Introduction: Managing thyroid storm requires aggressive multimodal therapy. However, options become exceptionally narrow when absolute contraindications to antithyroid drugs (ATDs) exist or standard therapy fails. In these refractory scenarios, therapeutic plasma exchange (TPE) serves as a critical rescue modality to optimize clinical and biochemical status. Despite its use, reported efficacy remains inconsistent. Cases: A 56-year-old female with Graves’ disease presented with thyroid storm (BWPS 60) complicated by high-output heart failure and distributive shock. Deterioration into acute liver failure (ALF) necessitated ATD discontinuation. TPE and Continuous Veno-Venous Hemofiltration (CVVH) were initiated at 40 hours. Following three TPE cycles, fT4 (freeT4) reduced by 6.7, 6.5, and 23% sequentially, leading to marked clinical stabilization and recovery. A 31-year-old female with Graves’ disease presented with thyroid storm (BWPS 90), pneumonia, and refractory tachycardia. Rising transaminases precluded ATD use. TPE was initiated at 48 hours, achieving a 55% fT4 reduction after 2 cycles and initial clinical stabilization. However, her course was complicated by a subdural hemorrhage requiring craniectomy; she eventually succumbed to nosocomial infection. A 27-year-old female with Graves’ disease presented with jaundice and altered sensorium (BWPS 45). Due to baseline ALF, ATDs were withheld. TPE was initiated early as a bridge to potential liver transplantation, achieving a significant 72% fT4 reduction after two cycles. Despite biochemical success, she succumbed to irreversible multi-organ failure. Conclusion Literature indicates that TPE achieves a mean fT4 reduction of 51.9% over four cycles. Our series demonstrated wide variability (23–72% over 2–3 cycles), reflecting unpredictable clearance dynamics. While TPE is an effective adjunctive tool for rapid biochemical optimization, the ultimate prognosis is heavily contingent on the timing of initiation. As seen in Cases 2 and 3, significant biochemical clearance may not reverse systemic damage once advanced neurological or hepatic failure ensues

Introduction. Vitamin B12 deficiency is more common among metformin-treated subjects although the prevalence is variable. Many factors have been associated with this. The aim of this study is to determine the prevalence of vitamin B12 deficiency and its associated factors among patients with type 2 diabetes mellitus (DM) who are on metformin. Methodology. A total of 205 patients who fit eligibility criteria were included in the study. A questionnaire was completed, and blood was drawn to study vitamin B12 levels. Vitamin B12 deficiency was defined as serum B12 level of ≤300 pg/ mL (221 pmol/L). Results. The prevalence of vitamin B12 deficiency among metformin-treated patients with type 2 DM patients was 28.3% (n=58). The median vitamin B12 level was 419 (±257) pg/mL. The non-Malay population was at a higher risk for metformin-associated vitamin B12 deficiency [adjusted odds ratio (OR) 3.86, 95% CI: 1.836 to 8.104, p<0.001]. Duration of metformin use of more than five years showed increased risk for metformin-associated vitamin B12 deficiency (adjusted OR 2.06, 95% CI: 1.003 to 4.227, p=0.049). Conclusion. Our study suggests that the prevalence of vitamin B12 deficiency among patients with type 2 diabetes mellitus on metformin in our population is substantial. This is more frequent among the non-Malay population and those who have been on metformin for more than five years.
Vitamin B 12 ; metformin ; Diabetes Mellitus, Type 2

A 31-year-old male, apparently well, presented with typical chest pain. His ECG showed ST-elevation from V1-V4 and echocardiogram revealed anteroseptal wall hypokinesia with an ejection fraction of 45%. Normal coronary arteries were seen on coronary angiogram. A thyroid function test showed elevated free T4 levels with suppressed thyroid stimulating hormone (TSH). Treatment with thionamides and beta-blockers improved symptoms. Upon review 4 months later he was well. Repeat echocardiogram showed good ejection fraction with no hypokinetic area.

An apparently well 27-year-old phenotypically male adult was seen at the endocrine clinic for gender assignment. Patient had been raised as a male and identifies as such. Abdominal CT scan showed a unilateral left adrenal mass and karyotyping revealed 46 XX female karyotype. She was diagnosed to have simple virilizing CAH and needed thorough counselling with subsequent management by a multidisciplinary team
17-alpha-Hydroxyprogesterone

A 58-year-old Malay female with underlying diabetes mellitus, presented with chronic skin lesions, associated with weight loss and anemia. There were erosive, scaling skin lesions over the extremities, gluteal region and perioral area. Skin biopsy histopathological examination revealed Necrolytic Migratory Erythema (NME). A CT scan of the abdomen revealed a pancreatic neck and body tumor with possible liver metastases. She was successfully treated with subcutaneous somatostatin and underwent distal pancreatectomy with wedge resection of liver nodule.
Glucagonoma ; Necrolytic Migratory Erythema ; Glucagon ; Somatostatin