Introduction: Cushing’s disease in adolescents is rare and frequently difficult to diagnose due to overlapping features with common pubertal and metabolic conditions. We present an adolescent who underwent inferior petrosal sinus sampling (IPSS) with possible cyclical Cushing’s disease, highlighting the diagnostic challenges and the interpretive value of IPSS. Case: A 16-year-old female presented with progressive weight gain, acne, hirsutism, secondary amenorrhea, proximal myopathy, violaceous striae, and facial plethora over 1 year. Her 24-hour urinary cortisol was >3,310 nmol/L with failure of suppression following a 1-mg overnight dexamethasone suppression test (701 nmol/L). Her adrenocorticotropic hormone (ACTH) was raised (77.9 pg/mL), consistent with ACTH-dependent Cushing syndrome. Her hemoglobin A1c was 5.9%, and she has low bone mass for age with a Z score of -2.9 at the Lumbar spine. Pituitary magnetic resonance imaging identified a rightsided microadenoma measuring 0.6 × 0.5 cm, while computed tomography of the thorax, abdomen, and pelvis showed no ectopic source. IPSS with desmopressin stimulation was performed to confirm the ACTH source. No steroidogenesis inhibitors were administered prior to testing. Notably, cortisol levels during IPSS were relatively low, with midnight cortisol of 91 nmol/L and morning cortisol of 200 nmol/L, suggesting testing during a trough phase of possible cyclical hypercortisolism. Despite this, IPSS demonstrated a significant central-to-peripheral ACTH gradient supporting a pituitary source. Conclusion This case highlights the diagnostic dilemma of interpreting IPSS in suspected cyclical Cushing’s disease. Fluctuating cortisol secretion may result in discordant biochemical findings and complicate localization studies. IPSS findings should be interpreted cautiously and integrated with clinical features, imaging, and serial biochemical monitoring. Recognition of cyclical disease patterns is essential to ensure appropriate management in adolescent patients.
Adolescent ; Humans ; Petrosal Sinus Sampling

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

Multiple endocrine neoplasia type 1 (MEN1) is a rare autosomal dominant disease caused by a mutation in the MEN1 gene. We present a 65-year-old man with MEN1 who has primary hyperparathyroidism, microprolactinoma, meningioma and gastrinoma. He had undergone parathyroidectomy followed by tumour excision of meningioma. The duodenal gastrinoma lesion was inoperable as it was close to the superior mesenteric artery with high surgery risk. Medical therapy with octreotide LAR had been initiated and showed good biochemical response as well as disease progression control. Chemoembolization was proposed if the duodenum lesion reduces in size on maintenance treatment with octreotide LAR. This case highlights the challenges in managing this rare condition and octreotide LAR has shown to be effective in controlling the disease progression in MEN1 with inoperable gastrinoma
meningioma ; octreotide ; gastrinoma