Efficacy of the BNT162b2 mRNA COVID-19 Vaccine in Patients with Chronic Lymphocytic Leukemia: A Serologic and Cellular Study.

BACKGROUND: Antibody response following SARS-CoV-2 vaccination is somewhat defective in chronic lymphocytic leukemia (CLL). Moreover, the correlation between serologic response and status of cellular immunity has been poorly studied. OBJECTIVE: This study was undertaken to assess humoral immune and cellular responses to the BNT162b2 messenger RNA (mRNA) COVID-19 vaccination in CLL. METHODS: The presence of the spike antibodies was assessed at a median time of 14 days from the second vaccine dose of SARS-CoV-2 in 70 CLL patients followed up at a single institution. RESULTS: The antibody response rate (RR) in CLL patients was 58.5%, compared to 100% of 57 healthy controls of the same sex and age (p < 0.0001). Treatment-naïve patients and those in sustained clinical remission after therapy had the highest RR (87.0% and 87.7%, respectively). In contrast, patients on therapy with a pathway inhibitor as monotherapy and those treated with an association of anti-CD20 antibody were unlikely to respond to the SARS-CoV-2 vaccine (52% and 10%, respectively). In multivariate analysis, early Rai stage (OR, 0.19 [0.05-0.79]; p = 0.02) and no previous therapy (OR, 0.06 [0.02-0.27]; p < 0.0001) were found to be independent predictors of vaccination response. An increase in absolute NK cells (i.e., CD16/CD56 positive cells) in patients with a serological response was found following the second dose of vaccine (p = 0.02). CONCLUSIONS: These results confirm that serological response to the BNT162b2 vaccine in patients with CLL is impaired. A third boosting vaccine dosage should be considered for these patients.

Open, uncontrolled, nonrandomized, 9-month, off-label use of bupropion to treat fatigue in a single patient with multiple sclerosis.

BACKGROUND: Improvement of fatigue in patients with multiple sclerosis (MS) who were given bupropion has been previously reported, but scales for lethargy and depression were not used. OBJECTIVE: This letter describes the course of chronic fatigue in a patient with MS who received off-label treatment with bupropion. METHODS: A 47-year-old white woman (weight, 56 kg) with a 7-year history of relapsing-remitting MS (Ex- panded Disability Status Scale score of 3), without previous use of medication for MS, presented with a complaint of irritability and chronic fatigue. The Fatigue Severity Scale (FSS) documented the presence of fatigue related to MS (score of 7). The Beck Depression Inventory scale excluded an association between depression and fatigue (score of 8; possible range, 0-24); both the Pittsburgh Sleep Quality Index (score of 4; possible range, 0-21) and the Epworth Sleepiness Scale (score of 6; possible range, 0-24) excluded nighttime and daytime sleep disturbances. The patient was started on amantadine (100 mg/d), with an increase to 100 mg every 12 hours 2 weeks later, for the persistence of fatigue. Three months later, the absence of clinical response was noted (FSS score of 7). Amantadine was discontinued and bupropion therapy was initiated at 300 mg/d. RESULTS: A repeat clinical evaluation conducted after 3 months of bupropion treatment indicated an improvement in fatigue (FSS score of 4) without changes in Beck Depression Inventory, Pittsburgh Sleep Quality Index, or Epworth Sleepiness Scale scores. The discontinuation and reinitiation of bupropion confirmed the effectiveness of bupropion for improving chronic fatigue in this patient. At the time of writing this report, 13 months after the resumption of bupropion treatment, the patient had experienced no further episodes of fatigue, and no adverse events had been reported. CONCLUSION: This patient with relapsing-remitting MS experienced improvements in chronic fatigue (as measured by FSS) after treatment with bupropion, but properly designed, randomized, active- and placebo-controlled clinical trials are needed to evaluate the efficacy and safety of bupropion in more patients with MS and fatigue.