Complications
Managed supportively, including pre-medication with hydroxycarbamide (for leukoreduction), prophylaxis with allopurinol, and hydration (for tumour lysis syndrome) for patients with very high white blood cell counts (>100 × 10⁹/L [>100,000/microlitre]).
Treated with aggressive supportive care.
Failure to recover haematological function, or loss after initial reconstitution, occurs in 5% to 11% of HLA-identical recipients.
Usually occurs within 60 days of transplant, although it may occur later.
Host T cells mediate an active immune response against minor alloantigens of donor cells.
Can be treated with donor lymphocyte infusion if donor cells can be detected in the bone marrow.
Otherwise, a second reconditioning regimen followed by donor stem cell infusion may be attempted. Outcomes in this setting are extremely poor.[73]
An established complication of haematopoietic stem cell transplantation (HSCT). VOD/SOS risk calculator may be used to predict risk.[76]
VOD/SOS occurs when hepatic vascular endothelial cells are damaged by the HSCT conditioning regimen. Fibrosis and occlusion of the terminal venules develops in late stage disease, leading to hepatic failure and potentially death.[77]
Defibrotide is reserved for severe or progressive VOD/SOS.
Includes a range of complications from pulmonary oedema or diffuse alveolar haemorrhage to interstitial pneumonitis.
Majority are probably due to viral infection. Previously considered idiopathic or attributed to aberrant inflammatory responses.
Adenovirus, respiratory syncytial virus (RSV), influenza, and parainfluenza have become more apparent.
Ribavirin with intravenous immunoglobulin is instituted in transplant patients with RSV pneumonia.
Can also be related to total body irradiation.[73]
Remains a major obstacle to allogeneic stem cell transplant.
Occurs acutely (<100 days after transplant) or chronically (>100 days after transplant, or 6 months after discontinuing immunosuppressives).
Acute and chronic GVHD can significantly increase the risk of mortality and morbidity.
Donor T cells target host antigens. The greater the degree of major and minor histocompatibility complex antigen disparity between donor and host, the more severe the resultant GVHD is likely to be.
Post-transplant, ciclosporin, methotrexate, and methylprednisolone have been successfully used as prophylaxis for acute GVHD. Antithymocyte globulin can effectively decrease the incidence of acute GVHD after HLA-matched sibling donor transplantation.[72]
Incidence of acute GVHD is inversely related to the intensity of immunosuppression.
Prevention is the key to the care of transplant patients.
Prophylaxis is generally provided to guard against fungal, viral, and bacterial pathogens.
Fluconazole reduces the incidence of systemic and superficial fungal infections.
Trimethoprim/sulfamethoxazole is given for prophylaxis of pneumocystis and pneumococcal infections.
Ganciclovir prophylaxis in cytomegalovirus-seropositive patients has largely eliminated this infection, which occurs in the first 3 months after transplant.
Aciclovir prophylaxis is routinely given, as the incidence of herpes simplex virus reactivation and related morbidity is common.[73]
The Infectious Diseases Society of America and American Society of Clinical Oncology have published joint guidelines on antimicrobial prophylaxis and managing neutropenic fever.[74][75]
Compared with imatinib, second- and third-generation tyrosine kinase inhibitors (e.g., dasatinib, nilotinib, and ponatinib) are associated with an increased risk of vascular occlusive events in patients with chronic myeloid leukaemia.[78]
ECGs should be monitored during nilotinib therapy.
If corrected QT >480 milliseconds, therapy should be withheld.[2]
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