A Case of Lupus Nephritis Improved by Molecular Targeted Drug Therapy for Multiple Intrapulmonary Metastasis of ROS-1 Gene-Positive Lung Cancer

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Introduction: Systemic lupus erythematosus is a multisystemic disease associated with genetic, environmental and epigenetic factors. The effect of tyrosine kinase inhibitors has only been reported in SLE model mice for imatinib. Here we report a case in which lupus nephritis was improved by a molecular targeted drug for multiple intrapulmonary metastases of ROS-1 gene-positive lung cancer. Case Description: Thirty-one-year-old woman, who was diagnosed with SLE at the age of 14 years, had been treated with immunosuppressive agents including corticosteroids, cyclophosphamide and mycophenolate mofetil, with frequent relapses. At the age of 30 years, she was admitted to our hospital due to development of systemic erythema, which was diagnosed as drug-induced eruption with increased SLE activities. She was treated with prednisolone (PSL) 50 mg/day and remission was achieved for SLE, however, during the systemic screening, lung adenocarcinoma was accidentally detected, and thoracoscopic right middle lobectomy was performed. Seven months after surgery, she had an exacerbation of erythema on the face and bilateral arms, arthralgia and urinary proteins, with elevated anti-ds-DNA antibodies and decreased serum complement levels. The dose of PSL was increased, but the symptoms did not improve, when multiple intrapulmonary metastases were detected, indicating recurrence of lung adenocarcinoma. The previous lung specimens revealed a high expression of PD-L1 and positive ROS-1 fusion gene, thus tyrosine kinase inhibitor (crizotinib) was selected as the anti-cancer therapy instead of anti-PD-L1 antibodies. Interestingly, urine protein and erythema/arthralgia improved as the size of lung tumor reduced. Discussion: Crizotinib is a molecular targeting agent with non-receptor-type tyrosine kinase inhibitory action that competitively binds to the ATP binding site of EML4-ALK tyrosine kinase, resulting in signal transduction inhibition. In this case, the molecular targeting drug induced improvement of lupus nephritis along with regression of lung cancer, suggesting that tyrosine kinase inhibition may be effective for lupus nephritis.

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