Introduction: Multiple daily insulin injections, while effective for glycemic control, impose considerable costs on healthcare systems and carry inherent risks including hypoglycemia, weight gain, and poor treatment adherence. This study evaluates the glycemic effects of insulin regimen de-escalation from multiple daily injections in poorly controlled type 2 diabetes mellitus (T2DM) patients and explores the predictors of successful insulin de-escalation. Methodology: This is a multi-centred, prospective observational study of adult T2DM patients on multiple daily insulin injections with hemoglobin A1c (HbA1c) 7–12% who underwent de-escalation to one or two injections. Patients were reassessed at 3 months and 6 months. Primary endpoint was change in HbA1c from baseline. Secondary endpoints were changes in body weight, hypoglycemia frequency, treatment adherence and predictors of successful insulin de-escalation defined by at least a 0.3% reduction in HbA1c while on de-escalated regimen. Results: A total of 80 patients were included. HbA1c improved from 9.23 to 8.52% (p <0.001) with total daily insulin dose reduction from 0.81 + 0.35 units per kg to 0.46 + 0.24 units per kg. Symptomatic hypoglycemia decreased from 22.5 to 5.0%. Insulin adherence improved from 50.0 to 92.3%. Body weight decreased by 1.4 kg. Forty-nine patients (61.3%) were successfully de-intensified. Factors associated with successful insulin de-escalation included a high baseline HbA1c, high fasting blood glucose and higher estimated glomerular filtration rate, while increased age, disease duration and being Indian were associated with unsuccessful insulin de-escalation. After adjustment of the confounders, only HbA1c (OR 2.07, 95% CI 1.23–3.46, p = 0.006) and the status of being Indian (OR 0.21, 95% CI 0.05–0.94, p = 0.041) remained as significant positive and negative predictors respectively for successful insulin de-intensification. Conclusion Insulin regimen de-escalation, when combined with optimized oral glucose-lowering agents, improved glycemic control and treatment adherence while reducing hypoglycemia and body weight. These findings support insulin therapy deescalation as a safe, effective strategy for poorly controlled T2DM patients taking multiple daily insulin injections.
Diabetes Mellitus, Type 2 ; Prospective Studies ; Insulins

Introduction: Pheochromocytoma is a catecholamine-secreting adrenal tumor associated with major perioperative hemodynamic instability. When concurrent major pelvic pathology requires surgery, operative planning becomes particularly challenging. We describe the successful single-stage management of pheochromocytoma and a giant uterine fibroid, highlighting the importance of multidisciplinary coordination and perioperative optimization. Case: A 49-year-old female with symptomatic uterine fibroid was found to have proliferative endometrium on a pipelle biopsy. Computed tomography (CT) abdomen incidentally detected a right adrenal mass alongside a large posterior uterine fibroid (11.9 × 17.4 × 14.6 cm). CT adrenal protocol demonstrated a heterogeneously enhancing right adrenal mass (6.9 × 6.9 × 9.6 cm) with high unenhanced attenuation. Biochemical evaluation revealed markedly elevated 24-hour urinary metanephrine (4.7× upper limit) and normetanephrine (2.4× upper limit). Following multidisciplinary discussions, a single-stage surgical approach was planned after careful assessment of feasibility and perioperative risk in view of the uncertain malignant potential of the pelvic mass and to minimize repeated exposure to anesthesia. Preoperative optimization included transitioning from terazosin to phenoxybenzamine, with subsequent addition of bisoprolol for hemodynamic control. The operative strategy prioritized pheochromocytoma resection first, given its potential for significant hemodynamic instability. Progression to hysterectomy was contingent upon achieving adequate intraoperative hemodynamic stability following adrenalectomy, with continuous reassessment by the anesthetic and surgical teams. Right adrenalectomy was performed first, followed by total abdominal hysterectomy with bilateral salpingooophorectomy. Significant hemodynamic lability occurred during tumor manipulation, with hypertensive surges managed using sodium nitroprusside and remifentanil infusions. Following adrenal vein ligation and tumor removal, hypotension was managed with noradrenaline and additional adrenaline support as required. Total operative time was approximately 6 hours. Postoperatively, transient noradrenaline support was required but was rapidly weaned as hemodynamic stability was achieved. Conclusion Single-stage adrenalectomy and major pelvic surgery can be safely performed in selected patients with pheochromocytoma when guided by meticulous preoperative optimization, clear intraoperative sequencing, and close multidisciplinary coordination.
Pheochromocytoma ; Adrenalectomy ; Leiomyoma ; Hysterectomy

Introduction: Adrenal incidentalomas are increasingly detected with the widespread use of imaging, whereby the large or heterogeneous lesions often raise concern for adrenocortical carcinoma (ACC). However, certain rare benign and infectious conditions may closely mimic malignant features, posing a diagnostic challenge. Case: A 64-year-old female with diabetes mellitus, hypertension, and dyslipidemia was noted to have progressively rising alkaline phosphatase during routine follow-up. She had non-specific gastrointestinal symptoms. A computed tomography abdomen pelvis showed a large, lobulated mass at the left flank, likely of adrenal origin. An adrenal protocol computed tomography revealed a large, heterogeneously enhancing left suprarenal mass measuring 10.7 × 10.3 × 10.7 cm, with a plain-phase attenuation of +81 Hounsfield Unit and absolute (28%) and relative (18%) washout. The right adrenal gland was normal, with no evidence of distant metastasis. Hormonal evaluation showed normal 24-hour urinary metanephrines, excluding pheochromocytoma. The overnight dexamethasone suppression test demonstrated cortisol of 89 nmol/L, suggestive of mild autonomous cortisol secretion, without clinical features of overt hypercortisolism. DHEA was low (0.371 µmol/L), and adrenocorticotropic hormone was suppressed (1.26 pg/mL). Evaluation for primary aldosteronism was not done due to the absence of resistant hypertension or hypokalemia. The gonadotropin profile was consistent with postmenopausal status (follicle-stimulating hormone (89 IU/L) and luteinizing hormone (28.9 IU/L) with low estradiol. The patient underwent open left adrenalectomy. Histopathology revealed an adrenal cavernous hemangioma with extensive hemorrhage and infarction, alongside necrotizing granulomatous inflammation with numerous intracellular fungal organisms and narrow-based budding yeast forms, highly suggestive of histoplasmosis, with no evidence of malignancy. She was subsequently comanaged with infectious disease team and commenced on intravenous amphotericin B. Conclusion This is a rare coexistence of an adrenal hemangioma and histoplasmosis, presenting as a large adrenal mass mimicking ACC. The limitations of imaging in differentiating benign from malignant adrenal lesions are revealed and emphasize the role of histopathological confirmation. Increased awareness of such entities can support the diagnosis and management.
Neoplasms

Introduction: Primary bilateral macronodular adrenal hyperplasia (PBMAH), characterized by bilateral adrenal macronodules >1 cm, is a rare genetic disease contributing to <2% of Cushing syndrome. Case: A 56-year-old male with underlying diabetes mellitus and hypertension presented with worsening proximal muscle weakness. Detailed neurological assessment was unremarkable. Re-assessment revealed more apparent cushingoid features, prompting referral to endocrinology. Basal cortisol was markedly elevated at 957 nmol/L (145.4– 619.4 nmol/L). Unsuppressed cortisol after 1 mg overnight dexamethasone and low-dose dexamethasone test confirmed Cushing Syndrome. Suppressed adrenocorticotropic hormone (ACTH <0.33 pmol/L) suggested autonomous cortisol secretion from adrenal glands. Computed tomography adrenal reported massively enlarged hypodense multinodular adrenal glands of varying sizes. Oral ketoconazole, an adrenal steroidogenesis inhibitor, was initiated. Despite careful titration to keep serum cortisol 400–500 nmol/L, he experienced glucocorticoid withdrawal syndrome. Bilateral adrenalectomy was planned but deferred as he continued to lose weight despite persistent hypercortisolism. Extensive investigations were conducted for possible opportunistic infections or malignancy. His chest X-ray revealed a suspicious right lung cavity. Positive serum galactomannan and bronchial alveolar lavage galactomannan suggested pulmonary aspergillosis. Voriconazole was introduced, with drug-drug interaction judiciously addressed. He underwent bilateral adrenalectomy and required lifelong glucocorticoid and mineralocorticoid replacement. Histopathological report confirms bilateral macronodular adrenocortical disease. A referral to a genetic clinic was made to explore the potential hereditary basis. Conclusion PBMAH is a highly heterogeneous disease with variable presentation and a wide spectrum of hypercortisolism. Definitive management remained controversial and individualized. Multidisciplinary discussion is crucial, and genetic study is highly recommended for long-term prognostication and familial screening.

Introduction: Diabetes literacy represents personal knowledge and competencies related to diabetes mellitus (DM) among people living with DM (PLWD). It is a crucial component for optimizing care and empowering effective selfmanagement. Methodology: A cross-sectional study was conducted at Hospital Tuanku Ja’afar Seremban (HTJS) and Klinik Kesihatan Seremban (KKS) using a validated simplified Diabetes Knowledge Test (DKT). DKT assessed understanding in six domains, namely, awareness, lifestyle modification, diet and monitoring, general knowledge, preventive screening, and insulin. A score of >75% was classified as adequate diabetes literacy. Significant predictive factors identified from univariate Pearson Chi Square were further analyzed using multivariate logistic regression. Results: A total of 250 PLWDs, with equal contribution from each centre, were recruited with a mean (SD) age of 50.3 (13.6) years, 58.4% female, and 43.2% Malays. A total of 21.2% demonstrated adequate diabetes literacy. The results demonstrated the highest proficiency in the preventive screening domain (92.6%) and the lowest in the awareness domain (50.2%). Unemployed PLWDs had significantly lower odds of adequate diabetes literacy (odds ratio [OR] = 0.20, p = 0.010). Similarly, PLWDs with hemoglobin A1c levels >10% exhibited approximately 2.6-fold lower odds of adequate diabetes literacy. In contrast, PLWDs who reported healthcare personnel as their primary source of diabetes-related information had significantly higher odds of adequate literacy (OR = 1.59, p = 0.017). No significant association was demonstrated between diabetes literacy and frequency of hospital admissions, medication adherence, and diabetes-related target organ damage Conclusion Diabetes literacy among PLWD in HTJS and KKS is suboptimal, with notable gaps in awareness of the disease. Targeted, culturally tailored education strategies are essential to address these disparities and to empower them for effective diabetes self-management.
Literacy ; Diabetes Mellitus

Introduction: Diabetic ketoacidosis (DKA) and thyroid storm are individually rare but potentially fatal endocrine crises in pregnancy. Each carries significant maternal and fetal morbidity, with mortality risk compounded when they occur concomitantly. Physiological and pharmacokinetic changes of pregnancy, combined with overlapping symptoms, necessitate urgent treatment strategies. Case: A 29-year-old G2P2 female at 29 weeks’ gestation, with poorly controlled type 2 diabetes mellitus (hemoglobin A1c 8.1%) on a basal–bolus insulin regimen and Graves’ disease managed with carbimazole, non-adherent to medications, presented with fever, vomiting, and dyspnea. On examination, she was tachycardic (HR 138 bpm), hypotensive (BP 94/60 mmHg), and hypoxic. Laboratory investigations revealed hyperglycemia (glucose 27.1 mmol/L), severe metabolic acidosis (pH 7.02, bicarbonate 4.9 mmol/L), and elevated serum ketones (4.6 mmol/L), consistent with DKA. Thyroid function tests showed suppressed thyroid-stimulating hormone (<0.005 mIU/L) and elevated free T4 (28.2 pmol/L), with a Burch–Wartofsky score of 70. Unfortunately, intrauterine fetal demise was confirmed upon the patient’s presentation to the emergency department. She was intubated and admitted to the intensive care unit, receiving fluid resuscitation judiciously according to the DKA regimen, with frequent assessment of volume status. Intravenous insulin and potassium supplements were commenced concurrently. Metabolic stabilization was achieved within 24 hours. Carbimazole, propranolol, Lugol’s iodine, and intravenous hydrocortisone were started for treatment of thyroid storm. A breech-assisted vaginal delivery was performed, and her postpartum course was uneventful. Conclusion The case reveals the catastrophic potential of concurrent DKA and thyroid storm in pregnancy, where rapid maternal deterioration and poor fetal outcomes can occur despite timely intervention. High clinical suspicion, early biochemical confirmation, and coordinated multidisciplinary management are vital. Precipitating factors, particularly medication non-adherence, must be addressed through intensive patient education and structured follow-up to prevent recurrence.
Female ; Pregnancy ; Diabetic Ketoacidosis ; Thyroid Crisis

Introduction: Giant parathyroid adenomas (GPAs), defined as lesions >3.5 g, are rare. Their size, biochemical severity, and compressive features often mimic carcinoma, creating diagnostic and surgical challenges. Case: A 33-year-old female was incidentally found to have hypercalcemia during evaluation after her newborn developed severe hypocalcemic seizures requiring NICU admission. Maternal calcium was 2.95 mmol/L with hypophosphatemia. Subsequent reviews showed persistent hypercalcemia (3.15–3.3 mmol/L), hypophosphatemia (0.32– 0.51 mmol/L), and markedly elevated intact parathyroid hormone (85–96 pmol/L). She had vitamin D deficiency, very high alkaline phosphatase (1,329 U/L), and progressive bone pain with reduced mobility. Bone mineral density revealed Z scores of −2.9 (hip) and −3.3 (lumbar spine). Multiphase computed tomography demonstrated a multilobulated 6.9 cm mass extending from C5 to T2, compressing the esophagus and raising suspicion for carcinoma. Endoscopic evaluation excluded mucosal invasion. She underwent en bloc left inferior parathyroidectomy with hemithyroidectomy. Intraoperative parathyroid hormone fell from 41.7 to 13.4 pmol/L, confirming complete excision. The gland measured 65 × 20 × 15 mm and weighed 18.4 g. Histopathology revealed a hypercellular parathyroid tumor with endocrine atypia but no invasion, consistent with a giant adenoma. Postoperatively, calcium was initially stable (1.99 mmol/L at discharge) but fell to 1.68–1.82 mmol/L at 2 weeks despite high-dose supplementation. Hypocalcemia persisted for 6 weeks, consistent with delayed hungry bone syndrome, likely precipitated by preoperative vitamin D deficiency, markedly elevated alkaline phosphatase, and low bone mineral density. With intensive supplementation, calcium gradually stabilized, and symptoms improved. Conclusion GPAs can closely mimic carcinoma, with endocrine atypia complicating histopathological interpretation. This case illustrates both diagnostic overlap and the unusual, delayed onset of hungry bone syndrome, emphasizing the need for preoperative risk assessment, correction of metabolic deficiencies, and extended postoperative monitoring. Rare presentations such as delayed hungry bone syndrome refine management strategies and improve outcomes in primary hyperparathyroidism.
Parathyroid Neoplasms

Introduction: Primary hyperparathyroidism (PHPT) is frequently asymptomatic or detected incidentally; however, delayed diagnosis may lead to severe skeletal complications. Early recognition is essential, as timely identification and management of parathyroid disease can prevent significant morbidity, although diagnosis may be challenging when clinical and imaging findings are inconclusive. Case: A 46-year-old female with severe bilateral hearing impairment presented to the orthopedic clinic with 3 years’ history of bilateral knee pain and was found to have a right intertrochanteric femur fracture following minimal trauma. She was referred for evaluation of suspected secondary osteoporosis. She has had intermittent constipation and long-standing oligomenorrhea since menarche. There was no history of childhood fractures or use of medications affecting bone metabolism. Examination revealed bilateral knee bowing. Initial evaluation considered metabolic bone disease, including Paget’s disease; however, skeletal survey showed no features suggestive of Paget’s disease or multiple myeloma. Biochemical investigations demonstrated persistent hypercalcemia (2.65–3.1 mmol/L) with inappropriately elevated intact parathyroid hormone (peak 7.62 pmol/L), consistent with PHPT. Serum phosphate was low-normal. Concomitant vitamin D deficiency (25-OH vitamin D 34.46 nmol/L) improved following replacement. Bone mineral density confirmed severe osteoporosis (lumbar spine T-score −5, z-score -4.1); (forearm −6.7, z-score -6.1) reflecting prolonged untreated disease. Neck ultrasound demonstrated a mixed solid-cystic lesion posterior to the right thyroid lobe, suggestive of a parathyroid adenoma. The TC-99 m Sestamibi scan showed no definite focal uptake. However, subsequent SPECT-CT revealed focal tracer uptake at the posterior right thyroid gland, consistent with a hyperfunctioning parathyroid gland. Parathyroidectomy was done. Postoperatively, the calcium level normalized. Conclusion Severe osteoporosis and fragility fracture occur, reflecting prolonged exposure to excess parathyroid hormone and significant skeletal morbidity. Early biochemical evaluation in unexplained severe osteoporosis is essential, as timely diagnosis and definitive management of parathyroid disease are critical to halt ongoing bone loss and prevent irreversible complications.
Hyperparathyroidism, Primary ; Osteoporosis

Introduction: Pituitary apoplexy is an acute endocrine emergency, as early recognition may influence the outcomes, often presenting with sudden headache, visual disturbances, ocular palsies, vomiting, or altered consciousness. Given that urgent surgical decompression is a common management, emerging evidence supports corticosteroid therapy in our patient with significant neuro-ophthalmic deficits. Case: A 65-year-old male with hypertension, dyslipidemia, type 2 diabetes mellitus, chronic kidney disease stage III, and ischemic heart disease presented with a 4-day history of fever, vomiting, bifrontal headache, and generalized abdominal pain. Initially, he was treated for presumed intraabdominal sepsis. On day 3 of admission, he developed acute right-sided complete ptosis with ophthalmoplegia involving cranial nerves III, IV, and VI. Prior to that, he had also reduced morning erections for 6 months before presentation. Biochemical evaluation revealed markedly reduced total testosterone (0.33 nmol/L) with inappropriately low–normal gonadotropins (luteinizing hormone 1.5 IU/L, follicle-stimulating hormone 2.3 IU/L), in keeping with secondary hypogonadism. Adrenocorticotropic hormone was suppressed, indicating secondary adrenal insufficiency. Thyroid function was preserved. Overall findings suggested partial hypopituitarism. Magnetic resonance imaging confirmed a cystic pituitary lesion measuring 1.4 × 2.6 × 1.8 cm with cavernous sinus involvement and features of pituitary apoplexy. His Pituitary Apoplexy Score was 4. He was offered surgical intervention but was not keen. He was treated with intravenous hydrocortisone, with rapid clinical improvement, including near-complete resolution of right eye ptosis and restoration of extraocular movements within 3 days, and was able to recover without surgery. The hydrocortisone was gradually tapered, and the patient was discharged well with Endocrine follow-up. Conclusion Timely corticosteroid therapy alone can result in rapid, near-complete neurological recovery in pituitary apoplexy, even with multiple cranial nerves involvement. In carefully selected patients without visual field compromise, conservative management may safely obviate the need for urgent surgical intervention, emphasizing the importance of early recognition and individualized treatment strategies.
Hydrocortisone ; Pituitary Apoplexy

Introduction: Painful Hashimoto's thyroiditis is a rare and atypical form of autoimmune thyroid disease characterized by thyroid pain and tenderness. It can closely resemble subacute thyroiditis and must be distinguished from other causes of thyroid pain, including hemorrhage into a cyst and thyroid abscess. This distinction is particularly important in pregnancy, where radionuclide imaging is not recommended. Case: A 27-year-old pregnant female (G4P3) at 24 weeks’ gestation, with Southeast Asian ovalocytosis and dietcontrolled gestational diabetes, was diagnosed with primary hypothyroidism at 14 weeks following evaluation of a painless goiter. Initial tests showed markedly elevated thyroid-stimulating hormone (>150 mIU/L), low free thyroxine (3.5 pmol/L), and positive anti-thyroid peroxidase antibodies (319 IU/mL), consistent with Hashimoto's thyroiditis. Levothyroxine therapy achieved biochemical euthyroidism. At 24 weeks, she developed acute right-sided anterior neck pain radiating to the ear, with dysphagia, odynophagia, and fever. Examination revealed a tender thyroid without lymphadenopathy. Ultrasound demonstrated diffuse enlargement with bilateral ill-defined hypoechoic avascular areas. Inflammatory markers showed markedly elevated C-reactive protein (184 mg/L) with a normal erythrocyte sedimentation rate (16 mm/h), while thyroid function remained within target range. Imaging and clinical findings made abscess and hemorrhage unlikely. The presence of pre-existing autoimmune thyroid disease, antibody positivity, and hypothyroidism before symptom onset supported painful Hashimoto's thyroiditis over subacute thyroiditis. This case highlights that normal thyroid function tests do not necessarily indicate disease remission, as inflammatory activity may persist independently of hormone levels. Conclusion Painful Hashimoto's thyroiditis should be considered in pregnant patients with known autoimmune thyroid disease presenting with acute thyroid pain despite normal thyroid function. Diagnosis requires integration of clinical, biochemical, and imaging findings to guide appropriate management.
Female ; Pregnancy ; Thyroiditis, Subacute