IntroductionEvidence on cancer drug wastage comes largely from high-income countries and generally excludes the pediatric setting. This study quantified consumption, leftover reuse and wastage in a chemotherapy compounding unit of the Brazilian public health system.MethodsProspective, observational, descriptive study covering every compounding episode performed between October and December 2024 in a public hospital serving adult oncology and adult and pediatric onco-hematology. Of 32 formulary injectable cytotoxic drugs, the 29 with activity were analyzed by quantity and cost. The daily balance was classified as reusable leftover or wastage by a 24-h stability threshold. Relative wastage (quantity discarded divided by quantity compounded) was calculated per drug.Results1298 patients were treated in 2030 compounding episodes. Compounded doses totaled 612,192 mg or IU (BRL 657,724.73), of which 5.5% by quantity came from reused leftovers. Wastage reached 53,996.45 mg or IU (BRL 30,391.78; USD 5206.84), equivalent to 8.8% of the compounded quantity, 4.6% of its value and 13.9 mg or IU per patient treated per month. Fluorouracil led both compounded quantity (29.5%) and wastage (27.1%), yet relative wastage was highest in low-volume drugs with short stability: fludarabine (158.9%), etoposide (134.0%) and azacitidine (95.5%). Pegaspargase, used predominantly in children, combined 57.5% relative wastage with the largest discard cost (BRL 15,402.00). Pertuzumab, the costliest drug compounded, generated none.ConclusionsWastage concentrated in drugs with short stability and vial sizes poorly matched to prescribed doses, whereas the greatest financial impact fell on high unit-cost biologics. Relative wastage reveals intervention targets that absolute volume does not.

Asparaginase treatment for acute lymphoblastic leukemia/lymphoblastic lymphoma is often discontinued or interrupted due to hypersensitivity reactions (HSRs) or silent inactivation, with inferior clinical outcomes. In those instances, consensus experts recommend switching to an immunogenically distinct asparaginase preparation. This case series details experiences of 4 adult patients who developed HSRs or silent inactivation while receiving modified Dana-Farber Cancer Institute (DFCI) protocols involving pegaspargase and consequently switched to crisantaspase (JZP458), a recombinant Erwinia asparaginase that was well tolerated without evidence of cross-immunological activity in 3 out of 4 cases, and with achievement of adequate serum asparaginase levels. Although limited to 4 patient cases, these data suggest that switching to crisantaspase after HSRs or silent inactivation of pegaspargase may represent a viable therapeutic option in adults, with close monitoring to ensure effective asparaginase levels. Dedicated clinical studies are needed to examine DFCI lymphoblastic leukemia protocols in more diverse patient populations.

Hypersensitivity reactions with pegylated Escherichia coli-derived asparaginase formulations are frequent and can complicate delivery of intended therapy for patients with acute lymphoblastic leukemia (ALL). On DFCI 16-001, which enrolled patients aged 1-21 years with newly diagnosed ALL, we piloted pegaspargase rechallenge after Grade 2 hypersensitivity reaction, including premedication and serum asparaginase activity (SAA) assessment. Among those who underwent rechallenge, the rechallenge dose was successfully administered (without reaction and with adequate SAA) in 41.3% of patients. This approach reduces the number of patients requiring switch to alternative asparaginase formulations, which have had limited availability and require frequent dosing.

Asparaginase is an integral component in the treatment of acute lymphoblastic leukemia. The asparaginase products available in our country are Escherichia Coli (E. Coli)-derived asparaginase (Leunase), pegaspargase (Oncaspar), and, to a lesser extent, Erwinia chrysanthemi-derived asparaginase. Hypersensitivity reactions (HSR) are reported less frequently in those receiving pegaspargase, ranging from 3% to 15%; however, these reactions can limit its use in this population.

A man in his early fifties was diagnosed with extranodal natural killer/T-cell lymphoma involving the nasal cavity and cervical lymph nodes. At the time of diagnosis, renal function was entirely normal. He was started on first-line combination therapy consisting of a PD-1 monoclonal antibody, pegaspargase, the histone deacetylase inhibitor chidamide, and systemic corticosteroids, with an early and favorable clinical response of the lymphoma. However, prior to the second treatment cycle, routine laboratory evaluation revealed new-onset proteinuria accompanied by a rising serum creatinine level. Subsequent renal biopsy demonstrated IgA-dominant immune complex deposition with crescent formation, consistent with rapidly progressive IgA glomerulonephritis. The immune checkpoint inhibitor was promptly discontinued, and high-dose corticosteroid therapy was initiated, followed by cyclophosphamide. Renal function showed partial but meaningful improvement. Given the renal toxicity, systemic immunotherapy was withheld, and the lymphoma was subsequently managed successfully with radiotherapy alone. At twelve months of follow-up, the patient remained in complete oncologic remission, with markedly improved renal parameters. This case highlights a rare presentation of rapidly progressive IgA nephropathy associated with PD-1 blockade in extranodal NK/T-cell lymphoma, a relationship that remains insufficiently characterized in current literature. It emphasizes the importance of close and regular monitoring of renal function and urinalysis during immunotherapy. Early recognition of renal involvement, together with timely discontinuation of the immune checkpoint inhibitor and appropriate immunosuppressive treatment, may preserve kidney function while still allowing effective control of the underlying malignancy.

Inherited fibrinogen disorders (IFDs) are rare, and limited evidence-based management guidelines exist, especially regarding haematological malignancies and haematopoietic stem cell transplantion (HSCT). This case highlights the successful multidisciplinary management of an adult patient with acute Philadelphia-negative B-cell lymphoblastic leukaemia (B-ALL) and IFD from induction through HSCT. A patient in his 20s with an IFD is diagnosed with B-ALL and receives induction chemotherapy, including dose-reduced pegaspargase (PEG-Asp), blinatumomab consolidative therapy and HSCT for post-induction measurable residual disease (MRD) positivity. Management involved prophylactic anticoagulation (AC) during induction and pharmacokinetic-guided fibrinogen replacement. Complications were iatrogenic intracranial hypotension and acute catheter-associated proximal deep vein thrombosis managed with therapeutic AC. One year post-HSCT, he remained MRD-negative with 100% donor chimerism. This case highlights a management strategy for patients with IFD requiring chemotherapy and/or HSCT and addresses a critical gap in knowledge.

Aggressive natural killer (NK) -cell leukemia (ANKL) is a rare hematological malignancy characterized by the abnormal proliferation of NK cells. It progresses rapidly and has a high mortality rate. This article reports the diagnosis and treatment of a rare case of a patient with ANKL and concurrent CD5(+)CD10(-) monoclonal B-cell lymphocytosis and hemophagocytic lymphohistiocytosis (HLH), and the relevant literature was reviewed. The patient was a 73-year-old male who presented with fever and lymphadenopathy in multiple areas without any obvious cause for over 1 month. Laboratory examinations, including bone marrow cell morphology and biopsy, revealed two distinct populations of abnormal cells. Flow cytometry, immunohistochemical staining, and gene testing confirmed the diagnoses of ANKL and CD5(+)CD10(-) monoclonal B-cell lymphocytosis, with concurrent HLH. The patient was initially treated with etoposide and dexamethasone. After receiving three courses of chemotherapy based on pegaspargase and other combination regimens, the patient's condition deteriorated. Resuscitation treatment was ineffective; the patient died due to multiple organ failure.