exam, there was mid-abdominal tenderness with a negative Murphy’s sign. Lipase level was 938 U/L (reference 12-53 U/L). His presentation and lipase levels met criteria to diagnose acute pancreatitis. A right upper quadrant ultrasound detected no gallstones or gallbladder thickening. Lipid panel was within normal limits, and the patient had not had any recent procedures. The patient was treated with continuous intravenous fluids, intravenous pain control, and anti-emetics. After a gradual recovery, the patient was discharged with recommendations to discontinue the emtricitabine/tenofovir alafenamide. Discussion: While tenofovir and emtricitabine are generally not considered high-risk for inducing pancreatitis, there have been rare reports of
pancreatitis potentially linked to combination therapies, including Bictegravir/emtricitabine/ tenofovir alafenamide. Additionally, clinical trials have noted elevated serum amylase and lipase levels in patients taking emtricitabine-including regimens, suggesting a contribution to pancreatic inflammation. In this case, the patient’s acute pancreatitis was of unknown origin, but the temporal relationship with emtricitabine/tenofovir alafenamide use raises the possibility of a drug-induced etiology. The patient’s recovery following discontinuation of the medication further supports this hypothesis. Clinicians should remain vigilant when managing patients on antiretroviral therapies, particularly in the setting of unexplained pancreatitis.
WHEN TRANSFUSION TURNS TOXIC: A CASE OF HYPERHEMOLYSIS SYNDROME IN A SICKLE CELL PATIENT Ramyashree Nyalakonda, Ricardo Vallejo-Calzada, Thomas Atkinson; Ochsner Clinic Foundation, New Orleans, LA.
Introduction: Hyperhemolysis syndrome (HS) is a severe hemolytic reaction that can occur following blood transfusion, characterized by a decline in hemoglobin levels that falls below the patient’s pre-transfusion baseline. Timely intervention is critical, as delayed treatment can result in significant mortality. Patients with sickle cell disease (SCD) are particularly more susceptible to HS, largely due to frequent and often inappropriate blood transfusions. Case: A 27-year-old female with sickle cell disease, avascular necrosis of the hips, and asthma presented with exacerbated left shoulder pain, pleuritic chest pain, and a productive cough. Initially treated conservatively for a vaso-occlusive pain crisis, she was then transfused a total of two units packed red blood cells (PRBCs) due to her ongoing symptoms and marginally low hemoglobin (Hgb) below her baseline of 7-9g/dL. Her Hgb was noted to not respond, and a decision was made for her to undergo exchange transfusion. Following her exchange transfusion, she experienced acute tachycardia, and her Hgb level dropped to 4.0 g/dL. Laboratory findings indicated a haptoglobin <10 mg/dL and an elevated
lactate dehydrogenase (LDH) level of 2,549 U/L, suggestive of hemolysis. Blood Bank was consulted, which suggested the patient was experiencing HS, noting auto and allo-antibodies against the red blood cells (RBCs) causing hemolysis. She was then given intravenous immunoglobulin (IVIG) and intravenous steroids without much improvement, and ultimately required plasma exchange (TPE) to remove her antibodies causing hemolysis. Discussion: Hyperhemolysis syndrome is a rare and serious complication associated with blood transfusions. HS can manifest as a severe transfusion reaction that can be life threatening to affected individuals. Early identification of HS is critical, necessitating prompt intervention with corticosteroids, IVIG, and even rituximab and TPE in some cases. Given the frequency of blood transfusions in patients with SCD, vigilance in monitoring for this condition is essential as the associated risks are often underestimated. Judicious transfusion of blood products remains the best way to avoid this rare complication.
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