Allogeneic Transplantation in Advanced Systemic Mastocytosis: a Single-Center Case Series Highlighting Gastrointestinal Toxicity and GvHD Risk 

Criscuolo M.1, Fianchi L.2,3, Chiusolo P.2,3, Sica S.2,3* and Pagano L.2,3*.

1 Dipartimento di Scienze di Laboratorio ed Ematologiche, Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma, Italy.
2 Sezione di Ematologia, Dipartimento di Scienze Radiologiche Ed Ematologiche, Università Cattolica del Sacro Cuore, Roma, Italy.
3 Dipartimento di Diagnostica Per Immagini, Radioterapia Oncologica Ed Ematologia, Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma, Italy.
* Both authors are considered last authors.






Correspondence to: Criscuolo M. Dipartimento di Scienze di Laboratorio ed Ematologiche, Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma, Italy. E-mail: marianna.criscuolo@policlinicogemelli.it

Published: July 01, 2026
Received: May 17, 2026
Accepted: June 16, 2026
Mediterr J Hematol Infect Dis 2026, 18(1): e2026060 DOI 10.4084/MJHID.2026.060

This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(https://creativecommons.org/licenses/by-nc/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Introduction

Systemic mastocytosis (SM) is a rare neoplastic disease characterized by clonal proliferation of altered mast cells (MCs). Involved organs are primarily skin and bone marrow, but the gastrointestinal (GI) tract, liver, and spleen are often infiltrated.[1] SM diagnosis relies on the identification of atypical MCs by morphological, histological, cytofluorimetric, and molecular analyses, the detection of D816V KIT mutation, and the presence of B or C findings defining organ involvement and dysfunction.[2-4] On this basis, five main clinical variants can be identified with different prognoses: indolent SM (ISM), smoldering SM (SSM), aggressive SM (ASM), SM with associated hematological neoplasm (SM-AHN), and mast cell leukemia (MCL). Treatment of ISM and SSM relies on controlling symptoms driven by mediator release, whereas TKIs are required for patients with AdvS.[5] When conventional treatments fail to control the disease, allogeneic transplantation could be a therapeutic option to discuss with younger patients, although long-term efficacy is questionable.[6] Recently, guidelines have been published to help guide decisions on the most favorable timing of transplant, adequate conditioning regimens, and stem cell source [7]. In this report, we aimed to discuss the indication for transplant, therapeutic options, and outcomes in three patients with AdvSM to provide further information for the management of these patients. Clinical characteristics of disease, conditioning regimen, GvHD prophylaxis, and engraftment are reported in Table 1. IWG-MRT-ECNM response criteria were considered for response assessment.[8]
Table 1
Table 1. Characteristics of patients.


Case 1: young patient with progressive MCL

A 32-year-old female patient was diagnosed with MCL in February 2013. She presented to the emergency room (ER) with fever, vomiting, and epigastric pain. Physical examination revealed diffuse brown papular skin lesions and hepatosplenomegaly. Laboratory tests showed grade II anemia and thrombocytopenia, with circulating MCs noted on peripheral blood smear and serum tryptase at 200 mcg/L. A bone marrow evaluation revealed 80% infiltration by a a multifocal cluster of CD2/CD25+ MCs, with the presence of the KIT D816V mutation, but no fibrosis. Upper endoscopy revealed only chronic inflammation, apparently without detectable MCs infiltration. She started subcutaneous pegylated (PEG) interferon 180 mcg weekly, and concomitant off-label dasatinib was initiated. Moreover, HLA typing and familiar donor screening were performed. In April 2013, she presented to the ER for abdominal pain, worsening of fever, and progressive leucocytosis: cytarabine 3000 mg intravenously for 4 days was started, and an application for compassionate use of midostaurin was completed. In June 2013, she started midostaurin 100 mg twice a day, with limited benefit over clinical symptoms and bone marrow infiltration. In September 2013, bone marrow evaluation demonstrated 90% infiltration by MCs and KIT D816V mutation: she underwent allogeneic transplant from an HLA-matched unrelated donor. The pre-engraftment period was complicated by urinary tract infection and flushing syndrome, which were resolved after appropriate antibiotic therapy and steroids, respectively. In October 2013, bone marrow evaluation did not show MCs infiltration and KIT D816V mutation, while full donor chimerism was reported; serum tryptase was 20 mcg/l. She developed cutaneous and intestinal GvHD, for which extracorporeal photopheresis, steroids, and two lines of immunosuppressive therapy were employed (infliximab, rituximab). She died in November 2013 from progressive intestinal GvHD and multiple infections.

Case 2: life-threatening GvHD

A 59-year-old male patient was diagnosed with ASM in January 2018. He had a previous diagnosis of tubular adenoma of the colon with low-grade dysplasia and Helicobacter pylori (Hp) related chronic gastritis. Since 2014, he has reported grade II neutropenia for which he has performed periodic blood count analysis. In December 2017, he presented to the ER with persistent fever: physical examination revealed splenomegaly confirmed by US evaluation (spleen 18 cm), and laboratory tests showed grade II anemia and grade IV neutropenia. Bone marrow evaluation revealed 25% infiltration by a a multifocal cluster of atypical CD2-/CD25+ MCs and grade I fibrosis, together with the presence of the KIT D816V mutation; serum tryptase was 100 mcg/L. In September 2018, he started midostaurin 100 mg twice daily, with limited benefit; in November 2020, bone marrow evaluation showed 40% MC infiltration and grade II fibrosis; concomitant serum tryptase was 132 mcg/L. Endoscopy revealed colon and gastro-duodenal infiltration of MCs (Figure 1, A to D), together with Hp infection. Cladribine 0.14 mg/kg daily infusion for 5 consecutive days was initiated; HLA typing and family donor screening were also performed. In March 2021, he presented to the ER with fever, nausea, vomiting, and scrotal abscess: he received multiple courses of antibiotic therapy and red blood cell transfusions. In July 2021, he underwent an allogeneic transplant from a haploidentical donor: bone marrow evaluation showed 75% MCs infiltration and grade III fibrosis. The pre-engraftment period was complicated by suspected veno-occlusive disease, diarrhea, and fever, which resolved after defibrotide and empiric antibiotic therapy. In August 2021, bone marrow evaluation detected a 25% MCs infiltration with persistent KIT D816V and grade II fibrosis. In September 2021, he came to the ER because of worsening diarrhea and vomiting, suspicious for intestinal GvHD. After a negative microbiological workup, extracorporeal photopheresis, steroids, and ruxolitinib were employed. Bone marrow evaluation revealed persistent 30% MCs infiltration and grade II fibrosis, and gastro-intestinal biopsies detected lamina propria inflammation suggestive of GvHD but no MCs infiltration or Hp infection (Figure 1, E-F). He experienced progressive worsening of clinical conditions after the onset of pleural effusion, hypotension requiring amine support, and abdominal pain with bloody vomiting. He was transferred to the intensive care unit (ICU) and died a few days later in November 2021 from progressive deterioration.
Figure 1 Figure 1. A. Hematoxylin and eosin (H&E) staining of colon (30x): MCs infiltration indicated by arrow. B. Tryptase antibody staining of colon (30x): yellow indicates triptase expression. C. H&E staining of stomach (20x): MCs infiltration indicated by arrow. D. Tryptase antibody staining of stomach (20x): yellow indicates triptase expression. E and F. H&E staining of colon and stomach (20x): inflammatory infiltrates suggestive of GvHD, no MCs infiltration has identified.


Case 3: late recovery of bone marrow function

 A 48-year-old male patient was diagnosed with ASM in July 2016. He complained of progressive fatigue and bone pain, associated with weight loss >10% in the previous 6 months. Physical examination revealed splenomegaly confirmed by US evaluation (spleen 17 cm), and laboratory tests showed grade III anemia. A bone marrow evaluation revealed infiltration by multifocal clusters of atypical CD2/CD25+ MCs and grade III fibrosis, together with the presence of KIT D816V mutation; serum tryptase was normal. Imatinib 100 mg daily was withdrawn after a few months due to an absent clinical response. In October 2018, the patient started midostaurin 100 mg twice a day with fluctuating clinical benefit. In December 2019, worsening of blood count and persistent bone pain and fatigue revealed BM infiltration by 60% MCs with persistent grade III fibrosis and KIT D816V mutation. Cladribine 0.14 mg/kg daily infusion for 5 consecutive days was initiated; HLA typing and family donor screening were also performed. In June 2020, the patient presented to the ER with a fever and received antibiotics as an inpatient for severe pulmonary infection. Bone marrow examination reported persistent 65% BM infiltration, grade III fibrosis, and KIT D816V mutation. In December 2020, avapritinib 200 mg daily was initiated in a compassionate program, with sustained improvement in platelet and absolute neutrophil counts and partial resolution of bone pain and fatigue. In February 2021, bone marrow evaluation showed sparse microaggregates of CD25+ MCs and an undetectable KIT D816V mutation, with persisting grade III fibrosis; he underwent allogeneic transplant from a sibling donor. The pre-engraftment period was complicated by a bloodstream infection caused by E. coli, which resolved after antibiotic therapy. The patient experienced prolonged incomplete recovery of platelet count and hemoglobin, for which weekly red blood cell transfusions were scheduled for 14 months. Periodic bone marrow evaluation revealed poor myelopoiesis with only sparse normally shaped MCs, full donor chimerism, and undetectable KIT mutation. In August 2022, 18 months after transplant, complete recovery of bone marrow function was obtained: at last follow-up in March 2026, full donor chimerism and undetectable KIT mutation were confirmed while bone pain and moderate asthenia persisted as the only symptoms.

Conclusions and Future Perspectives

Allogeneic transplant in AdvSM remains controversial, not only because of the rarity of the disease. The discovery of cKIT mutations and the subsequent availability of targeted therapy have changed the prognosis of AdvSM: disease control has improved, with median estimated 24-month OS rate of 76% overall.[9] Nevertheless, AdvSM may present as a rapidly progressive disease, or relapse may occur early after initial response: subsequent available treatments are limited, waiting for experimental drugs to be evaluated.
Comparing the three most considerable studies about transplant in AdvSM, OS, and PFS after transplant were largely overlapping: at 3 years, about 40-50% of patients progressed, and almost 50% died.[6,10,11] Some considerations could be discussed. First, the study's population includes mostly patients with SM-AHN, among whom the associated hematological neoplasm is often responsible for the indication to transplant. Different authors have reported a reduced efficacy of graft-versus-mast cell effect compared to other hematopoietic compartments. This is particularly prominent in extra-medullary disease, irrespective of the intensity of conditioning regimens,[6,10] as reported for most myeloid neoplasms.[12] Furthermore, single case reports have shown a delayed clearance of bone marrow MCs infiltration.[13,14] Second, the time of observation is wide and not directly comparable to today, when TKI are widely available for AdvSM treatment. Nevertheless, recent changes in transplant management have improved non-relapsed mortality and mitigated the severity of GvHD.
According to clinical conditions and age, the transplant option should be discussed early with patients to plan HLA typing and familiar/unrelated donor screening. Myeloablative conditioning (MAC) regimens are known to be highly effective in disease control, although a higher rate of drug toxicity and increased GvHD severity have been observed. In the last few years, the age limit for the procedure has progressively increased, following the introduction of reduced-intensity conditioning (RIC) regimens. A worse survival was reported following RIC among 57 patients transplanted between 1990 and 2013,[6] although RIC was used in patients with lower performance status. More recently, a retrospective analysis of 71 patients transplanted between 1999 and 2021 could not conclusively establish the superiority of one conditioning regimen over another, likely due to the wide range of regimens used.[10] In our patients, the use of MAC regimens obtained disease control in all cases and timely engraftment in 2/3 cases, while severe GvHD was fatal for two patients.
Transplant should be performed when the best disease control has been achieved: lack of response was reported to predict an adverse prognosis among 71 patients transplanted between 1999 and 2021.[10] In our third patient, the use of avapritinib before transplant reduced the burden of disease, while grade III fibrosis persisted at the time of transplant: the presence of fibrosis since diagnosis may have impaired bone marrow recovery irrespective of conditioning regimens, as for other myeloid neoplasms.[15]
In our case series, we reported a good tolerability of MAC with valuable disease eradication and variable timing of engraftment. A potential difficulty in GvHD control has emerged, especially if the target organ has been a site of disease involvement: prior GI mast-cell involvement may warrant careful pre-transplant assessment, as severe post-transplant GI GvHD/toxicity may be difficult to control. The limitations of this report are related to the small number of cases and the relatively long observation period, during which both therapeutic options and transplant procedures have advanced. More data are warranted to better understand the potential correlation between MC infiltration and the severity of GvHD.
In this case series, two patients reported symptoms predictive of MCs' infiltration of the GI tract at the onset of AdvSM. In the post-engraftment phase, both developed acute severe GI GvHD, irrespective of conditioning regimen and GvHD prophylaxis. Acute GvHD has been reported in 42% of patients in two studies,[6,10] while it was about 20% after wider use of RIC in a more recent study.[11] No apparent correlation with prior disease infiltration has been reported so far. Recently, different studies have identified elevated MCs infiltration in the GI tract in patients with unexplained chronic diarrhea, disorders of gut-brain interaction, and irritable bowel syndrome.[16,17,18] MC activation causes hypersecretion, alterations in intestinal motility, visceral hypersensitivity, and alterations in the gut epithelial barrier through the release of inflammatory mediators such as histamine, prostaglandins, serotonin, and tryptase.[19,20] Taken together, these observations may suggest a contributory role for mediators released from MCs after the graft-versus-mast cell effect, increasing local toxicity and ultimately causing damage. In patients with AdvSM, pre-transplant GI involvement may be a clinical warning sign requiring careful assessment and monitoring.

Acknowledgments

There are no acknowledgments to report.

Footnotes

The study was conducted in accordance with the Declaration of Helsinki. Ethical review and approval were waived for this study due to report of a case series with no formal analysis aiming to evaluate the efficacy of a therapeutic approach.
Informed consent to publication was obtained verbally from living patients and recorded in the medical record.

Author contributions

CM Conceptualization; Data curation; Writing – original draft. FL, CP, and SS Data curation; Writing – review & editing. PL Conceptualization; Data curation; Writing – review & editing.

Availability of data and materials

All data reported in the manuscript are available on request.


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