Introduction: Cushing’s disease (CD) in adolescents may present with subtle clinical features, resulting in a significant diagnostic challenge. We report a case of a young lady whose CD initially masqueraded as Type 2 diabetes (T2D), highlighting the difficulties in differentiating early hypercortisolism from T2D. Case: A 12-year-old female was incidentally diagnosed with diabetes during routine medical screening. Examination revealed an overweight female without the classical features of Cushing’s syndrome. Due to the presence of acanthosis nigricans, a diagnosis of T2D was initially made. Her diabetes remained well-controlled with a single oral glucose-lowering drug. The diagnostic challenge became apparent over time. She experienced delayed menarche at the age of 17, and a diagnosis of Cushing’s syndrome was suspected when she subsequently developed hypertension and reduced bone mineral density. Biochemical evaluation was consistent with adrenocorticotropic hormone (ACTH)- dependent hypercortisolism, evidenced by the failure of serum cortisol suppression on low dose and overnight dexamethasone suppression tests. Her 24-hour urinary cortisol was elevated twofold, and plasma ACTH was elevated (17.8 pmol/L). MRI demonstrated a right-sided pituitary microadenoma (0.3 × 0.5 × 0.3 cm), and inferior petrosal sinus sampling confirmed the diagnosis of CD. She underwent endoscopic transsphenoidal surgery 7 years later, which was complicated by panhypopituitarism and cranial diabetes insipidus. Postoperatively, CD was cured, with the resolution of her metabolic comorbidities. Conclusion Despite the increasing prevalence of T2D in adolescents, clinicians must recognize the diagnostic challenge of CD in this age group. Atypical manifestations in a presumed T2D patient should prompt consideration of Cushing’s syndrome.
Adolescent ; Humans ; Diabetes Mellitus, Type 2

Introduction: Atypical parathyroid adenoma is a rare cause of primary hyperparathyroidism and represents a borderline entity between benign adenoma and parathyroid carcinoma. Due to overlapping clinical, biochemical, and imaging features with carcinoma, diagnosis can be challenging and relies on histopathological evaluation to guide management and follow-up. Case: A 25-year-old male presented with a 3-month history of generalized bone pain and lethargy, with significant weight loss of 17 kg over 7 months. He denied headache, visual disturbance, or hypoglycemic episodes. There was no known family history of endocrine tumors. Examination revealed a palpable right-sided neck mass. Biochemical evaluation showed severe primary hyperparathyroidism with marked hypercalcemia (4.12 mmol/L), hypophosphatemia (0.6 mmol/L), markedly elevated intact parathyroid hormone (137 pmol/L) and alkaline phosphatase (1,958 U/L). Thyroid function was normal. Neck ultrasound demonstrated a right TIRADS 4 lesion, and fine-needle aspiration suggested parathyroid tissue. Sestamibi scan localized a hyperfunctioning right inferior parathyroid gland measuring 2.1 × 1.7 × 3.3 cm. During admission, he sustained low-impact fragility fractures of the left femur and humerus after a fall. Preoperatively, management of hypercalcemia proved challenging. Despite aggressive medical therapy and intensive intravenous hydration with up to 6 liters of normal saline per day, serum calcium levels remained persistently exceeding 3.0 mmol/L. He underwent right hemithyroidectomy with excision of the right inferior parathyroid gland. The postoperative course was complicated by hungry bone syndrome, necessitating intravenous calcium gluconate infusion for 1 week. Histopathological examination confirmed the diagnosis of an atypical parathyroid adenoma. On postoperative follow-up, serum calcium and phosphate levels normalized while he remained on calcium carbonate and calcitriol supplementation. Conclusion Severe primary hyperparathyroidism in young patients may indicate aggressive parathyroid pathology. Atypical parathyroid tumors can mimic carcinoma, and diagnosis requires histopathology with long-term follow-up due to uncertain malignant potential.
Carcinoma ; Adenoma

Introduction: A negative computed tomography (CT) scan does not preclude an insulinoma, as small lesions frequently remain undetected on conventional imaging. This case highlights the indispensable role of endoscopic ultrasound (EUS)— not just for localizing occult tumors, but as a definitive, minimally invasive therapeutic alternative to high-risk surgical resection. Case: A 39-year-old female with underlying hypertension presented with a 5-month history of predominantly fasting hypoglycemia (glucose <3.0 mmol/L) and neuroglycopenic symptoms, fulfilling Whipple’s triad. A supervised 72-hour fast confirmed endogenous hyperinsulinemic hypoglycemia at 31 hours, with a nadir glucose of 1.4 mmol/L, insulin 116 pmol/L, and C-peptide 821 pmol/L. Notably, contrastenhanced CT of the pancreas was reported as normal. To overcome this, EUS was performed, successfully identifying a hidden 19 × 18 mm lesion in the head of the pancreas, intimately abutting the main pancreatic duct. Despite medical therapy with diazoxide and strict dietary modifications, her hypoglycemia remained refractory. Given the tumor’s proximity to the main pancreatic duct, surgical enucleation carried a prohibitively high risk of complications. Consequently, she underwent EUS-guided radiofrequency ablation (RFA). Immediate post-procedure outcomes demonstrated near-complete resolution of the hypoglycemic episodes. Diazoxide was subsequently stopped. Outpatient continuous glucose monitoring confirmed sustained normoglycemia and marked symptom resolution, with no procedure-related complications. Conclusion The absence of a pancreatic lesion on CT demands persistent clinical suspicion in cases of biochemically proven hypoglycemia. EUS remains paramount for detecting occult lesions missed by standard imaging. Importantly, EUSRFA serves as a highly effective, tissue-sparing alternative to surgical resection for insulinomas, especially when conventional surgery poses prohibitive anatomical risks.
Insulinoma ; Tomography, X-Ray Computed

Background/Aims: Non-alcoholic fatty liver disease (NAFLD) is associated with the development of cardiovascular disease. While existing studies have examined cardiac remodeling in NAFLD, there has been less emphasis on the development of carotid atherosclerosis and stroke. We sought to conduct a meta-analysis to quantify the prevalence, risk factors, and degree of risk increment of carotid atherosclerosis and stroke in NAFLD. Methods: Embase and Medline were searched for articles relating to NAFLD, carotid atherosclerosis, and stroke. Proportional data was analysed using a generalized linear mixed model. Pairwise meta-analysis was conducted to obtain odds ratio or weighted mean difference for comparison between patients with and without NAFLD. Results: From pooled analysis of 30 studies involving 7,951 patients with NAFLD, 35.02% (95% confidence interval [CI], 27.36–43.53%) had carotid atherosclerosis with an odds ratio of 3.20 (95% CI, 2.37–4.32; P<0.0001). Pooled analysis of 25,839 patients with NAFLD found the prevalence of stroke to be 5.04% (95% CI, 2.74–9.09%) with an odds ratio of 1.88 (95% CI, 1.23–2.88; P=0.02) compared to non-NAFLD. The degree of steatosis assessed by ultrasonography in NAFLD was closely associated with risk of carotid atherosclerosis and stroke. Older age significantly increased the risk of developing carotid atherosclerosis, but not stroke in NAFLD. Conclusions This meta-analysis shows that a stepwise increment of steatosis of NAFLD can significantly increase the risk of carotid atherosclerosis and stroke development in NAFLD. Patients more than a third sufferred from carotid atherosclerosis and routine assessment of carotid atherosclerosis is quintessential in NAFLD.

Aim: To record the incidence and prevalence ofinflammatory bowel disease (IBD), its social demographics,clinical characteristics and treatment, in the state of Johor,Malaysia.Methods: Hospital Sultanah Aminah, Johor Bahru, is the onlypublic hospital in Johor with a Gastroenterology service.Data on all existing and new IBD patients managed by theGastroenterology Unit in 2016 were collected. Incidence andprevalence of IBD in 2016 were then calculated based on theestimated population of Johor and Johor Bahru.Results: Twenty-five new cases of IBD were diagnosed in2016. Among the 25 cases, 13 cases were Crohn’s disease(CD), 10 were ulcerative colitis (UC) and two were IBDUnclassified (IBDU). The crude incidence of IBD, CD, UC andIBDU were 0.68, 0.36, 0.27, and 0.05 per 100,000 populationrespectively. Ethnic Indians had the highest incidence of IBDat 4.21 followed by Malays and Chinese at 0.56 and 0.18 per100,000 population respectively. A total of 156 IBD caseswere captured. Amongst them, 85 cases were UC, 68 caseswere CD and three cases were IBDU, hence the prevalence ofIBD, UC, CD and IBDU were 4.27, 2.33, 1.86 and 0.08 per100,000 population respectively. Similarly, Indians had thehighest prevalence at 16.84, followed by Chinese at 4.06 andMalays at 3.44 per 100,000 population.Conclusions: The incidence of IBD in Johor is comparable tothat of a previous study in northern Peninsular Malaysia.The ethnicity preponderance is similar to the previousstudies conducted in Malaysia.