Disease relevance of Goiter

• This perinatal rat model can be used to study the mechanisms responsible for iodide-induced hypothyroidism and goiter in human newborns whose mothers received iodide-containing medications during pregnancy [1].
• In pregnant women, vaginitis should not be treated with povidone-iodine because of the possible development of iodine-induced goiter and hypothyroidism in the fetus and newborn [2].
• Thus, primarily colloid-rich goiters may form in the presence of continuously higher than normal thyrotropin levels without a previous stage of follicular hyperplasia [3].
• BRAF mutation at codon 599 was detected in 21 of 56 PTC (38%) but not in 18 follicular adenomas and 6 goiters [4].
• Inflammatory thyroid lesions associated with goiters, including Hashimoto's thyroiditis (6) and Graves' disease (8), showed moderate to intense expression of p21 as did multinodular goiters (4) [5].

Psychiatry related information on Goiter

• Antipsychotic exposure can produce extrapyramidal symptoms in the neonate and lithium has been associated with neonatal cyanosis, lethargy, flaccidity, and non-toxic goiter [6].
• Despite India's substantial progress in human development since its independence in 1947, 5-7% of its children have vitamin A deficiency disorders in selected geographic areas, 53% have iron deficiency anemia, and 9% have goiter [7].
• Two sisters and their mother had a syndrome of microcephaly, cleft palate, and variable anomalies such as unusual facial appearance, hypotelorism, abnormal retinal pigmentation, maxillary hypoplasia, goiter, camptodactyly, mild mental retardation, and abnormal dermatoglyphics [8].

High impact information on Goiter

• Efficacy was assessed by evaluating goiter size and measuring urinary iodine and serum thyroid hormone concentrations for 12 months [9].
• Among the 21 patients studied serially while receiving levothyroxine, thyrotropin-blocking antibodies disappeared in 15 (group 1), 7 of whom had goiter initially, and persisted in 6 (group 2), none of whom had goiter initially [10].
• Characteristically these patients exhibit hereditary congenital goiter with relatively low Tg levels that do not increase after stimulation with bovine TSH [11].
• Congenital goiter with defective iodide transport [12].
• Thyroglobulin and calcitonin in patients with nontoxic goiter [13].

Chemical compound and disease context of Goiter

• Goiters developed in all rats given amitrole (groups I-III) [14].
• The histological picture of the goiters was similar to that found in thiourea-treated teleosts and thiouracil-treated mammals [15].
• Goiter formation following prostaglandin administration in rats [16].
• Goiter was more common in patients treated with lithium for 1-5 years (44%) or more than 10 years (50%) than in patients who never received lithium (16%) [17].
• Treatment with amiodarone was continued; however, therapy with L-thyroxin was initiated, followed by a complete regression of the goiter [18].

Biological context of Goiter

• Since few hypothyroid patients had autoimmunity or goiter, lithium may affect the thyroid gland directly [17].
• We identified a homozygous missense mutation of A-->C at nucleotide +1060 in NIS complementary DNA in a male patient who was born from consanguineous marriage, had a huge goiter, and lacked the ability to accumulate iodide but was essentially euthyroid [19].
• The data support the possibility that the TG accumulated in the follicular lumen of nontoxic goiters together with relative iodine deficiency contributes to increased MHC expression in thyroid cells in vivo and that increased MHC gene expression contributes to the ability of thyroid antigens to trigger an autoimmune reaction [20].
• We report herein the study of two siblings (DESM and DSM) with hypothyroidism, goiter, and positive perchlorate discharge tests (50% and 70%) in a family (M) with no history of consanguinity [21].
• The point mutation is, thus, removed from a portion of the transcripts by the preferential accumulation in the goiter of a 171-nt-deleted Tg mRNA [22].

Anatomical context of Goiter

• Congenital hypothyroid goiter with deficient thyroglobulin. Identification of an endoplasmic reticulum storage disease with induction of molecular chaperones [23].
• Levothyroxine in non-thyroid-stimulating hormone-suppressive doses may also be indicated for patients with nontoxic multinodular goiter and for certain patients after lobectomy for benign thyroid nodules [24].
• Erythrocyte, plasma, and serum antioxidant activities in untreated toxic multinodular goiter patients [25].
• Intraamniotic fluid injections of 500 micrograms levothyroxine sodium (T4) every 10-14 days increased fetal serum T4 (59.2 nmol/L), decreased fetal serum TSH (14 mU/L), decreased amniotic fluid TSH, and decreased the size of the fetal goiter [26].
• In this work the presence of estrogen receptors alpha and beta in thyroid cells derived from human goiter nodules and in human thyroid carcinoma cell line HTC-TSHr was demonstrated [27].

Gene context of Goiter

• The congenital goiter mutation is linked to the thyroglobulin gene in the mouse [28].
• Here we report that the mRNA expression of PlGF, VEGF and their receptors is markedly enhanced in biopsies of goiters resected from Graves's patients [29].
• Linkage of familial euthyroid goiter to the multinodular goiter-1 locus and exclusion of the candidate genes thyroglobulin, thyroperoxidase, and Na+/I- symporter [30].
• By contrast, only three of five multinodular goiter samples were positive for IL-1 alpha mRNA; of these, two were also positive for IL-6, and 1 was positive for IL-8 mRNA [31].
• Levels of fibroblast growth factor 2 (FGF-2) and its receptor, FGFR1, are elevated in goiter, but whether this is a direct effect of TSH is unknown [32].

Analytical, diagnostic and therapeutic context of Goiter

• Northern blotting analysis of the goiter RNA with a thyroglobulin probe suggested that thyroglobulin mRNA size was slightly reduced [33].
• Indications for treatment were nontoxic goiter (n = 5) or thyroidectomy for differentiated thyroid cancer (n = 6) or nontoxic goiter (n = 3) [34].
• Immunohistochemistry was performed on formalin-fixed paraffin-embedded thyroid tissue specimens from patients with GD, Hashimoto's thyroiditis (HD), and multinodular goiter (MNG) as well as on normal thyroid tissue [35].
• Confocal microscopy revealed a 6-fold increase in intensity of FGFR-1 expression in follicular cells of multinodular goiter (P < 0.05) [36].
• In 29 patients with thyrotoxic Graves' disease treated with conventional long term antithyroid drug therapy, serum thyroglobulin (Tg) was serially determined by RIA and compared with clinical course, goiter shrinkage, and 131I uptake suppression [37].

References