Introduction: Pheochromocytoma is a catecholamine-secreting adrenal tumor associated with major perioperative hemodynamic instability. When concurrent major pelvic pathology requires surgery, operative planning becomes particularly challenging. We describe the successful single-stage management of pheochromocytoma and a giant uterine fibroid, highlighting the importance of multidisciplinary coordination and perioperative optimization. Case: A 49-year-old female with symptomatic uterine fibroid was found to have proliferative endometrium on a pipelle biopsy. Computed tomography (CT) abdomen incidentally detected a right adrenal mass alongside a large posterior uterine fibroid (11.9 × 17.4 × 14.6 cm). CT adrenal protocol demonstrated a heterogeneously enhancing right adrenal mass (6.9 × 6.9 × 9.6 cm) with high unenhanced attenuation. Biochemical evaluation revealed markedly elevated 24-hour urinary metanephrine (4.7× upper limit) and normetanephrine (2.4× upper limit). Following multidisciplinary discussions, a single-stage surgical approach was planned after careful assessment of feasibility and perioperative risk in view of the uncertain malignant potential of the pelvic mass and to minimize repeated exposure to anesthesia. Preoperative optimization included transitioning from terazosin to phenoxybenzamine, with subsequent addition of bisoprolol for hemodynamic control. The operative strategy prioritized pheochromocytoma resection first, given its potential for significant hemodynamic instability. Progression to hysterectomy was contingent upon achieving adequate intraoperative hemodynamic stability following adrenalectomy, with continuous reassessment by the anesthetic and surgical teams. Right adrenalectomy was performed first, followed by total abdominal hysterectomy with bilateral salpingooophorectomy. Significant hemodynamic lability occurred during tumor manipulation, with hypertensive surges managed using sodium nitroprusside and remifentanil infusions. Following adrenal vein ligation and tumor removal, hypotension was managed with noradrenaline and additional adrenaline support as required. Total operative time was approximately 6 hours. Postoperatively, transient noradrenaline support was required but was rapidly weaned as hemodynamic stability was achieved. Conclusion Single-stage adrenalectomy and major pelvic surgery can be safely performed in selected patients with pheochromocytoma when guided by meticulous preoperative optimization, clear intraoperative sequencing, and close multidisciplinary coordination.
Pheochromocytoma ; Adrenalectomy ; Leiomyoma ; Hysterectomy

Introduction: Adrenal incidentalomas are increasingly detected with the widespread use of imaging, whereby the large or heterogeneous lesions often raise concern for adrenocortical carcinoma (ACC). However, certain rare benign and infectious conditions may closely mimic malignant features, posing a diagnostic challenge. Case: A 64-year-old female with diabetes mellitus, hypertension, and dyslipidemia was noted to have progressively rising alkaline phosphatase during routine follow-up. She had non-specific gastrointestinal symptoms. A computed tomography abdomen pelvis showed a large, lobulated mass at the left flank, likely of adrenal origin. An adrenal protocol computed tomography revealed a large, heterogeneously enhancing left suprarenal mass measuring 10.7 × 10.3 × 10.7 cm, with a plain-phase attenuation of +81 Hounsfield Unit and absolute (28%) and relative (18%) washout. The right adrenal gland was normal, with no evidence of distant metastasis. Hormonal evaluation showed normal 24-hour urinary metanephrines, excluding pheochromocytoma. The overnight dexamethasone suppression test demonstrated cortisol of 89 nmol/L, suggestive of mild autonomous cortisol secretion, without clinical features of overt hypercortisolism. DHEA was low (0.371 µmol/L), and adrenocorticotropic hormone was suppressed (1.26 pg/mL). Evaluation for primary aldosteronism was not done due to the absence of resistant hypertension or hypokalemia. The gonadotropin profile was consistent with postmenopausal status (follicle-stimulating hormone (89 IU/L) and luteinizing hormone (28.9 IU/L) with low estradiol. The patient underwent open left adrenalectomy. Histopathology revealed an adrenal cavernous hemangioma with extensive hemorrhage and infarction, alongside necrotizing granulomatous inflammation with numerous intracellular fungal organisms and narrow-based budding yeast forms, highly suggestive of histoplasmosis, with no evidence of malignancy. She was subsequently comanaged with infectious disease team and commenced on intravenous amphotericin B. Conclusion This is a rare coexistence of an adrenal hemangioma and histoplasmosis, presenting as a large adrenal mass mimicking ACC. The limitations of imaging in differentiating benign from malignant adrenal lesions are revealed and emphasize the role of histopathological confirmation. Increased awareness of such entities can support the diagnosis and management.
Neoplasms

Introduction: Diabetic ketoacidosis (DKA) and thyroid storm are individually rare but potentially fatal endocrine crises in pregnancy. Each carries significant maternal and fetal morbidity, with mortality risk compounded when they occur concomitantly. Physiological and pharmacokinetic changes of pregnancy, combined with overlapping symptoms, necessitate urgent treatment strategies. Case: A 29-year-old G2P2 female at 29 weeks’ gestation, with poorly controlled type 2 diabetes mellitus (hemoglobin A1c 8.1%) on a basal–bolus insulin regimen and Graves’ disease managed with carbimazole, non-adherent to medications, presented with fever, vomiting, and dyspnea. On examination, she was tachycardic (HR 138 bpm), hypotensive (BP 94/60 mmHg), and hypoxic. Laboratory investigations revealed hyperglycemia (glucose 27.1 mmol/L), severe metabolic acidosis (pH 7.02, bicarbonate 4.9 mmol/L), and elevated serum ketones (4.6 mmol/L), consistent with DKA. Thyroid function tests showed suppressed thyroid-stimulating hormone (<0.005 mIU/L) and elevated free T4 (28.2 pmol/L), with a Burch–Wartofsky score of 70. Unfortunately, intrauterine fetal demise was confirmed upon the patient’s presentation to the emergency department. She was intubated and admitted to the intensive care unit, receiving fluid resuscitation judiciously according to the DKA regimen, with frequent assessment of volume status. Intravenous insulin and potassium supplements were commenced concurrently. Metabolic stabilization was achieved within 24 hours. Carbimazole, propranolol, Lugol’s iodine, and intravenous hydrocortisone were started for treatment of thyroid storm. A breech-assisted vaginal delivery was performed, and her postpartum course was uneventful. Conclusion The case reveals the catastrophic potential of concurrent DKA and thyroid storm in pregnancy, where rapid maternal deterioration and poor fetal outcomes can occur despite timely intervention. High clinical suspicion, early biochemical confirmation, and coordinated multidisciplinary management are vital. Precipitating factors, particularly medication non-adherence, must be addressed through intensive patient education and structured follow-up to prevent recurrence.
Female ; Pregnancy ; Diabetic Ketoacidosis ; Thyroid Crisis

Introduction: Primary hyperparathyroidism (PHPT) is frequently asymptomatic or detected incidentally; however, delayed diagnosis may lead to severe skeletal complications. Early recognition is essential, as timely identification and management of parathyroid disease can prevent significant morbidity, although diagnosis may be challenging when clinical and imaging findings are inconclusive. Case: A 46-year-old female with severe bilateral hearing impairment presented to the orthopedic clinic with 3 years’ history of bilateral knee pain and was found to have a right intertrochanteric femur fracture following minimal trauma. She was referred for evaluation of suspected secondary osteoporosis. She has had intermittent constipation and long-standing oligomenorrhea since menarche. There was no history of childhood fractures or use of medications affecting bone metabolism. Examination revealed bilateral knee bowing. Initial evaluation considered metabolic bone disease, including Paget’s disease; however, skeletal survey showed no features suggestive of Paget’s disease or multiple myeloma. Biochemical investigations demonstrated persistent hypercalcemia (2.65–3.1 mmol/L) with inappropriately elevated intact parathyroid hormone (peak 7.62 pmol/L), consistent with PHPT. Serum phosphate was low-normal. Concomitant vitamin D deficiency (25-OH vitamin D 34.46 nmol/L) improved following replacement. Bone mineral density confirmed severe osteoporosis (lumbar spine T-score −5, z-score -4.1); (forearm −6.7, z-score -6.1) reflecting prolonged untreated disease. Neck ultrasound demonstrated a mixed solid-cystic lesion posterior to the right thyroid lobe, suggestive of a parathyroid adenoma. The TC-99 m Sestamibi scan showed no definite focal uptake. However, subsequent SPECT-CT revealed focal tracer uptake at the posterior right thyroid gland, consistent with a hyperfunctioning parathyroid gland. Parathyroidectomy was done. Postoperatively, the calcium level normalized. Conclusion Severe osteoporosis and fragility fracture occur, reflecting prolonged exposure to excess parathyroid hormone and significant skeletal morbidity. Early biochemical evaluation in unexplained severe osteoporosis is essential, as timely diagnosis and definitive management of parathyroid disease are critical to halt ongoing bone loss and prevent irreversible complications.
Hyperparathyroidism, Primary ; Osteoporosis

Introduction: Pituitary apoplexy is an acute endocrine emergency, as early recognition may influence the outcomes, often presenting with sudden headache, visual disturbances, ocular palsies, vomiting, or altered consciousness. Given that urgent surgical decompression is a common management, emerging evidence supports corticosteroid therapy in our patient with significant neuro-ophthalmic deficits. Case: A 65-year-old male with hypertension, dyslipidemia, type 2 diabetes mellitus, chronic kidney disease stage III, and ischemic heart disease presented with a 4-day history of fever, vomiting, bifrontal headache, and generalized abdominal pain. Initially, he was treated for presumed intraabdominal sepsis. On day 3 of admission, he developed acute right-sided complete ptosis with ophthalmoplegia involving cranial nerves III, IV, and VI. Prior to that, he had also reduced morning erections for 6 months before presentation. Biochemical evaluation revealed markedly reduced total testosterone (0.33 nmol/L) with inappropriately low–normal gonadotropins (luteinizing hormone 1.5 IU/L, follicle-stimulating hormone 2.3 IU/L), in keeping with secondary hypogonadism. Adrenocorticotropic hormone was suppressed, indicating secondary adrenal insufficiency. Thyroid function was preserved. Overall findings suggested partial hypopituitarism. Magnetic resonance imaging confirmed a cystic pituitary lesion measuring 1.4 × 2.6 × 1.8 cm with cavernous sinus involvement and features of pituitary apoplexy. His Pituitary Apoplexy Score was 4. He was offered surgical intervention but was not keen. He was treated with intravenous hydrocortisone, with rapid clinical improvement, including near-complete resolution of right eye ptosis and restoration of extraocular movements within 3 days, and was able to recover without surgery. The hydrocortisone was gradually tapered, and the patient was discharged well with Endocrine follow-up. Conclusion Timely corticosteroid therapy alone can result in rapid, near-complete neurological recovery in pituitary apoplexy, even with multiple cranial nerves involvement. In carefully selected patients without visual field compromise, conservative management may safely obviate the need for urgent surgical intervention, emphasizing the importance of early recognition and individualized treatment strategies.
Hydrocortisone ; Pituitary Apoplexy

Introduction: Painful Hashimoto's thyroiditis is a rare and atypical form of autoimmune thyroid disease characterized by thyroid pain and tenderness. It can closely resemble subacute thyroiditis and must be distinguished from other causes of thyroid pain, including hemorrhage into a cyst and thyroid abscess. This distinction is particularly important in pregnancy, where radionuclide imaging is not recommended. Case: A 27-year-old pregnant female (G4P3) at 24 weeks’ gestation, with Southeast Asian ovalocytosis and dietcontrolled gestational diabetes, was diagnosed with primary hypothyroidism at 14 weeks following evaluation of a painless goiter. Initial tests showed markedly elevated thyroid-stimulating hormone (>150 mIU/L), low free thyroxine (3.5 pmol/L), and positive anti-thyroid peroxidase antibodies (319 IU/mL), consistent with Hashimoto's thyroiditis. Levothyroxine therapy achieved biochemical euthyroidism. At 24 weeks, she developed acute right-sided anterior neck pain radiating to the ear, with dysphagia, odynophagia, and fever. Examination revealed a tender thyroid without lymphadenopathy. Ultrasound demonstrated diffuse enlargement with bilateral ill-defined hypoechoic avascular areas. Inflammatory markers showed markedly elevated C-reactive protein (184 mg/L) with a normal erythrocyte sedimentation rate (16 mm/h), while thyroid function remained within target range. Imaging and clinical findings made abscess and hemorrhage unlikely. The presence of pre-existing autoimmune thyroid disease, antibody positivity, and hypothyroidism before symptom onset supported painful Hashimoto's thyroiditis over subacute thyroiditis. This case highlights that normal thyroid function tests do not necessarily indicate disease remission, as inflammatory activity may persist independently of hormone levels. Conclusion Painful Hashimoto's thyroiditis should be considered in pregnant patients with known autoimmune thyroid disease presenting with acute thyroid pain despite normal thyroid function. Diagnosis requires integration of clinical, biochemical, and imaging findings to guide appropriate management.
Female ; Pregnancy ; Thyroiditis, Subacute

Introduction: Muscle weakness in thyroid disease is commonly attributed to thyrotoxic myopathy or hypokalemic periodic paralysis. Nevertheless, autoimmune conditions such as idiopathic inflammatory myopathies (IIM) and myasthenia gravis (MG) should be considered, as they may coexist with Graves’ disease. Case: A 54-year-old female with hypertension and Graves’ disease, treated with carbimazole for 2 years, had her therapy discontinued after remission. She was restarted on low-dose carbimazole following symptom recurrence. Three weeks later, she developed progressive proximal weakness, dysphagia, hoarseness, anorexia, and weight loss. On examination, body mass index was 22 kg/m² with mild proptosis, symmetrical proximal weakness (MRC 4/5), and erythematous rashes on thighs and shins. Otorhinolaryngology evaluation confirmed bilateral vocal cord palsy. Investigations revealed markedly elevated creatine kinase (7,950 U/L), aspartate aminotransferase (349 U/L), and alanine aminotransferase (179 U/L), with euthyroid biochemistry (thyroid-stimulating hormone 5.21 mIU/L, free thyroxine 4 16.6 pmol/L). Hypokalemia correction failed to improve symptoms, excluding periodic paralysis. ANA, C3, and C4 were normal. Myositis panel showed strong anti-Cytosolic 5’-nucleotidase 1A positivity with borderline anti-Ro-52. A diagnosis of IIM with bulbar involvement was made. She was treated with intravenous methylprednisolone and intravenous immunoglobulin, with clinical improvement. Conclusion This case highlights the diagnostic challenge of muscle weakness in thyroid disease. While thyrotoxic myopathy is often presumed, markedly elevated creatinine kinase, rash, and bulbar involvement should prompt suspicion of IIM. Early immunosuppressive therapy is essential to achieve favorable outcomes.
Muscle Weakness ; Thyroid Diseases ; Muscular Diseases