Nivolumab
- PDF / 171,701 Bytes
- 1 Pages / 595.245 x 841.846 pts (A4) Page_size
- 49 Downloads / 162 Views
1 S
Late-onset giant cell myocarditis: case report A 57-year-old man developed late-onset giant cell myocarditis during treatment with nivolumab for metastatic renal cell carcinoma. The man, who had metastatic renal cell carcinoma, had been receiving second line treatment with immune checkpoint inhibitor (ICI) monotherapy nivolumab 3 mg/kg every 3 weeks [route not stated]. Following 27 courses of nivolumab, he presented with myalgias and dyspnoea. An ECG revealed sinus tachycardia, low QRS voltage with T-wave inversion in the anterior leads without STsegment changes. Cardiac biomarkers were found to be elevated. Left heart catheterisation showed normal coronary arteries. Cardiac magnetic resonance revealed severe and diffuse myocardial oedema with high T1 values and high extravascular volume. Also, severe biventricular dysfunction was noted. A right ventricular endomyocardial biopsy (EMB) was performed. The man was transferred to the ICU and was started on methylprednisolone within 24h, which was continued for 3 days. Then methylprednisolone was replaced with prednisone. On day 3 of hospitalisation, his troponin I was 5800 ng/L. Histopathological analysis of the EMB specimen revealed intense myocardial inflammation with numerous giant cells associated with many mononuclear cells and prominent myocyte necrosis. Immunohistochemistry revealed the inflammatory cells were mainly CD68-positive giant cells, macrophages and CD8-positive T-lymphocytes. Most of these cells had granzyme B, perforin and TIA1 cytotoxicity markers. Only inflammatory cells expressed programmed cell death ligand-1 (PD-L1) and not by cardiomyocytes. CD4 and CD20 lymphocytes along with NKp46-positive NK cells represented poorly. Based on these findings, he was diagnosed with late onset giant cell myocarditis [duration of treatment to reaction onset not stated]. His haemodynamics became stable with no cardiogenic shock. Additionally, gradual improvement in left ventricular ejection fraction (LVEF) was noted over 8 days in the ICU. The LVEF improved to 50% prior to discharge, despite there was right ventricular impairment. Eventually, on day-13, he was discharged on an unspecified angiotensin converting enzyme inhibitors and beta-blockers along with prednisone. ICI therapy was not restarted considering the high-risk and became withheld. Thereafter, he had close follow-up in the cardio-oncology clinic, where his angiotensin converting enzyme inhibitors and beta-blockers were titrated to maximum tolerable doses. Subsequently, the steroids were tapered. An ambulatory 24h Holter monitor revealed unremarkable rhythm or conduction disorders. An investigation of viral markers of cardiac infection performed on frozen EMB specimen showed enterovirus (EV) RNA genomes. The mean EV-B viral load was 6000 genome copies/mg of total nucleic acid extracted, which was suggestive of a moderate viral genomic replication load in the cardiac tissue. The sequence identities between the EMB virus isolate and the prototype echovirus-19 strain Burke revealed a homologous sero
Data Loading...
