-
Lakartidningen Oct 2004
Topics: Adult; Aged; Autoimmune Diseases; Diagnosis, Differential; Female; Goiter, Nodular; Graves Disease; Humans; Male; Thyroiditis, Autoimmune; Thyroiditis, Subacute; Thyrotoxicosis
PubMed: 15544131
DOI: No ID Found -
Clinical Endocrinology Mar 1995
Topics: Adenoma; Autoimmune Diseases; Clinical Protocols; Female; Goiter; Graves Disease; Humans; Pregnancy; Thyroid Neoplasms; Thyroiditis; Thyroiditis, Autoimmune; Thyrotoxicosis
PubMed: 7758237
DOI: 10.1111/j.1365-2265.1995.tb01880.x -
The American Journal of Medicine Apr 2005Subclinical hyperthyroidism is defined as normal serum free thyroxine (T4) and triiodothyronine (T3) concentrations and persistently suppressed thyroid stimulating... (Review)
Review
Subclinical hyperthyroidism is defined as normal serum free thyroxine (T4) and triiodothyronine (T3) concentrations and persistently suppressed thyroid stimulating hormone (TSH) concentrations. The most common cause of subclinical hyperthyroidism is the use of suppressive doses of L-thyroxine for treatment of hypothyroidism or, less commonly, diffuse nontoxic goiter or thyroid carcinoma (exogenous subclinical hyperthyroidism). Endogenous subclinical hyperthyroidism may be caused by a variety of thyroid disorders that result in overproduction and release of thyroid hormones from the gland with normal/high 24-hour thyroid radioiodine uptake or by inflammation in the thyroid resulting in release of excess thyroid hormones and low 24-hour thyroid radioiodine uptake. Several groups have investigated whether persistent endogenous or exogenous subclinical hyperthyroidism, like overt hyperthyroidism, causes symptoms, adverse effects on the cardiovascular and the skeletal systems, and increased mortality, whether endogenous subclinical hyperthyroidism evolves to overt thyrotoxicosis, and whether or not it should be treated. The present report reviews the most important and recent studies of subclinical hyperthyroidism and attempts to draw conclusions based upon the literature and the authors' experience.
Topics: Bone and Bones; Cardiovascular System; Humans; Thyrotoxicosis; Thyrotropin; Thyroxine; Triiodothyronine
PubMed: 15808130
DOI: 10.1016/j.amjmed.2005.01.004 -
Thyroid : Official Journal of the... Jun 2011
Topics: Adolescent; Antithyroid Agents; Child; Female; Graves Disease; Humans; Hyperthyroidism; Practice Guidelines as Topic; Pregnancy; Pregnancy Complications; Thyrotoxicosis
PubMed: 21663419
DOI: 10.1089/thy.2011.2106.ed2 -
Annals of Clinical Biochemistry Jul 2008
Topics: Diagnosis, Differential; Humans; Thyroglobulin; Thyrotoxicosis
PubMed: 18583641
DOI: 10.1258/acb.2008.080611 -
Endocrine Practice : Official Journal... 2008To report the case of a neonate presenting with nonautoimmune thyrotoxicosis and failure to thrive in whom an activating TSHR mutation was suspected. (Review)
Review
OBJECTIVE
To report the case of a neonate presenting with nonautoimmune thyrotoxicosis and failure to thrive in whom an activating TSHR mutation was suspected.
METHODS
We describe the clinical and laboratory findings in a neonate who presented with nonautoimmune thyrotoxicosis and failure to thrive, including results of DNA analysis of TSHR, which encodes the thyroid-stimulating hormone receptor (TSHR). Relevant literature is also reviewed.
RESULTS
The proband was born spontaneously at 35 weeks' gestation, and his early neonatal period was remarkable for meconium aspiration, pneumothorax, hepatomegaly with associated elevated transaminases, and direct hyperbilirubinemia. On days 9 and 11 of life, thyroid function studies revealed hyperthyroidism, which remained persistent on day 26 of life. On day 44 of life, the infant was admitted to the hospital. The mother reported he had an increased activity level, disturbed sleep, jitteriness, and exaggerated startle response. Weight was at the third percentile. After additional workup, Lugol's iodine solution, propanolol, and propylthiouracil were prescribed, which led to improvement in thyroid function. No TSHR antibodies were detected in the mother's or patient's sera. Analysis of the patient's DNA revealed a heterozygous T-to-C substitution at amino acid 568 in exon 10 (Ile568Thr), which predicts an isoleucine to threonine conversion in the second extracellular loop of TSHR. The mutation was not identified in the parents' DNA.
CONCLUSIONS
A mutation causing constitutive activation of TSHR was confirmed in this patient, a finding that has implications for genetic counseling and consideration of total thyroidectomy or long-term thionamide therapy followed by radioiodide ablation as treatment options. Although rare, TSHR mutations should be considered in an infant presenting with thyrotoxicosis in absence of demonstrable TSHR antibodies in serum.
Topics: DNA Mutational Analysis; Humans; Infant, Newborn; Male; Mutation, Missense; Receptors, Thyrotropin; Thyrotoxicosis
PubMed: 18558604
DOI: 10.4158/EP.14.4.479 -
International Clinical... Jul 2023The relationship between psychiatric symptoms and thyroid function has been well known and studied since antiquity. The common view is that clinical hypothyroidism is...
The relationship between psychiatric symptoms and thyroid function has been well known and studied since antiquity. The common view is that clinical hypothyroidism is associated with depressive symptoms, whereas the psychiatric manifestations of hyperthyroidism are agitation, emotional lability, hyperexcitability, occasionally accompanied by angry outbursts, and euphoria. The case here reported overturns this conventional medical knowledge. A 73-year-old Italian woman experienced a severe major depressive episode with psychotic and melancholic features during laboratory thyrotoxicosis. No classical clinical signs and symptoms of thyrotoxicosis were present. Psychiatric symptoms improved together with the resolution of the hyperthyroid state. Historically, different cases of so-called 'apathetic hyperthyroidism' have been described. Recent neuroimaging and animal studies provided possible neurobiological explanations, showing how the excess thyroid hormones could affect brain structures involved in the regulation of mood, leading to depression. A direct link between hyperthyroidism and depression seems to be likely. This insight may be relevant in facilitating early diagnosis of thyroid disease and the planning of therapeutic strategies.
Topics: Humans; Depression; Depressive Disorder, Major; Hyperthyroidism; Thyrotoxicosis; Female; Aged
PubMed: 36853810
DOI: 10.1097/YIC.0000000000000438 -
The Journal of Clinical Endocrinology... Jan 2021
Topics: Humans; Telemedicine; Thyrotoxicosis
PubMed: 33038240
DOI: 10.1210/clinem/dgaa723 -
Clinical Chemistry Jan 1996The generic term thyrotoxicosis defines the clinical syndrome of hypermetabolism associated with excess amounts of circulating free thyroxine (T4) and (or)... (Review)
Review
The generic term thyrotoxicosis defines the clinical syndrome of hypermetabolism associated with excess amounts of circulating free thyroxine (T4) and (or) triiodothyronine (T3) concentrations, irrespective of the source of the excess hormones. The term hyperthyroidism is reserved for those patients with thyrotoxicosis caused by increased synthesis and secretion of thyroid hormones from the gland due either to thyroid stimulators in the blood or to autonomously functioning thyroid nodules and is almost always associated with an increased radioactive iodine uptake (RAIU) by the thyroid. Another major cause of thyrotoxicosis is increased release of thyroid hormone from the gland, not associated with increased synthesis, caused by inflammatory changes, and always associated with a low thyroid RAIU. The most common miscellaneous cause of thyrotoxicosis is the exogenous ingestion of excess thyroid hormone, associated with a low thyroid RAIU. The serum concentration of thyrotropin (TSH) is low in all causes of thyrotoxicosis, except for TSH-secreting pituitary tumors and selective pituitary resistance to thyroid hormones. Anti-thyroglobulin and anti-thyroid peroxidase antibodies are present in patients with autoimmune thyroid disease, and serum thyroglobulin is increased in all patients with thyrotoxicosis except those with thyrotoxicosis facticia. A decreased serum TSH and normal concentrations of serum free T4 and T3 define the syndrome of subclinical thyrotoxicosis.
Topics: Female; Humans; Pregnancy; Thyroid Function Tests; Thyrotoxicosis; Thyrotropin
PubMed: 8565222
DOI: No ID Found -
Critical Care Clinics Jan 1991The thyrotoxic patient offers a considerable challenge to the critical care physician because the "obvious" diagnosis often will be a cardiac (or other nonthyroidal)... (Review)
Review
The thyrotoxic patient offers a considerable challenge to the critical care physician because the "obvious" diagnosis often will be a cardiac (or other nonthyroidal) problem, but the "correct" diagnosis will be an endocrinologic one. The importance of considering the diagnosis of thyrotoxicosis in any patient with tachyarrhythmias, new-onset congestive heart failure, weight loss, or change in mental status cannot be overstated. Treatment for presumed thyroid disease sometimes will have to be initiated prior to the availability of the results of diagnostic tests. Timely and appropriate treatment of the thyroid problem is vital for a successful outcome in treating patients with thyrotoxicosis.
Topics: Female; Humans; Middle Aged; Pregnancy; Thyrotoxicosis
PubMed: 2007220
DOI: No ID Found