HSCT is effective in patients with PSTPIP1-associated myeloid-related proteinemia inflammatory (PAMI) syndrome.


Journal

The Journal of allergy and clinical immunology
ISSN: 1097-6825
Titre abrégé: J Allergy Clin Immunol
Pays: United States
ID NLM: 1275002

Informations de publication

Date de publication:
07 2021
Historique:
received: 23 09 2020
revised: 06 11 2020
accepted: 12 11 2020
pubmed: 19 12 2020
medline: 13 10 2021
entrez: 18 12 2020
Statut: ppublish

Résumé

Proline-serine-threonine phosphatase-interacting protein 1-associated myeloid-related proteinemia inflammatory (PAMI) syndrome is a novel genetic disorder, causing hypercalprotectinemia and hyperzincemia with inflammatory complications accompanied by cytopenia. Immunosuppressive and/or anticytokine therapy is of limited effect. Because of cytokine production in nonhematopoietic tissues, the potential therapeutic effect of allogeneic hematopoietic stem cell transplantation (HSCT) in autoinflammatory disorders, including PAMI syndrome, has remained uncertain. Five patients with PAMI syndrome underwent allogeneic HSCT with myeloablative (4) or reduced-intensity (1) conditioning regimens. Lack of PAMI disease control served as indication for the HSCT in 4 patients and myelodysplastic syndrome development in 1. All 5 patients engrafted; however, 1 patient at day +13 developed hemophagocytic syndrome, followed by graft rejection at day +17. After 5.5 months, a second HSCT was performed from an alternative donor. A further patient at day +116 developed an intense inflammatory syndrome with significant serositis and severe mitral and aortic valve regurgitation, controlled with adalimumab, tacrolimus, and prednisone. No other noninfectious inflammatory episodes, or acute or chronic graft-versus-host disease, occurred in any patient. At the last follow-up (median, 2.2 years), all 5 patients have predominantly or complete donor chimerism and adequate immune recovery and are free of any PAMI symptoms. Allogeneic HSCT seems to be an effective option to cure cytopenia and severe autoinflammation in PAMI syndrome and may be a curative option for other proline-serine-threonine phosphatase-interacting protein 1-associated inflammatory disorders with poor therapeutic control.

Sections du résumé

BACKGROUND
Proline-serine-threonine phosphatase-interacting protein 1-associated myeloid-related proteinemia inflammatory (PAMI) syndrome is a novel genetic disorder, causing hypercalprotectinemia and hyperzincemia with inflammatory complications accompanied by cytopenia. Immunosuppressive and/or anticytokine therapy is of limited effect.
OBJECTIVES
Because of cytokine production in nonhematopoietic tissues, the potential therapeutic effect of allogeneic hematopoietic stem cell transplantation (HSCT) in autoinflammatory disorders, including PAMI syndrome, has remained uncertain.
METHODS
Five patients with PAMI syndrome underwent allogeneic HSCT with myeloablative (4) or reduced-intensity (1) conditioning regimens. Lack of PAMI disease control served as indication for the HSCT in 4 patients and myelodysplastic syndrome development in 1.
RESULTS
All 5 patients engrafted; however, 1 patient at day +13 developed hemophagocytic syndrome, followed by graft rejection at day +17. After 5.5 months, a second HSCT was performed from an alternative donor. A further patient at day +116 developed an intense inflammatory syndrome with significant serositis and severe mitral and aortic valve regurgitation, controlled with adalimumab, tacrolimus, and prednisone. No other noninfectious inflammatory episodes, or acute or chronic graft-versus-host disease, occurred in any patient. At the last follow-up (median, 2.2 years), all 5 patients have predominantly or complete donor chimerism and adequate immune recovery and are free of any PAMI symptoms.
CONCLUSIONS
Allogeneic HSCT seems to be an effective option to cure cytopenia and severe autoinflammation in PAMI syndrome and may be a curative option for other proline-serine-threonine phosphatase-interacting protein 1-associated inflammatory disorders with poor therapeutic control.

Identifiants

pubmed: 33338535
pii: S0091-6749(20)31764-4
doi: 10.1016/j.jaci.2020.11.043
pii:
doi:

Substances chimiques

Adaptor Proteins, Signal Transducing 0
Cytokines 0
Cytoskeletal Proteins 0
Immunosuppressive Agents 0
PSTPIP1 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

250-255.e1

Informations de copyright

Copyright © 2020 American Academy of Allergy, Asthma & Immunology. All rights reserved.

Auteurs

Alexandra Laberko (A)

Department of Immunology, Dmitry Rogachev National Medical Research Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russia; Translational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, United Kingdom. Electronic address: alexandra.laberko@gmail.com.

Vasiliy Burlakov (V)

Department of Immunology, Dmitry Rogachev National Medical Research Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russia.

Sarah Maier (S)

Division of Pediatric Stem Cell Transplantation and Immunology, Department of Pediatric Hematology and Oncology, University Medical Center Eppendorf, Hamburg, Germany.

Mario Abinun (M)

Translational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, United Kingdom; Great North Children's Hospital, Newcastle University, Newcastle upon Tyne, United Kingdom.

Roderick Skinner (R)

Translational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, United Kingdom; Great North Children's Hospital, Newcastle University, Newcastle upon Tyne, United Kingdom.

Anna Kozlova (A)

Department of Immunology, Dmitry Rogachev National Medical Research Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russia.

Deepti Suri (D)

Great North Children's Hospital, Newcastle University, Newcastle upon Tyne, United Kingdom.

Kai Lehmberg (K)

Division of Pediatric Stem Cell Transplantation and Immunology, Department of Pediatric Hematology and Oncology, University Medical Center Eppendorf, Hamburg, Germany.

Ingo Müller (I)

Division of Pediatric Stem Cell Transplantation and Immunology, Department of Pediatric Hematology and Oncology, University Medical Center Eppendorf, Hamburg, Germany.

Dmitry Balashov (D)

Department of Hematopoietic Stem Cell Transplantation, Dmitry Rogachev National Medical Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russia.

Galina Novichkova (G)

Department of Hematology, Dmitry Rogachev National Medical Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russia.

Dirk Holzinger (D)

Department of Pediatric Hematology-Oncology, University of Duisburg-Essen, Essen, Germany.

Andrew R Gennery (AR)

Translational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, United Kingdom; Great North Children's Hospital, Newcastle University, Newcastle upon Tyne, United Kingdom.

Anna Shcherbina (A)

Department of Immunology, Dmitry Rogachev National Medical Research Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russia.

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Classifications MeSH