The assessment of haematological pathologies following solid organ transplantation (SOT) must consider the specific issues that arise in the post-transplant period and influence the onset of these conditions. Cytopenias, haemophagocytic syndrome, transplant-associated thrombotic microangiopathy, and post-transplant lymphoproliferative disorders typically develop within a few months to a year after transplantation. Anaemia and cytopenias can occur due to various mechanisms, including drug-induced bone marrow suppression or the destruction of a subset of T cells by immunosuppressive agents. Persistence increases the risk of developing immunosuppression, which in turn increases the risk of transplant rejection.Early diagnosis of pancytopenia through bone marrow biopsy is warranted, as it is often the presenting symptom of one or more pathologies following bone marrow transplantation. These complications may have a better prognosis if early intervention is undertaken. Most of the published articles focus on specific topics such as PTLD, cytopenia, anaemia, and so on. These complications have various causes and can result from both immunosuppressive therapy and changes in immune system activity following transplantation.The clinical presentation of blood disorders is similar to that of non-transplanted individuals; however, the progression, prognosis, and treatment differ due to the anergic state in post-transplant patients. The accepted articles on this topic have explored the subject from a variety of perspectives. The impact of TBD-related haematological complications on the outcome of solid organ transplants is limited to small series of heart and kidney transplants. Conversely, the majority of existing evidence comes from lung transplant cohorts.Lung transplantation has served as a clinical "sentinel" for TBD, as a significant subset of patients with interstitial lung disease (ILD) carry pathogenic variants in telomererelated genes and exhibit telomere lengths below the first or tenth percentile. In several cohorts of patients with IPF or ILD who carry TERT, TERC, RTEL1, or PARN variants, post-transplant cytopenias are surprisingly common. Anaemia, neutropenia, and thrombocytopenia requiring transfusion occur in the vast majority of cases, often leading to a switch from triple to dual immunosuppressive therapy. In a series of cases, almost all carriers of the variant developed leukopenia and anaemia, and a significant proportion also developed thrombocytopenia. Complications were more common in patients with pre-transplant thrombocytopenia or a history of SMD, highlighting the limited bone marrow reserve typical of TBD.Similar concerns arise regarding liver transplantation in patients with short telomere syndromes. While positive transplant outcomes have been reported, these cases often involve a history of prior hematopoietic stem cell transplantation, ganciclovir-resistant CMV infection, and a persistent risk of hematological and immune complications. This confirms that, in highly selected candidates, relapse is not necessarily synonymous with graft failure. Furthermore, both cohorts experienced multiple episodes of infection, with no significant differences observed between the two groups.This study is necessarily limited by its small sample size, single-centre design, and the absence of routine biopsies to assess transplant damage caused by disease recurrence.Nevertheless, we can draw some important conclusions:-A pre-existing oncohaematological condition should prompt a more thorough assessment, rather than an automatic exclusion.-With a well-documented, stable disease, careful multidisciplinary supervision, and structured monitoring protocols, these patients can achieve excellent transplant survival, low rejection rates, and favourable long-term clinical outcomes.-Specific disease surveillance programmes before and after transplantation, including bone marrow assessment, imaging, and biomarker monitoring (e.g., light chains, JAK2or BCR-ABL status, minimal residual disease testing) tailored to each condition.-Immunosuppressive therapies that explicitly consider bone marrow reserve and the risk of relapse, avoiding unnecessary lymphodepletion Zheng et al. evaluated the effectiveness of treating acute GVHD following liver transplantation. Graft-versus-host disease (GVHD) is a rare complication following liver transplantation (LT), with an incidence of 0.5-2%. GVHD occurs when the donor's immune cells recognise the recipient's antigens as foreign and trigger an immune response. Transplants containing a higher number of immunocompetent donor lymphocytes, such as those involving hematopoietic stem cells, bone marrow, or peripheral blood stem cells, are associated with a high incidence of GVHD. Among solid organ transplants, intestinal transplantation has the highest incidence of GVHD, followed by liver transplantation. GVHD rates are lower after kidney, heart, or pancreas transplants.Early diagnosis of GVHD is important to reduce the severity of infections and mortality rates. Unfortunately, diagnosis can be delayed, as similar symptoms can be observed in Although limited by the sample size, these observations are noteworthy for several reasons:-Firstly, the study highlights the importance of early diagnosis, which integrates compatible clinical features, histological confirmation, and analysis of donor Tcell chimerism -a triad that can distinguish aGVHD from mimics.-Secondly, it leverages ATG's ability to deplete the donor's activated lymphocytes, potentially restoring immune balance with less collateral damage than prolonged high-dose corticosteroid therapy.The inclusion of ruxolitinib, a JAK1/2 inhibitor with proven efficacy in steroidrefractory aGVHD following hematopoietic transplantation, is another rational element. Case reports and small series have already suggested a role for ruxolitinib in GVHD following solid organ transplants, including liver transplants, although experience remains limited. By blocking JAK-STAT signalling downstream of multiple inflammatory cytokines, ruxolitinib can interrupt the "cytokine storm" that perpetuates tissue damage,.Tai and colleagues evaluated the influence of immunosuppression on the onset of haematological complications following SOT. They considered different types of immunosuppressive regimens applied after kidney transplantation.The era of "one-size-fits-all" maintenance immunosuppression in kidney transplantation is clearly ending, yet our routine tools to guide drug choice and intensity are still represented by creatinine, trough levels, DSA, and perhaps protocol biopsies. -firstly, it recognises that peripheral blood contains a rich, untapped archive of how different immunosuppressive treatments reprogram the immune system of KTRs; and -secondly, it insists that future clinical studies on treatment regimens integrate standardised, high-content peripheral immune monitoring as the primary endpoint, rather than as an additional exploratory component.Only by systematically linking these cellular signatures to rejection, infection, malignancy, and transplant longevity will we be able to move from descriptive immunophenotyping to truly mechanistic and patient-specific immunosuppression in kidney transplantation.In conclusion, blood disorders following organ transplantation remain a concerning condition, despite improved understanding of risk factors and their pathophysiology.Indeed, their treatment remains complex due to the wide variety of clinical forms and their progression. Treatment needs to be tailored to each situation. Furthermore, patients undergoing organ transplantation with a haematological condition are more vulnerable, and cytotoxic drugs should be used with caution.
Giovanbattista Ippoliti (Wed,) studied this question.