Introduction: Adrenocortical carcinoma (ACC) is an aggressive malignancy with high rates of recurrence even after surgical resection. Surgery remains the mainstay of treatment, while adjuvant options are limited. Mitotane is the only approved systemic therapy. Current guidelines recommend stereotactic body radiotherapy (SBRT) alongside adjuvant mitotane therapy in Rx, R1, R2 resections and in locally advanced disease. Case: We present a case of a 40-year-old female who presented with abdominal pain and was found to have a large heterogeneous left adrenal mass measuring 8.2 × 8.5 × 9.5 cm (Hounsfield Unit 63) on computed tomography (CT) imaging. Clinically, she was obese with a body mass index of 33.7 kg/m². No discriminatory feature of Cushing’s was present. Hormonal evaluation demonstrated autonomous cortisol secretion with failure of suppression on both overnight and low-dose dexamethasone suppression tests at 301 nmol/L and 313.6 nmol/L, respectively. DHEA, testosterone, and urinary metanephrine were within range. Hemoglobin A1c was 6.6%. She underwent open left adrenalectomy. Intra-operatively, a 12 × 10 cm adrenal tumor was identified with multiple areas of tumor rupture and spillage during mobilization. HPE confirmed high-grade ACC with high Weiss score of 8, Ki-67 index 60–80%, and mitotic count 54/50 hpf (pT2Nx). Post-operative CT imaging demonstrated a residual soft tissue lesion in the left adrenal bed (largest diameter 3.8 cm) with fluorodeoxyglucose avidity. We commenced adjuvant mitotane therapy, titrated to 2 g TDS with supraphysiological hydrocortisone replacement. Mitotane level was within therapeutic range (16 mcg/mL). She was deemed unsuitable for repeat surgery due to the proximity of the residual mass to the adjacent vessel and was planned for SBRT therapy after a multidisciplinary team discussion. Conclusion High-risk ACC with suspected residual disease remains a therapeutic challenge. While mitotane remains the cornerstone of adjuvant therapy, SBRT may represent a promising adjunctive local treatment modality in carefully selected patients. Further studies are required to define its role in improving local control and outcomes in ACC.
Adrenocortical Carcinoma ; Mitotane

Introduction: Permanent hypoparathyroidism is a recognized complication of total thyroidectomy, with an estimated incidence of 10.47%. Standard treatment involves supplementation with calcium and activated vitamin D. However, some patients remain refractory to conventional therapy and fail to achieve normocalcemia. During pregnancy, significant physiological changes occur in calcium-regulating hormones. Notably, the placenta increases the production of parathyroid hormone-related peptide (PTHrP), which acts as a calcitropic hormone, mimicking the effects of parathyroid hormone. Case: A 38-year-old female with a history of total thyroidectomy 14 years ago for follicular thyroid carcinoma presented with permanent hypoparathyroidism. Her condition was refractory to high-dose replacement therapy, which included calcium carbonate 3 g BD, alfacalcidol 4 mcg ON, calcitriol 1 mcg BD, and cholecalciferol 100,000 IU OD. Despite compliance, her serum calcium levels fluctuated between 1.7 and 1.93 mmol/L, necessitating intermittent intravenous calcium infusions. Laboratory investigations showed a phosphate level of 1.63 mmol/L and 24-hour urine calcium of 4.81 mmol/L. Her thyroid function remained stable on levothyroxine 150 mcg daily (T4: 12.0 pmol/L; thyroid-stimulating hormone: 2.93 mIU/L). While off-label use of teriparatide was being considered, she became pregnant. As the pregnancy progressed, her calcium levels stabilized. Calcitriol was discontinued at 26 weeks’ gestation when her calcium reached 2.5 mmol/L. By 30 weeks, the alfacalcidol dose was reduced to 3.5 mcg daily, with cholecalciferol dosing reduced to 50,000 IU OD. Her corrected calcium levels remained between 2.4 and 2.6 mmol/L until delivery. Similar reduction in supplementation requirements was noted during her previous pregnancy. Conclusion Elevated PTHrP during pregnancy likely contributed to improved calcium homeostasis by increasing maternal bone resorption and enhancing placental calcium transfer. This case underscores the necessity of individualized, dynamic adjustments to calcium and vitamin D therapy based on rigorous biochemical monitoring for pregnant patients with hypoparathyroidism.
Female ; Pregnancy ; Hypoparathyroidism ; Placenta

Introduction: Immunoglobulin G4-related hypophysitis (IgG4-RH) is a rare fibro-inflammatory disorder affecting the pituitary gland. Glucocorticoids remain the first-line therapy, but their use may be complicated in patients with significant metabolic comorbidities. We report a case of suspected IgG4-RH presenting with hyperosmolar hyperglycemic state (HHS), highlighting the challenges of balancing disease control against glucocorticoid metabolic toxicity adverse effects. Case: A 32-year-old female with obesity and newly diagnosed diabetes mellitus was admitted with HHS. Prior to admission, she reported weight fluctuations, episodic headaches, progressive visual disturbance, and secondary amenorrhea. Following resolution of HHS, persistent polyuria of 10–16 L/day prompted further evaluation and led to a diagnosis of arginine vasopressin deficiency. Anterior pituitary hormonal work-up revealed hypogonadotropic hypogonadism. Pituitary magnetic resonance imaging demonstrated infundibular thickening measuring 0.5 cm, with concomitant marked bilateral parotid enlargement. Serum IgG4 was elevated at 2.26 g/L (0.63–2.01), raising strong suspicion for IgG4-RH with systemic involvement. Histopathological confirmation from the parotid gland biopsy was consistent with sialadenosis. She was commenced on sublingual desmopressin and cyclical sex hormone replacement therapy. Given the provisional diagnosis of IgG4-RH, oral prednisolone 40 mg daily was initiated as a reduced induction regimen. However, treatment was poorly tolerated, with rapid weight gain from 93 to 100 kg and worsening glycemic control. Prednisolone was therefore tapered rapidly to 10 mg daily. Repeat imaging demonstrated interval improvement in infundibular thickening, but no functional endocrine recovery was observed. Conclusion This case illustrates the therapeutic challenge of managing IgG4-RH in the setting of pre-existing metabolic syndrome. Although glucocorticoids are effective for induction, their metabolic adverse effects may significantly restrict treatment tolerability. Early consideration of steroidsparing agents, such as rituximab or azathioprine, may be important to achieve remission while minimizing glucocorticoid-related adverse effects.
Autoimmune Hypophysitis

Introduction: Short stature and delayed puberty characterize Turner syndrome (TS). The 2024 international clinical practice guidelines recommend growth hormone (GH) for latediagnosed patients if epiphyses remain open. For patients with remaining growth potential, initiating GH alongside low-dose estrogen effectively balances linear growth with the need for timely pubertal induction. Case: A 15-year-old female, born prematurely at 6 months gestation, presented with delayed puberty, primary amenorrhea, and short stature. Examination revealed a height of 122 cm (<5th percentile), weight of 26 kg, with no syndromic facies, and Tanner stage 1. Investigations confirmed hypergonadotropic hypogonadism. Metabolic screening, including thyroid, renal, and liver profile, was normal. Her baseline insulin-like growth factor 1 (IGF-1) was low at 117.5 ng/mL (127.5–541.5). Karyotyping confirmed mosaic TS (45,X/46,Xr). Her skeletal bone age was delayed at 12 years, indicating a viable window for linear growth prior to complete epiphyseal fusion. Subcutaneous GH was initiated at 0.3 mg up titrated to 1.2 mg (0.45 µg/kg) daily over 4 weeks, then 1.35 mg (50 µg/kg) daily at month 5. Low-dose oral estradiol (0.5 mg three times weekly) was introduced for pubertal induction at month 4. After 9 months of combined GH and estrogen therapy, the patient achieved a height increment of 6 cm, reaching 128 cm without an adverse event. To achieve the clinical target of a 10–15 cm increment in the first year, her GH dose was further increased to 1.50 mg (55 µg/kg) daily. She showed an appropriate biochemical response with IGF-1 increased to 40.2 nmol/L (16.4–67.8) with a total height gain of 6 cm over the first 9 months of GH therapy. Conclusion Concomitant GH and estrogen therapy in late-diagnosed TS successfully induced clinically significant height gain. This dual approach maximized the limited window for linear growth, without delaying pubertal induction and compromising patient’s psychosocial well-being.
Turner Syndrome

Presentation of Cushing’s syndrome during pregnancy is extremely rare. We report a 21-year-old female with Cushing’s syndrome diagnosed at 23 weeks of gestation and had recurrent acute pulmonary oedema during the antepartum and postpartum period. She delivered prematurely via emergency caesarean section at 28 weeks of gestation. This case highlights the rare occurrence of recurrent acute pulmonary oedema during pregnancy and consequential premature birth in a patient with adrenal Cushing’s. She was diagnosed with adrenal Cushing’s during the postpartum period based on unsuppressed serum cortisol after overnight and low-dose dexamethasone suppression test with a suppressed ACTH. CT scan of the adrenal glands revealed a right adrenal cortical adenoma. The risk of complications in infants and mothers who suffer from Cushing’s syndrome needs to be handled carefully. The diagnosis of Cushing’s syndrome in pregnant women often overlaps and is difficult to establish in early pregnancy.
Pregnancy