Introduction: The identification of a significant adrenal mass in a patient without a biopsy-confirmed malignancy poses a diagnostic challenge: Is it a metastatic lesion or an underlying adrenal condition? Adrenal metastases are the second most common site of spread for lung adenocarcinoma; approximately 3–7% of adrenal masses represent benign adenomas. Diagnosis is even harder if there are signs of primary aldosteronism (PA). Case: We present a case of a 62-year-old Chinese female with a 10-year history of hypertension, managed on dual antihypertensive therapy, who presented for evaluation of suspected PA following the discovery of hypokalemia. Biochemical screening revealed an elevated aldosteronerenin ratio (ARR, 65). The overnight dexamethasone suppression test (20 nmol/L) and testosterone (0.79 nmol/L) were both within normal limits. Saline Suppression Test (SST) showed an indeterminate post-infusion aldosterone level (202.8 pmol/L). Cross-sectional imaging via computed tomography (CT) Adrenals identified a large, 6.4 × 5.4 × 6.2 cm heterogeneous left suprarenal mass with a low mean attenuation (8.6 Hounsfield Unit [HU]). Concurrently, an incidental left upper lobe pulmonary lesion was identified, and PET-CT was performed; the SUVmax of the lung was identical to that of the adrenal lesion. An ultrasoundguided biopsy of the pulmonary lesion confirmed estimated glomerular filtration rate-mutation-positive lung adenocarcinoma. The patient started on targeted therapy with dacomitinib. Follow-up CT imaging at 9 months demonstrated disease progression within the thorax, marked by the appearance of a new pulmonary nodule. Notably, however, the adrenal mass remained stable in size and morphology. Conclusion The absence of mixed androgen/glucocorticoid hypersecretion, combined with the radiographically static nature of the mass, suggests a lower probability of adrenocortical carcinoma. This case highlights that while size is a major risk factor for adrenocortical carcinoma, it must be interpreted in conjunction with hormonal activity, HU, and growth patterns. Identifying these “mimics” helps avoid over-staging lung cancer and ensures patients receive targeted therapy instead of unnecessary adrenalectomies.

Introduction: Paragangliomas are rare neuroendocrine tumors arising from extra-adrenal chromaffin cells, with an estimated incidence of 2–8 cases per million per year. These tumors originate from neural crest–derived cells of the sympathetic and parasympathetic paraganglia and may secrete catecholamines, resulting in malignant hypertension or symptoms such as headache, palpitations, and diaphoresis. They can occur anywhere along the paravertebral and para-aortic regions from the skull base to the pelvic floor. Case: We report a case of a 14-year-old male with no known premorbid conditions who presented with presyncope and a 1-month history of headache. On examination, he had severe hypertension (242/167 mmHg), tachycardia (127 bpm), and grade IV hypertensive retinopathy. Investigations showed preserved renal function with markedly elevated 24-hour urinary metanephrines (normetanephrine 90.75 µmol/L). Computed tomography revealed a lobulated, heterogeneously enhancing mass measuring 5.0 × 6.1 × 5.4 cm along the left margin of the abdominal aorta at the infrarenal level, suggestive of an extra-adrenal lesion. Gallium-68 PET scan demonstrated a somatostatin receptor–avid left peritoneal mass. The patient underwent exploratory laparotomy and tumor excision, complicated intraoperatively by blood pressure lability requiring nitroprusside and inotropic support. Postoperatively, he improved significantly and was able to wean off all antihypertensive medications. Histopathology confirmed left retroperitoneal paraganglioma. Conclusion Primary peritoneal paraganglioma is a rare but important cause of secondary hypertension, especially in young patients presenting with hypertensive emergency. High index of suspicion is essential for early diagnosis. Management requires a multidisciplinary approach with careful preoperative optimization to minimize perioperative complications. Surgical resection remains the definitive treatment and, as demonstrated in this case, can result in marked clinical improvement with resolution of hypertension.
Paraganglioma

Introduction: Brown tumors, also known as osteitis fibrosa cystica, are focal bone lesions resulting from increased osteoclastic activity and fibroblastic proliferation. They represent a rare complication of uncontrolled hyperparathyroidism (HPT) and may affect any part of the skeleton, including craniofacial bones. Case: We report a case of a 31-year-old Malay female diagnosed with primary HPT secondary to multiglandular disease, who initially presented with symptomatic hypercalcemia. Biochemical evaluation revealed elevated corrected calcium (2.84 mmol/L; reference range 2.2–2.6 mmol/L), low phosphate (0.63 mmol/L; reference range 0.8–1.6 mmol/L), and markedly elevated serum intact parathyroid hormone (iPTH) (286 pg/mL; reference range 14.9–56.9 pg/mL). Ultrasound parathyroid showed a large right extrathyroidal lesion, most likely suggestive of parathyroid adenoma, where sestamibi scan suggested multiglandular parathyroid adenomas with possible mediastinal involvement. She underwent exploratory parathyroidectomy on 19 June 2024, with excision of bilateral inferior parathyroid adenomas confirmed on histopathology. Despite surgery, she had persistent hypercalcemia (2.8–3.1 mmol/L) and rising iPTH levels (307 pg/mL on 24 June 2024, increasing to 413 pg/mL by 2 September 2024), consistent with persistent disease. Repeat imaging demonstrated hyperfunctioning parathyroid tissue in the anterior mediastinum. Subsequently, the patient developed progressive enlargement of the left upper gingiva associated with significant pain during mastication. Clinical and radiological evaluation revealed aggressive lesions with cortical expansion. Excisional biopsy of the gingival lesion confirmed the diagnosis of brown tumors involving the jaws. She later underwent a second parathyroidectomy with intraoperative parathyroid hormone monitoring at another centre. Postoperatively, normalization of serum calcium and iPTH levels was achieved, which led to marked clinical improvement and regression of the craniofacial brown tumor. Conclusion This case highlights that skeletal manifestations of HPT, including brown tumors, may regress following adequate biochemical control without additional local therapy. Early recognition and definitive surgical management of persistent or ectopic hyperfunctioning parathyroid tissue are essential to prevent progression and promote spontaneous bone healing processes.

Introduction: Accounting for less than 2% of all pituitary adenomas, TSHsecreting pituitary adenomas (TSHoma) are an uncommon cause of hyperthyroidism. Majority are macroadenomas with delayed diagnosis as most patients are unwittingly treated for primary hyperthyroidism. Recurring discordant thyroid function test (TFT) with elevated thyroidstimulating hormone (TSH) and Free T4 is a hint and warrants additional investigation to facilitate diagnosis. Case: We report a case of a 48-year-old female who was treated for primary hyperthyroidism since her late 20s with multiple admissions for recurrent congestive heart failure and atrial fibrillation. The cardiac issue was preceded by worsening thyrotoxicosis. Previous thyroid autoantibodies were negative. Of note, she had recurring discordant TFT results from two different assays (TSH:84.7, free thyroxine 4 [FT4]:75.43) (TSH:37.86, FT4:27.34) during admission, excluding assay interference and prompting toward TSHoma or Resistance to Thyroid Hormone (RTH). Examination revealed a large goiter (10 × 8 cm) hard in consistency, and pansystolic murmur over tricuspid area. No thyroid eye disease nor bitemporal hemianopia or clinical sign of acromegaly. Echocardiography showed dilated left atrium and mild to moderate tricuspid regurgitation with preserved ejection fraction. Thyroid-releasing hormone (TRH) stimulation test demonstrated blunted TSH response confirming TSHoma. Anterior pituitary hormone profile revealed normal insulin-like growth factor-1 level with suppressed sex hormones and prolactin, thus excluding co-secreting hormone. Sex hormone-binding globulin level, α-subunit, and T3 suppression test were not done due to unavailability. Magnetic resonance imaging pituitary uncovered pituitary mass measuring (2.6 × 3.3 × 2.2 cm) suggestive of macroadenoma with encasement of cavernous internal carotid arteries and cavernous sinus compression. Computed tomography neck revealed diffuse thyroid enlargement with compressive mass effects onto adjacent structure with trachea narrowing. After discussing with a multidisciplinary team, we planned her for total thyroidectomy followed by transsphenoidal surgery. Conclusion Late presentation and diagnosis in TSHoma remain a major challenge. TFT interpretation is fundamental in identifying the causes of secondary hyperthyroidism to avert detrimental sequalae and to guide optimal treatment.
Atrial Fibrillation ; Thyrotropin

Primary hyperparathyroidism (PHPT) is rare in pregnancy. This condition is challenging to diagnose and manage due to the limited diagnostic and therapeutic options that are safe during pregnancy. If not diagnosed and managed in a timely manner, serious maternal and foetal complications may occur. We report two cases, one with surgical intervention and one without, to show the importance of timely surgical intervention and discuss the challenges in the management of PHPT in pregnancy.
Hyperparathyroidism, Primary ; Pregnancy