyperkalaemia, pancytopenia, hypothyroidism, hyperglobulinaemia and hypoalbuminaemia with reversal of serum albumin/globulin ratio. The morning plasma cortisol was lower than normal and could not be appropriately stimulated after the Synacthen test. The bone marrow histopathology was suggestive of visceral leishmaniasis. He was diagnosed as a case of visceral leishmaniasis and HIV coinfection with primary adrenal insufficiency (Addison’s disease) and primary hypothyroidism, as a rare and unusual presentation.

Causes and laboratory investigation of hypothyroidism

2011 ◽  
pp. 530-537 ◽  
Author(s):  
Ferruccio Santini ◽  
Aldo Pinchera
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Thyroid Hormone Receptor ◽  
Hormone Secretion ◽  
Thyroid Tissue ◽  
Clinical Manifestations ◽  
Primary Hypothyroidism ◽  
Central Hypothyroidism ◽  
Resistance To Thyroid Hormones

Hypothyroidism is the clinical state that develops as a result of the lack of action of thyroid hormones on target tissues (1). Hypothyroidism is usually due to impaired hormone secretion by the thyroid, resulting in reduced concentrations of serum thyroxine (T4) and triiodothyronine (T3). The term primary hypothyroidism is applied to define the thyroid failure deriving from inherited or acquired causes that act directly on the thyroid gland by reducing the amount of functioning thyroid tissue or by inhibiting thyroid hormone production. The term central hypothyroidism is used when pituitary or hypothalamic abnormalities result in an insufficient stimulation of an otherwise normal thyroid gland. Both primary and central hypothyroidism may be transient, depending on the nature and the extent of the causal agent. Hypothyroidism following a minor loss of thyroid tissue can be recovered by compensatory hyperplasia of the residual gland. Similarly, hypothyroidism subsides when an exogenous inhibitor of thyroid function is removed. Peripheral hypothyroidism may also arise as a consequence of tissue resistance to thyroid hormones due to a mutation in the thyroid hormone receptor. Resistance to thyroid hormones is a heterogeneous clinical entity with most patients appearing to be clinically euthyroid while some of them have symptoms of thyrotoxicosis and others display selected signs of hypothyroidism. The common feature is represented by pituitary resistance to thyroid hormones, leading to increased secretion of thyrotropin that in turn stimulates thyroid growth and function. The variability in clinical manifestations depends on the severity of the hormonal resistance, the relative degree of tissue hyposensitivity, and the coexistence of associated genetic defects (see Chapter 3.4.8).

scholarly journals Thyroid Autoantibodies Are Rare in Nonhuman Great Apes and Hypothyroidism Cannot Be Attributed to Thyroid Autoimmunity

Endocrinology ◽  
2013 ◽  
Vol 154 (12) ◽  
pp. 4896-4907 ◽  
Author(s):  
Holly Aliesky ◽  
Cynthia L. Courtney ◽  
Basil Rapoport ◽  
Sandra M. McLachlan
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Autoimmunity ◽  
Great Apes ◽  
Normal Serum ◽  
Thyroid Peroxidase ◽  
Thyroid Autoantibodies ◽  
Free T4 ◽  
Hormone Levels ◽  
Free T3 ◽  
Thyroid Hormone Levels

The great apes include, in addition to Homo, the genera Pongo (orangutans), Gorilla (gorillas), and Pan, the latter comprising two species, P. troglodytes (chimpanzees) and P. paniscus (bonobos). Adult-onset hypothyroidism was previously reported in 4 individual nonhuman great apes. However, there is scarce information on normal serum thyroid hormone levels and virtually no data for thyroid autoantibodies in these animals. Therefore, we examined thyroid hormone levels and TSH in all nonhuman great ape genera including adults, adolescents, and infants. Because hypothyroidism in humans is commonly the end result of thyroid autoimmunity, we also tested healthy and hypothyroid nonhuman great apes for antibodies to thyroglobulin (Tg), thyroid peroxidase (TPO), and the TSH receptor (TSHR). We established a thyroid hormone and TSH database in orangutans, gorillas, chimpanzees, and bonobos (447 individuals). The most striking differences are the greatly reduced free-T4 and free-T3 levels in orangutans and gorillas vs chimpanzees and bonobos, and conversely, elevated TSH levels in gorillas vs Pan species. Antibodies to Tg and TPO were detected in only 2.6% of adult animals vs approximately 10% in humans. No animals with Tg, TPO, or TSHR antibodies exhibited thyroid dysfunction. Conversely, hypothyroid nonhuman great apes lacked thyroid autoantibodies. Moreover, thyroid histology in necropsy tissues was similar in euthyroid and hypothyroid individuals, and lymphocytic infiltration was absent in 2 hypothyroid animals. In conclusion, free T4 and free T3 are lower in orangutans and gorillas vs chimpanzees and bonobos, the closest living human relatives. Moreover, thyroid autoantibodies are rare and hypothyroidism is unrelated to thyroid autoimmunity in nonhuman great apes.

Technetium-99m pentavalent dimercaptosuccinic acid imaging in patients with pituitary adenomas

1995 ◽  
Vol 133 (1) ◽  
pp. 38-47 ◽  
Author(s):  
Secondo Lastoria ◽  
Annamaria Colao ◽  
Emilia Vergara ◽  
Diego Ferone ◽  
Paola Varrella ◽  
...  
Keyword(s):  
Pituitary Adenomas ◽  
Addison’S Disease ◽  
Primary Hypothyroidism ◽  
Dimercaptosuccinic Acid ◽  
Addison's Disease ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Technetium 99M ◽  
Before And After ◽  
Acth Secreting

Lastoria S, Colao A, Vergara E, Ferone D, Varrella P, Merola B, Lombardi G, Salvatore M. Technetium-99m pentavalent dimercaptosuccinic acid imaging in patients with pituitary adenomas. Eur J Endocrinol 1995;133:38–47. ISSN 0804–4643 We studied the tumor-seeking agent technetium-99m-labeled pentavalent dimercaptosuccinic acid ([99mTc](V)DMSA) to visualize 21 growth hormone (GH)-, nine prolactin (PRL)-, two mixed GH/PRL-, six adrenocorticotropin (ACTH)-secreting and 15 clinically non-functioning pituitary adenomas, three craniopharyngiomas and one dysgerminoma of the sella. All non-adenomas and 31 out of 53 adenomas were studied before treatment: 22 after surgery and/or radiotherapy. Eight cases of acromegaly were studied before and after chronic treatment with octreotide, whereas three cases of acromegaly, one of prolactinoma and two of non-functioning adenoma were imaged before and after adenomectomy. As a control group, 27 patients without any clinical evidence of pituitary adenoma were studied: 10 of them were operated on previously and treated with iodine-131 for metastatic thyroid carcinoma, 10 had brain tumors and the remaining seven patients had functional pituitary hypersecretion (four Klinefelter's syndrome, two primary hypothyroidism and one Addison's disease). The scintigraphy was repeated after testosterone in Klinefelter's syndrome, l-thyroxine in primary hypothyroidism and cortisone administration in Addison's disease. Seventeen GH-secreting (81%), seven PRL-secreting (78%), three ACTH-secreting (50%), 15 non-functioning (100%) and one (50%) mixed adenoma significantly concentrated [99mTc](V)DMSA, showing elevated tumor-to-background (T/B) ratios. The T/B ratios were similar in untreated and surgically treated adenomas (11.2 ± 5.6 vs 11.8 ± 6.2). Radiotherapy significantly lowered the [99mTc](V)DMSA uptake to 5.1 ± 2.8 (p < 0.1 vs untreated patients). Non-adenomatous lesions of the sella turcica did not concentrate [99mTc](V)DMSA in the pituitary as well as brain tumors and 8 out of 10 metastatic thyroid cancers. The treatment with octreotide normalized GH and insulin-like growth factor I levels and reduced [99mTc](V)DMSA from 15.7 ± 4.8 to 13.5 ± 3.9 (p < 0.05). Conversely, adequate substitutive therapy completely inhibited the uptake of the radiotracer in Klinefelter's syndrome, in primary hypothyroidism and in Addison's disease. The [99mTc](V)DMSA scintigraphy showed an overall sensitivity of 81% (43/53) in detecting pituitary adenomas, which was increased to 95% for lesions greater than 10 mm in size. High-quality images with minimal total body radiation were obtained, enabling a good in vivo characterization of viable adenomatous tissue as well as an accurate monitoring of the effects of different therapeutic regimens. Secondo Lastoria, Department of Nuclear Medicine, National Cancer Institute, Fondazione G Pascale, via M Semmola, 80131 Napoli, Italy

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