World journal of transplantation · 2025
Toxic agranulocytosis following nitazoxanide treatment for norovirus diarrhea in a kidney transplant recipient: A case report and review of literature.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Grépilloux Dorian, Guéneau Corentin, Weinhard Jules, Richaud Rémi, Chevallier Eloi, Jouve Thomas, Dusserre Julien, Rostaing Lionel
Аннотация
BACKGROUND: In France, nitazoxanide is available through compassionate use authorization, as there is no summary of product characteristics for this medication. However, it has been marketed in the United States for several years, with evidence supporting its use in the treatment of chronic norovirus infections in immunocompromised individuals. Due to its limited use, data on the efficacy and safety of this drug remain sparse.
CASE SUMMARY: We report the case of a 79-year-old immunocompromised patient, a renal transplant recipient undergoing treatment with mycophenolate mofetil and tacrolimus, who developed toxic agranulocytosis, as absolute neutrophil count dropped from 2.93 G/L to 0.09 G/L within 17 days following the introduction of nitazoxanide for the treatment of chronic diarrhea caused by norovirus infection. Clinical and laboratory findings suggest a toxic mechanism, most likely attributable to nitazoxanide.
CONCLUSION: This case highlights the potential of nitazoxanide to induce dose-dependent toxic agranulocytosis. While this adverse effect does not necessarily contraindicate reintroduction of the drug, it underscores the necessity for close hematological monitoring in such cases.
CASE SUMMARY: We report the case of a 79-year-old immunocompromised patient, a renal transplant recipient undergoing treatment with mycophenolate mofetil and tacrolimus, who developed toxic agranulocytosis, as absolute neutrophil count dropped from 2.93 G/L to 0.09 G/L within 17 days following the introduction of nitazoxanide for the treatment of chronic diarrhea caused by norovirus infection. Clinical and laboratory findings suggest a toxic mechanism, most likely attributable to nitazoxanide.
CONCLUSION: This case highlights the potential of nitazoxanide to induce dose-dependent toxic agranulocytosis. While this adverse effect does not necessarily contraindicate reintroduction of the drug, it underscores the necessity for close hematological monitoring in such cases.