Introduction: Skeletal disease in transfusion-dependent thalassemia is commonly attributed to reduced bone mineral density and managed with anti-resorptive therapy. However, chronic iron overload can induce progressive endocrine siderosis, disrupting anabolic pathways essential for bone homeostasis. This mechanism remains under-recognized and may underlie treatment failure in severe cases. Case: We describe a 34-year-old female with transfusiondependent HbE β-thalassemia, post-splenectomy, receiving regular transfusions and iron chelation, who sustained multiple pathological fractures following a trivial fall, including bilateral supracondylar femur fractures and a distal radius fracture. She had severe systemic iron overload (ferritin 2,621 ng/mL) complicated by hepatic cirrhosis, insulin-dependent diabetes, and hypogonadotropic hypogonadism. Bone mineral density assessment demonstrated severe osteoporosis (hip T-score −5.4) despite prolonged bisphosphonate therapy, with prior vertebral compression fracture. Endocrine evaluation revealed multiaxis dysfunction, including gonadal failure and probable growth hormone deficiency, consistent with pituitary and peripheral endocrine siderosis. Conclusion This case demonstrates that skeletal fragility in transfusiondependent thalassemia reflects an endocrine-driven failure of bone formation rather than isolated loss of bone mineral density. Iron overload–induced endocrine siderosis impairs osteoblast function and suppresses anabolic signaling, leading to profound skeletal vulnerability. The progression of osteoporosis despite anti-resorptive therapy highlights the limitation of conventional approaches and supports reframing thalassemia-associated bone disease as an endocrine disorder. Severe osteoporosis should prompt systematic endocrine evaluation, with early hormonal replacement and consideration of anabolic therapy to prevent catastrophic fractures and long-term disability.
Siderosis ; Thalassemia

Introduction: Autoimmune thyroid disease is frequently associated with other immune-mediated disorders; however, clinically significant pancytopenia is rare. In patients with Graves’ disease receiving antithyroid therapy, leukopenia raises concern for drug-induced agranulocytosis, a rare but potentially life-threatening complication characterized by severe neutropenia requiring immediate drug withdrawal. The coexistence of hemolytic anemia and thrombocytopenia may instead suggest Evans syndrome, defined by autoimmune hemolytic anemia with immune thrombocytopenia, with or without neutropenia. Importantly, uncontrolled thyrotoxicosis itself may cause immunemediated cytopenias, creating a diagnostic challenge. Case: We report a 55-year-old female with thyroid receptor antibody-positive Graves’ disease who presented with jaundice and pancytopenia while receiving carbimazole therapy. Laboratory evaluation demonstrated anemia with reticulocytosis and a positive direct antiglobulin test, thrombocytopenia and leukopenia. Complement testing revealed reduced C3 with normal C4, consistent with immune-mediated hemolysis. Peripheral blood film showed no blast cells or marrow infiltration, and autoimmune screening, including antinuclear antibodies and anti–double stranded DNA, was negative. The coexistence of Coombs-positive hemolysis and thrombocytopenia initially raised suspicion for Evans syndrome, while leukopenia during carbimazole therapy prompted concern for drug-induced agranulocytosis. However, neutropenia was not severe, and the absence of marrow infiltration or systemic autoimmune disease made alternative causes of pancytopenia less likely. Importantly, blood counts progressively improved following the optimization of thyroid control despite continuation of carbimazole at a reduced dose, without the use of immunosuppressive therapy. This clinical course supported the interpretation of thyrotoxicosis-associated immune cytopenia rather than primary Evans syndrome or carbimazole-induced agranulocytosis. Conclusion This case highlights thyrotoxicosis-associated immune cytopenia as an important mimic of Evans syndrome and carbimazole-related hematological toxicity. Recognizing this entity is essential to avoid unnecessary discontinuation of antithyroid therapy or inappropriate immunosuppressive treatment.
Evans Syndrome ; Carbimazole ; Pancytopenia ; Agranulocytosis ; Graves Disease

Introduction: Thyroid stimulating hormone (TSH) suppression following differentiated thyroid carcinoma is widely recommended to reduce recurrence risk. However, this strategy assumes cardiovascular tolerance to supraphysiologic thyroid hormone exposure. In patients with advanced structural heart disease, this assumption may fail, exposing a critical limitation of guideline-directed TSH suppression. Case: We report a 71-year-old male with end-stage renal failure on hemodialysis and severe ischemic cardiomyopathy (ejection fraction 23%) who presented with acute decompensation characterized by dyspnea, rapid atrial fibrillation, and non–ST-elevation myocardial infarction. He had a history of papillary thyroid carcinoma treated with total thyroidectomy and radioactive iodine over 20 years prior and was maintained on levothyroxine 200 mcg daily for TSH suppression. Despite biochemically euthyroid indices (TSH 1.8 mIU/L, free thyroxine 4 17 pmol/L), he developed recurrent arrhythmia with heart failure decompensation. This case highlights a dissociation between biochemical euthyroidism and tissue-level thyrotoxicity in a structurally compromised myocardium. Papillary thyroid carcinoma after definitive therapy typically follows an indolent course with low short-term mortality. In contrast, in severe left ventricular dysfunction, excess thyroid hormone increases adrenergic sensitivity and myocardial oxygen demand, precipitating arrhythmia and ischemia. This risk is amplified in end-stage renal disease, where altered hormone handling renders biochemical indices less reliable. Conclusion Biochemical euthyroidism does not equate to physiological safety. In patients with advanced cardiovascular disease, thyroid hormone therapy should be titrated to cardiovascular tolerance rather than oncologic targets alone, and routine TSH suppression may be inappropriate.
Thyroxine ; Heart Failure ; Thyrotropin

Introduction: Thyrotoxicosis following neck surgery is typically attributed to transient destructive thyroiditis from follicular disruption. In end-stage renal failure (ESRF), however, altered thyroid hormone kinetics, including reduced protein binding, impaired peripheral metabolism, and decreased clearance, can distort biochemical interpretation. This creates a high-risk scenario where laboratory values overestimate tissue thyrotoxicity, predisposing to inappropriate antithyroid therapy. We present a case demonstrating marked clinical–biochemical dissociation, reframing postoperative thyrotoxicosis in ESRF as a disorder of hormone handling rather than hormone overproduction. Case: A 45-year-old female with ESRF on maintenance hemodialysis and tertiary hyperparathyroidism underwent total parathyroidectomy. Preoperative thyroid function was consistently euthyroid. Within 48 hours postoperatively, she developed severe biochemical thyrotoxicosis (thyroidstimulating hormone 0.28 mIU/L, free thyroxine 4 [FT4] 68 pmol/L). Despite this, she remained clinically euthyroid, with stable hemodynamics, absence of adrenergic or neuropsychiatric features, and no evidence of thyroid eye disease. The temporal relationship strongly suggested destructive thyroiditis secondary to surgical manipulation, with passive release of preformed thyroid hormone. In the context of ESRF, impaired hormone clearance and altered binding likely amplified circulating free hormone levels without proportional end-organ effect, resulting in striking clinical–biochemical dissociation. A conservative strategy was adopted. Antithyroid drugs were withheld, given the non-synthetic mechanism of hormone excess, and the patient was managed with close monitoring and symptom-guided beta-blockade. Serial thyroid function demonstrated spontaneous improvement without complications. Conclusion Post-parathyroidectomy thyrotoxicosis in ESRF represents exaggerated biochemical derangement without true tissue toxicity. Management must prioritize physiology over laboratory values, as misclassification risks iatrogenic harm. This case demonstrates that in ESRF, elevated FT4 may not reflect true tissue thyrotoxicity, and reliance on biochemical severity alone can lead to inappropriate antithyroid therapy and iatrogenic harm.
Parathyroidectomy ; Hyperthyroidism ; Thyrotoxicosis

Introduction: N-Carboxymethyllysine (CML) is involved in diabetic nephropathy (DN) via production of oxidative stress, growth factors and cytokines. C-reactive protein (CRP) is an inflammatory marker associated with diabetes risk. This study is to determine the level of serum CML and CRP in Type 2 diabetes mellitus (T2DM) patients and healthy subjects and to determine the correlation between CML and CRP with glycated haemoglobin (HbA1c) in T2DM patients. Methods: This is a case-control study on 73 T2DM patients without nephropathy, 74 T2DM patients with nephropathy and 73 healthy subjects, aged from 18 to 65 years old. Fasting venous blood was taken and analysed for CML, CRP, HbA1c, and creatinine. The comparisons of serum CML and CRP among the three groups and the correlation between CML and CRP with HbA1c (in T2DM patients) were determined. Results: The differences in CML [median (Interquartile Range) (IQR)] between healthy subjects [131.80 (73.56) ng/ml] and T2DM patients without nephropathy [188.80 (55.95) ng/ml]; between healthy subjects and T2DM patients with nephropathy [237.70 (439.04) ng/ml] were statistically significant (P<0.001). The differences in CRP [median (IQR)] between healthy subjects [1.64 (1.91) ng/ml] and T2DM patients without nephropathy [2.15 (5.64) ng/ml]; between healthy subjects and T2DM patients with nephropathy [4.75 (6.91) ng/ml] were statistically significant (P<0.001). Logistic regression showed CML and CRP are independent predictors of diabetic groups. There was no correlation between HbA1c with CML and CRP in T2DM groups. Conclusion: Since serum CML and CRP are independent predictors of DN, their levels can be used to identify high-risk diabetic patients prone to developing DN.

Introduction: Suboptimal vitamin D levels are commonly presented by systemic lupus erythemathosus (SLE) patients. This is likely due to protection measures from sunshine exposure adopted by SLE patients to reduce the likelihood of SLE flares onset. In this study, we investigated the vitamin D level among SLE patients and its association with SLE Disease Activity (SLEDAI) scores and among groups of steroid and non-steroid usage. Methods: We recruited 84 SLE patients who attended the Rheumatology Clinic of Hospital Universiti Sains Malaysia from June 2018 until October 2018. Their clinico-demographic data were retrieved and serum vitamin D immunoassay was conducted to measure the vitamin D levels of each patient Vitamin D levels were categorized as normal (≥75nmol/L), insufficient (50-74 nmol/L) or deficient (<50 nmol/L). Comparison between the clinico-demographic parameters with vitamin D levels were conducted using the Fisher’s exact test (for categorical variables) and unpaired t-test (for continuous variables). Results: The mean vitamin D level among the subjects was 40.79 ± 20.2 nmol/L. Fifty-eight (69%) patients were vitamin D deficient, while 20 (23.8%) patients were vitamin D insufficient, and only 6 (7.1%) patients had sufficient level of vitamin D. Vitamin D status was not significantly associated with SLEDAI score (p=0.185) as well as between steroids and non-steroids groups (p=0.255). Conclusion: Vitamin D deficiency occurred in majority of our SLE patients. SLE disease activities were not associated with the status of vitamin D or steroid usage.

Introduction: Despite abundant sunshine for cutaneous vitamin D synthesis, low levels of vitamin D have been documented among the Malaysian population. The aim of this study was to characterise the effects of occupational sunlight exposure and monsoon season on serum 25-hydroxyvitamin D [25(OH)D] concentration. Methods: A comparative cross-sectional study was performed among Malay outdoor (n=119) and indoor workers (n=119) in Kelantan. Two-point data were collected on the same participants, first during non-monsoon season and second during the northeast monsoon season. Data collection comprised of anthropometry measurements (body mass index and body fat), fasting blood test [serum 25(OH)D concentration], and questionnaire (physical activity level, sun exposure, sun protection use, and vitamin D intake). Vitamin D classification was based on the 2011 Endocrine Society Clinical Practice Guidelines. Results: This study found that serum 25(OH)D concentrations were significantly higher in outdoor compared to indoor workers irrespective of season (p<0.001) and sex (p<0.001). Monsoonal differences in serum 25(OH)D concentration was only observed in male outdoor workers (mean difference=10.39 nmol/l, p<0.001). Significant association between vitamin D status and occupation was also observed (p<0.001). However, no significant association was found between vitamin D status and monsoon season [χ2(1)=0.076, p=0.783]. Conclusion: Seasonal and occupational factors should be considered while evaluating individual serum 25(OH)D concentration and in comparing community studies, especially among workers.

BACKGROUND: A qualitative study providing an in-depth exploration of people's view and the increasing burden of overweight and obesity is required. This study aimed to explore the understanding of dieting and previous experiences on weight loss attempts among overweight and obese government employees in Kelantan, Malaysia, prior to recruitment into the intervention program. METHODS: Thirteen focus group discussions involving 129 participants from a weight-loss intervention program were conducted within the first 1 month of recruitment. These discussions were moderated by two trained researchers in the Malay language and assisted by an interview guide. They were audio-recorded and transcribed verbatim. A thematic analysis was performed, and codes and themes from each discussion were constructed. RESULTS: The participants understood dieting with various meanings, including skipping meals and removing rice from daily diets. They applied numerous methods to lose weight and achieved various outcomes. Health and appearance, social support, and compliance with current trends were the factors motivating these participants to lose weight. Their determination to lose weight was limited by lack of self-control and motivation, experiences of unpleasant effects, influence on weight, and environmental and health factors. CONCLUSION: Real-life weight loss experiences and perceptions provided relevant insights into current weight loss management strategies. Some of these issues and misunderstandings should be emphasized in weight loss strategies during health promotion.
Compliance ; Diet ; Focus Groups ; Health Promotion ; Malaysia ; Meals ; Motivation ; Obesity ; Overweight ; Qualitative Research ; Self-Control ; Weight Loss