Introduction: Non-thyroidal illness syndrome commonly occurs during acute systemic illnesses and is characterized by suppressed or inappropriately normal thyroid-stimulating hormone with low or low-normal thyroid hormone levels. This biochemical pattern may obscure or delay the diagnosis of underlying hyperthyroidism, especially in mild or borderline cases. Acute stroke is a recognized trigger of non-thyroidal illness syndrome, yet its masking effect on hyperthyroidism is under-recognized in clinical practice. Case: A 58-year-old Malay male with cardiovascular risk factors presented with an acute ischemic stroke involving the left occipital lobe and right internal capsule. He developed new-onset atrial fibrillation (CHA₂DS₂-VASc 3) and mild left ventricular systolic dysfunction. Initial thyroid function tests during the acute stroke phase showed mildly suppressed thyroid-stimulating hormone (TSH) (0.30 mIU/L) with high-normal free T4 (21.2 pmol/L), interpreted in the context of acute illness. The patient was clinically stable without overt thyrotoxic features. One month post-stroke, repeat testing revealed further TSH suppression (0.09 mIU/L) and rising free T4 (27.6 pmol/L). Detailed history uncovered prior Graves’ disease in 2019 with treatment default. Examination revealed a small diffuse goiter without ophthalmopathy. The biochemical evolution following recovery from acute illness confirmed recurrent hyperthyroidism previously masked by nonthyroidal illness syndrome. Conclusion Acute stroke can induce cytokine-mediated suppression of the hypothalamic-pituitary-thyroid axis and altered peripheral deiodination, leading to misleading thyroid function tests. In this case, non-thyroidal illness syndrome blunted the biochemical severity of hyperthyroidism, delaying recognition despite high-risk features such as atrial fibrillation and prior Graves’ disease. Reliance on a single thyroid function test during acute illness may therefore result in underdiagnosis.
Euthyroid Sick Syndromes ; Ischemic Stroke ; Hyperthyroidism

Introduction: Thyrotoxicosis following neck surgery is typically attributed to transient destructive thyroiditis from follicular disruption. In end-stage renal failure (ESRF), however, altered thyroid hormone kinetics, including reduced protein binding, impaired peripheral metabolism, and decreased clearance, can distort biochemical interpretation. This creates a high-risk scenario where laboratory values overestimate tissue thyrotoxicity, predisposing to inappropriate antithyroid therapy. We present a case demonstrating marked clinical–biochemical dissociation, reframing postoperative thyrotoxicosis in ESRF as a disorder of hormone handling rather than hormone overproduction. Case: A 45-year-old female with ESRF on maintenance hemodialysis and tertiary hyperparathyroidism underwent total parathyroidectomy. Preoperative thyroid function was consistently euthyroid. Within 48 hours postoperatively, she developed severe biochemical thyrotoxicosis (thyroidstimulating hormone 0.28 mIU/L, free thyroxine 4 [FT4] 68 pmol/L). Despite this, she remained clinically euthyroid, with stable hemodynamics, absence of adrenergic or neuropsychiatric features, and no evidence of thyroid eye disease. The temporal relationship strongly suggested destructive thyroiditis secondary to surgical manipulation, with passive release of preformed thyroid hormone. In the context of ESRF, impaired hormone clearance and altered binding likely amplified circulating free hormone levels without proportional end-organ effect, resulting in striking clinical–biochemical dissociation. A conservative strategy was adopted. Antithyroid drugs were withheld, given the non-synthetic mechanism of hormone excess, and the patient was managed with close monitoring and symptom-guided beta-blockade. Serial thyroid function demonstrated spontaneous improvement without complications. Conclusion Post-parathyroidectomy thyrotoxicosis in ESRF represents exaggerated biochemical derangement without true tissue toxicity. Management must prioritize physiology over laboratory values, as misclassification risks iatrogenic harm. This case demonstrates that in ESRF, elevated FT4 may not reflect true tissue thyrotoxicity, and reliance on biochemical severity alone can lead to inappropriate antithyroid therapy and iatrogenic harm.
Parathyroidectomy ; Hyperthyroidism ; Thyrotoxicosis

Introduction: Gestational trophoblastic disease (GTD) is an uncommon but important cause of secondary hyperthyroidism, termed trophoblastic hyperthyroidism, resulting from the structural similarity between human chorionic gonadotropin (hCG) and thyroid-stimulating hormone (TSH). Excessively elevated hCG levels can stimulate the TSH receptor, leading to increased thyroid hormone production and clinically significant thyrotoxicosis. Early recognition is essential as uncontrolled hyperthyroidism may lead to serious perioperative complications. Case: We report a 50-year-old female who presented with persistent vaginal bleeding following a prior uterine evacuation. Clinical examination and ultrasonography revealed a uterine mass corresponding to approximately 14 weeks’ gestation. Serum β-hCG was markedly elevated at >1,000,000 IU/L. Histopathological evaluation confirmed choriocarcinoma. Thyroid function tests demonstrated severe biochemical hyperthyroidism, with suppressed TSH and elevated free thyroxine levels. Notably, the patient did not exhibit classic symptoms or signs of hyperthyroidism such as palpitations, tremor, goiter, or thyroid eye signs. She was started on beta-blockers and carbimazole for initial control. Given the underlying pathology, early definitive surgical management was planned with multidisciplinary input, and she subsequently underwent total abdominal hysterectomy with bilateral salpingo-oophorectomy successfully. Hyperthyroidism in GTD is well described, but patients may remain clinically asymptomatic despite significant biochemical derangement, as seen in this case. Markedly elevated β-hCG can mimic primary thyroid disease and may lead to misinterpretation if the underlying cause is not recognized. While antithyroid drugs such as carbimazole are commonly initiated, they may have limited effect in this setting, as the hyperthyroidism is driven by hCG rather than intrinsic thyroid overactivity. Beta-blockers play an important role in controlling symptoms and reducing peripheral conversion of T4–T3. Early definitive treatment of the underlying trophoblastic disease remains the key to resolution. Conclusion Trophoblastic hyperthyroidism is a reversible condition secondary to the underlying disease process. Treatment of the trophoblastic tumor results in resolution of the thyrotoxic state. Early recognition and appropriate preoperative optimization are essential to ensure safe patient outcomes.
Gestational Trophoblastic Disease ; Hyperthyroidism

Introduction: Hyperthyroidism in children and adolescents, although uncommon, has significant effects on growth, neurodevelopment, and quality of life. Local data in Malaysia are limited, and regional variations may influence disease presentation and outcomes. This study aimed to determine the incidence, clinical characteristics, and treatment outcomes of paediatric hyperthyroidism at a tertiary centre. Methodology: A retrospective cohort study was conducted at the Paediatric Endocrine Clinic, Universiti Malaya Medical Centre, from 2014 to 2024. Patients aged below 18 years with confirmed hyperthyroidism were included. Demographic, clinical, biochemical, and treatment data were analyzed. Descriptive statistics were used, and associations were tested using chisquare and Fisher’s exact tests, with p <0.05 considered significant. Results: Forty-three patients were included, representing 9.7% of paediatric thyroid disorders. The cohort was predominantly female (74.4%) and majority Malay, with a median age of 11.7 years. Most patients presented with typical features, including palpitations (72.5%), goiter (62.5%), weight loss (45.0%), and heat intolerance (40.0%). However, atypical presentations such as learning difficulties and psychological disturbances were also observed and, in some cases, constituted the chief complaints. Notably, 82.5% of patients presented with severe thyrotoxicosis. Grave’s disease was the predominant etiology. All patients received antithyroid drugs, mainly carbimazole, with 80.0% achieving disease control and a median time to euthyroid state of 2 months. The duration of antithyroid drug therapy prior to cessation was shorter than international recommendations, indicating a significant reduction in time to treatment completion. Relapse occurred in 25.0% and was significantly associated with poor disease control (p = 0.014), while no significant associations were found with demographic or biochemical factors. Definitive therapy was required in 35.0%, with older age, growth stunting, and prior relapse identified as significant predictors (p <0.05). Conclusion Paediatric hyperthyroidism in this Malaysian cohort is predominantly due to Graves’ disease and frequently presents with both classical and atypical manifestations, which may delay diagnosis. Despite a high proportion of severe thyrotoxicosis at presentation, antithyroid drug therapy was effective, with a shorter duration to treatment cessation compared to international standards. Poor disease control emerged as the strongest predictor of relapse, while older age, growth stunting, and prior relapse predicted progression to definitive therapy. Early recognition and individualized management are essential to optimize outcomes. Larger multicentre studies are needed to inform national clinical practice guidelines.
Adolescent ; Child ; Incidence ; Hyperthyroidism

INTRODUCTION

Hyperthyroidism was thought to lower thyroid cancer risk due to TSH suppression, potentially leading to overlooked diagnoses. This study examines clinical factors linked to thyroid cancer in hyperthyroid patients who have undergone thyroidectomy.

OBJECTIVE

This study determined the clinical factors associated with malignancy among patients with hyperthyroidism who underwent thyroidectomy in a tertiary hospital.

METHODS

This analytical cross-sectional study reviewed electronic biopsy results of adult patients who underwent thyroidectomy from January 2009 to December 2019 for hyperthyroidism secondary to Graves’ Disease, Solitary Toxic Adenoma or Multinodular Toxic Goiter. It considered factors linked to thyroid cancer, its prevalence, and clinical features associated with aggressive tumor behavior.

RESULTS

Sixty hyperthyroid patients who underwent thyroidectomy were included, 12 of whom have thyroid cancer. Each increase in the initial free thyroxine (FT4) leads to increased likelihood of thyroid cancer by 1.02 times (95% CI 1.001-1.03, p=0.044). The presence of thyroid nodule is associated with 24 times (95% CI 2.67-3275.62, p=0.002) higher risk of thyroid cancer, while every unit increase in mm for nodule diameter increases thyroid cancer odds by 1.04 times (95% CI 1.01-1.07, p=0.022). An FNAB pre-op diagnosis of malignancy is associated with having histopathologic diagnosis of thyroid cancer increased by 40 times (95% CI 2.42-6668.98, p=0.007). Although aggressive tumor behavior was noted among those with a younger age on average (36.35 vs 46.75 years), higher initial FT4 (95.97 vs 23.55 pmol/L), and those with sizeable diameter of multinodular goiter (95 mm vs 20 mm), only the high FT4 was statistically significant.

CONCLUSION

Initial FT4, thyroid nodules, nodule size, and pre-operative FNAB finding of a malignancy were the factors associated with thyroid cancer in hyperthyroid patients who underwent thyroidectomy. Furthermore, those with aggressive tumor behavior had higher initial FT4 levels.

Human ; Hyperthyroidism

Primary hyperparathyroidism is characterized by increased secretion of parathyroid hormone, leading to hypercalcemia and skeletal and renal complications. In the past, it was diagnosed when presenting with classical signs and symptoms. Currently, the most common clinical presentation of PHPT is asymptomatic hypercalcemia, often detected by routine screening tests. Due to the changing presentations, the diagnosis can become challenging.

We present BA, a 16-year-old female with a 2-year history of multiple fractures, progressive lytic bone lesions and pain, and kidney stones. She was initially managed as a case of polyostotic fibrous dysplasia. The workup also revealed low levels of vitamin D, hypercalcemia, increased alkaline phosphatase, and elevated intact parathyroid hormones. A neck ultrasound revealed two solid masses posterior to the right thyroid lobe.

She underwent right parathyroidectomy, and a biopsy confirmed a double parathyroid adenoma.

This report also highlights the management of the case in a low-resource setting and the importance of timely diagnosis of primary hyperthyroidism to prevent a delay in the management, which could cause unnecessary pain, bone deformities, and disability.

Human ; Female ; Adolescent: 13-18 Yrs Old ; Parathyroid Hormone ; Parathyroid Neoplasms ; Parathyroidectomy ; Phosphoric Monoester Hydrolases ; Fractures, Multiple ; Hypercalcemia ; Hyperparathyroidism ; Hyperthyroidism

OBJECTIVES

This study aimed to determine the clinical profile of non thyroidal cancer patients with thyroid dysfunction associated with tyrosine kinase inhibitor (TKI) therapy at the University of Santo Tomas Hospital (USTH), Philippines.

METHODOLOGY

This is a retrospective observational study of TKI initiated adult non-thyroidal cancer patients with thyroid function testing from 2013 to 2018.

RESULTS

Forty percent (95% CI: 26.2% - 58.61%) of the sixty individuals who had thyroid function tests (TFT) had incident thyroid dysfunction. Thirty percent had hypothyroidism (i.e., 25% overt [mean TSH 16.64 uIU/mL]; 5% subclinical [mean TSH 6.62 uIU/mL]). The median time at risk was 8 and 16 months for overt and subclinical hypothyroidism, respectively. Fifty-six percent had persistent hypothyroidism (median TSH 16.75, p = 0.009). The average time to recovery of transient hypothyroidism was 39 months. Ten percent had hyperthyroidism with a median time at risk of 1.5 months. Non-small cell lung cancer and renal cell carcinoma were possible associated risk factors of thyroid dysfunction.

CONCLUSION

TKI-induced thyroid dysfunctions are common. Screening and monitoring for thyroid abnormalities during TKI therapy is important.

Tyrosine Kinase Inhibitors ; Hypothyroidism ; Hyperthyroidism

Restless legs syndrome （RLS） is a common sensory-motor disorder of the nervous system， and its mechanism remains unknown， which may be related to neuropsychiatric diseases， nutritional and metabolic diseases， kidney diseases， and pregnancy. We report a special case of RLS which was diagnosed prior to hyperthyroidism and experienced worsening of the RLS symptoms. We aim to discuss the mechanism of hyperthyroidism aggravating RLS， helping clinicians have a better understanding of the influencing factors for RLS.
Hyperthyroidism ; Comorbidity

Objective: To investigate the risk factors of childhood systemic lupus erythematosus (SLE) with thyroid dysfunction and to explore the relationship between thyroid hormone and kidney injury of lupus nephritis (LN). Methods: In this retrospective study, 253 patients who were diagnosed with childhood SLE and hospitalized in the First Affiliated Hospital of Zhengzhou University from January 2019 to January 2021 were enrolled in the case group, and 70 healthy children were the control cases. The patients in the case group were divided into the normal thyroid group and the thyroid dysfunction group. Independent t-test, χ² test, and Mann-Whitney U test were used for comparison between the groups, Logistic regression analysis was used for multivariate analysis, and Spearman correlation. Results: A total of 253 patients, there were 44 males and 209 females in the case group, and the age of onset was 14 (12, 16) years; a total of 70 patients, 24 males and 46 females were in the control group, and the age of onset was 13 (10, 13) years. The incidence of thyroid dysfunction in the case group was higher than that in the control group (48.2% (122/253) vs. 8.6% (6/70), χ²=36.03, P<0.05). Of the 131 patients, there were 17 males and 114 females in the normal thyroid group, and the age of onset was 14 (12, 16) years. Of the 122 patients in the thyroid dysfunction group, 28 males and 94 females were in the thyroid dysfunction group, and the age of onset was 14 (12, 16) years. Of the 122 had thyroid dysfunction, including 51 cases (41.8%) with euthyroid sick syndrome, 25 cases (20.5%) with subclinical hypothyroidism, 18 cases (14.8%) patients with sub-hyperthyroidism, 12 cases (9.8%) with hypothyroidism, 10 cases (8.2%) with Hashimoto's thyroiditis, 4 cases (3.3%) with hyperthyroidism, and 2 cases (1.6%) with Graves disease. Compared to patients with normal thyroid function, the serum level of triglyceride, total cholesterol, urine white blood cell, urine red blood cell, 24 h urine protein, D-dimer, and fibrinogen, ferritin and systemic lupus erythematosus disease activity Index-2000 (SLEDAI-2K) score were higher in patients with thyroid dysfunction (Z=3.07, 3.07, 2.48, 3.16, 2.40, 3.99, 2.68, 2.55, 2.80, all P<0.05), while the serum level of free thyroxine and C3 were lower in thyroid disfunction patients (10.6 (9.1, 12.7) vs. 11.3 (10.0, 12.9) pmol/L, and 0.46 (0.27, 0.74) vs. 0.57 (0.37, 0.82) g/L, Z=2.18, 2.42, both P<0.05). The higher level of triglyceride and D-dimer were the independent risk factors for childhood SLE with thyroid dysfunction (OR=1.40 and 1.35, 95%CI 1.03-1.89 and 1.00-1.81, respectively, both P<0.05). There were 161 patients with LN in the case group, all of which were conducted with renal biopsies, including 11 cases (6.8%) with types Ⅰ LN, 11 cases (6.8%) with typesⅡLN, 31 cases (19.3%) with types Ⅲ LN, 92 cases (57.1%) with types Ⅳ LN, and 16 cases (9.9%) with types Ⅴ LN. There were significant differences in the level of free triiodothyronine and thyroid stimulating hormone among different types of kidney pathology (both P<0.05); compared with types I LN, the serum level of free triiodothyronine was lower in types Ⅳ LN (3.4 (2.8, 3.9) vs. 4.3 (3.7, 5.5) pmol/L, Z=3.75, P<0.05). The serum level of free triiodothyronine was negatively correlated with the acute activity index score of lupus nephritis (r=-0.228, P<0.05), while the serum level of thyroid stimulating hormone was positively correlated with the renal pathological acute activity index score of lupus nephritis (r=0.257, P<0.05). Conclusions: There is a high incidence of thyroid dysfunction in childhood SLE patients. The higher SLEDAI and more severe renal damage were found in SLE patients with thyroid dysfunction compared to these with normal thyroid functions. The risk factors of childhood SLE with thyroid dysfunction are the higher level of triglyceride and D-dimer. The serum level of thyroid hormone is possibly related to the kidney injury of LN.
Child ; Female ; Male ; Humans ; Lupus Nephritis/epidemiology* ; Triiodothyronine ; Retrospective Studies ; Lupus Erythematosus, Systemic/complications* ; Hypothyroidism/epidemiology* ; Hyperthyroidism ; Risk Factors

Studies have demonstrated the detrimental effects of overt hyperthyroidism on sexual functioning.Here,we comprehensively reviewed the studies that focused on the association between overt hyperthyroidism and erectile dysfunction (ED).After the systematic searching for relevant studies,we find that overt hyperthyroidism is significantly associated with the high risk of ED.The prevalence of ED in patients with hyperthyroidism ranges from 3.05% to 85%,while that in general population is 2.16% to 33.8%.A study reported that the erectile functioning of the hyperthyroidism patients was improved (International Index of Erectile Function:22.1±6.9 vs. 25.2±5.1) after the achievement of euthyroidism.The underlying mechanism of the increase in the risk of ED by overt hyperthyroidism might be correlated to the dysfunction of hypothalamus-pituitary-thyroid axis,dysregulation of sex hormones,abnormal expression of thyroid hormone receptors,and psychiatric or psychological disturbances (e.g.,depression,anxiety,and irritability).Since limited clinical trials have been conducted,additional well-designed cohorts with sizable samples are warranted to elucidate the evidence and mechanism of hyperthyroidism predisposing to ED.The present review indicates that overt hyperthyroidism and the risk of ED are associated,which reminds the clinicians should assess the thyroid stimulating hormone in hyperthyroidism patients presenting with ED,especially in those without positive conventional laboratory findings for causing ED.
Male ; Humans ; Erectile Dysfunction/etiology* ; Anxiety ; Hyperthyroidism/complications* ; Thyrotropin