Rhabdomyolysis after Intravenous Ferric Gluconate: A Case Report

Abstract

Patients with severe iron deficiency, malabsorption or intolerance to oral iron are frequently treated with intravenous iron replacement. We report the case of a 42-year-old woman with non-erosive oligoarticular arthritis with antiparietal cell antibodies and iron deficiency anemia secondary to menorrhagia and unresponsive to oral iron preparations. She was treated with an intravenous infusion of ferric gluconate. After the first infusion of 125 mg (in 250 mL saline), she developed transient pain in her knee and wrist joints. When the dose was subsequently halved, the patient showed no adverse symptoms in the next four infusions and had normalized hemoglobin levels and iron indices. However, after a subsequent 125 mg ferric gluconate infusion she developed severe leg pain, muscular and joint stiffness, and functional impairment of her hands, right foot, and ankle. Laboratory tests showed a progressive increase in creatine kinase, transaminase, and C-reactive protein that normalized several days after the infusion. Although rhabdomyolysis is not reported among endovenous iron-induced adverse events, our findings suggest that intravenous iron infusions might have increased free iron generation promoting oxidative joint and muscular injury, which would explain the joint pain and stiffness, and rhabdomyolysis. Greater attention should be paid to the more frequent cases of myalgia occurring after iron infusion, which may underlie a rhabdomyolytic event requiring clinical observation.

Rhabdomyolysis After Intravenous Iron Sucrose Infusion During Pregnancy

“…However, there are reports of rhabdomyolysis after iron administration in nonpregnant patients. Botti et al 12 published a case report of a 42-year-old patient with nonerosive oligoarticular arthritis and antiparietal cell antibodies who developed rhabdomyolysis after the second infusion of IV ferric gluconate. Foulkes et al 13 described a 59-year-old man with a severe malabsorptive state who developed rhabdomyolysis during treatment with intramuscular iron dextran.…”

“…The exact mechanism for IV iron-associated rhabdomyolysis is currently unknown. Botti et al 12 suggested that free iron generation promotes oxida-tive joint and muscular injury. Foulkes et al 13 postulated that profound deficiencies of vitamin E and selenium, which protect against oxidative injury, played a role.…”