Introduction: Endothelial dysfunction (ED) is an early marker of atherosclerosis and plays a role in the pathophysiology of cardiovascular complications in type 2 diabetes mellitus (T2DM). Metabolic factors such as adiposity and insulin resistance contribute to early vascular dysfunction, particularly in patients with preserved kidney function. This study aimed to identify factors associated with ED in T2DM and early-stage chronic kidney disease (CKD) Methodology: This study was conducted at Universiti Teknologi MARA (UiTM), Sungai Buloh, and involved 107 adults with T2DM and estimated glomerular filtration rate ≥60 mL/min/1.73 m² (CKD stages 1–2). Endothelial function was assessed using ultrasound-based brachial artery flow-mediated dilation (FMD), with ≤7.1% defining ED. Clinical, anthropometric, metabolic, and renal parameters were compared between groups. Logistic regression analyses were performed to identify independent predictors, with p-values <0.05 considered statistically significant. Results: Of the cohort, 48.6% (n = 52) had abnormal FMD. They tended to have higher BMI (31.36 vs 28.38 kg/m², p = 0.020), larger waist circumference (100.48 vs 94.53 cm, p = 0.026), and were more likely to be on insulin therapy (71.2 vs 49.1%, p = 0.020). The total daily insulin dose was higher in the abnormal FMD group (0.48 vs 0.35 U/kg), but this difference did not reach statistical significance (p = 0.140). There were no significant differences in hemoglobin A1c, blood pressure, or renal parameters. In multivariate analysis, BMI (adjusted OR 1.07, 95% CI 1.00–1.14, p = 0.037) and insulin therapy (adjusted OR 2.43, 95% CI 1.07–5.51, p = 0.034) remained independently associated. Conclusion In patients with T2DM and early CKD, higher BMI and insulin therapy are independently associated with ED. These findings highlight the role of obesity and insulin resistance in early vascular dysfunction, emphasizing the importance of weighttargeted strategies alongside glycemic control and further identifying high-risk individuals to reduce cardiovascular risk.
Diabetes Mellitus, Type 2 ;

Introduction: Disseminated histoplasmosis is a rare but important cause of adrenal insufficiency (AI), particularly in tuberculosis (TB)-endemic regions, where it may mimic granulomatous diseases. Adrenal involvement occurs in up to 80% of disseminated cases, although overt AI is less common. Reported cases described bilateral adrenal masses mimicking malignancy or TB, even in immunocompetent individuals. Addisonian crisis may be the initial manifestation, especially when the diagnosis is delayed. In TB-endemic settings, fungal infections are often overlooked, leading to delayed diagnosis and inappropriate therapy. Case: We reported a case of a 68-year-old male with underlying diabetes mellitus who presented with fever, cough, dysphagia, and weight loss for 1 month. He was empirically treated as smear-negative disseminated TB. On day 2 of therapy, he developed hypotension (80/50 mmHg), hypoglycemia (3.9 mmol/L), hyponatremia (Na 129 mmol/L), and hyperkalemia (K 5.1 mmol/L), suggestive of adrenal crisis, and was started on intravenous hydrocortisone. Serum cortisol prior to treatment was 61 nmol/L. Computed tomography (CT) imaging revealed bilateral lipid-poor adrenal lesions (right: 3.6 × 2.2 × 4.9 cm, Hounsfield Unit (HU) 36 and absolute washout 33%; left: 3.5 × 2.4 × 5.4 cm; HU 35 and absolute washout 17%), raising suspicion of infectious or malignant etiologies. Endoscopic ultrasound-guided biopsy demonstrated necrotizing granulomatous inflammation with budding fungal yeasts on Pituitary Apoplexy Score and GMS staining, consistent with Histoplasma capsulatum. TB and malignancy were excluded. He received amphotericin B for 14 days, followed by oral itraconazole for 1 year, and oral hydrocortisone replacement. At 1-year follow-up, adrenal lesions remained stable on CT images, and he continued to require hydrocortisone replacement. Conclusion This case highlights the importance of considering disseminated histoplasmosis as a differential diagnosis of bilateral adrenal masses with AI, especially with poor response to anti-TB therapy. Early tissue diagnosis is essential, as imaging findings are non-specific. Prompt recognition is critical to prevent life-threatening adrenal crisis and improve clinical outcomes.
Histoplasmosis ; Tuberculosis

Introduction: Diabetic peripheral neuropathy (DPN) is a common complication of type 2 diabetes mellitus (T2DM), with nerve conduction studies recognized as the diagnostic gold standard. Serum neuron-specific enolase (NSE) has been linked with DPN. This study aims to determine the prevalence of DPN among T2DM patients, evaluate clinical characteristics, and explore the relationship between NSE and DPN. Methodology: A cross-sectional study was conducted at Universiti Teknologi MARA Specialist Centre Sungai Buloh and Hospital Al-Sultan Abdullah, involving patients aged 18–60 years, diagnosed with T2DM for more than 5 years (n = 132). All participants underwent anthropometric measurement, completed the Michigan Neuropathy Screening Instrument evaluation, and biochemical parameters, including lipid profile, hemoglobin A1c, and serum creatine and NSE. The diagnosis of DPN was made based on positive NCS findings. Logistic regression was used to identify factors associated with DPN. Results: The study population had a mean age of 60.16 ± 10.28 years and a mean duration of diabetes of 14.82 ± 6.66 years. The prevalence of DPN was 51.5% (n = 68). Serum NSE levels were significantly higher (p = 0.003) and independently associated with the presence of DPN (adjusted odds ratio [OR] 1.033, 95% confidence interval [CI] 1.009–1.058, p = 0.006). Participants with DPN were also more likely to be on insulin therapy (p = 0.040). In addition, retinopathy (adjusted OR 3.567, 95% CI 1.528–8.329, p = 0.013) and elevated Urine Albumin-to-Creatinine Ratio levels indicating albuminuria (adjusted OR 1.031, 95% CI 1.002– 1.061, p = 0.037) were significantly associated with DPN. Conclusion More than half of the study population had DPN, which was significantly associated with both retinopathy and nephropathy, as well as with elevated serum NSE. This emphasizes the importance of early screening and highlights the role of NSE as a surrogate marker for neuropathy in diabetes.
Humans ; Diabetes Mellitus, Type 2 ; Diabetic Neuropathies ; Prevalence ; Phosphopyruvate Hydratase

Introduction: Type 2 diabetes mellitus (T2DM) and thyroid disorders are common endocrine conditions with a bidirectional relationship affecting glucose and lipid metabolism. Adiposity, particularly fat mass index (FMI), may influence thyroid function. but its association with thyroid dysfunction and glycemic control remains unclear, especially in Malaysia. This study aimed to determine the prevalence of thyroid dysfunction in T2DM and its association with glycemic control and FMI at Universiti Teknologi MARA (UiTM). Methodology: A cross-sectional study was conducted among patients with T2DM attending the Endocrine Clinic, UiTM, from December 2025 to March 2026. A total of 91 participants aged 18–70 years were recruited using convenience sampling. Demographic, clinical, anthropometric, and laboratory data were collected. Thyroid dysfunction was defined as thyroid-stimulating hormone (TSH) <0.38 or >5.33 mIU/L. Body composition was assessed using the InBody 380 to determine FMI. Data were analyzed using SPSS version 30 with descriptive statistics and Pearson correlation. Results: The prevalence of thyroid dysfunction among patients with T2DM was 7.7% (7/91), predominantly with low TSH levels. Mean hemoglobin A1c (HbA1c) in the overall study population was 7.59 ± 1.49%, and mean TSH was 1.42 ± 0.95 mIU/L, within the euthyroid range. Mean FMI was 11.95 ± 5.23 kg/m², exceeding normal ranges for both men (3–6 kg/m²) and women (5–9 kg/m²). FMI showed a positive correlation with TSH level (r = 0.379, p <0.001), indicating that higher adiposity was associated with higher TSH levels despite remaining within the euthyroid range. Pearson correlation showed a weak, non-significant negative correlation between HbA1c and TSH (r = −0.127, p = 0.229). Conclusion The prevalence of thyroid dysfunction among patients with T2DM in our cohort was relatively low at 7.7%. However, the significant correlation between FMI and TSH level, even within the euthyroid range, suggests that adiposity may exert a clinically relevant influence on thyroid function.
Diabetes Mellitus, Type 2 ; Prevalence ; Thyroid Gland ; Adipose Tissue

Introduction: Clinically important drug–drug interactions are a frequently overlooked cause of severe hypoglycemia in patients with type 2 diabetes mellitus (T2DM). Gliclazide is primarily metabolized via cytochrome P450 2C9 (CYP2C9), while fluconazole is a potent inhibitor of this enzyme.1,2 Concomitant administrations markedly increase gliclazide plasma concentration and prolong its hypoglycemic effect, substantially increasing the risk of severe and prolonged hypoglycemia. In some cases of refractory sulfonylureainduced hypoglycemia, octreotide may need to be considered early. Case: A 63-year-old Malay female with a 15-year history of T2DM on maximum-dose gliclazide (320 mg/day) presented with syncope and recurrent severe hypoglycemia 5 days after receiving a single oral dose of fluconazole 150 mg for a superficial fungal skin infection. Her other antidiabetic medications included metformin 1 g twice daily and vildagliptin 50 mg once daily. Her blood pressure on presentation was 151/74 mmHg, and her glucose level was 2.8 mmol/L. Her presentation was compounded by community-acquired pneumonia and acute kidney injury (estimated glomerular filtration rate 52 mL/min/1.73 m²). Biochemical evaluation excluded adrenal insufficiency, with normal serum cortisol (1,098 µg/dL), serum sodium (141 mmol/L), and serum potassium (4.6 mmol/L). Thyroid and liver function tests were normal. Despite repeated boluses of 50% dextrose and continuous infusion of 20% dextrose, recurrent hypoglycemia persisted for up to 48 hours after discontinuation of gliclazide, with glucose ranging from 1.7 to 5.1 mmol/L, reflecting prolonged sulfonylurea activity. Conclusion This case highlights a clinically significant yet preventable interaction between fluconazole and gliclazide, mediated through CYP2C9 inhibition, resulting in sustained hyperinsulinemic hypoglycemia. Gliclazide should be reduced or withheld prior to initiating fluconazole, and medication review should be performed at every consultation.
Fluconazole ; Gliclazide ; Hypoglycemia