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Adrenocortical carcinoma (ACC) is a rare malignant tumour originating from the adrenal cortex. Half of the cases are functional, with ACTH independent autonomous cortisol production being the most common. It is rare for ACC to present with markedly elevated metanephrine levels which is a typical characteristic of pheochromocytoma. We report a case of a large functioning adrenal tumour with overlapping biochemistry features of ACC and pheochromocytoma. Biopsy confirmed the histopathological diagnosis of metastatic ACC.

Abstract Background Managing treatment-resistant aggressive giant prolactinoma can be challenging, as the diagnosis is often complex, and treatment beyond dopamine agonists, surgery, and radiotherapy is limited. Case presentation A 21-year-old Malay woman first presented to our hospital at the age of 16 years with 1-year history of reduced vision and 2 years of amenorrhea. Her baseline prolactin level was 255,894 µIU/mL with secondary hypogonadism, and pituitary magnetic resonance imaging revealed a giant prolactinoma (2.8 × 3.2 × 4.2 cm3) with suprasellar extension and optic chiasmal compression. She was initially treated with cabergoline, and reductions in the prolactin level and tumor mass were achieved, leading to vision improvement and resumption of normal menstruation. However, she developed recurrent tumor growth and hyperprolactinemia, causing relapse of symptoms, and she needed surgery. Eventually, despite three tumor debulking surgeries and escalation of cabergoline doses up to 1 mg/day, her tumor progressed with aggressive characteristics. Following a multidisciplinary meeting, the patient is initiated on temozolomide therapy after considering the long-term side effects of radiotherapy in her case. Conclusion This case highlights the importance of early identification of treatment-resistant prolactinoma and the need for a multidisciplinary approach in managing aggressive prolactinoma in young patients, particularly regarding timely implementation of temozolomide therapy.

Objective. To evaluate the effect of adding DPP4 inhibitor (DPP4-I) on glycemic variability (GV) in patients with type 2 diabetes mellitus (T2DM) treated with premixed human insulin (MHI). Methodology. We conducted a prospective study in patients with T2DM on twice-daily MHI with or without metformin therapy. Blinded continuous glucose monitoring was performed at baseline and following 6 weeks of Vildagliptin therapy. Results: Twelve patients with mean (SD) age of 55.8 (13.1) years and duration of disease of 14.0 (6.6) years were recruited. The addition of Vildagliptin significantly reduced GV indices (mmol/L): SD from 2.73 (IQR 2.12-3.66) to 2.11 (1.76-2.55), p=0.015; mean amplitude of glycemic excursions (MAGE) 6.94(2.61) to 5.72 (1.87), p=0.018 and CV 34.05 (8.76) to 28.19 (5.36), p=0.010. In addition, % time in range (3.9-10 mmol/l) improved from 61.17 (20.50) to 79.67 (15.33)%, p=0.001; % time above range reduced from 32.92 (23.99) to 18.50 (15.62)%, p=0.016; with reduction in AUC for hyperglycemia from 1.24 (1.31) to 0.47 (0.71) mmol/day, p=0.015. Hypoglycemic events were infrequent and the reduction in time below range and AUC for hypoglycemia did not reach statistical significance. Conclusion. The addition of DPP4-I to commonly prescribed twice-daily MHI in patients with T2DM improves GV and warrants further exploration.

Acollision tumor involving metastasis to a pituitary adenoma is rare. We describe a case of a 68-year-old Bidayuh woman with underlying treatment-responsive lung adenocarcinoma, who presented with mass effect, panhypopituitarism and polyuria. Her initial imaging study reported pituitary macroadenoma, and she was treated with hormone replacement therapy. She then underwent transsphenoidal tumor debulking surgery with subsequent histopathological findings of a collision tumor of an adenocarcinoma with metastasis to a non-functioning pituitary adenoma.

Abstract Background Hypokalemia in the presence of hypertension is often attributed to primary hyperaldosteronism as a cause of secondary hypertension, however secondary hyperaldosteronism may present similarly. Accessory renal arteries are variants in the vascular anatomy which are often thought to be innocuous but in some circumstances can cause renovascular hypertension leading to secondary hyperaldosteronism. Case presentation We report 2 cases of hypertension with secondary hyperaldosteronism associated with accessory renal arteries. Both patients presented with hypokalemia and further investigations revealed hyperaldosteronism with unsuppressed renin levels. Imaging studies showed the presence of accessory renal artery. Conclusion Accessory renal arteries are a potential cause renovascular hypertension which can be detected via CT angiography or magnetic resonance angiography. Hormonal evaluation should be undertaken to determine whether its presence contributes to hypertension in the patient as targeted treatment such as aldosterone antagonist can be initiated. Surgical intervention or renal denervation may be considered in resistant cases.

Background: Neuropathic pain is chronic and debilitating. Early and accurate diagnosis is important for appropriate management. The painDETECT questionnaire (PDQ) is an effective screening tool for presence of neuropathic pain. We tested the validity and reliability of the translated Malay version of PDQ (PDQ-M). Methods: This was a multi-center cross-sectional study conducted over 24 months. The original English version of PDQ was translated into Malay version following international guidelines. Subsequently, patients with chronic pain were administered PDQ-M and Malay version of SF36 at baseline and 2-4 weeks later. The reliability, construct and criterion validity of PDQ-M were evaluated. Clinician diagnoses were used as gold standard for comparison of diagnostic accuracy. Multiple regression analysis was performed to determine correlation between PDQ-M and SF-36 scores. Results: A total of 97 patients were included in the study (53 with neuropathic pain, 44 with nociceptive pain). The EFA of PDQ-M produced three factors which explained 58.3% of the variance. It exhibited fair consistency with Cronbach’s alpha coefficient of 0.719 (for all 9 items) and 0.755 (for 7-item with Likert scale). PDQ-M is reliable with Cronbach’s alpha coefficient of 0.719 and 0.852 for test-retest reliability. A score of ≥17 was the best cut-off value for discriminating between neuropathic and non-neuropathic pain in PDQ-M (79.2% sensitivity, 50.0% specificity). Multiple regression analysis exhibited total PDQ-M score to have significant negative correlation with all components of SF-36 scores except role limitation due to physical health. Conclusions: PDQ-M is a reliable and valid self-administered screening tool for neuropathic pain. [ABSTRACT FROM AUTHOR]