A 65-year-old man was referred to the department of oncology with complaints of right chest and back pain, cough, expectoration, and dyspnea for more than 9 months and had been diagnosed with PPSCC by another hospital. He was also diagnosed with type 2 diabetes for 7 years, with a past history of varicose veins in both lower extremities. No other family history of cancer was reported.
A review of the patient's medical history showed that the initial symptoms of the patient were pain in the right chest and back, with cough and expectoration; however, subsequently, the patient was inadvertently found to have multiple lymph nodes of different sizes in the left neck, which was neglected by the patient. With progressive enlargement of the lymph nodes and aggravation of the cough, sputum, and chest pain, he visited a local hospital. After paracentesis of the pleura, immunohistochemistry revealed that the tumor tissue (TT) was a poorly differentiated squamous cell carcinoma, and the final pathological diagnosis was PPSCC. No abnormality was found in head magnetic resonance imaging and bone scan. Computed tomography (CT) scan showed extensive inhomogeneous thickening of the right and interlobar pleuras that invade the right pericardial invasion with mediastinal lymph nodes surrounding the superior vena cava. Therefore, he received radiotherapy for mediastinum as well as chemotherapy. The treatment of cisplatin plus paclitaxel systemic chemotherapy was terminated after two cycles of the chemotherapy, since the patient could not tolerate severe gastrointestinal distress. L858R mutation in epidermal growth factor receptor (EGFR) exon 21 and EML4-anaplastic lymphoma kinase (ALK) fusion gene mutation was found in genetic testing. Due to economic reasons, the patient first chose gefitinib instead of the ALK inhibitor. Tumor progression was observed after the patient received gefitinib as the targeted therapy for 4 months. However, both lung and liver metastasis were detected by CT scan. During the treatment, the patient's dyspnea was not alleviated, and the general condition of the patient was exacerbated with a weight loss of 10 kg within 6 months.
Subsequently, the patient was transferred to our hospital for further treatment. On examination, vital signs of the patient were within normal limits at the time of admission. Following physical examination of the patient, multiple enlarged lymph nodes were found (approximately 4 cm) in the left neck with partial fusion, hard texture, irregular shape, smooth surface, poor mobility, but no tenderness. The patient had obvious dyspnea, cough, expectoration, and laboratory tests (Table 1) (Figure 2) showed platelet aggregation, hypoproteinemia, and abnormal coagulation function. The CT scan showed (Figure 1) bilateral pleural thickening with bilateral pleural effusion, which were consistent with pleural malignant tumor. The family members of the patient showed a strong willingness for active treatment. We decided to detect the expression of PD-L1 by needle biopsy again. However, after evaluation by an anesthesiologist, various factors, such as severe pulmonary infection and pleural effusion with dyspnea precluded transthoracic fine needle biopsy, were considered. Moreover, the patient was accompanied by coagulation dysfunction and platelet aggregation. It was considered that the risk of malignant thrombosis in perioperative period was extremely high, and the pulmonary function was poor, which could be life threatening. Therefore, only the left cervical lymph node biopsy was performed. The immunohistochemical results supported the neuroendocrine function of squamous cell carcinoma (Figure 3): Ki67 (+, 70%), CD56 (-), Syn (++), P40 (+++), P63 (++), CD20 (-), Vim (-), EMA (++), TTF1 (++), NaspinA (-), CD99 (-), and PD-L1 (+, 80%). After retesting the hematological samples, no mutations were observed in the EGFR and ALK genes of the patient. Hence, targeted therapy was not selected. Fortunately, the tumor had a high expression of PD-L1; thus, we decided to administer camrelizumab according to the recommended intravenous dose of 200 mg (once every 3 weeks) for a total of six times from October 20, 2019 to February 11, 2020 (Figure 4).
After the first administration of camrelizumab, the symptoms of dyspnea were significantly relieved, which boosted our confidence in continuing the treatment. Re-examination of CT after the fifth treatment showed that the pleural effusion, pleural nodules, pulmonary lesions, and lymph nodes were smaller than before. The patient developed cough, expectoration, and dyspnea 1 month after the end of the treatment. However, the novel coronavirus (COVID-19) outbreak delayed the patient's access to treatment. The patient had massive pericardial effusion. Laboratory tests on the last admission showed that the infection was serious and that cardiac function deteriorated. We observed that a number of elevated cytokines revealed that the patient's immune system was destroyed due to ICIs (Table 2). Eventually, the patient died as result of respiratory and circulatory failure.