Introduction: Accurate preoperative localization is essential for the surgical management of primary hyperparathyroidism (PHPT). Although ultrasound, technetium-99m sestamibi scintigraphy, and 4D-CT provide high localization rates, a subset of patients have non-localizing or discordant imaging. Selective parathyroid venous sampling (PVS) is an invasive adjunct that measures regional parathyroid hormone (PTH) gradients to aid localization in challenging cases. We present a threepatient case series demonstrating the utility of PVS in diagnostically complex PHPT. Cases: We retrospectively reviewed three female patients (ages 44–63) with biochemically confirmed PHPT who underwent selective PVS following negative or discordant imaging. Venous sampling was performed via femoral access with catheterization of bilateral internal jugular, brachiocephalic, and bilateral thyroidal veins. PTH levels were measured at each site and compared to peripheral levels to identify regional gradients. Surgical findings, intraoperative parathyroid hormone monitoring (IOPTH), histopathology, and postoperative biochemical outcomes were recorded. All patients had non-localizing or discordant preoperative imaging (USG, sestamibi, 4D-CT). PVS identified significant PTH gradients, guiding focused parathyroidectomy. IOPTH monitoring confirmed successful excision in all operated patients. Histopathology confirmed parathyroid adenoma in two cases; in the third case, the parathyroid tissue was identified within the thyroid gland. Postoperative PTH levels suppressed (range 0.79–1.48 pg/mL) in keeping with successful parathyroidectomy. Conclusion PVS effectively lateralized disease in imaging-negative PHPT and directly guided surgical management. When conventional imaging fails, PVS combined with intraoperative PTH monitoring enables targeted surgery and favorable biochemical outcomes.
Humans

Introduction: Hemorrhagic suprarenal masses presenting with hypertensive emergency pose a significant diagnostic challenge, particularly when biochemical and radiological findings are inconclusive. The clinical presentation may mimic catecholamine-secreting tumors, necessitating consideration of a broad differential diagnosis, including pheochromocytoma, adrenocortical carcinoma, retroperitoneal hemorrhage, and hematological-related extramedullary lesions. Accurate diagnosis is essential, as management strategies differ significantly. Case: We report a 48-year-old male smoker with no known prior medical illness who presented with sudden left-sided chest pain radiating to the epigastrium, associated with vomiting. On arrival, he was markedly hypertensive (207/131 mmHg). He reported a 1-year history of paroxysmal palpitations, headaches, migraines, and intermittent diaphoresis. Computed tomography angiography excluded aortic dissection but demonstrated a left retroperitoneal hemorrhage with non-visualization of the adrenal gland, suggestive of adrenal or tumor-related hemorrhage. He was initially managed empirically as a pheochromocytoma while undergoing biochemical evaluation; however, urinary metanephrines were only mildly elevated. Repeat imaging demonstrated interval enlargement of a non-enhancing suprarenal mass, raising concern for tumor-related hemorrhage. Subsequent ultrasonography, however, favored a liquefied hematoma, and percutaneous drainage yielded 750 mL of sanguineous fluid, resulting in marked clinical improvement. Notably, an elevated hematocrit prompted further evaluation for erythrocytosis. Subsequent testing confirmed JAK2 mutation-positive polycythemia rubra vera, providing a unifying explanation for both the erythrocytosis and spontaneous adrenal hemorrhage. The patient was commenced on hydroxyurea and referred for hematology follow-up. Conclusion Adrenal hemorrhage may closely mimic pheochromocytoma in hypertensive emergencies. A systematic, multidisciplinary approach integrating clinical, biochemical, and imaging findings is essential to avoid misdiagnosis and guide appropriate management, particularly in patients with underlying hematological disorders.
Hypertensive Crisis ; Pheochromocytoma ; Polycythemia Vera ; Hematoma

Introduction: Primary adrenal lymphoma (PAL) is a rare extranodal lymphoma, accounting for less than 1% of cases. It often presents with non-specific constitutional symptoms and features of adrenal insufficiency. The absence of pathognomonic findings frequently leads to delayed diagnosis, by which time the disease is often advanced, contributing to poor prognosis. Case: A 59-year-old male with type 2 diabetes mellitus and previously treated pulmonary tuberculosis presented with 1 month of lethargy, anorexia, weight loss, and abdominal pain. He was cachectic but hemodynamically stable (BP 120/81 mmHg; glucose 5.1 mmol/L), with otherwise unremarkable systemic examination. Laboratory evaluation revealed hyponatremia (120 mmol/L), hyperkalemia (6.0 mmol/L), and severe hypercalcemia (4.4 mmol/L). A short Synacthen test confirmed adrenal insufficiency. Computed tomography demonstrated marked bilateral adrenal enlargement with bulky masses (8.9 × 8.7 × 8.7 cm right; 9.9 × 7.6 × 10.2 cm left), suggestive of malignant infiltration. Adrenal protocol imaging revealed indeterminate lesions with attenuation >40 Hounsfield Unit and relative washout <40%. Ultrasound-guided biopsy of the right adrenal gland was performed. The patient was discharged on hydrocortisone replacement with plans for early follow-up. One week later, he presented again in adrenal crisis with severe hypoglycemia (1.1 mmol/L) and cardiovascular collapse. Despite resuscitative efforts, he succumbed. Histopathology subsequently confirmed diffuse large B-cell lymphoma, activated B-cell subtype, consistent with PAL. Conclusion This case highlights the diagnostic pitfalls of PAL, particularly when constitutional symptoms mimic chronic infections such as tuberculosis. It underscores the need for high clinical suspicion in patients with bilateral adrenal masses and adrenal insufficiency. Early recognition, adequate steroid replacement including mineralocorticoid therapy, and prompt tissue diagnosis are critical to prevent rapid deterioration and improve outcomes.
Lymphoma

Introduction: Diabetic ketoacidosis (DKA) is a common complication of type 1 diabetes mellitus (T1DM). Neurological complications of DKA are rare in adults. We report a case of young lady with T1DM who presented with severe DKA and complicated with subarachnoid hemorrhage (SAH). Case: A 19-year-old female was diagnosed with T1DM following an admission for DKA 2 months earlier. Her hemoglobin A1c was 17.2%, and autoimmune markers showed positive anti-glutamic acid decarboxylase (anti-GAD) antibodies (71 IU/mL) with negative anti-insulinoma-associated antigen 2 (anti-IA2) and islet cell antibodies. Her C-peptide level was low at 69 pmol/L. She was discharged with basal bolus insulin analogues, but she defaulted on her medications. She presented to the hospital 2 months later with a history of epigastric pain, vomiting, and breathlessness for 2 days, and was then found unconscious at home. There was no history of trauma. She was intubated for a poor Glasgow Coma Scale (E1V1M1). Blood results showed severe DKA with glucose 25 mmol/L, blood gas pH 6.572, bicarbonate 2.6 mmol/L, and ketone more than 8.8 mmol/L. She was started on insulin infusion and fluid resuscitation. DKA resolved after 24 hours. Computed tomography (CT) of the brain showed SAH in the right frontal and left frontotemporal regions. CT angiography of the brain reported no evidence of an intracranial aneurysm. She was extubated on day 4 of admission. Subsequent cerebral digital subtraction angiography was unremarkable. The patient achieved complete neurological recovery on follow-up. Conclusion This case highlights that severe DKA may rarely be associated with spontaneous SAH, which increases morbidity and mortality. Proposed mechanisms include vascular injury, oxidative stress from severe ketoacidosis, and endothelial dysfunction related to inflammatory mediators. Clinicians should have a high suspicion and consider neuroimaging in DKA patients with unexplained reduced consciousness or atypical neurological findings.

Introduction: Osteoporosis is associated with increased fracture risk, leading to significant morbidity and mortality. Despite established clinical guidelines, a substantial gap remains between recommended and actual prescribing practices. Patients at very high fracture risk have poorer outcomes and are recommended to receive anabolic or parenteral antiresorptive therapies. However, access to these treatments is limited in Malaysian government hospitals due to cost constraints. Methodology: This retrospective clinical audit evaluated osteoporosis treatment prescriptions among very high-risk patients attending the Osteoporosis Endocrine Clinic at Hospital Queen Elizabeth II from 2020 to 2025. Very high fracture risk was defined according to the American Association of Clinical Endocrinologists criteria, including recent fractures, fractures on therapy, multiple fractures, high fall risk, glucocorticoid use, very high FRAX probability (>30% major osteoporotic fracture or >4.5% hip fracture), or very low bone mineral density (T-score <−3.0). Results: A total of 120 patients were included, with a median age of 68 years (interquartile range [IQR] 62–73). Most were of Chinese ethnicity (60%, n = 72), with a median body mass index of 22.6 kg/m² (IQR 19.6–26). Secondary osteoporosis was present in 70% of patients, commonly due to aromatase inhibitor use (45%), glucocorticoid-induced osteoporosis (13.3%), thyroid disorders (10.8%), and vitamin D insufficiency (9.2%). Only 12% of patients (n = 14) received anabolic or parenteral antiresorptive therapy, while 88% (n = 106) were treated with oral alendronate. Among those on alendronate, 19.8% (n = 21) developed adverse outcomes, including treatment failure (n = 13), gastrointestinal side effects (n = 6), and atypical femoral fractures (n = 2). Conclusion The uptake of guideline-recommended therapy in very high-risk osteoporosis patients remains low. A notable proportion of patients treated with oral alendronate experienced adverse outcomes or suboptimal responses. Addressing financial and systemic barriers is crucial to improving access to advanced therapies and optimizing patient outcomes.
Prescriptions ; Osteoporosis

Non-islet cell tumor-induced hypoglycemia (NICTH) secondary to phyllodes tumor is extremely rare but potentially life threatening if not treated promptly. We report a case of a 46-year-old Indian female without underlying diabetes mellitus who presented with a large breast tumor and recurrent severe symptomatic hypoglycemia. Investigations supported the diagnosis of NICTH. The hypoglycemia only resolved after corticosteroids and mastectomy. This case highlights the importance of considering NICTH in the evaluation of patients with voluminous tumor and hypoglycemia.
Hypoglycemia ; Insulin-Like Growth Factor II ; Phyllodes Tumor ; Mastectomy ; Adrenal Cortex Hormones

Thyrotoxicosis is a well-recognized cause of myopathy, but rarely presents as acute flaccid quadriparesis. We report a 25-year-old female with underlying uncontrolled Graves’ disease who presented with thyroid storm and acute flaccid quadriparesis due to thyrotoxic myopathy. She showed marked clinical improvement with subsequent normalization of her thyroid parameters. Besides highlighting this rare association, this report underscores the importance of considering thyrotoxic myopathy in the evaluation of patients with acute flaccid quadriparesis.
Thyroid Crisis ; Quadriplegia