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Immune checkpoint inhibitor atezolizumab is
currently FDA approved for the treatment of locally advanced or metastatic
transitional cell carcinoma (TCC). Exceptionally, it can induce adverse effects
related to the immune system. AIHA is a rare complication of atezolizumab but
it must be taken into account because secondary effects related to the
hematopoietic system have been recently reported.
Given the current and increasing indications for
these drugs, it is essential for all physicians to become well versed with
their common adverse effects in order to address early detection and better
management.
We report a case of autoimmune hemolytic anemia in a
patient with CCT and lymphatic node treated with atezolizumab.
Keywords: Atezolizumab,
Programmed death receptor 1 (PD-L1), Autoimmune hemolytic anemia (AIHA)
INTRODUCTION
Atezolizumab is a
humanized monoclonal antibody that belongs to the family of checkpoint
inhibitors. It can bind directly to the ligand of the programmed death receptor
1 (PD-L1), providing PD-L1/PD-1 mediated inhibition of the immune response and
reactivation of the antitumor response without inducing the cell-dependent
cytotoxicity of antibody. Currently, it is approved for the treatment of locally
advanced or metastatic transitional cell carcinoma (TCC). Exceptionally, it can
induce adverse effects related to the immune system such as pneumonitis,
colitis, pruritus and hepatitis. Recently, secondary effects related to the
hematopoietic system have been reported, such as autoimmune hemolytic anemia
(AIHA).
OBJECTIVE
To present a case of AIHA in a patient with
CCT under treatment with Atezolizumab.
CASE REPORT
A 57 year old woman with CCT and lympatic
node affectation diagnosis in November 2017 who started chemotherapy
(CDDP-gemcitabine) in April 2018. After performing the last cycle of first-line
chemotherapy (July 2018), persistence of hyper metabolic lymph nodes was
evidenced, so cystectomy and lymphadenectomy were rejected. Three months later,
given the adenopathic progression, it was decided to start treatment with
Atezolizumab. One week after the third cycle (January 2019), the patient went
to the Emergency Department with syncope, presenting hemoglobin (Hb) of 5.1
mg/dL that required transfusional support. The pre-transfusion tests showed:
positive irregular antibody screening, nonspecific agglutination for a panel of
11 cells with presence of positive self-control, direct positive Coombs test
(polyspecific 2+, IgG 2+ and negative Cd3) and eluted with nonspecific
panglutination. After treating the sample with PEG, the presence of
alloantibodies was ruled out. An erythrocyte genotyping was also performed
using BloodChip technology. Finally, in accordance with the results obtained,
it was transfused with isophenotype blood and negative cross-tests. The
analytical results founded were compatible with an AHAI (reticulocytes:
274.3•109/L, haptoglobin <8.06 mg/dL, lactate dehydrogenase: 948
U/L, bilirubin 5.8 mg/dL).
Due to the absence of other causes and the
recent administration of the drug, AIHA was suspected as a secondary
complication of the anti-PD-L1. The Atezolizumab interruption and initiation
of corticosteroid
CONCLUSION
AIHA is a rare complication of Atezolizumab
but it must be taken into account because it can put the patient's life at
risk. Further research and documentation on this manifestation would be
justified in order to address early detection and better management.
In our case, given the suspicion of AIHA due
to Atezolizumab, it was decided to change the treatment to Rituximab. After
three infusions the patient presented a notable analytical recovery (Hb: 10.5
mg/dL).
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