Introduction: Nonfunctioning pituitary adenomas (NFPA) may cause central hypothyroidism due to pituitary compression, often presenting with low thyroid-stimulating hormone (TSH). However, suppressed TSH in this setting should not automatically be attributed to pituitary dysfunction, as primary hyperthyroidism—such as Graves’ disease—may rarely coexist. Distinguishing between these disorders is essential to avoid misdiagnosis and inappropriate management. Case: A 42-year-old female presented with intermittent headache, visual field impairment, palpitations, fine tremors, and weight loss. Physical examination revealed visual field deficits and no goiter. Laboratory evaluation showed cortisol level of 1 µg/dL (normal: 3.7–19.4 µg/dL), luteinizing hormone 1.62 mU/L (normal: 2.4–12.6 mU/L), follicle-stimulating hormone 5.01 mU/L (normal: 3.5–12.5 mU/L), free thyroxine 4 28.32 pmol/L (normal: 12–22 pmol/L), TSH 0.02 µIU/mL (normal: 0.27–4.2 µIU/mL), and prolactin 70.84 ng/mL. Thyrotropin receptor antibody (TRAb) was 3.53 IU/L, confirming Graves’ disease. Contrast-enhanced brain magnetic resonance imaging demonstrated a pituitary macroadenoma (2.13 × 2.28 × 3.05 cm) with optic chiasm compression. The patient was diagnosed with NFPA, Graves’ disease, secondary adrenal insufficiency, possible hypogonadotropic hypogonadism, and hyperprolactinemia likely due to the stalk effect. Preoperative management included hydrocortisone replacement and antithyroid therapy. The patient subsequently underwent transsphenoidal surgery with appropriate perioperative care. Postoperatively, no new pituitary hormone deficiencies were observed. She was maintained on thiamazole 10 mg daily with clinical improvement and remains under regular follow-up. Conclusion This case highlights a rare but clinically important coexistence of NFPA and Graves’ disease. Suppressed TSH in patients with pituitary adenoma should not be assumed to reflect pituitary dysfunction without thorough evaluation. Comprehensive thyroid assessment is crucial to ensure accurate diagnosis and appropriate management.
Pituitary Neoplasms ; Graves Disease

Introduction: Autoimmune thyroid disease is frequently associated with other immune-mediated disorders; however, clinically significant pancytopenia is rare. In patients with Graves’ disease receiving antithyroid therapy, leukopenia raises concern for drug-induced agranulocytosis, a rare but potentially life-threatening complication characterized by severe neutropenia requiring immediate drug withdrawal. The coexistence of hemolytic anemia and thrombocytopenia may instead suggest Evans syndrome, defined by autoimmune hemolytic anemia with immune thrombocytopenia, with or without neutropenia. Importantly, uncontrolled thyrotoxicosis itself may cause immunemediated cytopenias, creating a diagnostic challenge. Case: We report a 55-year-old female with thyroid receptor antibody-positive Graves’ disease who presented with jaundice and pancytopenia while receiving carbimazole therapy. Laboratory evaluation demonstrated anemia with reticulocytosis and a positive direct antiglobulin test, thrombocytopenia and leukopenia. Complement testing revealed reduced C3 with normal C4, consistent with immune-mediated hemolysis. Peripheral blood film showed no blast cells or marrow infiltration, and autoimmune screening, including antinuclear antibodies and anti–double stranded DNA, was negative. The coexistence of Coombs-positive hemolysis and thrombocytopenia initially raised suspicion for Evans syndrome, while leukopenia during carbimazole therapy prompted concern for drug-induced agranulocytosis. However, neutropenia was not severe, and the absence of marrow infiltration or systemic autoimmune disease made alternative causes of pancytopenia less likely. Importantly, blood counts progressively improved following the optimization of thyroid control despite continuation of carbimazole at a reduced dose, without the use of immunosuppressive therapy. This clinical course supported the interpretation of thyrotoxicosis-associated immune cytopenia rather than primary Evans syndrome or carbimazole-induced agranulocytosis. Conclusion This case highlights thyrotoxicosis-associated immune cytopenia as an important mimic of Evans syndrome and carbimazole-related hematological toxicity. Recognizing this entity is essential to avoid unnecessary discontinuation of antithyroid therapy or inappropriate immunosuppressive treatment.
Evans Syndrome ; Carbimazole ; Pancytopenia ; Agranulocytosis ; Graves Disease

Introduction: Graves’ disease is associated with various hematological abnormalities, including anemia, leucopenia, and thrombocytopenia. However, pancytopenia involving all three cell lines is a rare and often under-recognized manifestation of thyrotoxicosis. We present a case of newly diagnosed Graves’ disease complicated by pancytopenia, in which cell counts normalized rapidly following carbimazole initiation. Case: A 51-year-old female with underlying type 2 diabetes mellitus, hypertension, and dyslipidemia presented with dysphagia for 3 months, significant weight loss (from 95 to 75 kg over 6 months), and a 1-week history of fever, palpitations, tremors, orthopnea, and bilateral lower limb swelling. On examination, she was febrile (38.2°C) with bibasal crepitations, pitting edema up to the midshins, bilateral hand tremors, and a multinodular neck mass moving with deglutition. Investigations confirmed thyrotoxicosis (thyroid-stimulating hormone [TSH] 0.01 mIU/L, free T4 130.1 pmol/L, T3 >30.8 pmol/L) with positive autoantibodies (thyroid receptor antibody 31.9 IU/L, anti-thyroid peroxidase 195 IU/mL). Full blood count showed pancytopenia: white cell count 2.73 × 10⁹/L, hemoglobin 10.3 g/dL, and platelets 108 × 10⁹/L. Peripheral blood film suggested normocytic normochromic anemia with leucopenia and thrombocytopenia. Chest radiography showed cardiomegaly with fluid overload, and echocardiography revealed an ejection fraction of 77%. She was treated for impending thyroid storm secondary to pneumonia with Lugol’s iodine, hydrocortisone, propylthiouracil, and intravenous antibiotics. She was discharged on day 3 with a transition to carbimazole. At outpatient follow-up approximately 9 days later, thyroid function had improved significantly (free thyroxine 4 reduced from 130.1 to 29.34 pmol/L with suppressed TSH), and repeat full blood count demonstrated complete normalization of all three cell lines. Conclusion This case illustrates that pancytopenia can be a direct consequence of severe thyrotoxicosis and may reverse completely with effective antithyroid therapy. The temporal relationship between biochemical improvement and hematological recovery supports a causal link. Clinicians should be aware of this rare association to avoid misdiagnosis and unnecessary invasive investigations.
Pancytopenia ; Graves Disease ; Thyrotoxicosis

Introduction: Beta-blockers are frequently used as adjunctive therapy in hyperthyroidism to manage adrenergic symptoms, yet their potential to precipitate secondary Raynaud’s phenomenon remains under-recognized. This adverse effect is attributed to β2-adrenoceptor blockade, which impairs peripheral vasodilation and promotes reflex vasoconstriction. Nonselective agents such as propranolol carry this particular risk. Case: A 22-year-old female presented with a 6-month history of palpitations, 11 kg weight loss, and fine tremors. There was no personal or family history of autoimmune or connective tissue disease. She denied any malar rash, joint swelling, alopecia, myopathy, oral ulcers, or uveitis. She also denied using any supplements or any herbal or traditional remedies. Examination revealed tachycardia, fine tremors, and Graves’ ophthalmopathy, but no acropachy or organomegaly. Investigations confirmed Graves’ disease: Free T4 of 73 pmol/L, thyroid-stimulating hormone <0.05 mIU/L, with elevated anti-thyroid peroxidase and antithyroglobulin antibodies. Full blood count, renal, and liver function were unremarkable. She was commenced on carbimazole 20 mg daily and propranolol 40 mg three times daily. After 8 months of treatment, she developed cold-induced digital color changes and skin tightening consistently, suggestive of Raynaud’s phenomenon. Dose reduction of propranolol to 20 mg BD only yielded partial improvement. Propranolol was subsequently substituted with verapamil, a nondihydropyridine calcium channel blocker, resulting in significant resolution of Raynaud’s phenomenon. Conclusion Propranolol-induced Raynaud’s phenomenon is an underrecognized complication in the management of Graves’ disease, and this case illustrates that it may develop insidiously after months of therapy and can persist despite dose reduction. Substitution with verapamil achieves rate control without β2-adrenergic antagonism. Clinicians should maintain a low threshold for recognizing this adverse effect and consider early substitution with verapamil in affected patients. While verapamil does not confer the same adrenergic blockade as propranolol, its vasodilatory properties make it a rational and effective alternative in this context.
Raynaud Disease ; Graves Disease

Introduction: Cystic fibrosis (CF) is an autosomal recessive disorder caused by mutations in the CFTR gene. Complications such as cystic fibrosis–related diabetes (CFRD) are well recognized. The association between CF and autoimmune thyroid disease, however, is rare and poorly understood. We report a case of CFRD complicated by Graves’ disease. Case: A 22-year-old male was diagnosed with CF at age 5, confirmed by a positive sweat chloride test. Following the diagnosis, lifelong pancreatic enzyme replacement therapy (Creon) was initiated to treat exocrine pancreatic insufficiency. In 2021, he developed type 3c diabetes, attributed to endocrine pancreatic insufficiency, and required regular basal insulin therapy. In early 2024, he developed hypokalemic periodic paralysis with proximal myopathy, despite potassium correction, and was admitted to the hospital. On admission, examination revealed a fine tremor and diffuse bilateral neck swelling. Biochemical evaluation showed thyrotoxicosis with Free T4 of 37 pmol/L and thyroid-stimulating hormone (TSH) <0.01 mIU/L. He started a tapering dose of carbimazole and propranolol. An urgent neck ultrasound showed a heterogeneous thyroid parenchyma with increased vascularity and no nodules. Elevated anti-thyroid peroxidase (anti-thyroid peroxidase, >600 IU/mL) and TSH receptor antibodies (thyrotropin receptor antibody, 2.57 IU/L) confirmed a diagnosis of Graves’ disease. During follow-ups, he had issues with compliance with the antithyroid therapy. However, the latest thyroid function test in February 2026 showed Free T4 of 20.5 pmol/L with suppressed TSH of <0.01 mIU/L. He remains clinically euthyroid throughout the follow-up. Conclusion This case highlights a rare but clinically relevant coexistence. Clinicians managing symptomatic CF patients should vigilantly screen for thyroid dysfunction to ensure early diagnosis and timely intervention. Early recognition and treatment may improve patient outcomes. Further research is needed to clarify the immunological link between CF and autoimmunity.
Cystic Fibrosis ; Graves Disease

Introduction: Graves’ disease is typically managed with antithyroid drugs (ATDs) and beta-blockers like propranolol. While allergic reactions to ATDs are common, beta-blockers are rarely identified as allergens. Case: A 42-year-old female with Graves’ disease was started on carbimazole 5 mg daily and propranolol 40 mg daily. She developed mild itchiness, which was tolerable. One month later, liver enzyme derangement led to the discontinuation of carbimazole. Propylthiouracil (PTU) 300 mg daily was initiated while continuing propranolol, but caused generalized urticaria, necessitating its cessation. Prednisolone was started, but her thyroid function worsened. Alternative therapies were proposed but declined by the patient. Upon resolution of urticaria, PTU was reintroduced at 50 mg daily without adverse effects, and propranolol was discontinued. Her cutaneous symptoms did not recur, implicating propranolol as the allergen. Conclusion In hyperthyroidism, increased hepatic clearance reduces plasma propranolol levels, minimizing the risk of adverse effects. However, as thyroid function normalizes, propranolol clearance slows, leading to drug accumulation and increased susceptibility to side effects. Clinicians should consider all medications as potential allergens and understand how thyroid states affect drug metabolism to optimize treatment.
Graves Disease ; Allergens

Introduction: Neuropsychiatric manifestations of thyrotoxicosis range from mild anxiety to severe psychosis. While the BurchWartofsky Point Scale (BWPS) reliably identifies systemic thyroid storms, an isolated “cerebral storm”—where profound thyrotoxic encephalopathy presents without peripheral autonomic signs—remains a diagnostic challenge. This case highlights the neuromodulatory pathogenesis of thyrotoxic psychosis and the critical role of biochemical control for psychiatric resolution. Case: A 31-year-old male with Graves’ disease and poor medication adherence presented with a 2-week history of aggressive behavior and auditory hallucinations. Initial investigations revealed overt thyrotoxicosis (thyroidstimulating hormone <0.01 mIU/L; free thyroxine 4 (FT4) 59.53 pmol/L) and an unremarkable computed tomography brain. Despite his severe neuropsychiatric decompensation, a BWPS of 20 precluded a clinical diagnosis of systemic thyroid storm. His symptoms remained refractory to aggressive psychotropic polypharmacy, including haloperidol, olanzapine, lithium, and diazepam. Management was therefore focused on the underlying thyrotoxicosis with an optimized antithyroid regimen of carbimazole and propranolol. Clinical resolution of psychotic symptoms was achieved only after FT4 declined significantly to 20.46 pmol/L, allowing the successful tapering of all psychiatric medications. He was discharged in a stable, clinically euthyroid state with integrated medical and psychiatric follow-up. Conclusion The failure of standard antipsychotics suggests that thyrotoxic psychosis is driven by distinct neuromodulatory mechanisms rather than primary dopaminergic dysfunction. The chronic thyrotoxic state secondary to prolonged treatment non-adherence likely upregulates and sensitizes dopamine receptors while simultaneously suppressing inhibitory GABAergic pathways. This neurochemical imbalance lowers the neurological threshold, precipitating an isolated cerebral storm. This case illustrates the limitations of the BWPS in purely neuropsychiatric presentations and reinforces that restoring euthyroidism is the definitive treatment for thyrotoxic psychosis.
Graves Disease ; Psychotic Disorders

We report a case of an uncommonly aggressive presentation of the rare entity of synchronous papillary (PTC) and follicular thyroid carcinomas (FTC) in a 67-year-old woman initially presenting with thyrotoxicosis from Graves’ disease. She was found to have two thyroid nodules with extensive intra-cardiac tumour thrombus, symptomatic left pelvis bony metastasis with pathological fracture, pulmonary metastases and mediastinal lymph node metastases. Further investigations suggested a diagnosis of synchronous papillary and metastatic follicular thyroid cancer. Treatment with radical surgery followed by adjuvant therapeutic radioiodine ablation was proposed, but the patient declined all forms of cancer-specific therapy and was elected solely for a palliative approach to treatment. We discuss the diagnostic considerations in arriving at the diagnosis of synchronous thyroid malignancy – in this case the clear features of PTC and the strong probability of FTC due to invasiveness and metastatic follicular lesions. This case underscores potential limitations of the ACR TI-RADS system, notably with certain ultrasonographic features suggesting malignancy that might not be adequately captured. Notably, the aggressive presentation of DTC in this case may be contributed by the concurrent presence of Graves’ Disease, suggesting heightened vigilance when assessing potential thyroid malignancies in such patients.
Papillary Thyroid Carcinoma ; Thyroid Cancer, Papillary ; Follicular Thyroid Carcinoma ; Adenocarcinoma, Follicular ; Graves Disease

Humans ; Child ; Methimazole/adverse effects* ; Graves Disease/drug therapy*

OBJECTIVE: To report the clinical and genetic characteristics of a rare case of Gitelman syndrome with comorbid Graves disease and ACTH-independent adrenocortical adenoma. METHODS: A patient who had presented at the Nanchong Central Hospital on December 21, 2020 was selected as the study subject. Clinical data of the patient was collected. Whole-exome sequencing was carried out on DNA extracted from peripheral venous blood samples from the patient and her family members. RESULTS: The patient, a 45-year-old woman, was found to have Graves disease, ACTH-independent Cushing syndrome, hypokalemia and hypomagnesemia following the discovery of an adrenal incidentaloma. MRI scan had revealed a 3.8 cm × 3.2 cm mass in the left adrenal gland. The mass was removed by surgery and confirmed as adrenocortical adenoma. DNA sequencing revealed that the patient and her sister have both harbored compound heterozygous variants of the SLC12A3 gene, namely c.1444-10(IVS11)G>A and c.179(exon1)C>T (p.T60M), which were respectively inherited from their father and mother. Based on the guidelines from the American College of Medical Genetics and Genomics (ACMG), the c.1444-10(IVS11)G>A and c.179(exon1)C>T (p.T60M) were respectively classified as a variant of uncertain significance (PM2_Supporting+PP3) and a likely pathogenic variant (PM3_Strong+PM1+PP3). CONCLUSION The conjunction of Gitelman syndrome with Graves disease and adrenal cortex adenoma is rather rare. The newly discovered c.1444-10(IVS11)G>A variant of the SLC12A3 gene, together with the heterozygous variant of c.179(exon1)C>T (p.T60M), probably underlay the pathogenesis in this patient.
Humans ; Female ; Middle Aged ; Gitelman Syndrome/genetics* ; Adrenocortical Adenoma ; Hypokalemia ; Graves Disease/genetics* ; Mothers ; Mutation ; Solute Carrier Family 12, Member 3