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Case history

image A 55-year-old woman presented with small volume metastatic disease 2 years after radical nephrectomy for a T3 clear cell renal cell carcinoma (RCC). At first oncological assessment she was of good performance status with no significant medical comorbidities and was deemed suitable for first line treatment with high-dose interleukin-2 (HD IL-2) therapy.

She was admitted for the first cycle of treatment and completed 19 doses of HD IL-2. Reassessment CT imaging at 3 months revealed a partial response to treatment and she was readmitted for a second course of eight doses, without complications. She developed central chest pain at rest 24 h after her final dose. Although her ECG revealed no acute abnormality, troponin I was elevated at 0.25 μg/l (<0.017 μg/l). She was assessed by the cardiology team and both echocardiography and coronary angiography were normal. Her troponin I normalized over 48 h and she experienced no further chest pain. No clear causes for these symptoms were identified.

She started a third cycle of HD IL-2 therapy, as her symptoms had resolved, cardiac investigations were normal and CT imaging at 6 months revealed an ongoing excellent response to treatment with almost complete resolution of her metastatic disease. Again, this was initially well tolerated and she completed eight doses. After her ninth dose, however, she developed dysarthria and left-sided facial droop. Intracranial imaging revealed an area of abnormality in the right hemisphere consistent with an embolic infarct. Investigations revealed elevated troponin I. New T wave inversion on ECG and transthoracic echo confirmed a left atrial thrombus with impaired left ventricular systolic function. She was commenced on therapeutic anticoagulation. Cardiac magnetic resonance (CMR) imaging with late gadolinium enhancement revealed non-ischaemic mid-wall late enhancement in keeping with acute oedema caused by myocarditis. Other causes of myocarditis were excluded and a diagnosis of HD IL-2-induced myocarditis was made. Medical therapy with beta-blockade was commenced.

Over the next 48 h her neurological symptoms completely resolved. Repeat echocardiography 3 months after the acute event revealed resolution of the atrial thrombus, and a repeat CMR demonstrated normally enhancing myocardium with restoration of systolic function. Cardiac medications were subsequently stopped. CT imaging over 4 years after completion of HD IL-2 therapy confirmed ongoing sustained response. She remains under active surveillance.

What is the current evidence for the use of HD IL-2 in the management of metastatic RCC?

How is HD IL-2 administered?

What are the frequent toxicities of HD IL-2?

How is treatment-induced myocarditis diagnosed and treated?

In this era of targeted immunotherapies, is there a continued role for HD IL-2 in the future management of RCC?

What is the current evidence for the use of HD IL-2 in the management of metastatic RCC?

Cytokines play an integral role in immune biology, and attempts have been made to harness their potential as anticancer therapies. IL-2 has a wide range of effects on a variety of immune cells, and T ...

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