Nova Scotia (NS) began offering CAR T-cell therapy as a third-line standard of care for eligible patients with relapsed or refractory large B-cell lymphoma (r/r LBCL) in 2022. Recipients of CAR T-cell therapy often experience acute toxicities, including cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS), which require close monitoring and prompt management. This retrospective review aimed to describe the characteristics of adult patients with r/r LBCL deemed eligible to receive CAR T-cell therapy with axicabtagene ciloleucel in NS between January 2022 and June 2024, the toxicities experienced and toxicity management, hospital visits and intensive care unit (ICU) admissions, the utilization of toxicity management guidelines, and general efficacy outcomes. Twenty-seven patients received axicabtagene ciloleucel. All patients experienced CRS (7.4% grade ≥ 3), and 55.6% developed ICANS (25.9% grade ≥ 3). The median hospital stay was 18 days, with 40.7% requiring ICU admission. There was one treatment-related mortality. Most CRS (85.2%) and ICANS (80.0%) cases were managed according to the guidelines. By day +100, the best objective response rate was 81.5% (44.4% complete responses). Patients who received CAR T-cell therapy in NS, Canada, experienced comparable toxicities and efficacy to those reported in pivotal clinical trials and other real-world experiences.

Cancer-associated venous thromboembolism is a devastating complication of cancer and is associated with significant morbidity and mortality. The cornerstone of cancer-associated venous thromboembolism treatment is anticoagulation, and in recent years, there have been notable randomized clinical trials that have revealed insights into the efficacy and safety of direct oral anticoagulants and low-molecular-weight heparin in the treatment of cancer-associated thrombosis. Deciding on the ideal anticoagulation treatment plan for a patient with a cancer-associated thrombosis is a complex task that requires an understanding of clinical trial data, society guidelines, and, most importantly, consideration of many cancer-related, treatment-related, and patient-related factors. This article summarizes important factors to consider when deciding on anticoagulation therapy for a patient with cancer-associated thrombosis.

Rationale: Alemtuzumab is a monoclonal antibody approved for the treatment of relapsing-remitting multiple sclerosis (RRMS). Many autoimmune-mediated adverse events have been associated with alemtuzumab, including renal-limited anti-glomerular basement membrane (GBM) disease. Presenting concern: A 52-year-old female with RRMS presented with acute kidney injury 39 months after receiving 1 cycle of alemtuzumab. She had a history of alemtuzumab-associated hypothyroidism and thrombocytopenia, urinary tract infections, and chronically abnormal urinalyses. Diagnosis: A diagnosis of renal-limited anti-GBM disease was made based on renal biopsy and positive anti-GBM serology. Alemtuzumab was thought to be the trigger of the anti-GBM disease as there were no other exposures or serologic findings suggesting other causes. Interventions: She was treated with corticosteroids, cyclophosphamide, and plasmapheresis. She required hemodialysis for acute renal failure. Outcomes: Despite treatment, the patient’s renal function did not recover. She remained dialysis-dependent and anti-GBM antibody titers remained elevated 6 months after presentation. Teaching points: Anti-GBM disease is a life-altering adverse event that can be associated with alemtuzumab. Our case highlights the limitations of monitoring urinalyses as a trigger for anti-GBM antibody testing in patients who have received alemtuzumab and have baseline abnormal urinalyses; such patients may require further protocolized anti-GBM antibody testing, although the optimal frequency of such antibody screening remains unclear.

TERC variant telomere biology disorders (TBDs) are a rare, heterogenous group of disorders that arise from germline variants in TERC, a gene that encodes for the RNA component of telomerase. Variants in TERC lead to accelerated telomere attrition and can manifest as many different phenotypes. In this case series, we aimed to add to the literature describing TERC variant TBDs by reporting cases from two unrelated families from Atlantic Canada. The first case, a previously described germline TERC variant, n.107G>T (NR_001566.1), was identified in a young woman with myelodysplastic syndrome (MDS) and found to segregate with cytopenias in the family. This case represents a unique phenotypic presentation: this variant has not previously been described in patients with MDS and adds important segregation data to the literature. The second case, a novel TERC n.437T>G variant, was identified in a patient with both aplastic anemia and pulmonary fibrosis manifesting in his early 30s. We report these novel cases of germline TERC variants in order to help clinicians recognize TBDs, as well as to add important supporting information for the pathogenicity of these variants.