BACKGROUND: Sodium ferric gluconate complex (SFGC) is a safe and effective drug administered to patients with iron deficiency anemia. Infusion of standard dose 125 mg SFGC can induce calculated transferrin iron saturation levels of greater than 100% and therefore elevation of “free” or non-transferrin bound iron (NTBI). The administration of iron can also impair host immunity including neutrophil function and the antibacterial effect of cytokines. Iron is essential for bacterial survival and increased NTBI facilitates microbial growth and virulence. The following cases are illustrative of these physiological principles and the theoretical concern that increased NTBI promotes infection.
CASE REPORTS: The first patient is a 27-year-old man with Crohn’s disease complicated by enterovesical fistula and iron deficiency anemia but not infection. His baseline labs include hemoglobin 9.1 g/dL and MCV 76 fL, iron 11 mcg/dL, iron saturation 3%, transferrin 270 mg/dL, TIBC 402 mcg/dL, ferritin 9 ng/mL, ESR 86 mm/hr. He was to receive weekly infusions of 125 mg SFGC in order to improve his anemia prior to fistula repair. Within 48 hours of the first dose he developed fever and abdominal pain requiring hospitalization. On exam he was hypotensive and tachycardic, and his abdomen was diffusely tender. His urine and blood cultures grew Escherichia coli, and no new abnormalities were found on CT scan of the abdomen and pelvis. His infection cleared with intravenous antibiotics and supportive care. Thereafter he resumed weekly parenteral SFGC infusions without incident. The second patient is a 53-year-old woman with a history of cystectomy and ileal conduit complicated by enterocutaneous fistula, recurrent wound infections, and persistent anemia mandating frequent blood transfusions. Her baseline labs include hemoglobin 7.8 gm/dL and MCV 82 fL, iron 17 mcg/dL, iron saturation 4%, transferrin 269 mg/dL, TIBC 401 mcg/dL, ferritin 12 ng/mL, ESR 52 mm/hr. She was to receive weekly infusions of 125 mg SFGC for her iron deficiency and intolerance to oral preparations. Her first dose was given one week after completing a course of antibiotics for a wound infection. At the time of infusion she was in general good health and her abdominal wound and ostomy sites were non-tender and without erythema. Within 48 hours, however, she was admitted to the hospital febrile and hypotensive. On exam she had no new changes to her fistula and ostomy sites. Cultures from her central venous catheter and peripheral blood, but not her wound, grew Staphylococcus aureus. Her catheter was removed and subsequently replaced, and she was successfully treated with a course of antibiotics. Two weeks later, on the day of her third SFGC infusion, fever and bacteremia recurred with coagulase-negative Staphylococcus. Her central venous catheter was again removed and she was treated with additional antibiotics.
CONCLUSIONS: Both patients had chronic medical conditions putting them at increased risk for infection. Both were severely iron deficient and became septic following their first standard dose of SFGC. It is postulated that the development of sepsis was due to these underlying risk factors, in addition to the experimental evidence that iron administration can induce oversaturation of transferrin, impaired host immunity and enhanced bacterial growth and virulence. Physicians are encouraged to carefully consider the recipient’s risk factors for infection prior to administering SFGC. The frequency of parenteral SFGC-induced sepsis cannot be established with case reports.
Disclosure: No relevant conflicts of interest to declare.
