Disease relevance of Thyroiditis, Subacute

• Serum angiotensin-converting enzyme. Alterations in hyperthyroidism, hypothyroidism, and subacute thyroiditis [1].
• Release of thyroglobulin by follicular disruption probably resulted in hyperthyroxinemia and suppression of TSH and radioactive iodine uptake, as occurs in subacute thyroiditis [2].
• The serum triiodothyronine/thyroxine ratio (T3/T4) was greater than 20 ng/microgram in Graves' disease but less than 20 in all patients with subacute thyroiditis and 9 of 11 patients with autoimmune thyroiditis [3].
• It is concluded that the mechanism of thyrotoxicosis is analogous to that of subacute thyroiditis: rapid tissue necrosis with resultant release of thyroid hormone [4].
• Except for asymptomatic bacteriuria in one patient (who remained febrile despite appropriate antibiotic therapy) infection was ruled out in all cases, and fever was attributed to "masked" thyrotoxicosis, triiodothyronine (T3) toxicosis, subacute thyroiditis, primary adrenal insufficiency, secondary adrenal insufficiency and pheochromocytoma [5].

High impact information on Thyroiditis, Subacute

• A diagnosis of subacute thyroiditis was made, prednisone therapy was tapered over 3 weeks, and treatment with beta blockers was instituted [6].
• The serum VEGF levels in untreated patients with subacute thyroiditis were significantly higher than those in patients with untreated GD or HT [7].
• The rise in serum IL-6 levels in untreated patients with subacute thyroiditis in this study is compatible with previous reports [8].
• In the patients with subacute thyroiditis, serum T3 levels also significantly decreased after TRH administration [9].
• Five hyperthyroid patients (two men and three women) with typical features of subacute thyroiditis were treated with sodium ipodate (Oragrafin; 0.5 g, orally daily or every other day) for 15-60 days; the treatment was stopped when both serum T4 and T3 levels were normal [10].

Chemical compound and disease context of Thyroiditis, Subacute

• During prednisolone treatment the RBC Zn in patients with subacute thyroiditis remained at the normal level and did not change significantly, although it was slightly decreased at 2 and 4 weeks of treatment [11].
• Serum free thyroxine and triiodothyronine concentrations in subacute thyroiditis [12].
• We previously reported that immunosuppressive acidic protein (IAP), an alpha 1-acid glycoprotein, is increased during the acute phase of subacute thyroiditis (SAT) [13].
• Increased cortisol-binding globulin in a patient with subacute thyroiditis [14].
• Technetium-99m tetrofosmin imaging in patients with subacute thyroiditis [15].

Anatomical context of Thyroiditis, Subacute

• Histological examination of the patients' thyroid glands revealed amyloid deposition and no evidence of subacute thyroiditis [16].
• CA 19-9 and CEA could be demonstrated occasionally in multinucleated giant cells of subacute thyroiditis, which may suggest that these giant cells are of either histiocytic or follicular cell origin [17].
• We present the first reported case of subacute thyroiditis in a patient who had been on chronic lithium therapy as well as long-term immunosuppression, with cyclosporin and prednisolone, following an allogeneic bone marrow transplant [18].
• Serum concentrations of granulocyte colony-stimulating factor (G-CSF) determined by a highly-sensitive chemiluminescent immunoassay during the clinical course of subacute thyroiditis [19].

Gene context of Thyroiditis, Subacute

• None of the five TSHR peptides caused the proliferation of PBL from patients with Hashimoto's thyroiditis, subacute thyroiditis, or RA and from normal volunteers [20].
• Although high concentrations of crude thyroid-soluble fraction and purified thyroglobulin gave strongly positive responses in the radioreceptor assay, concentrations of thyroglobulin over the range found in the sera of patients with subacute thyroiditis could not be shown to give positive responses [21].
• Allele 2 of interleukin-1 receptor antagonist gene increases the risk of thyroid peroxidase antibodies in subacute thyroiditis [22].
• Immunohistochemical investigation with antibodies against CA 19-9 and CEA may help to histomorphologically define subacute granulomatous thyroiditis [17].
• The normal concentrations of SHBG in the hyperthyroid phase of subacute thyroiditis most likely reflects the shorter duration of exposure to increased thyroid hormone in this condition [23].

Analytical, diagnostic and therapeutic context of Thyroiditis, Subacute

• MATERIALS AND METHODS: Thirty-four patients with a variety of thyroid disorders (24 Graves disease; five subacute thyroiditis; five Hashimoto thyroiditis) were examined using T1-, T2-, and diffusion-weighted magnetic resonance (MR) imaging and thyroid scintigraphy with Tc-99m pertechnetate [24].

References