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

BACKGROUND: To investigate the molecular basis for invasion of malignant gliomas, proteomic analysis approach was carried out using two human glioma cell lines, U87MG and U343MG-A that demonstrate different motility and invasiveness in in vitro experiments. METHODS: High-resolution two-dimensional gel electrophoresis and matrix-assisted laser-desorption/ionization time-of-flight mass spectrometry analysis were performed. RESULTS: Nine distinct protein spots that were recognized with significant alteration between the two cell lines. Five of these protein spots were up-regulated in U87MG and four were up-regulated in U343MG-A. CONCLUSION: Among these proteins, cathepsin D was shown to be one of the important proteins which are related with glioma invasion. However, further studies are necessary to reveal the exact role and mechanism of cathepsin D in glioma invasion.
Cathepsin D ; Cell Line* ; Electrophoresis, Gel, Two-Dimensional ; Glioma* ; Humans ; Mass Spectrometry ; Proteomics