Introduction: Empty sella (ES) is characterized by herniation of the subarachnoid space into the sella turcica, leading to pituitary flattening. Although often considered incidental, ES is increasingly recognized as a radiological marker of idiopathic intracranial hypertension (IIH) which classically presents with headache and visual loss. Importantly, IIH may also present with otolaryngological manifestations such as pulsatile tinnitus, hearing loss, and vertigo. Audiovestibular symptoms have been reported in up to 88.9% of patients with primary ES, with sensorineural hearing loss being the most frequent, while pulsatile tinnitus occurs in approximately 58% of IIH cases. Case: A 51-year-old female presented with 3 months of progressively worsening headaches, rapid deterioration of left-sided hearing, and a 20-kg weight gain over 1 year. Audiometry confirmed moderate left sensorineural hearing loss. Examination revealed a normotensive female with a body mass index of 35 kg/m² and diplopia on left upward gaze without evidence of ophthalmoplegia. The rest of the neurological examination was unremarkable. There was no evidence of papilledema or Cushingoid features. Repeat magnetic resonance imaging brain in 2025 showed persistent partial ES and loss of the posterior pituitary bright spot without an intracranial mass lesion or venous sinus thrombosis. There was no biochemical evidence of hypopituitarism or Cushing’s syndrome. Autoimmune markers were unremarkable. Lumbar puncture demonstrated a mildly elevated opening pressure of 23 mmHg with normal CSF composition. Based on the clinical and radiological findings, early IIH was diagnosed. She was treated with acetazolamide, and prescribed tirzepatide for weight reduction, resulting in improvement in headache and tinnitus. Conclusion IIH can manifest with partial ES and audiovestibular symptoms related to raised intracranial pressure. Early recognition is important, and IIH should be suspected in patients with pulsatile tinnitus or progressive sensorineural hearing loss. Acetazolamide and weight management remain the mainstay of treatment, with emerging evidence supporting a potential role for glucagon-like peptide-1 receptor agonists in reducing intracranial pressure.
Pseudotumor Cerebri ; Tinnitus ; Hearing Loss

Introduction: Polycystic ovary syndrome (PCOS) is the most common cause of hyperandrogenism in women of reproductive age. However, several endocrine disorders, particularly Cushing disease (CD), can closely mimic the clinical, biochemical, and radiological features of PCOS. This overlap may lead to misdiagnosis and delayed recognition of hypercortisolism, with significant metabolic and reproductive consequences. Case: We report a 24-year-old female with young-onset diabetes mellitus who was referred for endocrine co-management during admission for recurrent mons pubis and labial abscesses with poorly controlled glycemia. She had a 5-year history of progressive hirsutism, oligomenorrhoea, scalp hair loss, significant weight gain, and insulin resistance, and had previously been labelled as having PCOS during adolescence, with subsequent default of follow-up. On examination, she was obese (body mass index 33 kg/ m²) with plethoric facies, acanthosis nigricans, proximal myopathy, and hirsutism (Ferriman–Gallwey score 10), without overt virilization or acromegalic features. Biochemical evaluation demonstrated severe hyperandrogenism with markedly elevated total testosterone (7.05 nmol/L), suppressed gonadotropins, and adrenocorticotropic hormone (ACTH)-dependent hypercortisolism. Cortisol failed to suppress on low-dose dexamethasone testing, and 24-hour urinary free cortisol was markedly elevated (>4,900 nmol/24 h). Pelvic ultrasonography and computed tomography imaging showed polycystic ovarian morphology without evidence of an ovarian mass. Pituitary magnetic resonance imaging revealed a small right-sided pituitary microadenoma measuring 2.6 × 3.7 mm. Inferior petrosal sinus sampling demonstrated a central-to-peripheral ACTH gradient with adequate prolactin ratios, confirming pituitary CD. Conclusion This case highlights how Cushing disease can closely mimic PCOS, including polycystic ovarian morphology and hyperandrogenism. Progressive symptoms, severe biochemical androgen excess, and marked insulin resistance should prompt evaluation for secondary causes of hyperandrogenism, particularly hypercortisolism, to avoid delayed diagnosis and prolonged morbidity.
Female ; Hyperandrogenism ; Pituitary ACTH Hypersecretion ; Polycystic Ovary Syndrome

Introduction: Acromegaly is usually diagnosed by elevated age- and sex-adjusted insulin-like growth factor-1 (IGF-1) levels reflecting chronic growth hormone (GH) excess. IGF-1 is preferred as a screening biomarker due to its longer half-life and reduced pulsatility compared with GH. However, IGF1 levels may be disproportionately low or only modestly elevated in certain clinical contexts, leading to diagnostic uncertainty. Pituitary apoplexy is one such condition in which acute tumor hemorrhage or infarction may disrupt sustained GH secretion and attenuate IGF-1 production Case: A 48-year-old female with hypertension, type 2 diabetes mellitus, and dyslipidemia presented with a 2-day history of severe headache, vomiting, and visual disturbance, on a background of progressive acral enlargement over 2 years. Examination revealed coarse facial features, prognathism, enlarged hands, and cranial nerve involvement. Magnetic resonance imaging demonstrated an invasive sellar– suprasellar pituitary macroadenoma with optic chiasmal compression and cavernous sinus encasement. Intravenous dexamethasone was initiated pre-operatively due to a significant mass effect. Biochemical evaluation showed markedly elevated random GH levels (>50 ng/mL) with only mildly elevated IGF-1 at 1.19 times the upper limit of normal, below the threshold at which confirmatory oral glucose tolerance testing may be omitted according to current guidelines. Other pituitary axes suggested evolving hypopituitarism. During admission, she developed severe hyperglycemia with marked insulin resistance, requiring high-dose insulin therapy (approximately 1.5 U/kg/day). She underwent urgent transsphenoidal surgery, with histopathology confirming a pituitary neuroendocrine tumor with extensive hemorrhage and infarction, consistent with pituitary apoplexy. Postoperatively, GH levels were suppressed to <5 ng/mL, insulin requirements decreased markedly, and hormone replacement was initiated for secondary adrenal insufficiency and central hypothyroidism. Conclusion This case highlights that IGF-1 levels below conventional diagnostic thresholds do not exclude clinically significant acromegaly, particularly in the setting of pituitary apoplexy. Integration of clinical phenotype, GH levels, and imaging findings is essential to avoid diagnostic delay and ensure timely management.
Acromegaly ; Insulin Resistance ; Pituitary Apoplexy

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

Thyroid crisis is a life-threatening form of thyrotoxicosis characterized by multi-system dysfunction. Therapeutic plasma exchange has been reported to be effective in removing excessive circulating thyroid hormones. We present a 46-year-old female with recently diagnosed Graves’ disease associated with thyrotoxic cardiomyopathy admitted for thyroid crisis complicated by propranolol-induced circulatory collapse, acute kidney injury and ischemic hepatitis. The tachyarrhythmia was refractory to conventional therapy. Initiation of TPE resulted in rapid clinical and biochemical stabilization.
Thyroid Crisiscirculatory collapse ; Shock ; Cardiomyopathies ; Propranolol