Objective To discuss the clinical complications caused by inferior vena cava abnormality and their interventional management. Methods The clinical data and interventional therapeutic results of 4 patients with complications due to abnormalities of the inferior vena cava were retrospectively analyzed. Results Duplicate inferior vena cava deformity was confirmed in two cases; one of them was complicated by right inferior vena cava with deep venous thrombosis of right lower extremity;and the other case had bilateral inferior vena cava thrombosis secondary to tumor thrombus within the intrahepatic segment of inferior vena cava, for which interventional treatment was not employed. Left-sided inferior vena cava was observed in 2 cases; clinically, one showed microscopic haematuria and lower back pain, and interventional treatment was not adopted; the other case had abdominal pain, and the symptom showed no obvious improvement after receiving stent implantation in the crossing segment of the left-sided inferior vena cava. Conclusion Clinically, the complications caused by abnormalities of inferior vena cava are rare. The diagnosis and the treatment of its complications should be based on the imaging manifestations, the related clinical symptoms, blood flow dynamics, etc. and the misdiagnosis and mistreatment should be avoided.

Objective Todiscusstheangiographicfeaturesofhepaticneuroendocrineneoplasm(NEN),and to analyze the survival time of patients.Methods The clinical data of 60 patients with hepatic NEN were retrospectively reviewed.Transcatheter arterial chemoembolization (TACE),used as main therapy,was employed in 17 patients,22 patients received palliative treatment with no use of TACE,and 21 didn't receive any related treatment.The angiographic features of hepatic NEN were analyzed.Kaplan-Meier method was used to calculate the survival rate,and the survival prognostic factors were evaluated by Cox multivariate analysis method.Results Angiography showed that most neuroendocrine tumors (NETs) were characterized by hypovascular lesion,while neuroendocrine carcinomas (NECs) were manifested as hypervascular mass.The median overall survival time of 60 patients was 13.8 months.The 6-month,one-,2-and 3-year cumulative survival rates were 85.0％,52.0％,40.0％ and 33.8％,respectively.Cox regression analysis indicated that pathological grade of tumor (P=0.001) and treatment mode (P＜0.001) were the independent prognostic factors.Conclusion The rich or poor vascularity of hepatic NEN is helpful for the judgment of tumor grading.Patients whose hepatic NENs belong to high pathological grade (grade Ⅲ) usually have a poor prognosis.TACE is an effective therapy for hepatic NEN.

A 61-year-old male patient was simultaneously diagnosed with lung adenocarcinoma and inflammatory myofibroblastic tumor (IMT). The lung adenocarcinoma and IMT harbored two distinct types of ALK translocation, LOC101927285-ALK, and TPM3-ALK, respectively. The ALK Ventana showed strong positivity on both lesions. The patient was therefore given an endobronchial cryotherapy and ALK inhibitor crizotinib. The tumors showed durable response however the left lung adenocarcinoma relapsed at 17th month post-crizotinib treatment. Tissue re-biopsy on the resistant tumor revealed an ALK exon 23 C1156Y missense mutation in addition to LOC101927285-ALK mutation. Further RNA-based sequence uncovered that the noncoding region rearrangement is the fusion mutation of EML4-ALK. The patient was therefore received alectinib, and the tumor exhibited partly response. Overall, it is very rare that two types of pulmonary tumors exist in one patient driven by two distinct ALK fusions, which emphasizes the necessity of gene sequencing in clinical decision-making and individualized therapy.

A 61-year-old male patient was simultaneously diagnosed with lung adenocarcinoma and inflammatory myofibroblastic tumor (IMT). The lung adenocarcinoma and IMT harbored two distinct types of ALK translocation, LOC101927285-ALK, and TPM3-ALK, respectively. The ALK Ventana showed strong positivity on both lesions. The patient was therefore given an endobronchial cryotherapy and ALK inhibitor crizotinib. The tumors showed durable response however the left lung adenocarcinoma relapsed at 17th month post-crizotinib treatment. Tissue re-biopsy on the resistant tumor revealed an ALK exon 23 C1156Y missense mutation in addition to LOC101927285-ALK mutation. Further RNA-based sequence uncovered that the noncoding region rearrangement is the fusion mutation of EML4-ALK. The patient was therefore received alectinib, and the tumor exhibited partly response. Overall, it is very rare that two types of pulmonary tumors exist in one patient driven by two distinct ALK fusions, which emphasizes the necessity of gene sequencing in clinical decision-making and individualized therapy.