Disease relevance of Thyrotoxicosis

• Amiodarone hydrochloride, an iodine-rich drug used in the treatment of tachyarrhythmias, is responsible for the development of thyrotoxicosis in approximately 10% of patients who reside in areas of moderate iodine deficiency [1].
• Treatment of amiodarone-induced thyrotoxicosis is difficult since the drug has a prolonged half-life, cardiac decompensation due to underlying heart disease occurs often, and discontinuation of amiodarone therapy may not be possible [1].
• If hyperthyroidism masked by beta-blockade is not recognized before withdrawal of propranolol therapy in patients with ischemic heart disease, the sudden appearance of thyrotoxicosis may lead to symptoms of increased myocardial ischemia [2].
• We conclude that T4 and T3 can directly stimulate bone resorption in vitro at concentrations approaching those which occur in thyrotoxicosis [3].
• Mild clinical hypothyroidism associated with low levels of serum total thyroxine (T4) and tri-iodothyronine (T3) and raised levels of serum thyroid-stimulating hormone (T.S.H.) has been observed in 14 of 40 patients (35%) in the early months after a subtotal thyroidectomy for thyrotoxicosis under cover of propranolol [4].

Psychiatry related information on Thyrotoxicosis

• CONCLUSIONS: These findings demonstrate an unusual pattern of thyroid alterations, featuring substantial elevations in total T3, free T3, and T4-binding globulin levels, in combat-related PTSD that differs from established endocrinopathies, such as classic hyperthyroidism, T3 thyrotoxicosis, or chronic T4-binding globulin elevation [5].
• Both the thyrotoxicosis and a catabolic state due to the hyperemesis were thought to have induced a vitamin B1 deficiency, causing the Wernicke encephalopathy [6].
• In particular it illustrates the derangements of thyroid function seen in pregnant women with eating disorders and reminds us that when a cause for thyrotoxicosis remains obscure, thyroxine abuse should be considered and explored [7].

High impact information on Thyrotoxicosis

• Whatever target organ is examined, there is tissue thyrotoxicosis if the serum thyrotropin concentration is low, even if the serum triiodothyronine and thyroxine concentrations are normal [8].
• Low serum thyroglobulin as a clue to the diagnosis of thyrotoxicosis factitia [9].
• Variable plasma propranolol levels in thyrotoxicosis [10].
• Perchlorate has a fast turnover in the body and requires frequent daily doses for therapy of thyrotoxicosis [11].
• Thyroidectomy for amiodarone-induced thyrotoxicosis [1].

Chemical compound and disease context of Thyrotoxicosis

• Many patients with thyrotoxicosis have clinical features that reflect the effects of excess thyroid hormone on the cardiovascular system [12].
• We report a patient with severe thyrotoxicosis who received amiodarone for 34 months [1].
• Thyrotoxicosis after a single ingestion of levothyroxine [13].
• Letter: Lithium in thyrotoxicosis [14].
• The THPP group had significantly higher fasting insulin concentrations (27.6 [3.6] vs 13.4 [1.8] mU/l; p less than 0.005) and a higher overall insulin response to oral glucose (p less than 0.001 by ANOVA) than the thyrotoxicosis group [15].

Biological context of Thyrotoxicosis

• These results suggest that the pharmacokinetics of propranolol are significantly altered in thyrotoxicosis [16].
• Four months later, with a normal hematocrit reading, thyrotoxicosis recurred, with noticeable elevation of T4 and T3 [17].
• Two young adults presented with thyrotoxicosis after increased iodide ingestion in the course of backpacking trips to Central and South America, during which each of them used an iodinated preparation for water purification [18].
• The down-regulation of sterol regulatory element binding protein-1c, a transcription factor controlling lipogenic gene expression, may constitute a link between thyrotoxicosis and insulin resistance [19].
• Resistance to thyroid hormone does not abrogate the transient thyrotoxicosis associated with gestation: report of a case [20].

Anatomical context of Thyrotoxicosis

• Thyroid function after surgical treatment of thyrotoxicosis. A report of 100 cases treated with propranolol before operation [21].
• Because D2 converts T4 to T3, the active form of thyroid hormone, the D2 TG mouse exhibits mild, chronic thyrotoxicosis that is limited to the myocardium [22].
• Forty-one patients showed thyrotoxicosis relapse; of these, 22 (54%) showed peripheral eosinophil increase, and 14 (34%) had attacks of allergic rhinitis [23].
• Leukocyte DNA from two littermates with familial feline thyrotoxicosis did not harbor mutations of this region of the TSHR gene [24].
• Thyrotoxicosis is associated with increased skeletal muscle glucose metabolism and lipid oxidation in the fasted state [25].

Gene context of Thyrotoxicosis

• Clinical thyrotoxicosis is directly caused by autoantibodies that activate the thyrotropin receptor (TSHR) [26].
• GH peak values (mean +/- SE; micrograms per L) were significantly lower in hyperthyroid patients compared to those in control subjects after GHRH alone (9.0 +/- 1.3 vs. 27.0 +/- 5.2) and GHRP-6 plus GHRH (22.5 +/- 3.5 vs. 83.7 +/- 15.2); a lack of the normal synergistic effect of the association of both peptides was observed in thyrotoxicosis [27].
• Moreover, thyrotoxicosis was accompanied by a 3-fold increase in beta 2-adrenoceptor number (P < 0.005), but unchanged beta 1-adrenoceptor levels [28].
• On the other hand, we were able to identify the R83H mutation in the KCNE3 gene in one sporadic case of THypoKPP, a man who had been asymptomatic until developing thyrotoxicosis caused by Graves' disease; we confirmed the disease-causing mutation in 2 of 3 descendants [29].
• CONCLUSION: Adult-onset type 1 diabetic patients some years post-diagnosis from central Africa show GAD, IA2 or TPO Abs; and surprisingly, patients with thyrotoxicosis had a similar frequency of diabetes-associated autoantibodies [30].

Analytical, diagnostic and therapeutic context of Thyrotoxicosis

• To test the hypothesis that there is an abnormal serum insulin response to a carbohydrate load in thyrotoxic hypokalaemic periodic paralysis (THPP), 18 men with THPP and 15 with uncomplicated thyrotoxicosis were studied during an oral glucose tolerance test [15].
• After treatment of thyrotoxicosis there was a fall (P less than 0.05) in the oral clearance of both total (4.2 +/- 0.6 to 2.7 +/- 0.4 L/min, mean +/- SEM) and free (30.5 +/- 4.7 to 25.5 +/- 4.1 L/min) propranolol although the half-life of propranolol did not change significantly [16].
• Signs and symptoms of apathetic thyrotoxicosis developed on two occasions, once within a week after exposure of the wound to povidone-iodine soaks and again following repeated Hubbard tank debridement with added povidone-iodine [31].
• In vivo SPECT quantitation of bone metabolism in hyperparathyroidism and thyrotoxicosis [32].
• There may be associated liver function test abnormalities and abnormal thyroid function tests, with biochemical thyrotoxicosis with raised free thyroxine levels and/or suppressed thyroid-stimulating hormone levels [33].

References