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Background: PGF is historically associated with high morbidity and mortality after allogeneic hematopoietic stem cell transplantation (allo‐HSCT). Methods: In this study, we report our multicenter experience on stem cell boost (SCB) for PGF, or incomplete donor engraftment, in 16 pediatric patients. Donors were HLA‐matched siblings (n = 4), unrelated donors (n = 11), or haploidentical family members (n = 1). Ten patients had two‐lineage cytopenia, 5 had one‐lineage cytopenia, and 1 had poor immunological reconstitution together with a low percentage of donor cell engraftment. A median of 6.6x106 selected CD34+/Kg was infused after 194 days from allo‐HSCT (48‐607). Results: In 4 out of 5 patients, one‐lineage cytopenia was resolved, while among the 10 patients with two‐lineage cytopenia, 4 resolved both cytopenia, 5 resolved one‐lineage, and one did not respond. All patients reverted their mixed chimera to full donor chimera. OS was 56%, transplant‐related mortality (TRM) 32%, and RI 12%. The main causes of failure were related to infections with 4 out of 7 deaths caused by this. Conclusions: SCB may rescue over 50% of patients with PGF after allo‐HSCT. An earlier treatment may reduce the infectious complications and improve survival. [ABSTRACT FROM AUTHOR]

Background: Autoimmune diseases may occur after allogeneic hematopoietic stem cell transplantation (allo‐HSCT) and inflammatory bowel disease (IBD or Crohn disease) is rarely described. We describe a child who developed CD after allo‐HSCT, successfully treated with thalidomide. Case report: A child affected by mucopolysaccharidosis type I received two allogeneic HSCTs for rejection after the first one. After cutaneous and intestinal chronic GvHD and 6 months after HSCT, the patients developed a trilinear autoimmune cytopenia successfully treated with rituximab and sirolimus. Due to persisting intestinal symptoms, colonoscopies were performed and histological findings demonstrated a picture of CD. Based on this observation and according to the recommendations for the treatment of CD, thalidomide was started. A complete stable clinical response was obtained 8 weeks after start of thalidomide. Colonoscopy performed 4.8 years later demonstrated a complete endoscopic and histological remission of CD. Discussion: In this case, the diagnosis of CD after HSCT was based on histological findings. Indeed, repeated colonscopies were necessary for diagnosis, since both clinical and endoscopic features are often common to chronic GvHD and CD. Thalidomide was started at the dose of 1.7 mg/Kg/day, and it was well tolerated. Mild peripheral neurotoxicity occurred 5 years later but disappeared completely with the dose reduction. Currently, the patient is in complete remission from CD, despite the discontinuation of all the immunosuppressive therapies. Conclusions: Thalidomide could represent a therapeutic option to treat CD as autoimmune disease after allogeneic HSCT. [ABSTRACT FROM AUTHOR]