Introduction: Large, rapidly enlarging adrenal masses typically mandate surgical intervention given the high probability of adrenocortical carcinoma (ACC). However, benign processes can mimic these aggressive growth kinetics, creating a diagnostic challenge for clinicians. Case: A 74-year-old male with hypertension, atrial fibrillation on rivaroxaban, and prostate cancer was referred for evaluation of a right adrenal incidentaloma detected on computed tomography imaging performed for prostate cancer staging. The well-defined mass measured 8.9 × 7.8 × 7.5 cm (AP × W × CC) with areas of calcification. Mean attenuation was +40 Hounsfield Unit, with no significant washout. Biochemical evaluation confirmed a non-functioning lesion (24-hour urine metanephrines 756 mcg/24 hours [N 246–753 mcg/24 hours]; serum cortisol 62 nmol/L post overnight dexamethasone suppression test). The patient was otherwise asymptomatic and declined surgical intervention. Repeat imaging 4 months later demonstrated interval enlargement of the mass to 9.8 × 8.8 × 10.7 cm. Due to this rapid growth, which was highly concerning for ACC, the patient underwent laparoscopic right adrenalectomy. Histopathological examination unexpectedly revealed an adrenal hematoma without evidence of an underlying tumor or malignancy. This case illustrates the difficulty in differentiating aggressive cortical tumors from atypical hemorrhagic events. Larger series on adrenal hemorrhage reported trauma and procedural complications as the leading causes, with a median size of 3–4 cm. Idiopathic large adrenal hematomas presenting as rapidly expanding “pseudotumors” are exceptionally rare, with fewer than 20 cases reported in which surgical resection was performed due to high preoperative suspicion of malignancy. Additionally, adrenal hemorrhage attributed to anticoagulant therapy often occurs bilaterally. Unilateral lesion, especially when large, can pose a diagnostic challenge as highlighted in this case. Conclusion In patients on anticoagulation, rapid interval growth of an adrenal mass does not always equate to malignancy. Recognizing this mimicry in the era of widespread Direct Oral Anticoagulant use is essential for refining treatment decision regarding surgical intervention, as most cases exhibited a self-limiting process with spontaneous resolution.

Introduction: Type 2 diabetes mellitus is a major healthcare problem worldwide, yet high percentage of patients are undiagnosed. There is a dire need for effective screening strategies. We examine the use of modified Asian FINDRISC (M-FINDRISC) and POCT random capillary blood glucose (rCBG) for the detection of dysglycemia Methodology: This cross-sectional, observational study included 151 adults aged ≥30 years without a prior history of diabetes in healthcare and community settings. Hemoglobin A1c of ≥6.3% was used for the diagnosis of diabetes, and 5.7– 6.2% for prediabetes. Areas under the receiver operating curve (ROC-AUC) for M-FINDRISC were analyzed. The sensitivity and specificity of the combined use of M-FINDRISC and rCBG for the detection of dysglycemia were evaluated. Results: The mean age of the participants was 44.6 ± 11.0 years. They had high body mass index (27.8 ± 4.9 kg/m²). Most were sedentary (only 25.2% reported physical activities of ≥30 min/day). A total of 52.3% had first-degree relatives with diabetes, but less than 12% were taking antihypertensive medication. Out of 151 participants, 3.3% (n = 5) were diagnosed with diabetes mellitus and 37.7% (n = 57) with prediabetes, giving an overall prevalence of 41.1% for dysglycemia. The mean age of participants with dysglycemia was significantly older (47.9 vs. 42.3 years, p-value 0.002). Other parameters were not statistically different for the two groups. Mean M-FINDRISC score was 9.7 ± 3.9 in the normal and 10.8 ± 4.0 in the dysglycemic group, while rCBG was 6.4 ± 1.1 mmol/L and 7.1 ± 3.1 mmol/L, respectively. ROC-AUC of M-FINDRISC for dysglycemia was 0.561. A combined screening strategy (M-FINDRISC score ≥7.5 and CBG ≥7.8 mmol/L) yielded high specificity (89.9%) but low sensitivity (17.7%) for dysglycemia. Conclusion While the combined screening strategy utilizing M-FINDRISC and POCT random CBG improves specificity, M-FINDRISC showed limited predictive value for dysglycemia in this specific cohort, making it a less ideal tool for screening.

Introduction: The increasing prevalence of diabetes represents a significant global health challenge. Modifiable risk factors, including physical inactivity, unhealthy dietary habits, and obesity contribute substantially to this rising burden. In conjunction with the 2025 World Diabetes Day (WDD) campaign focusing on “diabetes and the workplace,” we assessed diabetes risk among healthcare workers in our hospital using the Modified Asian Finnish Diabetes Risk Score (ModAsian FINDRISC). Methodology: Healthcare workers from various departments were invited to participate in the hospital WDD celebration. A total of 286 attendees underwent anthropometric measurements and completed the ModAsian FINDSRIC questionnaire. Descriptive statistics were used to summarize the prevalence of risk factors and overall diabetes risk. Results: The participants included doctors, nurses, allied healthcare professionals, as well as hospital support and administrative staff. The majority of participants (74.8%) were aged below 45 years. 39.2% were overweight while 30.8% were obese. One-third (37.4%) had increased waist circumference (WC) (≥90 cm for men, ≥80 cm for women). Additionally, 20% of respondents reported being on antihypertensive medication, and 23.8% had previously recorded high blood glucose. A family history of diabetes mellitus (DM) was reported by 62.6% of respondents. Additionally, about onethird were sedentary with less than 30 minutes of daily exercise or physical activity, another one-third did not consume fruits or vegetables on a daily basis. The median ModAsian FINDRISC score was 8, with approximately 30% of them classified as having moderate to very high risk of developing DM (moderate: 17.5%; high: 10.8%; very high: 2.8%). Conclusion These results revealed high metabolic risk in healthcare workers and highlight the need for targeted workplace health promotion strategies to reduce the risk of developing diabetes.
Tertiary Care Centers ; Health Personnel ; Diabetes Mellitus

Introduction: Repaglinide, a meglitinide analogue, has a rapid onset and short duration of action. It offers prandial glucose control while reducing hypoglycemia risk compared to sulfonylureas. We describe its use in our special cohorts of diabetic patients where repaglinide was prescribed to reduce hypoglycemia in vulnerable patients or to optimize glycemic control through pharmacotherapy intensification or deintensification. Cases: Cohort A comprised 12 elderly patients with multiple comorbidities (mean age: 70.3 years; mean DM duration: 18.3 years) characterized by high glucose variability and problematic hypoglycemia. In seven patients, low-dose gliclazide was replaced with repaglinide with reduction in hypoglycemic episodes. One patient on low-dose premixed insulin was successfully switched to preprandial repaglinide. Two patients on basal insulin were able to reduce their insulin requirements and stabilize their glucose levels. A younger patient with autonomic dysfunction had hypoglycemia while on insulin glulisine, while its omission led to severe hyperglycemia. Substituting glulisine with repaglinide resolved the glucose variability. Repaglinide effectively reduced hypoglycemic episodes while maintaining glycemic stability, with a mean hemoglobin A1c (HbA1c) reduction of 0.36% over 3–6 months. Cohort B consisted of six younger patients (mean age: 35.3 years) with focus on optimizing HbA1c and improving treatment adherence. Two patients on basal-bolus regimes success-fully transitioned off bolus insulin to repaglinide, significantly improving compliance. One patient on basal insulin was successfully transitioned to an all-oral regimen. Three patients on existing oral hypoglycemic agents were started on repaglinide to close the glycemic gap. Cohort B achieved a robust mean HbA1c reduction of 2.1% within 3–6 months. Conclusion Repaglinide remains an important armamentarium in personalized diabetes management. Its pharmacokinetics and flexible dosing allow intensification of glycemic control while minimizing the risk of hypoglycemia. It also offers a viable strategy for selected patients struggling with complex insulin regime.
Repaglinide

Introduction: Severe hypercalcemia is most commonly caused by primary hyperparathyroidism (PHPT) and malignancy. While standard therapies are effective in most cases, a subset of patients have persistent or refractory hypercalcemia. We present a retrospective case series detailing the clinical characteristics, biochemistry, and outcomes of patients treated with denosumab for hypercalcemia. Cases: Seven patients with severe hypercalcemia were identified, comprising five with PHPT and two with malignancyassociated hypercalcemia. The mean age was 70.4 years (range 55–86), with 71% female (n = 5) and 29% male (n = 2). Baseline corrected calcium ranged from 2.92 to 4.59 mmol/L, with a mean of 3.26 mmol/L. In the PHPT cohort, parathyroid hormone (PTH) levels were significantly elevated (16.7–168 pmol/L), while malignancy patients had suppressed PTH (0.6 and 0.9 pmol/L). Prior to denosumab, 4/7 patients (57%) received bisphosphonates, 3/7 (43%) received calcitonin, and 1/7 (14%) was treated with cinacalcet. Denosumab resulted in a mean reduction in corrected calcium of 0.22 mmol/L from 3.26 to 3.03 mmol/L. Biochemical response was observed in 5/7 patients (71%). Of these, 3 patients (43%) achieved normocalcemia, while 2 patients (29%) demonstrated a partial response. The remaining 2/7 patients (29%) showed no significant improvement in calcium levels. Among responders, the mean time to calcium reduction to <3.0 mmol/L was 27 days (range 7–47). Repeat dosing was required in the majority of patients, with a mean of 1.7 doses per patient (range 1–4), indicating variability in both onset and durability of response. Among patients with PHPT, four underwent parathyroidectomy, and one declined surgery. Both patients with malignancy were managed nonsurgically. Conclusion Denosumab achieved normocalcemia in 43% of patients, with additional partial responses. Its effects were variable, with delayed response and frequent need for repeat dosing, supporting its role as an adjunctive or bridging therapy rather than as a definitive treatment.
Denosumab ; Hypercalcemia ; Retrospective Studies

Introduction: Hypercalcemic crisis, a decompensated state characterized by multiorgan dysfunction and a corrected serum calcium (CCa) level typically >3.5 mmol/L, is a rare but lifethreatening endocrine emergency that requires prompt recognition and aggressive multimodal management. We report a fatal case of hypercalcemic crisis secondary to primary hyperparathyroidism, which was refractory to multiple lines of medical therapy. Case: A 55-year-old female with diabetes mellitus, hypertension, and chronic kidney disease (creatinine 159 umol/L; estimated glomerular filtration rate 33 mL/min) presented with 3 days of confusion, profound fatigue, and constipation, preceded by a 1-month history of polyuria and polydipsia. Her Glasgow Coma Scale (GCS) was E4V3M5. Physical examination was unremarkable, with no palpable neck swelling. Significant laboratory findings included severe hypercalcemia with markedly elevated serum intact parathyroid hormone (iPTH) (CCa 4.49 mmol/L; phosphate 1.01 mmol/L; iPTH 60.1 pmol/L [N 1.6–6.0]; creatinine 149 umol/L). Saline diuresis was initiated together with subcutaneous calcitonin, resulting in an initial biochemical response, with CCa decreasing to a nadir of 3.61 mmol/L. However, the CCa subsequently rebounded to 5.00 mmol/L. Hemodialysis was performed, followed by administration of subcutaneous denosumab 60 mg. Nonetheless, the CCa decreased only modestly to 4.28 mmol/L. She became increasingly drowsy, and her clinical course was further complicated by aspiration pneumonia and lung collapse, leading to respiratory failure requiring intubation and inotropic support. Despite intensive care, additional sessions of hemodialysis and continuous renal replacement therapy, her CCa remained persistently above 4.0 mmol/L, peaking at 5.35 mmol/L. Due to her critical condition, imaging for lesion localization could not be performed. She eventually succumbed to her illness on day 10 of admission, before definitive surgery could be undertaken. Conclusion This case highlights the potentially fatal course of hypercalcemic crisis secondary to primary hyperparathyroidism. The reported mortality rate is high, at around 60%. Early recognition and intensive management, including emergency parathyroidectomy in resistant cases, have been shown to be crucial in improving outcomes.
Hyperparathyroidism, Primary

Introduction: Ectopic ACTH secretion (EAS) is a rare cause of Cushing’s syndrome, accounting for 5–15% of cases. Pulmonary neuroendocrine tumors are the most frequent cause. However, primary tumor localization remains a significant diagnostic challenge, delaying effective treatment. Case: A 59-year-old female with diabetes mellitus presented with refractory hypertension and hypokalemia. Initial laboratory findings revealed a baseline cortisol of 1,164 nmol/L and morning adrenocorticotropic hormone (ACTH) of 19.5 pmol/L (normal <10.2 pmol/L), with an overnight dexamethasone suppression test cortisol of 624 nmol/L. Pituitary magnetic resonance imaging (MRI) and computed tomography (CT) scans of the thorax, abdomen, and pelvis were initially unremarkable. A PET scan identified mild hypermetabolism in the left adrenal gland and gastrointestinal tract, though colonoscopy revealed only chronic colitis. An intravenous desmopressin stimulation test demonstrated a 181% rise in ACTH and a 35% rise in cortisol, pointing toward pituitary Cushing’s. However, repeat pituitary MRI remained normal. A high-dose dexamethasone suppression test showed approximately 34% cortisol suppression (cortisol 1,128 nmol/L to 745 nmol/L), suggesting ectopic Cushing’s syndrome. Bilateral inferior petrosal sinus sampling demonstrated a peak central-to-peripheral ACTH ratio of 1.8 on the right and 1.6 on the left, pointing toward ectopic Cushing’s. Localization with DOTATATE PET-CT identified a 7 × 9 × 8 mm nodule in the right middle lobe. A wedge resection was performed. Histopathology confirmed a typical carcinoid tumor with clear resection margins. Immunohistochemistry revealed tumor cells positive for CK AE1/ AE3, synaptophysin, chromogranin, and INSM-1, with weak positivity for ACTH. The latest 8 am cortisol was 117 nmol/L and ACTH 1.74 pmol/L, confirming biochemical cure. Hypokalemia resolved, with improvement in her metabolic profile. Conclusion This case highlights the diagnostic complexities of EAS, particularly when initial imaging is inconclusive and biochemical tests yield conflicting results. Timely, precise localization of the causative tumor is crucial for successful surgical intervention and to prevent severe complications of hypercortisolism, thereby improving patient outcomes.
ACTH Syndrome, Ectopic

Introduction: Electrolyte imbalance is common in central nervous system infections. Arginine vasopressin deficiency (AVP-D), Cerebral Salt Wasting (CSW), and Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH) are important etiologies that can cause opposing extremes of serum sodium, posing diagnostic and therapeutic challenges. We report a rare case of transient central AVP-D followed by CSW secondary to tuberculous meningitis (TBM). Case: An 18-year-old female presented with a 1-month history of fever, reduced responsiveness, and visual hallucinations. Her Glasgow Coma Scale was E4V1M4 with neck stiffness and upper motor neuron signs. Initial investigations revealed severe hyponatremia (119 mmol/L) and communicating hydrocephalus with third ventricle ballooning on brain imaging. Coupled with a positive tuberculosis contact, anti-tuberculous therapy was initiated for probable TBM alongside 3% saline correction prior to insertion of external ventricular drain (EVD). Her condition deteriorated on day 5, requiring intubation for aspiration pneumonia. Repeated imaging showed worsening hydrocephalus, necessitating EVD revision. She subsequently developed polyuria (urine output [UO] 150–300 mLs/hour), with biochemical findings consistent with AVP-D (serum sodium 154 mmol/L; urine osmolality 96 mOsm/kg; urine sodium <20 mmol/L). Intravenous desmopressin 1 mcg was administered, and UO reduced to 30 mLs/hour. However, polyuria recurred on Day 9, accompanied by tachycardia, hypotension, and a rapid decline in serum sodium to 120 mmol/L. Diagnosis of CSW was established (urine sodium 204 mmol/L; urine osmolality 470 mOsm/kg). Oral fludrocortisone was initiated and titrated to 0.4 mg daily to maintain serum sodium >130 mmol/L. Due to persistent hydrocephalus, right ventriculoperitoneal shunt was inserted on Day 22, after which her UO gradually decreased, allowing tapering of fludrocortisone. She remains on fludrocortisone 0.1 mg daily with ongoing rehabilitation. Conclusion TBM can be complicated by SIADH, AVP-D, or CSW. Concurrent AVP-D and CSW have not been reported. This case highlights the dynamic electrolyte disturbances in TBM which may lead to diagnostic confusion and therapeutic error. Early recognition and tailored therapy, alongside definitive management to reduce intracranial pressure, are essential for optimal outcomes.
Hypernatremia ; Hyponatremia ; Tuberculosis, Meningeal

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.
Adrenocortical Carcinoma ; Pheochromocytoma

Purpose: Varicoceles can be a source of elevated seminal oxidative stress (OS) and sperm DNA fragmentation (SDF). However, it remains unclear whether varicocele repair (VR) could reduce these parameters. This systematic review and meta-analysis (SRMA) aims to investigate the impact of VR on SDF and seminal malondialdehyde (MDA). Materials and Methods: A literature search was performed in Scopus, PubMed, Ovid, Embase, and Cochrane databases. This SRMA included randomized controlled trials and observational studies reporting the pre- and postoperative levels of SDF and seminal OS in infertile men with clinical varicocele that underwent VR. Subgroup analyses included techniques of VR and SDF testing. The effect size was expressed as standardized mean difference (SMD). Results: Out of 1,632 abstracts assessed for eligibility, 29 studies with 1,491 infertile men were included. The analysis showed a significant reduction in SDF after VR, compared to preoperative values (SMD −1.125, 95% confidence interval [CI] −1.410, −0.840; p<0.0001) with high inter-study heterogeneity (I2=90.965%). Reduction in SDF was evident with microsurgical technique and non-microsurgical inguinal approaches (SMD −1.014, 95% CI −1.263, −0.765; p<0.0001, and SMD −1.495, 95% CI −2.116, −0.873; p<0.0001), respectively. Reduction in SDF was significant irrespective of testing was done by sperm chromatin dispersion (SMD −2.197, 95% CI −3.187, −1.207; p<0.0001), sperm chromatin structure assay (SMD −0.857, 95% CI −1.156, −0.559; p<0.0001) or TUNEL (SMD −1.599, 95% CI −2.478, −0.719; p<0.0001). A significant decrease in seminal MDA levels was observed following VR (SMD −2.450, 95% CI −3.903 to −0.997, p=0.001) with high inter-study heterogeneity (I2=93.7%). Conclusions Using pre- and post-intervention data, this SRMA indicates a significant reduction in SDF and seminal MDA levels in infertile men with clinical varicocele treated with VR. These findings may have important implications for the future management of this selected group of infertile patients.