scholarly journals Metastatic Follicular Thyroid Carcinoma Secreting Thyroid Hormone and Radioiodine Avid without Stimulation: A Case Report and Literature Review

2014 ◽  
Vol 2014 ◽  
pp. 1-6
Author(s):  
Syed A. Abid ◽  
Brendan C. Stack ◽  
Donald L. Bodenner
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Carcinoma ◽  
Follicular Thyroid Carcinoma ◽  
Cervical Vertebrae ◽  
Lung Nodule ◽  
Thyroid Stimulating Hormone ◽  
Whole Body ◽  
Rapid Progression ◽  
Free T4 ◽  
Metastatic Lesions

Introduction. This is an extremely rare case of a patient with metastatic follicular thyroid cancer who continued to produce thyroid hormone and was iodine scan positive without stimulation after thyroidectomy and radioiodine (I-131) therapy.Patient Findings. A 76-year-old Caucasian male was diagnosed with metastatic follicular thyroid carcinoma on lung nodule biopsy. Total thyroidectomy was performed and he was ablated with 160 mCi of I-131 after recombinant human thyrotropin (rhTSH) stimulation. Whole body scan (WBS) after treatment showed uptake in bilateral lungs, right sacrum, and pelvis. The thyroglobulin decreased from 2,063 to 965 four months after treatment but rapidly increased to 2,506 eleven months after I-131. Thyroid stimulating hormone (TSH) remained suppressed and free T4 remained elevated after I-131 therapy without thyroid hormone supplementation. He was treated with an additional 209 mCi with WBS findings positive in lung and pelvis. Despite I-131, new metastatic lesions were noted in the left thyroid bed and large destructive lesion to the first cervical vertebrae four months after the second I-131 dose.Conclusions. This case is exceptional because of its rarity and also due to the dissociation between tumor differentiation and aggressiveness. The metastatic lesions continued to secrete thyroid hormone and remained radioiodine avid with rapid progression after I-131 therapy.

Thyroid Hormone Therapy and Incident Stroke

2021 ◽  
Author(s):  
Maria Papaleontiou ◽  
Deborah A Levine ◽  
David Reyes-Gastelum ◽  
Sarah T Hawley ◽  
Mousumi Banerjee ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Thyroid Hormone ◽  
Hormone Treatment ◽  
Population Based ◽  
Thyroid Stimulating Hormone ◽  
Prior History ◽  
Veterans Health ◽  
Health Administration ◽  
Free T4 ◽  
Increased Risk

Abstract Context Stroke is a leading cause of death and disability and there is a need to identify modifiable risk factors. Objective Determine the relationship between thyroid hormone treatment intensity and incidence of atrial fibrillation and stroke. Design Retrospective cohort study using data from the Veterans Health Administration between 2004 and 2017, with a median follow-up of 59 months. Setting Population-based. Participants 733,208 thyroid hormone users aged ≥18 years with at least two thyroid stimulating hormone (TSH) measurements between thyroid hormone initiation and incident event or study conclusion (406,030 thyroid hormone users with at least two free T4 measurements). Main Outcome Measures Incident atrial fibrillation and stroke. Results Overall, 71,333/643,687 (11.08%) participants developed incident atrial fibrillation and 41,931/663,809 (6.32%) stroke. In multivariable analyses controlling for pertinent factors such as age, sex and prior history of atrial fibrillation, low TSH or high free T4 levels (i.e., exogenous hyperthyroidism; e.g., TSH<0.1 mIU/L, OR 1.33, 95% CI 1.24-1.43) and high TSH or low free T4 levels (i.e., exogenous hypothyroidism; e.g., TSH>5.5 mIU/L, OR 1.29, 95% CI 1.26-1.33; free T4<0.7 ng/dL, OR 1.29, 95% CI 1.22-1.35) were associated with higher incidence of stroke compared to euthyroidism (TSH >0.5-5.5 mIU/L and free T4 0.7-1.9 ng/dL). Risk of developing atrial fibrillation and stroke was cumulative over time for both patients with exogenous hyperthyroidism and hypothyroidism. Conclusions Both exogenous hyper- and hypothyroidism were associated with increased risk of stroke, highlighting the importance of patient medication safety.

scholarly journals 99mTc-DMSA (V) in Evaluation of Osteosarcoma: Comparative Studies with 18F-FDG PET/CT in Detection of Primary and Malignant Lesions

ISRN Oncology ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-11
Author(s):  
G. P. Bandopadhyaya ◽  
Priyanka Gupta ◽  
Archana Singh ◽  
Jaya Shukla ◽  
S. Rastogi ◽  
...  
Keyword(s):  
Fdg Pet ◽  
Lung Nodule ◽  
Inflammatory Lesion ◽  
Primary Site ◽  
Whole Body ◽  
Metastatic Lesions ◽  
Pet Ct ◽  
Malignant Lesions ◽  
Fdg Pet Ct

To evaluate the role of 99mTc-DMSA (V) and [18F]FDG PET-CT in management of patients with osteosarcoma, 22 patients were included in our study. All patients underwent both 99mTc-DMSA (V) and whole-body [18F]FDG PET-CT scans within an interval of 1 week. 555–740 MBq of 99mTc-DMSA (V) was injected i.v. the whole-body planar, SPECT images of primary site and chest were performed after 3-4 hours. [18F]FDG PET-CT images were obtained 60 minutes after i.v. injection of 370 MBq of F-18 FDG. Both FDG PET-CT (mean SUVmax = 7.1) and DMSA (V) scans showed abnormal uptake at primary site in all the 22 patients (100% sensitivity for both). Whole-body PET-CT detected metastasis in 11 pts (lung mets in 10 and lung + bone mets in 1 patient). Whole-body planar DMSA (V) and SPECT detected bone metastasis in one patient, lung mets in 7 patients and LN in 1 patient. HRCT of chest confirmed lung mets in 10 patients and inflammatory lesion in one patient. 7 patients positive for mets on DMSA (V) scan had higher uptake in lung lesions as compared to FDG uptake on PET-CT. Three patients who did not show any DMSA uptake had subcentimeter lung nodule. Resuts of both 99mTc-DMSA (V) (whole-body planar and SPECT imaging) and [18F]FDG PET-CT were comparable in evaluation of primary site lesions and metastatic lesions greater than 1 cm. Though 99mTc-DMSA (V) had higher uptake in the lesions as compared to [18F]FDG PET-CT, the only advantage [18F]FDG PET-CT had was that it could also detect subcentimeter lesions.

scholarly journals Invasive follicular thyroid carcinoma infiltrating trachea

2011 ◽  
Vol 68 (10) ◽  
pp. 891-894
Author(s):  
Aleksandar Filipovic ◽  
Ljiljana Vuckovic ◽  
Milan Mijovic
Keyword(s):  
Thyroid Cancer ◽  
Thyroid Carcinoma ◽  
Radioiodine Therapy ◽  
Follicular Thyroid Carcinoma ◽  
Radical Resection ◽  
Left Lobe ◽  
Whole Body ◽  
Suppressive Therapy ◽  
Tracheal Resection ◽  
Serum Thyroglobulin

Introduction. Although follicular thyroid carcinoma is a rare malignant tumor, up to 20% of the patients are threatened by potential complications resulting from infiltrating tumor growth into surrounding tissues. Case report. A 66- year-old female came to hospital with the presence of a growing thyroid nodule of the left lobe. Ultrasonic examination showed a 8 cm hypoechoic nodule in the left lobe. Thyroid scintigraphy showed a cold nodule. CT scan and tracheoscopy showed tracheal infiltration without tracheal obstruction. An extended total thyroidectomy was done, with the left jugular vein, strap muscles and tracheal 2 cm long circular resection. The pathologist confirmed invasive follicular thyroid cancer. After the surgery the patient was treated with radioiodine therapy and permanent TSH suppressive therapy. The patient was followed with measurements of the thyroid hormone and serum thyroglobulin level every six months, as well as the further tests (chest xray, ultrasound of the neck and a whole body scintigraphy) were done. After more than three years the patient had no evidence of the recurrent disease. Conclusion. Radical resection of the tracheal infiltrating thyroid cancer with circular tracheal resection and terminoterminal anastomosis followed by radioiodine therapy should be considered the treatment of choice.

scholarly journals Thyroid Hormone Resistance With Concurrent Papillary Thyroid Cancer

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A961-A962
Author(s):  
Dhivya Pahwa ◽  
Michael Howard Shanik
Keyword(s):  
Thyroid Cancer ◽  
Thyroid Hormone ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Thyroid Hormone Receptor ◽  
Hormone Resistance ◽  
Papillary Thyroid ◽  
Free T4 ◽  
Thyroid Hormone Resistance ◽  
History Of

Abstract Introduction: Thyroid hormone resistance is a genetic mutation resulting in decreased receptor responsiveness. We present a case of thyroid hormone resistance with concurrent papillary thyroid cancer. Clinical Case: A 34-year-old man with a history of papillary thyroid carcinoma status post total thyroidectomy and radioactive iodine. He had transferred his care after moving to our area. He presented with persistently elevated TSH despite ongoing treatment with Levothyroxine 400 mcg daily. Upon presentation the patient reported intermittent palpitations and tremor. Vital signs revealed height of 74 inches, weight of 235 pounds, blood pressure of 112/64, and heart rate of 48. Physical examination revealed a well -healed scar on the neck without palpable lymphadenopathy. Bloodwork revealed TSH of 15.28 mIU/L and Free T4 of 2.8 ng/dL. The patient was maintained on Levothyroxine 400 mcg daily and educated on proper administration of the medication. Two months later, bloodwork revealed a TSH of 9.22 mIU/L with a Free T4 of 3.3 ng/dL. MRI of the pituitary revealed a 4mm hyper-intensity which likely represented a microadenoma. Resistance Thyroid Hormone (RTH) Mutation analysis was ordered which revealed a heterozygous mutation for the Thyroid Hormone Receptor (THR)-Beta gene. The mutation was detected at pArg438His indicating a single nucleotide substitution leading to the replacement of arginine by histidine at the p.438 of the translated protein on exon 10. The patient was maintained on Levothyroxine at 400 mcg daily. Discussion: Thyroid hormone resistance describes a constellation of symptoms from decreased tissue responsiveness to thyroid hormones. Literature reveals the prevalence of THR to be 1 in 40,000 individuals. It occurs due to mutation on the thyroid hormone receptor, most often found on the alpha or beta subunit. Frequently patients present with tachycardia and hyperactivity but it can also present with symptoms suggestive of hypothyroidism and goiter. Risk factors include family history of RTH mutation often with an autosomal dominant inheritance pattern. Patients with an elevated Free T4 with a non-suppressed TSH should be investigated with a genetic analysis of Resistance Thyroid hormone. A positive mutation would confirm the diagnosis. Close monitoring of symptoms as well as thyroid function tests should guide treatment. The concurrent diagnosis of thyroid hormone resistance in conjunction with papillary thyroid carcinoma in our patient is unique and makes management a challenge. The literature reveals few cases reported. Reference: DynaMed. (2018, November 30). Thyroid Hormone Resistance. Retrieved October 2, 2020, from https://www-dynamed-com.arktos.nyit.edu/topics/dmp~AN~T912485 Igata M, et al. Coexistence of resistance to thyroid hormone and papillary thyroid carcinoma. Endocrinol Diabetes Metab Case Rep. 2016;2016:160003. doi:10.1530/EDM-16-0003

THYROID PROFILE IN CHILDREN WITH NEPHROTIC SYNDROME

2021 ◽  
pp. 75-77
Author(s):  
Meiyappan Kavitha ◽  
Mallaiyan Manonmani
Keyword(s):  
Nephrotic Syndrome ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Thyroid Stimulating Hormone ◽  
The Body ◽  
Urinary Protein ◽  
Creatinine Ratio ◽  
Free Triiodothyronine ◽  
Free T4 ◽  
Renal Disorder

Objectives: Nephrotic syndrome is a common renal disorder seen in children, with proteinuria as the hallmark. Growth retardation is a known feature of nephrotic syndrome, either due to the disease or treatment with steroids. Thyroid hormone strongly inuences growth of the body. So, the present study was undertaken with the objective to assess the thyroid prole in children with nephrotic syndrome Methods: The study involved 41 cases of nephrotic syndrome and 41 age and sex matched controls. Serum total triiodothyronine (T3), total thyroxine (T4), free triiodothyronine (T3), free thyroxine (T4) and thyroid stimulating hormone (TSH) were assessed in these subjects. The thyroid hormones were correlated with urinary protein creatinine ratio. The cases were followed up after one month and the levels of thyroid hormones were reassessed. Results: Total T3, total T4, free T3 and free T4 are signicantly decreased and TSH signicantly increased among cases when compared to controls. TSH is positively correlating with urinary protein creatinine ratio in cases. After one month of treatment, total T3 and total T4 are signicantly increased in cases. Conclusions: The thyroid hormone levels are altered in children with nephrotic syndrome during the episode. A state of subclinical hypothyroidism exists during the nephrotic stage. The alteration is normalized with remission and does not require treatment.

scholarly journals Growth Activation Alone Is Not Sufficient to Cause Metastatic Thyroid Cancer in a Mouse Model of Follicular Thyroid Carcinoma

Endocrinology ◽  
2010 ◽  
Vol 151 (4) ◽  
pp. 1929-1939 ◽  
Author(s):  
Changxue Lu ◽  
Li Zhao ◽  
Hao Ying ◽  
Mark C. Willingham ◽  
Sheue-yann Cheng
Keyword(s):  
Thyroid Hormone ◽  
Mouse Model ◽  
Thyroid Carcinoma ◽  
Focal Adhesion ◽  
Follicular Thyroid Carcinoma ◽  
Gene Knockout ◽  
Metastatic Cancer ◽  
Genetic Alterations ◽  
Human Thyroid ◽  
Migration And Invasion

TSH is the major stimulator of thyrocyte proliferation, but its role in thyroid carcinogenesis remains unclear. To address this question, we used a mouse model of follicular thyroid carcinoma (FTC) (TRβPV/PV mice). These mice, harboring a dominantly negative mutation (PV) of the thyroid hormone-β receptor (TRβ), exhibit increased serum thyroid hormone and elevated TSH. To eliminate TSH growth-stimulating effect, TRβPV/PV mice were crossed with TSH receptor gene knockout (TSHR−/−) mice. Wild-type siblings of TRβPV/PV mice were treated with an antithyroid agent, propylthiouracil, to elevate serum TSH for evaluating long-term TSH effect (WT-PTU mice). Thyroids from TRβPV/PVTSHR−/− showed impaired growth with no occurrence of FTC. Both WT-PTU and TRβPV/PV mice displayed enlarged thyroids, but only TRβPV/PV mice developed metastatic FTC. Molecular analyses indicate that PV acted, via multiple mechanisms, to activate the integrins-Src-focal adhesion kinase-p38 MAPK pathway and affect cytoskeletal restructuring to increase tumor cell migration and invasion. Thus, growth stimulated by TSH is a prerequisite but not sufficient for metastatic cancer to occur. Additional genetic alterations (such as PV), destined to alter focal adhesion and migration capacities, are required to empower hyperplastic follicular cells to invade and metastasize. These in vivo findings provide new insights in understanding carcinogenesis of the human thyroid.

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