Introduction: Adrenocortical carcinoma (ACC) is a rare and aggressive malignancy with a predilection for metastasis to the liver, lungs, and lymph nodes. Bone involvement is less common and typically occurs alongside widespread disease. Isolated skeletal progression without visceral involvement is unusual and not well characterized. Case: A 60-year-old female underwent left adrenalectomy in 2019 for an incidentally detected adrenal mass, which was reported as a benign adrenal cortical adenoma (Ki67 <3%). In 2022, she presented with persistent low back pain. Imaging demonstrated fluorodeoxyglucoseavid lesions involving the T12 vertebra and right ilium, without evidence of local recurrence or visceral metastases. Histopathological evaluation of a bone biopsy initially suggested a neuroendocrine neoplasm based on synaptophysin positivity. Following multiple expert reviews and integration of clinical, radiological, and immunohistochemical findings, a consensus diagnosis of metastatic ACC was established. She received palliative radiotherapy to symptomatic skeletal sites and subsequently completed six cycles of etoposide, doxorubicin, and cisplatin chemotherapy in 2023, achieving disease stabilization. Surveillance imaging in May 2025 demonstrated progression confined to the axial and appendicular skeleton, with no involvement of the adrenal bed or visceral organs. Mitotane therapy was initiated in December 2025. Ongoing management focuses on systemic disease control, symptom palliation, and multidisciplinary supportive care. Conclusion This case illustrates an uncommon pattern of ACC progression characterized by bone-dominant metastases in the absence of visceral disease. It also highlights the importance of reconsidering the initial histopathological diagnosis when clinical behavior is discordant. Vigilance for atypical metastatic patterns is warranted, even years after resection of an adrenal lesion initially classified as benign.
Adrenocortical Carcinoma

Introduction: Diabetic ketoacidosis (DKA) is a life-threatening complication associated with significant morbidity and healthcare burden. Despite advances in diabetes care, recurrent DKA remains common, often reflecting gaps in treatment adherence and patient education. Identifying predictors of recurrence is crucial for risk stratification and targeted intervention. Methodology: We conducted a retrospective observational study of all adult DKA admissions to a tertiary centre between 2001 and 2025. Electronic medical records were reviewed for demographic data, biochemical parameters, precipitating factors, and clinical outcomes. DKA was defined using standard biochemical criteria. Recurrent DKA was defined as ≥2 admissions during the study period. Factors associated with recurrent DKA admissions were analyzed. Patients under the age of 18 years and those with missing vital information were excluded. Results: A total of 667 DKA admissions, comprising 566 patients, were identified, of which 101 admissions (15.1%) were recurrent, involving 65 patients. Among recurrent DKA episodes, the most common precipitating factors were infection (64.4%) and insulin omission (62.4%). After multivariate analyses, patients with type 1 diabetes mellitus (T1DM) were more likely to develop recurrent DKA compared to those with type 2 diabetes mellitus (aOR 4.16; 95% confidence interval [CI] 2.58–6.70; p <0.001). Insulin omission was strongly associated with recurrent DKA (aOR 2.29; 95% CI 1.46–3.60; p <0.001). In contrast, baseline glycated hemoglobin and chronic kidney disease were not significantly associated with recurrence. Diabetic counseling during the first DKA admission did not reduce recurrent DKA. There were no significant differences in mortality (3.9% vs 6.2%, p = 0.524) or critical care admission rates (40.6% vs 38.7%, p = 0.718) between recurrent and first DKA episodes. Conclusion Recurrent DKA accounts for a substantial proportion of DKA admissions and is strongly associated with insulin omission and T1DM. Our findings suggest that recurrent DKA is driven predominantly by behavioral and adherencerelated factors, indicating the need for multidisciplinary interventions beyond standard inpatient counseling.
Diabetic Ketoacidosis ; Retrospective Studies

Introduction: The rising incidence of diabetic ketoacidosis (DKA) in type 2 diabetes mellitus (T2DM) represents a paradigm shift from its traditional recognition as a hallmark complication of type 1 diabetes mellitus (T1DM). However, contemporary data comparing clinical presentation, precipitating factors, and outcomes between these two populations remain limited. Methodology: In this retrospective observational study, all adult DKA admissions with T1DM or T2DM at a tertiary centre between 2001 and 2025 were studied. DKA was defined according to standard biochemical criteria. Electronic medical records were reviewed to extract demographic data, biochemical parameters, precipitating factors, management details, and clinical outcomes of all adult DKA admission in T1DM and T2DM. Patients aged <18 years or those with incomplete data were excluded. Results: A total of 601 DKA episodes were analyzed, comprising 130 (21.6%) in patients with T1DM and 471 (78.4%) in those with T2DM. Mean age was 26.9 ± 0.71 years for T1DM and 52.1 ± 0.7 years for T2DM. Gender distribution was balanced (male 48.3%, female 51.7%). Mean hemoglobin A1c (HbA1c) was 11.3 ± 0.3% in T1DM and 12.1 ± 0.2% in T2DM. Infection was the most common precipitating factor overall (69.0%), occurring more frequently in T2DM than in T1DM (74.7% vs. 56.2%), followed by medication non-adherence (62.4% vs. 43.8%). Significant differences were observed between groups in admission pH, bicarbonate (both p <0.001), blood ketones (p = 0.028), and HbA1c (p = 0.010), whereas anion gap (p = 0.056) and blood glucose levels (p = 0.755) did not differ significantly. Clinical outcomes were comparable with respect to intensive care unit (ICU) admission rates (40.0% in T1DM vs. 39.0% in T2DM, p = 0.779) and median resolution time (p = 0.462). However, the median length of hospital stay was significantly longer in T2DM (8.2 ± 0.32 vs. 5.4 ± 0.4 days; p <0.001). Overall mortality was 6.0%, with substantially higher mortality in T2DM compared to T1DM (7.4% vs. 0.8%, p = 0.013). Conclusion In this large regional series of adult DKA, most episodes occurred in T2DM. Despite similar ICU admission rates and time to resolution, T2DM was associated with more frequent infection-related precipitants, longer hospital stays, and higher mortality, underscoring the need for targeted preventive strategies in this population.
Adult ; Diabetes Mellitus, Type 1 ; Diabetic Ketoacidosis ; Diabetes Mellitus, Type 2

Introduction: Diabetic ketoacidosis (DKA) in pregnancy is an uncommon yet life-threatening emergency, with disproportionate risks to both mother and fetus. Pregnancy-specific physiological changes predispose patients to rapid metabolic decompensation, often with atypical presentations. Despite this, local data remain limited. We describe the clinical profile, precipitating factors, and outcomes of DKA in pregnancy in a tertiary centre, with emphasis on potentially preventable triggers. Cases: Nine pregnant patients with DKA were identified from a retrospective review of all cases admitted for DKA from 2002 to 2025. Mean age was 31.67 ± 5.20 years; all were Malay. The majority had type 2 diabetes mellitus (55.6%), followed by type 1 diabetes (33.3%) and latent autoimmune diabetes in adults (11.1%). The mean period of amenorrhea was 19.67 ± 12.62 weeks. Infection was the leading precipitant (44.4%), with additional triggers including insulin omission (22.2%), hyperemesis gravidarum, preterm labor, steroid exposure, and perioperative fasting. Most diagnoses were made in the emergency department (55.6%). Biochemical parameters reflected significant severity (mean bicarbonate 7.89 ± 2.98 mmol/L; anion gap 25.00 ± 5.81), with 88.9% classified as severe DKA. Intensive Care Unit (ICU) care was required in 77.8% of cases. The majority (77.8%) were admitted to the ICU unit, with a median time to resolution of 13.00 ± 12.00 hours (interquartile range [IQR]), and the median hospital length of stay was 7.00 ± 5.00 days (IQR). Complications during treatment included hypokalemia (33.3%), acute kidney injury (22.2%), and hypoglycemia (11.1%). Rebound DKA occurred in one-third of patients. All patients were discharged clinically stable. Outcome data demonstrated pregnancy loss in three cases and one preterm birth. Conclusion DKA in pregnancy remains a severe and resource-intensive condition. This series highlights missed opportunities in prevention, with modifiable precipitants such as infection and insulin omission commonly identified. The high severity at presentation suggests delays in recognition. Early detection, optimized metabolic care, and targeted preventive strategies are crucial to improving maternal and fetal outcomes.
Female ; Pregnancy ; Diabetic Ketoacidosis

Introduction: Bullous pemphigoid (BP) is the most common autoimmune blistering disease. Drug-induced BP has been increasingly reported, with dipeptidyl peptidase-4 (DPP-4) inhibitors, particularly vildagliptin, emerging as a notable cause. The pathogenesis is thought to involve the disruption of immune tolerance and epitope spreading, leading to a broader autoimmune response against basement membrane antigens beyond the classic NC16A domain of BP180. This case series highlights the variable clinical spectrum and therapeutic challenges in vildagliptin-induced BP. Case: A 74-year-old male with type 2 diabetes mellitus (T2DM), hypertension, dyslipidemia, and a history of stroke presented with a 2-month history of recurrent, pruritic, tense bullae. He had been on vildagliptin for 36 months. Histopathology confirmed subepidermal blistering, and direct immunofluorescence demonstrated linear IgG/C3 deposition at the dermo-epidermal junction, with positive anti-BP180 antibodies, diagnosing BP. Discontinuation of vildagliptin and initiation of systemic corticosteroids resulted in significant clinical improvement, allowing a rapid prednisolone taper to 5 mg daily without new bullae formation. A 62-year-old female with T2DM and dyslipidemia presented with bullous eruptions 3 months after initiating vildagliptin. Skin biopsy confirmed BP, revealing subepidermal blistering with eosinophils and linear C3/IgG deposition at the basement membrane zone. Vildagliptin was discontinued. Despite initial management with systemic corticosteroids, the disease course was refractory. The patient experienced a flare upon steroid taper and had persistent blistering on prednisolone 20 mg daily, necessitating the addition of azathioprine as a steroidsparing agent. Conclusion This case series illustrates the variable clinical course of vildagliptin-induced BP in which the therapeutic trajectories diverged significantly. Recognition of BP as a potential adverse effect of DPP-4 inhibitors is critical, and management should be individualized.