ResearcherID - CLICK HERE Scientific Journal Impact Factor (SJIF-2020) - CLICK HERE

TITLE:

INCREASED FREQUENCY OF ANTI-MA2 ENCEPHALITIS ASSOCIATED WITH IMMUNE CHECKPOINT INHIBITORS

AUTHORS:

Dr Muhammad Wajih Ansari, Dr Arva Zubair Khan, Dr Malik Naveed Hassan, Dr Ali Sattar, Dr Syed Haris Mustafa Zaidi, Dr Azhan Jamal Bukhari

ABSTRACT:

Introduction: Therapy with monoclonal antibodies (Abs) targeting immune checkpoints, including cytotoxic T lymphocyte–associated antigen 4 (CTLA-4), the programmed death-1 receptor (PD-1), and its ligand PD-L1, has led to a paradigm shift in the treatment of numerous types of cancer. Aims and objective: The basic aim of the study is to analyse the increased frequency of anti-Ma2 encephalitis associated with immune checkpoint inhibitors. Material and methods: This descriptive study was conducted in Baqai Medical University, Karachi During March 2019 till November 2019. Data was collected from those patients who observed with anti-Ma2-PNS after treatment with ICIs. All patients underwent a comprehensive laboratory examination for suspected PNS. Demographic and clinical features of patients with Ma2-PNS triggered by ICIs were compared with those of the overall cohort of patients with Ma2-PNS unrelated to ICI treatment diagnosed in hospital. Results: Most of the patients were male (83%), with a median age of 63 years (range: 47–79 years). All were Caucasians. Four of them had an associated non–small-cell lung cancer, 1 a pleural mesothelioma, and the last one a renal clear cell carcinoma. At the time of ICI introduction, a median of 6.5 months (range: 0.5–25) after cancer diagnosis, all the patients except 1 (patient 2) had a metastatic disease, which included brain involvement in 2 cases. Conclusion: It is concluded that motor neuron involvement could complicate Ma2-Ab-associated PNS in almost 10% of patients and must be carefully studied to adapt treatment.

Top
  • Follows us on
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.