Undetectable Thyrotropin Research Articles

From routine to rescue: Thyroidectomy for life-threatening thyrotoxicosis.

Thyroidectomies are routinely same-day elective procedures. The aim of this study was to investigate outcomes in patients who underwent uncommon urgent thyroidectomy. We retrospectively reviewed patients diagnosed with thyrotoxicosis at a quaternary medical center between 2011 and 2023. Included patients were admitted nonelectively with thyroidectomies performed during same hospital stay. Patient demographics, comorbidities, hospital course, and operative outcomes were analyzed. Thirty patients met the inclusion criteria. The majority were female (60%) and Black (60%) with a mean age of 41±14years. At admission, 76.6% had undetectable thyrotropin levels (<0.01µU/mL) and 26.7% were diagnosed with thyroid storm. Common presenting comorbidities included atrial fibrillation (53.3%), heart failure (40%), and liver failure (16.7%). Graves' disease was diagnosed in 83.3% of patients, while 13.3% had amiodarone-induced thyrotoxicosis. Median hospital stay before surgery was 8days (interquartile range: 4-16). Indications for surgery were adverse medication events (30%), inadequate therapeutic effect by medication (30%), and worsening heart failure (26.7%). Postoperatively, 6.7% required reoperation for neck hematoma, 13.3% experienced temporary hypoparathyroidism, and 6.7% had hoarseness. Following surgery, 50% of patients with atrial fibrillation experienced resolution and 50% with heart failure with reduced ejection fraction showed ultrasonic improvement. Within 30days, 20% visited the emergency department, none due to thyroidectomy complications, and 13.3% were readmitted for comorbidities. One patient (3.3%) died from liver failure. Patients who require an urgent thyroidectomy often have life-threatening comorbidities particularly cardiac disease. Performing thyroidectomy in these patients can potentially create clinical homeostasis for further management of their comorbidities.

FRI555 A Misdiagnosis Of TSH-secreting Adenoma With Thyrotoxicosis In A Patient With Graves’ Disease

Abstract Disclosure: J. Huynh: None. A. Makawi: None. G. Elshimy: None. Introduction: Modern healthcare relies on laboratory and imaging results for accurate diagnosis and medical decision-making. However, the collection and distillation of laboratory results is a multi-step process with the potential for error at each stage. This may result in diagnostic errors. A review of salient cases is one avenue to improving awareness of the risk for failure in the laboratory assessment process. We present one such case of a patient initially referred to neurosurgery for management of a thyroid stimulating hormone (TSH) secreting microadenoma, which is a rare disease and accounts for less than 1% of all pituitary adenomas, with incongruent laboratory presentation including elevation in TSH and free T4. Endocrinology consultation prompted further investigations which led to the diagnosis of Graves’ disease with a concomitant nonfunctional pituitary microadenoma. Case Presentation: This is a case of a 61-year-old white male who presented with 30-lb weight loss, insomnia, palpitations, and diaphoresis. Initial thyroid stimulating hormone (TSH) from outside facility was &amp;gt; 90 mcIU/mL with elevated free T4 of 23.4 pg/mL. MRI of the brain shows a 3x3 mm pituitary microadenoma raising concern for an atypical case of TSH-secreting adenoma. The patient referred to Neurosurgery for evaluation by primary care. Endocrinology was consulted for evaluation prior to any surgical intervention. A large goiter was noted on exam. Clinical presentation was highly concern for Graves’ disease. Repeated labs included undetectable TSH with FT4 of 4.4 pg/mL and free T3 12.9 pg/ml. TPO-ab was elevated at 17.1 IU/mL. TSIg index was low. Ultrasound of the thyroid gland revealed a normal thyroid without nodules. He was diagnosed with Graves’ disease and was initiated on methimazole and propranolol with symptomatic improvement. His pituitary panels continued to show suppressed TSH pre and post treatment with no other significant pituitary abnormalities hence the diagnosis of a concomitant nonfunctional pituitary microadenoma was made. Discussion: Ultimately, the initial TSH-secreting microadenoma has deemed a misdiagnosis and he was subsequently treated appropriately for Graves’ disease with normalization of thyroid functions. Standard of care for any laboratory abnormalities is to assess for reproducibility of the result. In our patient, subsequent in-house and outside assays were unable to demonstrate elevation of both TSH and FT4. Instead, the patient had suppressed TSH with elevated FT4, without evidence of nodules consistent with Graves’ disease. Treatment of Graves’ disease differs greatly from the treatment of TSH-secreting pituitary adenoma, which includes surgical resection, radiotherapy, and/or, a somatostatin analog based on the clinical picture. Correct diagnosis prevented our patients from unnecessary surgical complications and lifelong morbidity. Presentation: Friday, June 16, 2023

Code Pseudo Stroke - A Case of Hypokalaemic Periodic Paralysis Mimicking Stroke.

Hypokalaemic periodic paralysis is an acute flaccid paralysis secondary to hypokalaemia, triggered by hyperthyroidism, environmental elements such as a high carbohydrate intake or rest after intense exercise, and an underlying genetic component with mutations in the muscle ion channels.The pursuit of code stroke protocol in the in-patient setting must bear in mind reversible but potentially fatal and disabling alternative diagnoses such as stroke mimics including hypokalaemic periodic paralysis.Stroke mimics defined as acute onset neurological deficits that are not related to vascular cause are a true challenge, multiple scales have been created to distinguish them from an actual stroke, such as the Recognition of Stroke in the Emergency Room (ROSIER) scale.

Acute ST-Elevation Myocardial Infarction in Patient with Severe Uncontrolled Hyperthyroidism Complicated by Thyroid Storm

Acute ST-elevation myocardial infarction is a life-threatening medical emergency that needs to be recognized early and treated properly to prevent deleterious complications, including death. A thyroid storm (TS) is a rare but severe manifestation of uncontrolled hyperthyroidism that might present with serious cardiovascular or neurological problems. We described a case of a 40-year-old male patient, known to have uncontrolled hyperthyroidism, who presented with acute onset of central chest pain, agitation, tachycardia, and pulmonary congestion. Fast atrial fibrillation with ST-segment elevation in anterior leads was detected on electrocardiogram. Thyroxin level (T4) was very high with undetectable thyroid stimulating hormone. Initially, the patient refused any type of coronary revascularization; therefore, he was admitted to the cardiology intensive care unit, and medical treatment was commenced for both TS and acute coronary syndrome. High-risk coronary angiography was done 2 h later because he had worsening persistent chest pain and started to develop signs of heart failure. It showed embolic occlusion of the distal left anterior descending artery that was treated medically with anti-coagulation. There were no complications. Chest pain and thyroid function tests settled down during his hospital stay with close cardiology and endocrinology follow-up.

Diagnosis and management of intraoperative thyroid storm in a child with undiagnosed Graves’ disease: a case report

BackgroundThyroid storm is a life-threatening manifestation of thyrotoxicosis and presents with fever, diaphoresis, tachycardia, hypertension, and widened pulse pressure.Case presentationWe present a case of intraoperative thyroid storm in a 12-year-old female undergoing posterior spinal fusion. Despite adequate depth of anesthesia and analgesia, the patient was persistently tachycardic and hypertensive. The surgical procedure was uneventful. A thyroid panel drawn immediately after surgery showed undetectable thyroid stimulating hormone (TSH) and high free thyroxine (T4) consistent with thyroid storm.ConclusionsIntraoperative thyroid storm in a pediatric patient is extremely rare with nonspecific clinical symptoms. Low to undetectable TSH and elevated free T4 is diagnostic.

Management Consideration for Anterior Mediastinal Mass in a Patient With Grave's Disease.

A 36-year-old active duty female presented to an outside hospital emergency department for the evaluation of chest pain and weakness. Per report, comprehensive evaluation ruled out acute cardiopulmonary conditions. A computerized tomography scan revealed a large homogeneous anterior mediastinal mass. The patient was referred to a cardiothoracic surgeon who discussed treatment options, including surgery. She was subsequently referred to an interventional radiologist, who performed a biopsy. Findings were consistent with thymic hyperplasia without evidence of malignant cells. Follow-up with her primary care physician revealed an undetectable thyroid-stimulating hormone (TSH) level, and she was subsequently diagnosed with Graves' disease (GD). The primary care physician referred her to an endocrinologist who initiated treatment with methimazole. The patient's GD responded well to medication therapy; the thymic mass size decreased and her exercise tolerance increased. Notably, testing for TSH levels upon initial presentation could have avoided the need for biopsy.

TSHB R75G is a founder variant and prevalent cause of low or undetectable TSH in Indian Jews.

ObjectiveBi-allelic loss-of-function mutations in TSHB, encoding the beta subunit of thyroid-stimulating hormone (TSH), cause congenital hypothyroidism. Homozygosity for the TSHB p.R75G variant, previously described in South Asian individuals, does not alter TSH function but abrogates its detection by some immune detection-based platforms, leading to erroneous diagnosis of hyperthyroidism. We set out to identify and determine the carrier rate of the p.R75G variant among clinically euthyroid Bene Israel Indian Jews, to examine the possible founder origin of this variant worldwide, and to determine the phenotypic effects of its heterozygosity.DesignMolecular genetic studies of Bene Israel Jews and comparative studies with South Asian cohort.MethodsTSHB p.R75G variant tested by Sanger sequencing and restriction fragment length polymorphism (RFLP). Haplotype analysis in the vicinity of the TSHB gene performed using SNP arrays.ResultsClinically euthyroid individuals with low or undetectable TSH levels from three apparently unrelated Israeli Jewish families of Bene Israel ethnicity, originating from the Mumbai region of India, were found heterozygous or homozygous for the p.R75G TSHB variant. Extremely high carrier rate of p.R75G TSHB in Bene Israel Indian Jews (~4%) was observed. A haplotype block of 239.7 kB in the vicinity of TSHB shared by Bene Israel and individuals of South Asian origin was detected.ConclusionsOur findings highlight the high prevalence of the R75G TSHB variant in euthyroid Bene Israel Indian Jews, demonstrate that heterozygosity of this variant can cause erroneous detection of subnormal TSH levels, and show that R75G TSHB is an ancient founder variant, delineating shared ancestry of its carriers.

Case Report of Hyperthyroidism on Molar Pregnancy

The hydatidiform mole in its partial or total form is a common cause of thyrotoxycosis during pregnancy. The structural homology of the placental hormone choriogonadotropin (hCG) and the hormone thyroid stimulating hormone (TSH) produced by the pituitary gland is the cause. The diagnosis of hyperthyroidism secondary to Gestational trophoblastic diseases is made in the face of low or undetectable TSH, high T4l compared to high hCG level and a suggestive image on pelvic ultrasound. The clinical signs relating to thyropathies are often absent. This is a resolving table after uterine extraction.

Development of Graves' disease during drug-free remission of juvenile dermatomyositis.

We report a Japanese boy with Graves' disease (GD) which developed during drug-free remission of juvenile dermatomyositis (JDM). He had been diagnosed with JDM at the age of 6years by typical skin rashes, muscle weakness, elevated serum transaminase levels, and typical findings of both magnetic resonance imaging and muscle biopsy. Although anti-melanoma differentiation antigen 5 autoantibody was positive, there was no complication of interstitial lung disease. He showed good response to methylprednisolone pulse therapy followed by oral prednisolone in combination with weekly methotrexate (MTX) and achieved drug-free remission after 3.5 years of treatment. Nevertheless, serum levels of soluble interleukin-2 receptor (sIL-2R) gradually elevated to 3185 U/ml despite no signs of relapse or malignancy. Hyperactivity and attention deficit was also noted. One year and 3 months after the cessation of MTX, he presented with abdominal pain, tachycardia, and apparent goitre. Laboratory tests showed elevated free triiodothyronine, undetectable thyroid stimulating hormone (TSH), and positive anti-TSH receptor antibodies. 99mTc scintigraphy showed high levels of thyroid uptake. He was diagnosed with GD and treated with 15 mg/day of thiamazole. Although transient drug eruption was observed, his thyroid functions are currently well-controlled on 5 mg/day of thiamazole. In conclusion, to our knowledge, this is the first report in English literature describing complication of GD with JDM. Unexpected elevation of sIL-2R could be a clue to the diagnosis of GD during the follow-up of JDM.

48-Year-Old Woman With Dyspnea and Chest Pain

48-Year-Old Woman With Dyspnea and Chest Pain

A case report of acute myopericarditis associated with Graves' thyrotoxicosis.

Background The effects of hyperthyroidism on the heart are well documented, primarily consisting of supraventricular tachycardias, congestive heart failure, and dilated cardiomyopathy. Acute myopericarditis resulting from a hyperthyroid state is an uncommon but recognized association.Case summary A 29-year-old man with a history of Graves’ disease presented with chest pain and electrocardiogram changes suggestive of an infero-lateral ST-elevation myocardial infarction. However, emergent coronary angiography and bedside echocardiography were normal. Troponin-I was found to be >25 000 ng/L (normal value <57). Thyroid function tests showed a significantly raised free T4 and undetectable thyroid-stimulating hormone. Cardiovascular magnetic resonance (CMR) showed extensive myocardial oedema and late gadolinium enhancement (LGE) in keeping with acute myopericarditis, alongside an enlarged thyroid gland consistent with goitre. Propylthiouracil in combination with an angiotensin-converting enzyme inhibitor and beta-blocker were commenced and eventually definitive treatment with thyroidectomy was performed. Follow-up CMR at 6 months showed complete resolution of the prior noted oedema and a reduction in the location and extent of LGE with significant residual fibrosis.Discussion Acute myopericarditis is a common diagnosis in young patients presenting with symptoms of chest pain with elevated troponin and is frequently related to a viral illness. Hyperthyroid states are also associated with acute myopericarditis and should be particularly considered in patients with a pre-existing thyroid condition or in those with symptoms suggestive of hyperthyroidism. Given the specific treatments required in a case of myopericarditis associated with hyperthyroidism, it is important to be aware of this association and consider screening where appropriate.

Massive Thymic Hyperplasia Secondary to Graves Disease

Graves disease (GD) has a well-known association with thymic hyperplasia, which is seen histo-logically in up to 38% of patients with GD. However, there have only been approximately 100 documented cases of Graves-associated massive thymic hyperplasia. Potential mechanisms of thymic pathology are reviewed. A 24-year-old female presented to the emergency department with dyspnea, palpitations, tachycardia, anxiety, and weight loss. She was evaluated for hyperthyroidism using labs (thyroid-stimulating hormone, free thyroxine, thyroid-stimulating immunoglobulins) and imaging (radioactive iodine uptake [RAIU] scan), leading to treatment with radioiodine. A computed tomography angiogram of the chest was also performed to evaluate for pulmonary embolism given the patient's presenting symptoms. Our patient was found to have undetectable thyroid-stimulating hormone, elevated free thyroxine (2.9 ng/dL), and elevated thyroid-stimulating immunoglobulins (399%). Diagnosis of GD was confirmed on RAIU scan. The computed tomography chest angiogram demonstrated a significant anterior mediastinal mass (7.9 × 6.9 × 6.3 cm). Treatment with radioiodine led to reduction of the mass by 76% in volume. While the patient's thyroid labs and RAIU scan were consistent with GD, the presence of massive thymic hyperplasia was atypical. However, the resolution of thymic hyperplasia after radioiodine therapy, without the use of thymectomy, was similar to other reported cases.

Subclinical hyperthyroidism

Subclinical hyperthyroidism (SH) is a relatively common disorder; it is defined as a condition in which the thyroid hormones thyroxine (T4) and triiodothyronine levels (T3) are normal with low or even undetectable thyroid-stimulating hormone (TSH) levels. SH may be caused by exogenous or endogenous factors with TSH suppressive therapy in differentiated thyroid cancer or unintentional over-replacement L-T4 therapy being the most common causes. Frank symptoms of hyperthyroidism is most often absent. Patients often present with goitre or for other symptoms of mild thyroid hormone excess such as headache, reduced feeling of well-being, and inability to concentrate. SH leads to increased risk of cardiovascular morbidity and mortality, it may accelerate the development of osteoporosis, and increase bone vulnerability to trauma, especially in postmenopausal women and elderly. It reduces the quality of life, affecting both the psycho and somatic components of wellbeing. Diagnosis of SH is confirmed by repeated testing of TSH spaced months apart in the presence of normal free T3 and T4 concentrations. Radionuclide uptake scan aids us in the diagnosis of the cause of SH. The treatment of SH is similar to the treatment of overt hyperthyroidism, it should be based on the underlying etiology.

Subclinical thyroid dysfunction and cardiovascular diseases: 2016 update.

Subclinical thyroid dysfunction comprises subclinical hypothyroidism (SHypo), defined as elevated thyroid-stimulating hormone (TSH) by normal free thyroxine (FT4), and subclinical hyperthyroidism (SHyper) with decreased or undetectable TSH and normal FT4. Up to 10% of the elderly have SHypo, which is usually asymptomatic. Individual participant data (IPD) analyses of prospective cohort studies from the international Thyroid Studies Collaboration show that SHypo is associated with increased coronary heart disease (CHD) mortality [hazard ratio (HR) 1,58 for TSH ≥ 10 mIU/L, 95% CI 1.10-2.27), as well as increased risk of stroke, and heart failure (HF) for both higher and lower TSH. Small studies found that SHypo affects carotid intima media thickness (CIMT), diastolic function, peripheral vascular resistance, endothelial function, and lipid profile. SHyper is associated with increased risk of atrial fibrillation (AF) (HR 1.68, 95% CI 1.16-2.43) and CHD events (HR 1.21, 95% CI 0.99-1.46). The TSH threshold for initiating treatment is unclear. In the absence of large randomized controlled trials, the best evidence suggests SHypo therapy should be started at TSH ≥ 10 mIU/L, and SHyper therapy at TSH < 0.1 mIU/L. Recommendations on screening are discordant, but most guidelines advocate that thyroid function should be checked in those at risk for hypothyroidism, those over 60, and those with known CHD and HF. This review updates current evidence on the association between thyroid dysfunction and cardiovascular disease, as well as on screening and treatment of subclinical thyroid dysfunction.

A case of masked toxic adenoma in a patient with non-thyroidal illness

BackgroundNon-thyroidal illness (NTI) refers to changes in thyroid hormone levels in critically ill patients in the absence of primary hypothalamic-pituitary-thyroid dysfunction, and these abnormalities usually resolve after clinical recovery. However, NTI can be accompanied by primary thyroid dysfunction. We report herein a case of a woman with NTI accompanied by primary hyperthyroidism.Case presentationA 52-year-old female was admitted to the intensive care unit with heart failure and atrial fibrillation. She had a longstanding thyroid nodule, and a thyroid function test revealed low levels of triiodothyronine and free thyroxine as well as undetectable thyroid stimulating hormone (TSH). She was diagnosed with NTI, and her TSH level began to recover but not completely at discharge. The thyroid function test was repeated after 42 months to reveal primary hyperthyroidism, and a thyroid scan confirmed a toxic nodule.ConclusionThis case suggests that although NTI was diagnosed, primary hyperthyroidism should be considered as another possible diagnosis if TSH is undetectable. Thyroid function tests should be repeated after clinical recovery from acute illness.

Heparin-Induced Hyperkalemia in a Patient Diagnosed with Thyroid Storm

To describe a case of heparin-induced hyperkalemia and the role for transtubular potassium gradient (TTKG) to guide fludrocortisone therapy. A 52-year-old white male developed hyperkalemia after receiving intravenous unfractionated heparin (UFH) for atrial fibrillation during thyroid storm. Admission laboratory results were noteworthy for normal potassium levels, undetectable thyroid-stimulating hormone, and mild transaminitis. Treatment for thyroid storm was initiated but UFH was stopped because the international normalized ratio was subsequently found to be elevated. Rising potassium levels developed just 24 hours after UFH discontinuation, without exogenous potassium supplementation, renal dysfunction, or acidosis. A TTKG was low, reflecting a hypoaldosterone state. In addition, the Naranjo probability scale indicated probable medication-associated hyperkalemia. Heparin-induced hyperkalemia (HIH) was suspected and oral fludrocortisone 0.2 mg was given daily alongside serial TTKG measurements. TTKG and hyperkalemia normalized with 2 days of treatment. UFH is commonly used; therefore, clinicians must be cautious of hyperkalemia. Although HIH usually resolves after discontinuation of heparin, it may persist despite discontinuation of the drug, as highlighted by this case. In this setting, a TTKG should be determined, which can be used to guide fludrocortisone therapy. HIH can occur despite discontinuation of heparin, and TTKG can be helpful in guiding fludrocortisone treatment in this circumstance.

Sporadic congenital nonautoimmune hyperthyroidism caused by P639S mutation in thyrotropin receptor gene

Germline mutations of thyrotropin receptor (TSHR) gene determining a constitutive activation of the receptor were identified as a molecular cause of familial or sporadic congenital nonautoimmune hyperthyroidism (OMIM: 609152) (Nat Genet 7:396-401, 1994; N Engl J Med 332:150-154, 1995; Acta Endocrinol (Copenh) 100:512-518, 1982). We report the case of an Italian child subjected to the first clinical investigation at 24months for an increased growth velocity; biochemical investigation showed high FT4 and FT3 serum values and undetectable thyrotropin in the absence of anti-thyroid antibodies; the thyroid gland was normal at ultrasound examination. Treatment with methimazole was started at the age of 30months when her growth velocity was high and the bone age was advanced. DNA was extracted from her parents', brother's, and the patient's blood. Exons 9 and 10 of the TSHR gene were amplified by polymerase chain reaction and subjected to direct sequencing. In proband, a heterozygous substitution of cytosine to thymine determining a proline to serine change at position 639 (P639S) of the TSHR was detected while the parents and brothers of the propositus, all euthyroid, showed only the wild-type sequence of the TSHR gene. This mutation was previously described as somatic in patients affected by hyperfunctioning thyroid nodules and as germline in a single Chinese family affected by thyrotoxicosis and mitral valve prolapse. This constitutively activating mutation is able to activate both the cyclic AMP and the inositol phosphate metabolic pathways when expressed in a heterologous system. In conclusion, we describe the first case of sporadic congenital nonautoimmune hyperthyroidism caused by de novo germinal P639S mutation of TSHR.

Circulating thyrotropin receptor messenger RNA for evaluation of thyroid nodules and surveillance of thyroid cancer in children

Purpose The aim of this study was to determine the role of thyrotropin receptor messenger RNA as a novel blood test for evaluation of thyroid nodules and cancer in children. Methods We reviewed thyroid disease management of patients younger than 18 years with thyrotropin receptor messenger RNA measurements identified from a prospective, institutional review board-approved registry during 2008 to 2010. Results Thirty-nine thyrotropin receptor messenger RNA measurements were made in 21 female patients (12-17 years old; median, 16 years). Four patients with fine-needle aspiration only had benign thyroid cytology, and 3 of 4 had undetectable thyrotropin receptor messenger RNA. Seventeen patients underwent 22 thyroid operations. Preoperative thyrotropin receptor messenger RNA was measured in 9 patients: 3 of 4 with thyroid cancer had elevated levels and 3 of 5 with goiters undetectable. Postthyroidectomy surveillance (median, 16 months; range, 6-24) of 11 thyroid cancer patients (8 papillary, 3 follicular) showed that thyrotropin receptor messenger RNA was concordant with thyroglobulin in 14 (73%) of 19 measurements. In 3 (16%) of 19 measurements, thyrotropin receptor messenger RNA was the only blood test useful for disease assessment because of elevated antithyroglobulin antibodies. Overall, to predict thyroid cancer, thyrotropin receptor messenger RNA demonstrated 73% sensitivity, 82% specificity, 62% positive predictive value, 88% negative predictive value, and 79% accuracy. Conclusion Thyrotropin receptor messenger RNA provides complementary evaluation to thyroglobulin and fine-needle aspiration for pediatric thyroid nodule management.

Evaluation of Predictors for the Diagnosis of Hyperthyroidism in Cats

In humans, subclinical hyperthyroidism is diagnosed when serum thyroid hormone concentrations are within the reference range but thyroid stimulating hormone (TSH) concentration is subnormal. In a previous study, a higher prevalence of thyroid nodular disease was found in euthyroid geriatric cats with undetectable TSH (<0.03 ng/mL) compared to those with detectable TSH concentrations, suggesting subclinical hyperthyroidism might also exist in cats. Euthyroid cats with undetectable TSH concentrations have subclinical hyperthyroidism and may subsequently develop overt signs of hyperthyroidism. One-hundred four client-owned cats. In this prospective cohort study, euthyroid geriatric (≥ 9 years) cats were recruited during routine health checks. Plasma biochemistry was performed at baseline and every 6 months thereafter. Total thyroxine and TSH concentrations were determined annually. Short-term follow-up data (within 14 months of recruitment) were used to detect variables at entry that were predictive of the diagnosis of hyperthyroidism, using univariable analysis followed by multivariable logistic regression analysis. Log rank analysis was used to test the association of initial TSH concentration with diagnosis of hyperthyroidism during the total available follow-up. Median (range) follow-up was 26 (0-54) months and annual incidence of hyperthyroidism during the study was 7.4%. Cats that became hyperthyroid within 14 months had higher ALKP activity (P = 0.02) and higher prevalence of goiter (P = .03) at baseline than controls. Cats with undetectable TSH at baseline (29/104; 28%) were significantly (P < .001) more likely to be diagnosed with hyperthyroidism. However, not all cats with undetectable TSH became hyperthyroid during the study.

Papillary Thyroid Carcinoma in an Autonomous Hyperfunctioning Thyroid Nodule: Case Report and Review of the Literature

Whereas thyroid nodules are less common among children than among adults, the anxiety generated by the finding of a thyroid nodule is high because 20% of nodules found in children contain thyroid cancer. Discovery of a nodule in the context of hyperthyroidism is usually comforting due to the presumption that the nodule represents a benign toxic adenoma. An 11-year-old girl presented with heavy menses, fatigue, and a right thyroid mass. Laboratory evaluation revealed elevated triiodothyronine and undetectable thyroid-stimulating hormone. Thyroid ultrasonography revealed a 3.5 cm nonhomogenous nodule, and scintigraphy was consistent with an autonomous hyper-functioning nodule. Fine-needle aspiration biopsy could not rule out malignancy, and patient underwent right hemithyroidectomy and isthmusectomy. Pathology was consistent with papillary thyroid carcinoma. We report the discovery of papillary thyroid carcinoma in an autonomously hyperfunctioning nodule in an 11-year-old girl. Detection of an autonomously functioning thyroid nodule in children and adolescents does not exclude the possibility of thyroid carcinoma and warrants careful evaluation and appropriate therapy.