Quercetin is a natural flavonoid that occurs in fruits and vegetables. Retinal inflammation is an important cause of vision loss. The study was aimed to analyze the effects of oral...

Rationale: Transcatheter arterial chemoembolization (TACE) is a widely adopted treatment for advanced stage hepatocellular carcinoma (HCC). Nevertheless, several complications may occur, such as hepatic artery injury, nontarget embolization, pulmonary embolism, hepatic abscess, biloma, biliary strictures, and hepatic failure. However, bronchobiliary fistula is rarely mentioned before. Patient concerns: A 65-year-old man with HCC underwent the TACE procedure, and then he encountered fever, dyspnea, abdominal pain, and abundant yellowish purulent bronchorrhea. Diagnosis: Bronchobiliary fistula was diagnosed based on the computed tomography (CT) scan of his chest, which revealed the right lower lobe of his lung was connected to a hepatic cystic lesion. Interventions: Percutaneous transhepatic cystic drainage was performed, and we obtained yellowish bile, showing the same characteristics as the patient’s bronchorrhea. Outcomes: We kept drainage of his biloma and provided supportive care as the patient wished. Unfortunately, the patient passed away due to progressive right lower lobe pneumonia 2 weeks later. Lessons: This case exhibits a typical CT scan image that was helpful for the diagnosis of post-TACE bronchobiliary fistula. Post-TACE bronchobiliary fistula formation hypothesis includes biliary tree injuries with subsequent biloma formation and diaphragmatic injuries. Moreover, the treatment of bronchobiliary fistula should be prompt to cease pneumonia progression. Therefore, we introduce this rare complication of post-TACE bronchobiliary fistula in hopes that future clinicians will keep earlier intervention in mind.

Introduction: Factor VII deficiency is a rare inherited autosomal recessive bleeding disorder with a global prevalence of 1/500,000. Most cases remain asymptomatic, and cases with severe clinical presentation are rarely reported.Case Presentation: A newborn male with no relevant maternal antenatal history, delivered via vacuum-assisted cesarean section, presented with a large cephalohematoma after delivery. Poor appetite, pale appearance, and bulging fontanelles were observed 2 days later, progressing to hypovolemic shock. Further imaging examination revealed a large intracranial hemorrhage. Serial laboratory examination revealed remarkable coagulopathy with prolonged prothrombin time and factor VII deficiency (<1%, severe type). The patient was genetically confirmed to have the FVII:c 681+1 G>T homozygous mutation. Brain hemorrhage was resolved with high-dose factor VII replacement therapy with recombinant activated factor VII. However, repeated hemothorax and intracranial hemorrhage were detected. Therefore, the patient was under regular factor VII supplementation with a rehabilitation program for cerebral palsy.Conclusions: A case of factor VII deficiency with large cephalohematoma and intracranial hemorrhage after birth is described herein, which was treated with high-dose replacement therapy. Variants of the FVII:c 681+1 G>T (IVS6+1G>T) homozygous genotype may present with a severe phenotype at the neonatal stage. We aim to share a unique neonatal presentation with a certain genotype and treatment experience with initial replacement therapy, followed by regular prophylactic dosage.