Hemophagocytic Syndrome as Uncommon Cause of Severe Pancytopenia After Liver Transplantation

Valenzuela, Esteban Fuentes; García, Ana Campano; García-Pajares, Félix; Tejada, Javier Tejedor; Muñoz, Rodrigo Nájera; Martín, Carlos M.; Delgado, Laura Sánchez; Martín, Carmen; Álvarez, Carolina Almohalla; Fernández-Fontecha, Elena; Sánchez-Antolín, Gloria

doi:10.1016/j.transproceed.2020.02.060

Cited by 4 publications

(1 citation statement)

References 6 publications

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“…7 A negative Toxoplasma serostatus prior to transplantation has been found to be the only independent risk factor of toxoplasmosis in SOT patients, 6 because both sensitivity (58%-83%) and specificity (60%) of bone marrow aspiration are questionable. 12 Our search strategy allowed us to retrieve 125 cases in SOT recipients, secondary to a variety of causes [66][67][68][69][70][71][72][73][74][75][76][77] (Figure 2). Results are presented in Tables 1 and 2.…”

Section: Discussionmentioning

confidence: 99%

Hemophagocytic syndrome triggered by donor‐transmitted toxoplasmosis as a complication in same‐donor recipients of renal transplantation: Case report and review of the literature

Franci

Flores

Candel

et al. 2021

Transplant Infectious Dis

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Background Hemophagocytic syndrome (HPS) is an infrequent complication of transplantation caused by an inflammatory response with a benign proliferation of macrophages and defective lytic capability of T lymphocytes and NK cells that can lead to multiorgan failure. Transplant patients are particularly exposed as a result of the increased risk of both infections and malignancies derived from immunosuppressive drugs. There is no consensus for therapy or immunosuppression; mortality is high. We report a case and present a review of all cases of HPS occurring in solid organ transplant recipients. Case report We report two cases of infection by Toxoplasma gondii transmitted by the kidney allograft. One of the recipients was seronegative before transplantation and developed disseminated primary toxoplasmosis. An immune reaction compatible with an HPS ensued. Both were treated with Trimethoprim/sulfamethoxazole, immunosuppression was tapered, and after a 2‐week period a complete response was obtained. Conclusion HPS presents therapeutic challenges in the context of transplantation. If HPS is suspected, the search of a very likely underlying infection should be central to the management.

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