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M. Griesshammer
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P3.02c - Poster Session with Presenters Present (ID 472)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Advanced NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 12/07/2016, 14:30 - 15:45, Hall B (Poster Area)
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P3.02c-044 - Nivolumab-Response in a Patient with Advanced Squamous NSCLC Occurring Simultaneously with SIAD (ID 4659)
14:30 - 14:30 | Author(s): M. Griesshammer
- Abstract
Background:
Nivolumab is a human IgG4 monoclonal antibody that binds to the PD-1 receptor and blocks its interaction with PD-L1 and PD-L2, releasing PD-1 pathway-mediated inhibition of the immune response- including the anti-tumor immune response. Due to the novelty of the mechanism of action and the limited treatment experience all checkpoint inhibitors can potentially induce treatment related AEs in any organ system that have not been noticed until now. The Syndrome of Inappopriate Antidiuresis (SIAD)-leading to hyponatremia with variant symptoms of CNS affection- is a frequent paraneoplastic syndrom in patients with advanced cancer, especially small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC), but can also be induced by a large number of anticancer drugs, however, not reported for Nivolumab until now.
Methods:
We report a 56year old heavily pretreated patient who was first diagnosed with squamous NSCLC in 2012. After symptomatic progression he started 4[th] line therapy on Nivolumab treatment (3mg/kg, q2w) in August 2015 after EMA licensing.
Results:
After 3 months of treatment we noted disease stabilization with a radiographic minor response together with a slight improvement of tumor symptoms. Thus, therapy was continued. After 6 months treatment CT scan showed for the first time a partial response, however patient reported a clinical deterioration with onset of new symptoms (headache, dizziness, fatigue, nausea, blurred vision). Lab results showed severe hyponatremia (nadir 116mmol/l) caused by SIAD (serum osmolality 254 mOsm/kg), possibly induced by Nivolumab as other potential causes were excluded. No signs of intracranial progression or hypophysitis (brain MRI, CSF cytology, endocrinology lab) were detected. In the phase III registration trial the median time to response was 2.2 months. In our patient hyponatremia occurred in a timely relationship with partial response of the disease (after 6 months of treatment). After 2 months Tolvaptan treatment (an oral ADH antagonist) sodium levels normalized, accompanied by improvement of hyponatremia-symptoms. The patient is still in PR on Nivolumab treatment without treatment interruptions with normal sodium levels.
Conclusion:
We report a patient case (squamous NSCLC) where chemotherapy was not able to induce long lasting radiographic remissions or clinical benefit. After switching to Nivolumab therapy the patient achieved a partial remission after 6 month of continous Nivolumab with a simultaneous onset of hyponatremia. To the best of our knowledge, this is the first report of a Nivolumab response occuring simultaneously with SIAD. Therefore we speculate that hyponatremia might be a predictor for Nivolumab treatment response.
