Introduction: Severe hypercortisolism is associated with profound impairment of both innate and adaptive immune responses, predisposing affected individuals to opportunistic infections. Excess glucocorticoids alter leukocyte trafficking, suppress pro-inflammatory cytokine production, and impair cellular immunity, increasing susceptibility to bacterial, viral, and fungal pathogens. In some cases, severe infections may precede the diagnosis of Cushing syndrome and represent the initial clinical manifestation. Early recognition is important as untreated hypercortisolism can lead to substantial morbidity and mortality. Case: A young adolescent male presented with progressive facial fullness and facial hyperpigmentation for 4 months, followed by 1 month of intermittent fever, cough, lower limb weakness, and hallucinations. On examination, he was tachypneic with cushingoid features including moon facies, pigmented acne over the face and chest, and nail bed hyperpigmentation. He was hypertensive and had severe hypokalemia with lymphopenia. Radiological imaging demonstrated multiple cavitary lung lesions and intracranial tuberculomas. Bronchoalveolar lavage identified multiple opportunistic pathogens, including Pneumocystis jirovecii, Aspergillus fumigatus, and Haemophilus influenzae, while cerebrospinal fluid testing was positive for cytomegalovirus. Given the unusual combination of infections, an underlying immunocompromised state was suspected. Endocrine evaluation revealed markedly elevated serum cortisol, with loss of diurnal rhythm and elevated adrenocorticotropic hormone (ACTH). Twenty-four-hour urinary cortisol was significantly increased, confirming severe ACTHdependent Cushing syndrome. Magnetic resonance imaging of the pituitary gland and computed tomography imaging of the thorax, abdomen, and pelvis did not identify the source of ACTH secretion. Conclusion This case highlights that overwhelming opportunistic infections may be the first manifestation of severe Cushing syndrome in children. Excess cortisol disrupts host defenses by impairing neutrophil chemotaxis and macrophage phagocytosis, suppressing T-cell-mediated immunity, and reducing cytokine signaling necessary for pathogen clearance. These mechanisms contribute to susceptibility to simultaneous bacterial, fungal, and viral infections. Clinicians should therefore consider underlying hypercortisolism in patients presenting with multiple or unusual opportunistic infections to enable earlier diagnosis and appropriate multidisciplinary management.
Cushing Syndrome ; Opportunistic Infections

Introduction: Malaysia has one of the highest diabetes prevalence rates in Asia (1 in 5), with >50% fail to achieve optimal glycemic control. Continuous glucose monitoring (CGM) provides detailed insights beyond hemoglobin A1c (HbA1c), capturing daily glucose fluctuations and variability. Realworld data describing CGM patterns and their clinical associations in Malaysian adults with type 2 diabetes mellitus (T2DM) are limited. Methodology: This cross-sectional study analyzed CGM data from 25 Malaysian adults with T2DM, standardized over 14 days. CGM metrics included time in range (TIR), time above range (TAR), time below range (TBR), mean glucose, and coefficient of variation (CV). Weekday–weekend comparisons were performed, and correlations with age, diabetes duration, HbA1c, body mass index (BMI), treatment regimen, and complications were assessed. Results: Participants had a mean age of 56.2 ± 13.2 years (52% male), mean HbA1c 9.4 ± 2.7%, diabetes duration 10.7 ± 9.0 years, and BMI 29.8 ± 9.4 kg/m². Mean TIR, TAR, TBR, mean glucose, and CV were similar between weekdays and weekends (p >0.34 for all). TIR >70% was achieved by 52% of participants on weekdays and 48% on weekends, with no statistically significant difference (p = 0.75). Longer diabetes duration correlated with lower TIR (r = −0.62, p <0.001), higher mean glucose (r = 0.58, p = 0.002), and greater variability (r = 0.54, p = 0.004). Older age was associated with lower TIR (r = −0.48, p = 0.014) and higher mean glucose (r = 0.44, p = 0.025). Higher HbA1c correlated with lower TIR (r = −0.36, p = 0.04), higher TAR (r = 0.35, p = 0.05), greater variability (r = 0.51, p = 0.006), and increased target organ damage (ρ = 0.55, p = 0.004). BMI was not associated with TIR (r = −0.18, p = 0.38). Participants with ≥2 complications had lower TIR (55.8 ± 28.4% vs 76.7 ± 19.2%, p = 0.073), while insulin the Conclusion In Malaysian adults with T2DM, CGM metrics were similar between weekdays and weekends, indicating lifestyle differences had minimal impact on glycemic control. Longer diabetes duration, older age, higher HbA1c, multiple complications, and insulin therapy identified patients at highest risk for poor glycemic control, greater variability, and hypoglycemia. These findings support the use of CGM for risk stratification, individualized monitoring, and therapy optimization to reduce complications and hypoglycemia risk.
Adult ; Blood Glucose ; Blood Glucose Self-Monitoring ; Continuous Glucose Monitoring ; Diabetes Mellitus, Type 2

Introduction: Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) induce clinically meaningful weight reduction in patients with type 2 diabetes mellitus (T2DM), but real-world data in Southeast Asian populations are limited. This study evaluated the effectiveness of GLP-1 RAs in achieving clinically significant weight loss in Malaysian patients with obesity and T2DM. Methodology: A retrospective cohort study was conducted among adults with T2DM and obesity attending the Endocrinology Clinic at Hospital Sultan Abdul Aziz Shah between January 2023 and December 2024. Patients receiving GLP-1 RAs (semaglutide or liraglutide) were compared with those on standard care. Anthropometric outcomes were assessed over 6–12 months, with weight loss thresholds of ≥3, ≥5, and ≥10%. Between-group comparisons used Fisher’s exact test, and odds ratios (OR) were calculated. Results: Eighty-five patients were included (GLP-1, n = 47; control, n = 38). The GLP-1 group achieved significantly higher rates of any weight loss (70.0% vs 41.2%; OR = 3.33, p = 0.019) and ≥3% weight loss (42.5% vs 14.7%; OR = 4.29, p = 0.011). Number needed to treat was 3–4 patients. Proportions achieving ≥5 and ≥10% weight loss were higher in the GLP-1 group but did not reach statistical significance. Conclusion GLP-1 RA therapy significantly improves the likelihood of clinically meaningful weight loss in Malaysian patients with obesity and T2DM. These findings support the integration of GLP-1 RAs into routine obesity management strategies in Southeast Asia.
Humans ; Diabetes Mellitus, Type 2 ; Glucagon-Like Peptide-1 Receptor Agonists ; Weight Loss

Introduction: While Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are effective for weight reduction in type 2 diabetes mellitus (T2DM), interindividual variability exists. Lifestyle factors, particularly baseline physical activity, may modify weight loss outcomes. This study examined whether baseline activity influences GLP-1 RA efficacy in Malaysian patients. Methodology: A retrospective cohort of adults with obesity and T2DM receiving GLP-1 RAs (semaglutide or liraglutide) from January 2023 to December 2024 was analyzed. Baseline physical activity was classified as active or inactive. Primary outcomes were achievement of ≥3 and ≥5% weight loss over 6–12 months. Associations were assessed using Fisher’s exact test and logistic regression. Results: Among GLP-1-treated patients, those reporting baseline physical activity were more likely to achieve ≥3% weight loss and demonstrated trends toward higher, ≥5%, weight loss. Logistic regression suggested baseline activity increased the odds of clinically meaningful weight reduction, though statistical significance was limited by sample size. Conclusion Baseline physical activity may enhance GLP-1 receptor agonist-mediated weight loss in obese patients with T2DM. Integrating lifestyle interventions with pharmacotherapy may optimize treatment outcomes. Larger prospective studies are warranted to confirm these findings.
Humans ; Glucagon-Like Peptide-1 Receptor Agonists ; Exercise ; Weight Loss ; Obesity ; Diabetes Mellitus, Type 2

Introduction: Uterine fibroids are common in reproductive-age women and are associated with obstetric complications. Their potential contribution to maternal metabolic disturbances is poorly described. We report a case of maternal hypoglycemia in the setting of a large uterine fibroid and fetal overgrowth, suggesting a possible endocrine–metabolic interaction. Case: A 39-year-old multiparous female with no history of diabetes or endocrine disease had a large lower-segment uterine fibroid measuring 8 × 10 cm. Pregnancy was otherwise uncomplicated until 39 weeks, when she underwent classical Caesarean section for transverse lie and delivered a large-for-gestational-age infant. Postpartum, she developed recurrent symptomatic hypoglycemia despite normal hemoglobin A1c (5.0%) and preserved thyroid and adrenal function. There was no evidence of sepsis, liver disease, medication exposure, or insulinoma. Hypoglycemia resolved spontaneously following delivery. Postnatal imaging showed persistence of the fibroid (6 × 9 cm). She remains under follow-up, considering interval laparoscopic myomectomy with bilateral tubal ligation. The coexistence of maternal hypoglycemia and fetal overgrowth raises the possibility of altered maternal– fetal glucose dynamics. Large mesenchymal tumors may produce insulin-like growth factor 2 (IGF-2), causing non–islet cell tumor hypoglycemia. Fibroid-related uteroplacental hemodynamic changes or increased fetal glucose demand may also contribute. While causality cannot be established, the temporal resolution post-delivery suggests a contributory role of the fibroid in metabolic disturbance. Conclusion This case highlights a rare but clinically relevant association between a large uterine fibroid, maternal hypoglycemia, and fetal overgrowth. In pregnant patients with unexplained hypoglycemia, uterine fibroids may represent an overlooked factor. Multidisciplinary follow-up and further research into IGF signaling and placental–tumor interactions are warranted.
Diabetes, Gestational ; Fetal Macrosomia ; Leiomyoma ; Hypoglycemia

Introduction: Non-thyroidal illness syndrome commonly occurs during acute systemic illnesses and is characterized by suppressed or inappropriately normal thyroid-stimulating hormone with low or low-normal thyroid hormone levels. This biochemical pattern may obscure or delay the diagnosis of underlying hyperthyroidism, especially in mild or borderline cases. Acute stroke is a recognized trigger of non-thyroidal illness syndrome, yet its masking effect on hyperthyroidism is under-recognized in clinical practice. Case: A 58-year-old Malay male with cardiovascular risk factors presented with an acute ischemic stroke involving the left occipital lobe and right internal capsule. He developed new-onset atrial fibrillation (CHA₂DS₂-VASc 3) and mild left ventricular systolic dysfunction. Initial thyroid function tests during the acute stroke phase showed mildly suppressed thyroid-stimulating hormone (TSH) (0.30 mIU/L) with high-normal free T4 (21.2 pmol/L), interpreted in the context of acute illness. The patient was clinically stable without overt thyrotoxic features. One month post-stroke, repeat testing revealed further TSH suppression (0.09 mIU/L) and rising free T4 (27.6 pmol/L). Detailed history uncovered prior Graves’ disease in 2019 with treatment default. Examination revealed a small diffuse goiter without ophthalmopathy. The biochemical evolution following recovery from acute illness confirmed recurrent hyperthyroidism previously masked by nonthyroidal illness syndrome. Conclusion Acute stroke can induce cytokine-mediated suppression of the hypothalamic-pituitary-thyroid axis and altered peripheral deiodination, leading to misleading thyroid function tests. In this case, non-thyroidal illness syndrome blunted the biochemical severity of hyperthyroidism, delaying recognition despite high-risk features such as atrial fibrillation and prior Graves’ disease. Reliance on a single thyroid function test during acute illness may therefore result in underdiagnosis.
Euthyroid Sick Syndromes ; Ischemic Stroke ; Hyperthyroidism

Introduction: Carbimazole is a first-line therapy for thyrotoxicosis and is generally well tolerated. Drug-induced liver injury is rare (<1%) and typically presents as cholestatic hepatotoxicity, in contrast to propylthiouracil, which more commonly causes hepatocellular injury. Clinical presentation may mimic obstructive jaundice, and delayed recognition can lead to unnecessary investigations and interruption of definitive thyroid management. : A 70-year-old female with toxic multinodular goiter developed painless jaundice 4 weeks after starting carbimazole 20 mg daily for thyrotoxicosis precipitated by urinary tract infection. She had no prior liver disease or alcohol exposure. Examination revealed isolated icterus without features of chronic liver disease. Initial thyroid function tests showed suppressed thyroidstimulating hormone (<0.01 mIU/L) with markedly elevated free T4 (>100 pmol/L), improving after 4 weeks (free T4 29.1 pmol/L). She subsequently developed progressive jaundice without abdominal pain, fever, pruritus, or encephalopathy. Liver biochemistry demonstrated a cholestatic pattern (R factor 1.1) with conjugated hyperbilirubinemia (peak bilirubin 227 µmol/L), mild transaminitis, and elevated alkaline phosphatase. Imaging, including hepatobiliary ultrasonography, contrast computed tomography, and endoscopic ultrasound, excluded biliary obstruction. Viral, autoimmune, and structural causes were negative. Carbimazole-induced cholestatic jaundice was diagnosed based on temporal association and exclusion of alternatives. Carbimazole was discontinued, ursodeoxycholic acid was initiated, and radioactive iodine therapy was performed, followed by gradual recovery. Conclusion Carbimazole-induced hepatotoxicity (0.1–0.2%) is likely idiosyncratic and not dose dependent. Differentiating drug-induced liver injury from thyrotoxicosis-related liver dysfunction is critical, as restoration of euthyroidism alone may normalize liver enzymes. Diagnosis relies on the exclusion of obstruction and recognition of drug chronology. Early drug withdrawal and multidisciplinary management are essential to prevent progression while ensuring timely definitive therapy.
Thyrotoxicosis ; Cholestasis

Introduction: Endogenous Cushing syndrome is a rare manifestation of chronic cortisol excess. It may present with severe hypercortisolism complicated by life-threatening opportunistic infections. Surgical management of a cortisol-secreting tumor is the mainstay of therapy. However, when the source is not found or when surgery is not feasible, medical therapies may be employed for rapid control of hypercortisolism. CASE: A 13-year-old male presented with breathlessness for one day. He also had a cough associated with weight loss, weakness, and hallucinations for 1 month. On presentation, he was tachypneic and had moon facies, acne, fine moustache, limb wasting, and pigmented nail beds. He was also hypertensive and developed an episode of seizure during admission. Investigation results showed severe hypokalemia and lymphopenia. Radiological examination revealed pneumothorax with multiple lung cavitations and brain tuberculomas. Bronchoalveolar lavage (BAL) was positive for Aspergillus fumigatus. However, both BAL and CSF PCR and culture for TB were negative. Serum ACTH was 379 pg/mL (0–46), and morning serum cortisol was 2,948 nmol/L with loss of diurnal rhythm. His 24-hour urine cortisol was 14,252 nmol/24 hour (31.7–282). This is consistent with ACTH-dependent Cushing syndrome. He was started on anti-TB and anti-fungal treatment. Serum cortisol levels were persistently high while on high-dose intravenous dexamethasone treatment for TB meningitis. An MRI pituitary and a CT scan thorax, abdomen, and pelvis could not reveal an ACTH-secreting tumor source. Metyrapone was started and titrated upwards to control the hypercortisolism. Serum cortisol reduced to 200–300 nmol/L after 1 month, and 24-hour urinary cortisol was down to 22.4 nmol/24 hour after 4 months, requiring weaning of metyrapone doses. Conclusion Metyrapone is effective in the rapid control of severe hypercortisolism with life-threatening complications, as illustrated in this case. However, it warrants careful monitoring and titration.
Child ; Cushing Syndrome

Fecal occult blood test (FOBT) screening has been shown to decrease the incidence and mortality of colorectal cancer (CRC). The sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of the immunochemical fecal occult blood test (i-FOBT) in diagnosing CRC were assessed among the patients in a tertiary referral hospital in Malaysia. A total sample of 814 patients aged 16 to 85 years old who performed i-FOBT and endoscopic screenings was obtained. The patients were recruited for a retrospective investigation. Sensitivity, specificity, PPV, and NPV were derived for the CRC screenees. Out of the 814 patients screened using i-FOBT, half of them were above 59 years old (49.6%), and 36% had positive i-FOBT. Gender distribution was almost equal, where 53.4% of the patients were female, and 46.6% were male. Majority of the patients were Malays (56.6%), followed by Chinese (24.0%), Indians (16.5%), and others (2.9%). Among the 71 patients referred for colonoscopy, 57.7% and 42.3% corresponded to positive and negative i-FOBT cases, respectively. Polyps were found to be most common among the patients (25.6%), 7.0% were found positive for invasive CRC, and 35.2% had normal colonoscopic findings. There was a significant association between colonoscopic finding and positive i-FOBT (p=0.001). The sensitivity, specificity, PPV, and NPV for CRC detection were 66.7%, 43.0%, 9.8%, and 93.3%, respectively. The results indicate that i-FOBT is a useful tool in the detection of abnormalities in the lower gastrointestinal tract and therefore serves as a cornerstone for potential large-scale screening programmes.

Background: Diabetes Mellitus (DM), characterised by chronic hyperglycaemia, exposes patients to acute and chronic complications, such as hypoglycaemia and vascular complications, respectively. The latter is associated with the degree of glycaemic control. Glycated haemoglobin (HbA1c) indicates long-term glycaemic control of the preceding 2-3 months. The practice of self-monitoring blood glucose (SMBG) is essential for insulin-treated diabetic patients to achieve optimum glycaemic control and prevent hypoglycaemia. Aim: The study aimed to determine the SMBG practice and frequency and its association with HbA1c and factors in insulin-treated diabetic patients. Methods: This was a cross-sectional study of insulin-treated diabetic patients attending follow-up at the diabetic clinic of Hospital Serdang from April 2015 to August 2015. Consented eligible patients completed validated selfadministered questionnaires. Patients’ HbA1c results were obtained from the hospital information system. Results: Ninetyone of 137 (66%) patients practiced SMBG and 46 (34%) did not. Although 82% had seen diabetic nurses, 54% of patients did not alter their treatment accordingly. Neither the practice nor the frequency of SMBG was significantly associated with differences in HbA1c levels (p=0.334 and p=0.116 respectively). Ethnicity and household income significantly affected SMBG practice. The presence and frequency of hypoglycaemia significantly increased the likelihood of SMBG practice (p<0.001) and frequency (p<0.001). Conclusions: The prevalence of SMBG practice in diabetic patients on insulin was 66%. However, SMBG was not followed by proper treatment alteration in 54% of patients. There was no association between SMBG practice and frequency with good glycaemic control. Hypoglycaemia significantly affected the practice and frequency of SMBG.
Insulin