Introduction: Primary adrenal insufficiency is rare and potentially lifethreatening, with an estimated prevalence of five cases per million in Southeast Asia. Local data remain limited, and diagnosis is frequently delayed due to non-specific clinical manifestations. Widespread use of traditional medication in Malaysia may further undermine recognition, particularly when steroid exposure is concealed. We report a female on prolonged use of traditional remedies presented with classic features of Addison’s disease rather than cushingoid features, confirmed by biochemical results. Case: A 65-year-old female with underlying dyslipidemia and osteoarthritis presented with 4 days of giddiness, poor intake, nausea, and diarrhea. Further history revealed prolonged use of multiple traditional Chinese medicines, discontinued months prior, raising suspicion of prior steroid exposure. She claimed her skin has become darker over the past 2 months. She denied any infectious symptoms, contact with PTB patients, or exposure to birds. There was no family history of autoimmune disease. Clinically, she was dehydrated and hypotensive. Her blood pressure improved after fluid resuscitation. There was hyperpigmentation involving the face, extremities, tongue, and buccal mucosa. Investigation results showed severe hyponatremia (119 mmol/L), hyperkalemia (4.93 mmol/L), with normal creatinine and negative infective markers. Hyponatremia persisted despite adequate hydration. Thyroid function test was normal (Free T4 12.28 pmol/L and thyroid-stimulating hormone 4.16 µIU/mL). Morning cortisol was suppressed (37 nmol/L) with markedly elevated adrenocorticotropic hormone levels (1,134 pg/mL), confirming the diagnosis of primary adrenal insufficiency. Hence, hydrocortisone was commenced, and serum sodium was normalized 2 days later. The underlying etiology remains under evaluation, although autoimmune adrenalitis is the most likely cause. Conclusion Primary adrenal insufficiency should be considered in patients presenting with unexplained hyponatremia and hypotension. In a setting where traditional medication use is prevalent, unrecognized steroid exposure may further complicate diagnosis. A thorough clinical and appropriate biochemical assessment is crucial to differentiating primary from secondary adrenal insufficiency.
Hyponatremia

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