Evaluation of thyroxine resistance in patients with hypothyroidism: a laboratory study

Thyroid Disorders.

Thyroid storm as a result of functioning metastatic thyroid carcinoma is exceedingly rare. 1 We describe a patient with functioning distant metastases from adenocarcinoma of the thyroid in whom thyroid storm developed in the course of care for extensive burns.

It is presumed that free T4 and thyroid-stimulating hormone (TSH) levels are related to obesity, but the findings are inconsistent. In this study we evaluated T4 and TSH concentrations between normal children and those with obesity and possible correlations between body mass index (BMI) and these markers. In this prospective study, 190 children who were overweight and obese and 133 children without obesity of the same age and sex were evaluated. Thyroid function tests (TSH, total T4, free T4 and free T3) were measured in all subjects in both groups. Thyroid antibodies (thyroid peroxidase and thyroglobulin) were determined among those with elevated TSH levels. Levels of TSH and total T4 were significantly higher in children with obesity compared with the control group. Subclinical hypothyroidism was significantly higher in children with obesity (14.7%) compared with normal subjects (6.8%, p = 0.02). Among children with obesity and increased TSH levels, 10.7% had positive thyroid peroxidase and thyroglobulin antibodies. There was significantly positive correlation between BMI z score and TSH level (r = 0.198, p < 0.001) and T4 level (r = 0.18, p = 0.001). TSH and total T4 levels are increased in children who are overweight or obese and are a common finding in these children, but the incidence of thyroid antibodies is low in these patients and so could not be accounted for by thyroid autoimmunity. Due to these findings it is possible that increased TSH and total T4 levels are a consequence of obesity and could be reduced by decreasing BMI.

Euthyroid Hyperthyroxinemia

Antidepressant-Resistant Depression in Patients With Comorbid Subclinical Hypothyroidism or High-Normal TSH Levels.

Thyroid function is impaired by diabetes, resulting into thyroid disorders, accompanied by the alteration of thyroid-stimulating hormone (TSH) and thyroxine (T4) levels. The aim of this study was to investigate the role of vitamin D supplementation on TSH and total T4 levels in serum of Libyan patients suffering from type 2 diabetes mellitus (T2DM) with thyroid disorders. A total of 180 subjects were recruited and distributed into two groups: 80 participants in control group (43 females and 37 males), with an age range of 26-72 years, and 100 participants in T2DM patient group (54 females and 46 males), with an age range of 26-63 years. Each T2DM patient received a monthly intramuscular injection of 200000 ng/ml vitamin D for three months. Glucose, vitamin D, total T4 and TSH levels were determined in serum samples of healthy subjects and of T2DM patients (pre- and post-administration of vitamin D). After the T2DM group received vitamin D supplementation, the mean of vitamin D level increased in the T2DM, while the mean of glucose level decreased. Most importantly, the mean of total T4 level for patients increased significantly (p ˂ 0.05) from 1.34 to 8.23 mg/dL, both of which were lower than the control group mean 10.99 mg/dL. In contrast, the mean of TSH level for patients decreased significantly (p ˂ 0.05) from 11.77 to 2.71 mU/L, and both values were greater than the control group mean 2.01 mU/L. ANOVA results showed that age, gender, and body mass index had no significant individual interactions (p &gt; 0.05) with vitamin D supplementation on total T4 and TSH levels. Vitamin D supplementation had a beneficial role on total T4 and TSH levels in serum of Libyan T2DM patients with thyroid disorders. Keywords: T2DM, thyroid disorder, total T4, TSH, vitamin D supplementation, ANOVA, t test.

Thyroid hormonal disturbances related to treatment of hepatitis C with interferon-alpha and ribavirin

Endocrinology| September 01 2008 “False-Positive” Newborn Thyroid Screen May Predict Future Subclinical Hypothyroidism AAP Grand Rounds (2008) 20 (3): 31–32. https://doi.org/10.1542/gr.20-3-31-a Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation “False-Positive” Newborn Thyroid Screen May Predict Future Subclinical Hypothyroidism. AAP Grand Rounds September 2008; 20 (3): 31–32. https://doi.org/10.1542/gr.20-3-31-a Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search nav search search input Search input auto suggest search filter All PublicationsAll JournalsAAP Grand RoundsPediatricsHospital PediatricsPediatrics In ReviewNeoReviewsAAP NewsAll AAP Sites Search Advanced Search Topics: false-positive results, subclinical hypothyroidism, thyroid screening, thyrotropin, hyperthyrotropinemia, thyroid function tests Source: Leonardi D, Polizzotti N, Carta A, et al. Longitudinal study of thyroid function in children with mild hyperthyrotropinemia at neonatal screening for congenital hypothyroidism. J Clin Endocrin Metab. Rapid Electronic Publication first published on April 29, 2008; doi:10.1210/jc.2007-2612 To better understand the natural history of children with unexplained transient increase in thyroid stimulating hormone (TSH) in the newborn period, researchers from the University of Catania in Catania, Italy, followed children who had a “false positive” newborn thyroid screen into late childhood. This study was an extension of previously published work describing children with transient increase in TSH who, when studied at 16–44 months of age, demonstrated a high incidence (50%) of subclinical hypothyroidism.1 Infants with Down syndrome, prematurity, small for gestational age, and newborns of thyroid autoimmunity-positive mothers were excluded. Thyroid function and morphology in children with transient unexplained hyperthyrotropinemia in infancy were compared with control children who had normal newborn TSH levels at three time periods: age 16–44 months, age 4.1–6.6 years, and age 7.2–9.5 years. Measures of function included TSH, free T4 (FT4), free T3 (FT3), anti-thyroglobulin (anti-Tg), and anti-thyroperi-oxidase (anti-TPO) antibodies. Morphology was evaluated by ultrasound and thyroid volume was calculated and compared with reference values. A total of 44 children were followed until an average age of eight years. At age 16–44 months all children had a normal serum FT4, but mean serum TSH and FT3 levels were significantly higher than those of controls. Based on TSH levels at this time, children were divided in two groups: group 1 (16 patients) had normal serum TSH levels of <4.0mU/L and group 2 (28 patients) had slightly elevated serum TSH (4.0–10.1 mU/L). Levothyroxine treatment was given to reduce TSH in 20 of 28 children in group 2. At age 4.1–6.6 years, serum FT4 was within normal range in all children, with average values similar in groups 1 and 2. Serum TSH was within normal range in all 16 group 1 children and in nine of 28 group 2 children (group 2a); however, when the 25 children with normal serum TSH were compared with the control group, their average TSH levels were significantly higher. In the remaining 19 of 28 group 2 children, serum TSH was persistently elevated (group 2b). FT3 values were significantly higher compared with controls. Anti-thyroid antibodies (anti-TPO and/or anti-Tg) were slightly positive in 11 of 44 children in early childhood; however, they were weakly positive in only one child in group 2 at 30 months of age. At age 7.2–9.5 years, TSH serum values remained in the normal range in all group 1 children and in the nine group 2a children. Of the 19 group 2b children, TSH remained elevated in 14 but normalized in five children. Of the eight children treated with levothyroxine, seven had persistent elevation of TSH. Out of these seven children, six were determined to have genetic and/or morphological abnormalities of the thyroid as the possible cause of their... You do not currently have access to this content.

Unusual Case of Hypothyroidism in an Infant With Hepatic Hemangioma

Introduction Hypothyroidism requires lifelong thyroid hormone replacement with levothyroxine. For most hypothyroid patients fasting during Ramadan, compliance with the administration procedure is a challenge. This study aimed to determine the impact of different administration times of levothyroxine on thyroid-stimulating hormone (TSH) and free T4 (FT4) levels before and after the holy month of Ramadan. Materials and Methodology. Hypothyroid patients taking levothyroxine were randomized to 3 groups during Ramadan: group 1, 30 minutes before the iftar meal; group 2, 3-4 hours after the iftar meal, with no food taken for at least 1 hour after the meal; group 3, they were not given specific instructions for taking levothyroxine during Ramadan. Thyroid function tests were performed within 2 weeks before Ramadan and within 2 weeks after Ramadan. Pre- and post-Ramadan TSH and free T4 levels were compared. Mixed-effects analyzes were performed to identify factors associated with changes in TSH and FT4 levels. Results Compliance was lower in patients taking levothyroxine 3-4 hours after iftar. In addition, the majority of patients who had not received a specific recommendation took levothyroxine 30 minutes before iftar. There was a statistically significant increase in TSH (P=0.006) and FT4 (P=0.044) levels after Ramadan. In multivariate analysis, the cause of hypothyroidism (Hashimoto's; postthyroidectomy; compared to postradioactive iodine) and levothyroxine dose significantly affected FT4 levels. In contrast, no variable was significantly associated with TSH level. The timing of levothyroxine intake during Ramadan did not significantly affect TSH or FT4 levels. Conclusion TSH and FT4 significantly increased after Ramadan. However, the timing of levothyroxine intake per se had no influence on TSH or free T4 levels. Therefore, hypothyroid patients might take levothyroxine either 30 minutes or 3-4 hours after iftar with no meal for 1 hour, depending on preference.

Exposure to endocrine disruptors has a sufficient impact in rise of thyroid disorders. Iodine accumulation by the thyroid is provided by sodium iodide symporter, a glycoprotein, located in the basolateral membrane of thyroid cells. Therefore, sodium iodide symporter might be a putative target for endocrine disruptors. Objective of the research – investigation of sodium iodide symporter production after long-term exposure to endocrine disruptor dichlorodiphenyltrichloroethane (DDT) in different periods on postnatal development. Newly borne and 7-week old male Wistar rats were exposed to low doses of DDT during 6 and 10 weeks. Expression of sodium iodide symporter in thyroid cells was evaluated by immunohistochemistry. Quantification of sodium iodide symporter, thyroid hormones (T3 and T4) and thyroid stimulating hormone (TSH) in serum was performed by enzyme-linked immunosorbent assay. The investigation also included morphological examination of thyroid slides and morphometry. Adult rats after 6 weeks of exposure showed diminished level of total T4 and increase in T3 production, associated with significantly lowered TSH and sodium iodide symporter serum concentration. Rats, exposed to endocrine disruptor since birth, demonstrated slight decrease in T4 and sodium iodide symporter. Reduced level of free T3 and elevated serum TSH were found in adult rats after 10 weeks of exposure. Exceeded level of serum sodium iodide symporter was revealed. It was provided by increased number of thyroid cells, producing this protein, due to formation of numerous microfollicles in the thyroid gland. Young rats after 10 weeks of exposure demonstrated diminished total and free T3 levels and elevated TSH. No up-regulation of sodium iodide symporter expression was found. Morphological examination revealed enlarged follicles and no microfollicular rearrangement of thyroid parenchyma. Considered that low dose exposure to endocrine disruptor DDT irreversibly depresses expression of membrane glycoprotein sodium iodide symporter, which provides iodine uptake by the thyroid gland. After-birth exposure impairs compensatory activation of proliferation and increase in number of sodium iodide symporter-producing cells.

70-Year-Old Woman With Rash and Muscle Weakness

Annals for Educators - 2 June 2020

This study compared the use of radioimmunoassay (RIA) and chemiluminescent immunoassay (CLIA) to measure serum thyroid hormone levels in green-winged macaws (Ara chloropterus). The sample group comprised 20 male and 13 female (n = 33) healthy, captive green-winged macaws of reproductive age but outside of breeding season. Mean free triiodothyronine (T3), total T3, and free thyroxine (T4) measured by CLIA and RIA corresponded to 5.11 and 5.08 pmol/L (3.33 and 3.31 pg/mL), 1.59 and 1.56 nmol/L (103.5 and 101.5 ng/dL), and 8.25 and 8.82 pmol/L (0.64 and 0.69 ng/dL), respectively. Mean total T4 by RIA corresponded to 6.29 nmol/L (0.49 µg/dL). Mean free T4 and thyroid-stimulating hormone (TSH) levels differed according to immunoassay method, with higher values measured by RIA compared with CLIA. Sex influence was statistically significant in immunoassay results only on free T3 levels. Free T3 levels measured by RIA were higher than levels measured by CLIA in male birds, but this difference was not found with the female bird samples. Conversely, free T3 levels measured by CLIA were higher in the female macaws compared with male birds. Comparative analysis of thyroid hormone measurements in this study revealed that RIA and CLIA are equivalent methods to measure free T4 and total T3 levels but not TSH levels. These findings support the use of CLIA for free T4 and total T3 level determinations in green-winged macaws. However, the CLIA kit used in this study provided invalid total T4 level results for the macaws sampled. Radioimmunoassay and CLIA were equally ineffective for determining TSH levels in this species.

The presence of antibodies to thyroglobulin (Tg) is associated with fetal loss even in the absence of thyroid dysfunction. The aim of this study was to examine whether active immunization with Tg could elicit anti-Tg autoantibodies and reproductive failure without interfering with thyroid function. BALB/c mice that were immunized with human Tg in complete Freund's adjuvant (CFA) or injected with only CFA were studied for the development of antibodies to Tg, T4, dsDNA, ssDNA and cardiolipin. Total T4, free T4 and thyroid-stimulating hormone (TSH) levels were also assessed before and during pregnancy. Percentages of resorbed fetuses (the equivalent to human missed abortion) were compared and autoantibody presence on the placentae and fetuses was examined. Following immunization, high levels of anti-Tg were observed in mice immunized with Tg, compared with mice injected with CFA [0.83 +/- 0.23 versus 0.012 +/- 0.016 respectively; mean +/- SD optical density (OD) at 405 nm; P < 0.001]. The specificity of binding to Tg was confirmed by competition assay. Although total T4 levels were increased in comparison with control mice, this was associated with the presence of antibodies to T4. Indeed, free T4 levels and TSH were similar to control mice. Mice were killed after 14 days of pregnancy. The thyroid function and the histology of the thyroid glands were normal. Increased fetal wastage was found among the Tg-immunized mice compared with the CFA-injected mice (P = 0.04), with lower fetal and placental weights (fetal weights: 194 +/- 4 mg versus 240 +/- 6 mg; placental weights: 105 +/- 2 mg versus 130 +/- 3; P < 0.001 for both). Antibodies to Tg were demonstrated only on the placentae of Tg-immunized mice. Immunization with Tg results in the production of Tg antibodies and fetal resorption. These effects occur in the absence of thyroid dysfunction.