Environmental and Health Impacts of Pesticide-Based Malaria Control in Low- and Middle-Income Countries: A Scoping Review Introduction Malaria remains a major public health challenge in tropical and subtropical regions, necessitating effective vector control strategies. This scoping review aims to evaluate the environmental and health impacts of pesticide-based malaria control in low-and middle-income countries (LMICs). Methods A comprehensive search was conducted across Scopus, Web of Science and PubMed for studies published between 2004 and 2024, using a predefined search string based on the PEO framework. Inclusion criteria focused on studies addressing malaria control programmes and their effects on the environment and human health. Data extraction followed PRISMA 2020 guidelines. Results 12 studies were included, most of which focused on indoor residual spraying (IRS) and insecticide-treated nets (ITNs). The review identified significant direct and indirect impacts. While effective in reducing malaria transmission, IRS and ITNs pose substantial risks. Direct health effects included acute poisoning and long-term neurodevelopmental issues linked to pesticide exposure, with residues detected in breast milk. Environmental impacts included soil and water contamination, biodiversity loss and ecological disruption. The overlap of pesticide use in malaria control and agriculture was found to exacerbate insecticide resistance in mosquito populations. Conclusions Pesticide-based malaria control, while crucial, carries significant unintended consequences for human health and the environment. The findings underscore the urgent need for Integrated Vector Management (IVM) strategies that reduce reliance on chemical pesticides, mitigate resistance, and ensure environmental sustainability and public health safety.

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: Severe hypertriglyceridemia, though rare in pregnancy, is a clinically significant condition that poses substantial maternal and perinatal risks. Case: We present a case of a 42-year-old pregnant female with class I obesity and pre-existing type 2 diabetes mellitus, with a booking hemoglobin A1c 12.1%. Her poorly controlled diabetes was complicated by nephrotic syndrome, with a 24-hour urine protein 4.9 g/day. She also had bilateral diabetic retinopathies requiring multiple sessions of panretinal photocoagulation. Throughout the pregnancy, her triglycerides rose progressively, peaking at 30 mmol/L by 33 weeks. Investigations revealed normal thyroid function, urea 4.8 mmol/L, creatinine 66 umol/L, and albumin 26 g/dL. The patient was hospitalized at 33 weeks of gestation and started on an intravenous insulin infusion along with a very low-fat, low-carbohydrate diet prescribed by a dietitian. Pulmonary embolism was diagnosed during evaluation for maternal tachycardia, and subcutaneous enoxaparin was initiated. One week after admission in 35 weeks of gestation, the baby was delivered via emergency Caesarean section due to fetal distress. The baby was small for gestational age, with a birth weight of 1.9 kg, below the 10th percentile for gestational age, and required admission to the neonatal intensive care unit with oxygen support for pneumonia-related respiratory distress. Post-delivery, intravenous insulin infusion and dietary control were continued, reducing her triglyceride level to the lowest level of 8.3 mmol/L. Both mother and baby were discharged well. Lipid-lowering agents such as rosuvastatin and fenofibrate were started after breastfeeding stopped, aiming to normalize her triglyceride levels. Conclusion Hypertriglyceridemia in this patient was the result of uncontrolled diabetes mellitus with nephrotic-range proteinuria. Severe hypertriglyceridemia can cause acute pancreatitis and/or hyperviscosity syndrome, both of which are life-threatening to the mother and baby. Thus, rapid reduction of triglyceride levels is crucial. This case highlights the importance of achieving good diabetes control prior to pregnancy, with strict adherence to treatment and enhanced patient education.
Female ; Pregnancy ; Glycemic Control ; Hypertriglyceridemia

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: Incidental hyperparathyroidism with hypercalcemia is not uncommon. However, parathyroid carcinoma is an extremely rare endocrine malignancy, accounting for less than 1% of cases of primary hyperparathyroidism. Case: A 57-year-old Malay female with well-controlled type 2 diabetes was incidentally found to have hypercalcemia during hospitalization for pyelonephritis. She was asymptomatic, with no history of calcium supplementation or family history of endocrine disorders. Physical examination revealed no obvious neck swelling, and other systemic examinations were unremarkable. Investigations showed elevated serum calcium (2.87–3.4 mmol/L), low phosphate (0.34–0.76 mmol/L), and elevated intact parathyroid hormone (iPTH) (6.81 pmol/L). Her 25-OH vitamin D was deficient (45.58 nmol/L). Ultrasound of the neck revealed a solid lesion (1.6 × 2.0 × 2.8 cm) posterior to the right thyroid lobe with bilateral thyroid nodules, with the highest TR4, and normal cervical lymph nodes. Sestamibi scan showed multinodular goiter with cold nodules in bilateral thyroid lobes and a soft tissue lesion posterior to the right thyroid lobe. Subsequently, she underwent right hemithyroidectomy with intraoperative nerve monitoring and right inferior parathyroidectomy with intraoperative iPTH monitoring; the intraoperative iPTH level dropped appropriately from 24 to 2.4 pmol/L. Histopathological examination of the excised right parathyroid gland revealed parathyroid carcinoma, while the right thyroid lobe showed nodular hyperplasia. Postoperatively, calcium and iPTH levels normalized, and she remained well under follow-up. Conclusion Parathyroid carcinoma typically presents with markedly elevated calcium and iPTH levels, often alongside a palpable neck mass. However, in this patient, serum iPTH was only slightly above the upper limit of normal, with tumor size less than 3 cm, no lymph node or surrounding structures involvement from pre-operative evaluation imaging. This highlights the variability in both physical and biochemical presentations of parathyroid carcinoma and the challenges in distinguishing it from benign parathyroid tumors preoperatively.
Parathyroid Neoplasms

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

Introduction: Muscle weakness in thyroid disease is commonly attributed to thyrotoxic myopathy or hypokalemic periodic paralysis. Nevertheless, autoimmune conditions such as idiopathic inflammatory myopathies (IIM) and myasthenia gravis (MG) should be considered, as they may coexist with Graves’ disease. Case: A 54-year-old female with hypertension and Graves’ disease, treated with carbimazole for 2 years, had her therapy discontinued after remission. She was restarted on low-dose carbimazole following symptom recurrence. Three weeks later, she developed progressive proximal weakness, dysphagia, hoarseness, anorexia, and weight loss. On examination, body mass index was 22 kg/m² with mild proptosis, symmetrical proximal weakness (MRC 4/5), and erythematous rashes on thighs and shins. Otorhinolaryngology evaluation confirmed bilateral vocal cord palsy. Investigations revealed markedly elevated creatine kinase (7,950 U/L), aspartate aminotransferase (349 U/L), and alanine aminotransferase (179 U/L), with euthyroid biochemistry (thyroid-stimulating hormone 5.21 mIU/L, free thyroxine 4 16.6 pmol/L). Hypokalemia correction failed to improve symptoms, excluding periodic paralysis. ANA, C3, and C4 were normal. Myositis panel showed strong anti-Cytosolic 5’-nucleotidase 1A positivity with borderline anti-Ro-52. A diagnosis of IIM with bulbar involvement was made. She was treated with intravenous methylprednisolone and intravenous immunoglobulin, with clinical improvement. Conclusion This case highlights the diagnostic challenge of muscle weakness in thyroid disease. While thyrotoxic myopathy is often presumed, markedly elevated creatinine kinase, rash, and bulbar involvement should prompt suspicion of IIM. Early immunosuppressive therapy is essential to achieve favorable outcomes.
Muscle Weakness ; Thyroid Diseases ; Muscular Diseases

Introduction: Early identification of patients at risk for severe multisystem inflammatory syndrome in children (MIS-C) is essential for favourable clinical outcomes. This study aims to identify the clinical characteristics, factors and outcomes associated with severe MIS-C. Materials and methods: In this retrospective cohort study involving 14 major hospitals in Malaysia, children <15 years who met the United States Centres for Disease Control and Prevention case definition for MIS-C were included. Severe MIS-C was defined as children who required inotropic support, ventilatory support (invasive or non-invasive ventilation), or left ventricular ejection fraction of <55%. The factors investigated for severe MIS-C were demographic characteristics, the presence of comorbidities, clinical characteristics, and laboratory measures. Multivariable logistic regression was used to compute the adjusted odds ratio (aORs) of factors associated with severe MIS-C. Results: Among the 155 patients, 91 (58.7%) presented with severe MIS-C. Severe MIS-C was more likely in patients aged ≥5 years old (aOR 2.13, 95% confidence interval [CI] 1.08-4.21), with dehydration (aOR 3.80, 95% CI 1.53-9.45), lethargy (aOR 2.02, 95% CI 0.97-4.18), tachycardia (aOR 8.33, 95% CI 3.27-21.22), albumin <30g/L (aOR 3.36, 95% CI 1.58-7.13), creatine kinase >200U/L (aOR 3.68, 95% CI 1.57-8.64), D-dimer >3.0µg/mL (aOR 2.11, 95% CI 1.08-4.13), ferritin >500ng/mL (aOR 3.77, 95% CI 1.88-7.55), prothrombin time >12.7 seconds (aOR 3.22, 95% CI 1.61-6.43), and urea >6mmol/L (aOR 5.09, 95% CI 2.04-12.71). Conclusion: Identification of these associated factors of severity in MIS-C could aid in early recognition and prompt escalation of care, leading to better outcomes.