Introduction: Swyer syndrome (46, XY gonadal dysgenesis) is a rare disorder of sex development, characterized by a phenotypic female with streak gonads and hypergonadotropic hypogonadism. It presents with primary amenorrhea and delayed puberty. Overlapping clinical features with Turner syndrome may cause diagnostic uncertainty, highlighting the role of karyotypic evaluation in diagnosis. Case: A 35-year-old phenotypic female was first evaluated at age 27 during admission for an acute viral illness, when incidental findings of primary amenorrhea, short stature (height 131 cm), webbed neck, pectus excavatum, and absent secondary sexual characteristics raised suspicion of Turner syndrome. She had hypertension, with initial imaging suggesting coarctation of the thoracic aorta. CT angiography showed focal narrowing of the descending aorta; multidisciplinary review favored aortic folding, and she was managed conservatively. Endocrine evaluation demonstrated hypergonadotropic hypogonadism, with markedly elevated follicle-stimulating hormone (FSH 108.6 IU/L) and luteinizing hormone (LH 23.16 IU/L) in the presence of low estradiol levels. Pelvic imaging revealed an atrophic uterus with absence of bilateral ovaries, consistent with gonadal dysgenesis. Karyotypic analysis was performed, demonstrating a 46, XY genotype with confirmed SRY gene presence, establishing the diagnosis of Swyer syndrome. DEXA scan demonstrated osteoporosis, in keeping with prolonged hypogonadism. She was commenced on hormone replacement therapy, resulting in the development of secondary sexual characteristics and regular withdrawal bleeding. She remains under structured multidisciplinary follow-up, with endocrine-led management of hypothyroidism and osteoporosis, alongside cardiology follow-up and gynecological surveillance. Conclusion This case highlights the diagnostic complexity of disorders of sex development with overlapping phenotypes and the need for re-evaluation when clinical progression is atypical. Diagnosis enables hormone replacement therapy for induction of secondary sexual characteristics and preservation of bone health. Integration of clinical, biochemical, and genetic data within a multidisciplinary framework is essential to achieve diagnostic accuracy and optimize outcomes.
Turner Syndrome

Introduction: The 2021 IDF-DAR risk calculator had been previously evaluated in multiple studies and subsequently widely accepted and applied in clinical practice as a practical standardized tool for patient risk stratification. Recently updated, the 2026 IDF-DAR Risk calculator enables a more individualized, evidence-related evaluation of patientrelated and disease-related risk factors, incorporating modern diabetes technologies, including continuous glucose monitoring (CGM), automated insulin delivery (AID) systems, and advanced insulin formulations to enhance risk stratification. This tool allows medical professionals to tailor Ramadan practices based on overall factors toward promoting safe fasting. Methodology: This prospective multicentre observational study recruited adults with Type 1 and Type 2 diabetes attending public hospitals nationwide. People with diabetes (PwD) intending to perform Ramadan fasting were invited to participate and assessed using the 2026 IDF-DAR Risk Calculator in the 6-week pre-Ramadan period between 30th January and 19th March 2026. Results: A total of 458 PwD were evaluated and stratified into low (15.7%), moderate (41%), and high risk (43.3%) categories. Most participants had Type 2 diabetes (83.6%), with 60.3% having a disease duration exceeding 10 years and 43% exhibiting poor glycemic control (hemoglobin A1c >9%). Insulin therapy was used by 76.4% of participants, including two individuals with Type 1 diabetes using AID systems. Most participants reported no recent hypoglycemia (76.4%), 81.0% performed glucose monitoring, and 3.3% used CGM. Severe comorbidities were uncommon, with 1.1% having unstable macrovascular disease and 4.4% advanced chronic kidney disease (estimated glomerular filtration rate <30). Notably, 72.2% received structured Ramadan education. Conclusion Majority of PwD attending tertiary diabetes clinics were in the moderate- to high-risk category and intended to fast despite medical advice against fasting in some cases. Although most participants were on insulin therapy, hypoglycemia was low in the pre-Ramadan period. Integration of modern technologies, advanced insulin therapies, and structured education may support safer fasting practices.
Risk Assessment ; Diabetes Mellitus ; Hospitals ; Fasting

Introduction: Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) improve glycemic control, promote weight loss, reduce insulin requirements, and confer cardiometabolic benefits in type 2 diabetes mellitus (T2DM). This audit evaluated glycemic and metabolic outcomes of GLP-1 RAs in T2DM patients at a single-centre diabetes clinic. Methodology: This audit included T2DM patients who initiated GLP1 RAs between January 2022 and March 2025 at Hospital Sultan Abdul Halim. Primary outcomes were changes in hemoglobin A1c (HbA1c), body weight, and body mass index (BMI) at 3 and 12 months. Secondary outcomes included percentage weight loss, changes in systolic blood pressure (SBP), insulin total daily dose (TDD), low-density lipoprotein (LDL) cholesterol, gastrointestinal adverse effects, and treatment discontinuation. Results: Sixteen patients were included; median age was 58.5 years (interquartile range [IQR] 47.5–65), and 56.3% were female. Median diabetes duration was 15 years (IQR 11.5–20.3). Median HbA1c decreased from 9.7% (IQR 8.6–10.4) at baseline to 8.8% (IQR 7.7–9.1) at 3 months and 7.8% (IQR 7.0–8.5) at 12 months. Body weight decreased from 88.1 kg (IQR 79.5–122.1) at baseline to 85.0 kg (IQR 75.9–113.7) at 3 months and 82.0 kg (IQR 74.8–117.3) at 12 months. BMI decreased from 37.8 kg/m² (IQR 31.7–47.1) to 37.3 kg/m² (IQR 30.7–45.5) at 3 months and 36.0 kg/m² (IQR 30.1–45.6) at 12 months. At 12 months, weight loss was 5.8% (IQR 3.0–8.0), with 56.5% achieving >5% weight reduction. In all, 93.8% achieved >1% HbA1c reduction. Mean SBP decreased by 10 ± 20 mmHg, LDL cholesterol 0.29 mmol/L (IQR -0.77 to 0.07), and insulin TDD 8 units/day (IQR -13 to 10). No gastrointestinal adverse effects reported. Three patients (18.8%) discontinued treatment due to excessive weight loss, treatment plateau, and limited drug availability. Conclusion From our single-centre experience, the observed improvements in glycemic and metabolic outcomes support the benefits of GLP-1 RAs in managing T2DM.
Diabetes Mellitus, Type 2 ; Glucagon-Like Peptide-1 Receptor Agonists ; Clinical Audit

Introduction: Severe hypertriglyceridemia increases the risk of pancreatitis and cardiovascular events. Therapies such as insulin, heparin, and plasmapheresis have been used. We present two cases of severe hypertriglyceridemia with distinct clinical presentations and management approaches. Cases: We first describe a 26-year-old female with hypertriglyceridemia who presented with acute epigastric pain radiating to the back. She had a prior admission 3 years earlier for acute pancreatitis complicated by acute respiratory distress syndrome, during which severe hypertriglyceridemia was diagnosed (triglycerides 13.5 mmol/L) but was not treated at that time. She had no history of alcohol use, diabetes, or family history of hypercholesterolemia. On admission, she was hemodynamically stable. Serum triglycerides were markedly elevated at 32.3 mmol/L, total cholesterol was 8.6 mmol/L, and non-HDL cholesterol was 8.1 mmol/L. Serum amylase was elevated (1,606 U/L). Computed tomography (CT) abdomen demonstrated acute interstitial pancreatitis with peripancreatic fluid collection. She was managed conservatively with intravenous fluids and bowel rest. Triglycerides declined rapidly to 6.1 mmol/L by day 8 without intravenous insulin therapy. She was discharged on lipid-lowering therapy. The second case involved a 57-year-old female with underlying hypertension, dyslipidemia, and poorly controlled diabetes mellitus who had not been on treatment for 3 years and presented with acute left-sided weakness. Brain CT confirmed a right cerebral infarction. Laboratory tests revealed triglycerides of 23.2 mmol/L, total cholesterol 9.9 mmol/L, non-HDL cholesterol 9.8 mmol/L, and hemoglobin A1c 11.2%. Intravenous insulin therapy was initiated, resulting in a progressive triglyceride reduction (Day 2: 18.7 mmol/L; Day 3: 13.1 mmol/L; Day 4: 11.0 mmol/L; Day 6: 6.9 mmol/L; Day 8: 4.2 mmol/L). Fenofibrate and high-intensity rosuvastatin were commenced, and glycemic control was optimized before discharge Conclusion Severe hypertriglyceridemia may present variably, from acute pancreatitis to ischemic stroke. Individualized management led to a successful reduction of triglycerides. Early recognition, tailored therapy, and ongoing metabolic care are essential to reduce recurrence and long-term complications.
Hypertriglyceridemia

: Introduction Retatrutide is an investigational triple agonist targeting glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, and glucagon receptors. Early clinical trials have demonstrated promising weight loss effects. Gastrointestinal side effects are common and dose-dependent; however, severe complications such as gastroparesis leading to starvation ketoacidosis are rarely reported. Increasing public interest in emerging anti-obesity pharmacotherapies has led to unsupervised access to investigational medications through unregulated channels. We report a case of starvation ketoacidosis associated with retatrutide-induced gastroparesis following unsupervised use of medication obtained from unregulated sources. Case: A 39-year-old female healthcare worker with prediabetes (hemoglobin A1c 5.7%), class I obesity (body mass index 31.2 kg/m²), and endometriosis presented with persistent vomiting and diarrhea. She reported using retatrutide for weight loss, initially obtained from an informal source, although the authenticity and origin of the medication could not be verified. She self-titrated retatrutide over 7 weeks, escalating from 1 mg twice weekly to 6 mg weekly, with only mild nausea. Subsequently, she purchased the medication from another unverified online source. Following this change, she developed worsening nausea at the 6 mg weekly dose, prompting a dose reduction to 5 mg weekly. Two days after the most recent dose, she developed intractable vomiting and diarrhea. On presentation, she was clinically dehydrated. Venous blood gas revealed metabolic acidosis (pH 7.33, bicarbonate 18.8 mmol/L) with elevated serum ketones (4.5 mmol/L) and normal lactate (1.2 mmol/L). Blood glucose was 4.5 mmol/L, and serum amylase was normal. She was treated with intravenous fluids, fixed-rate insulin infusion, and antiemetics. Ketoacidosis resolved by day 3, with improvement of gastrointestinal symptoms by day 5. Conclusion This case highlights a serious complication associated with retatrutide and underscores the risks of unsupervised use of investigational weight-loss therapies obtained from unregulated sources. It also emphasizes pharmacovigilance as emerging antiobesity therapies become widely used. Careful dose titration, close clinical monitoring, and use within regulated medical channels are essential for patient safety.
Gastroparesis ; Ketosis

Introduction: Prolactinomas are the most common functioning pituitary adenomas, accounting for 50% of all pituitary tumors. Microprolactinomas (<10 mm) are the most frequent subtype and usually follow a benign course, with tumor progression reported in only 5% of cases. We report a rare case of microprolactinoma that progressed to macroprolactinoma over 16 years. : A 39-year-old female was initially diagnosed with a microprolactinoma at the age of 23 during evaluation for irregular menses since menarche. Baseline pituitary magnetic resonance imaging (MRI) at that time revealed a lesion measuring 2 × 2 × 0.8 mm. She was treated with bromocriptine for 2 months but subsequently lost to followup. The patient had been married for 10 years without conceiving and continued to have irregular menses. She decided to repeat prolactin before seeking fertility treatment after 16 years. Laboratory investigations revealed markedly elevated serum prolactin (>42,000 mIU/L) with suppressed gonadotropins, while thyroid and adrenal axes were normal. She reported no galactorrhea, headache, or visual disturbances and notably did not develop amenorrhea. Visual field assessment was normal. Repeat pituitary MRI demonstrated that the previously diagnosed microprolactinoma had progressed to a macroprolactinoma, measuring 2.1 × 2.3 × 1.6 cm, with extension into the left cavernous sinus and encasement of the left internal carotid artery, without optic chiasm compression. Oral cabergoline 0.25 mg twice weekly was initiated. She was counselled regarding potential risks of dopamine agonist therapy and advised to use mechanical contraception during treatment. At the 2-week follow-up, she tolerated therapy well. Follow-up imaging and prolactin monitoring were planned at 3 months to assess treatment response and guide fertility planning. Conclusion This case highlights the rare progression of microprolactinoma to macroprolactinoma, underscoring the importance of long-term monitoring in patients with prolactinoma. A careful balance between tumor control and fertility management is essential for optimizing care in women of reproductive age.
Prolactinoma

Introduction: Central diabetes insipidus (CDI) is characterized by impaired arginine vasopressin secretion, resulting in hypotonic polyuria and hypernatremia. In patients with coexisting diabetes mellitus, persistent polyuria may be misattributed to hyperglycemia, delaying recognition of a concurrent water balance disorder. CDI without identifiable structural abnormalities may be overlooked, leading to delayed diagnosis and complications. Case: We report a 30-year-old Malay female with underlying type 2 diabetes mellitus and premorbid obesity who presented with hyperosmolar hyperglycemic state, accompanied by persistent polyuria, polydipsia, weight gain, and amenorrhea. Despite resolution of hyperglycemia, she had ongoing polyuria with hypernatremia, raising suspicion of a concomitant water balance disorder. Biochemical evaluation demonstrated a hyperosmolar state with serum osmolality 334 mOsm/kg and inappropriately dilute urine (urine osmolality 254 mOsm/kg), supporting impaired vasopressin activity. A modified water deprivation test showed a >50% rise in urine osmolality following desmopressin, consistent with CDI. Diabetes autoantibody screening was negative. Anterior pituitary function was preserved, with normal thyroid and adrenal axes (thyroidstimulating hormone 3.30 mIU/L, cortisol 290.6 nmol/L), and gonadotropins not suggestive of hypopituitarism (luteinizing hormone 6.8 IU/L, follicle-stimulating hormone 24.6 IU/L). Neuroimaging with computed tomography brain showed no structural hypothalamic–pituitary lesion. Magnetic resonance imaging of the pituitary demonstrated absence of the posterior pituitary bright spot, with preserved gland morphology and no focal lesion, supporting CDI without an identifiable structural cause. Her clinical course was complicated by severe hospitalacquired infection leading to septic shock, requiring intensive care support, mechanical ventilation, and renal replacement therapy. She was commenced on desmopressin, with subsequent clinical and biochemical improvement, alongside multidisciplinary management. Conclusion In patients with type 2 diabetes mellitus, persistent polyuria may obscure an underlying water balance disorder. This case highlights the importance of considering alternative causes of polyuria and a systematic endocrine approach to ensure accurate diagnosis and appropriate management.
Diabetes Mellitus, Type 2 ; Hyperglycemic Hyperosmolar Nonketotic Coma ; Diabetes Insipidus

Introduction: Cranial nerve palsies have been reported in patients with uncontrolled hypothyroidism. We describe a case of overt hypothyroidism due to treatment disruption following radioiodine therapy, presented with a unilateral lower motor neuron seventh cranial nerve palsy. Case: A 32-year-old female presented with hypertension, dyslipidemia, class III obesity, and Graves’ disease post radioiodine therapy. She had stable thyroid function test with levothyroxine replacement post radioiodine. She presented with a 3-day history of right-sided facial droop associated with lethargy, weight gain, and constipation. She reported inadequate levothyroxine supply due to 2-month lapses in follow-up. On examination, there was a right-sided lower motor neuron 7th cranial nerve palsy with delayed ankle reflexes. No additional neurological deficits, goiter, cutaneous rashes, or vesicular lesions were noted. There was no preceding viral illness or otologic symptoms. Thyroid function tests showed overt hypothyroidism with thyroid-stimulating hormone 38 mIU/L, free thyroxine <5.4 pmol/L with a deranged lipid profile (total cholesterol: 8.8 mmol/L, low-density lipoprotein: 5.72 mmol/L, triglyceride: 1.77 mmol/L). Renal and liver function tests were within normal limits, with no leukocytosis. Neuroimaging of the brain was unremarkable. She was commenced on a short course of high-dose prednisolone, with no improvement in symptoms. Levothyroxine replacement therapy initiated led to progressive restoration of thyroid function, accompanied by symptom recovery. Conclusion Isolated lower motor 7th nerve palsy has been reported as a manifestation of hypothyroidism. This case underscores the importance of early recognition to enable timely and appropriate management, as patients with hypothyroidisminduced isolated seventh nerve palsy demonstrate marked recovery with adequate levothyroxine replacement.
Facial Nerve ; Hypothyroidism ; Motor Neurons ; Paralysis

Introduction: The coexistence of thyroid storm and Guillain–Barré syndrome (GBS) is rare, with few reported cases. A shared autoimmune mechanism has been suggested, although the exact pathophysiology remains unclear. In severe thyrotoxicosis, new neurological symptoms may be overlooked or attributed to metabolic causes, delaying diagnosis and posing a diagnostic and therapeutic challenge. We report a case of a 43-year-old female with Graves’ disease complicated by thyroid storm and Acute Motor Axonal Neuropathy (AMAN), a variant of GBS, highlighting the importance of early recognition and multidisciplinary management. Case: A 43-year-old female with no prior medical illness presented with fever, generalized weakness, fine tremors, and 10 kg weight loss over 5 months. On arrival, she was lethargic, febrile (40.2°C), and tachycardic (148 bpm), consistent with thyroid storm by Burch–Wartofsky criteria. She denied preceding diarrheal illness or upper respiratory tract symptoms. The thyroid function test showed markedly elevated free thyroxine 4 (>64.35 pmol/L) and suppressed thyroid-stimulating hormone (TSH) (<0.008 mIU/L). Subsequent testing revealed elevated TSH receptor antibodies (>40 IU/L), confirming Graves’ disease. Her course was complicated by anaphylactic shock with transient cardiac arrest, followed by acute kidney injury and respiratory failure requiring intensive care unit admission and mechanical ventilation. Following extubation, symmetrical limb weakness with generalized areflexia and bilateral foot drop was observed. Nerve conduction studies demonstrated a symmetrical axonal motor-predominant polyneuropathy consistent with AMAN. She received five sessions of plasma exchange and showed marked neurological improvement, while thyroid and renal function normalized at discharge. Conclusion This case highlights a rare and potentially life-threatening association of thyroid storm and AMAN. Severe thyrotoxicosis can precipitate atypical autoimmune complications, underscoring the need for vigilance. Clinicians should consider neurological evaluation in patients with severe thyrotoxicosis presenting with newonset motor weakness.
Thyrotoxicosis