Journal of Interventional Medicine最新文献

Background

Hepatic tumors with complex vascular supply or poor relative perfusion are prone to decreased rates of objective response. This is compounded in the setting of Yttrium-90 (Y90) transarterial radioembolization (TARE), which is minimally embolic and flow-dependent, relying on high threshold dose for complete response.

Objective

We describe our experience with intrahepatic flow diversion (FD) prior to TARE of hepatocellular carcinoma (HCC) with challenging vascular supply.

Materials and methods

Between April 2014 and January 2020, 886 cases of coinciding MAA or TARE and bland embolization or temporary occlusion were identified. Intraprocedural embolizations performed for more routine purposes were excluded. FD was performed by bland embolization or temporary occlusion of vessels supplying non-malignant parenchyma in cases where flow was not preferential to target tumor. Lesion characteristics, vascular supply, treatment approach, angiography, and adverse events (AEs) were reviewed. Radiographic response was assessed using mRECIST criteria.

Results

22 cases of FD of focal HCC were identified. Embolics included calibrated microspheres (n ​= ​11), microcoils (n ​= ​4), gelfoam (n ​= ​3), temporary balloon occlusion (n ​= ​2) and temporary deployment of a microvascular plug (n ​= ​1). Post-treatment SPECT-CT dosimetry coverage was concordant with target lesions in all cases. Mean follow-up was 16.7 months (1.4–45 ​mos). Tumor-specific response per mRECIST was 41% complete response, 50% objective response, and 59% disease control rate. No major adverse events or grade 3/4 hepatotoxicity were reported.

Conclusion

Our findings suggest that FD prior to TARE is safe and potentially effective in treating HCC with complex vascular supply or poor tumor perfusion.

Background

To investigate the underlying molecular mechanisms of radiofrequency hyperthermia (RFH)-enhanced direct chemotherapy of pancreatic cancers.

Method

Rat ductal PaCa cell line DSL-6A/C1 and orthotopic pancreatic cancers of Lewis rats were divided into four study groups with various treatments: i) phosphate-buffered saline (PBS) as a control; ii) RFH alone; iii) intratumoral chemotherapy alone (gemcitabine); and (iv) combination therapy of gemcitabine plus intratumoral RFH at 42 ​°C for 30 ​min. In the in-vitro confirmation experiments, the viability and apoptosis of DSL-6A/C1 cells in each treatment group were evaluated using cell live/dead staining, flow cytometry, and Western blot. In the in vivo validation experiments, related proteins were evaluated by immunohistochemistry (IHC) staining of tumors.

Results

Of the in-vitro experiments, the lowest cell viability and more apoptotic cells were shown in the group with combination therapy compared to other treatments. Western blot data showed elevated Bax/Bcl-2, Caspase-3, and HSP70 expressions in DSL cells with combination therapy, compared to other treatments. Of the in vivo experiments, IHC staining detected the significantly increased expressions of HSP70, IL-1β, TNF-ɑ, Bax, and Caspase-3 in pancreatic cancer tissues of the animal group treated by combination therapy of gemcitabine with RFH.

Conclusion

Molecular imaging-guided interventional RFH can significantly enhance the chemotherapeutic effect on pancreatic cancers via potential molecular mechanisms of up-regulating Bax/caspase-3-dependent apoptosis pathways.

Cases of low-grade cerebral arteriovenous malformations (cAVMs) showing dynamic changes and large areas of brain edema on short-term MRI follow-up have rarely been reported. This report describes an incidentally discovered and initially misdiagnosed cAVM in a patient with malignancies. The presence of abnormal signals surrounded by large areas of brain edema combined with tortuous or dilated vessels indicates the possibility of an AVM, especially in young people.

We report two cases of hepatic encephalopathy caused by molecular targeted drugs after the Transjugular intrahepatic portosystemic shunt (TIPS) procedure in our center. The liver toxicities and anti-angiogenic effects induced by targeted drugs may generate an imbalance in ammonia metabolism, elevating blood ammonia levels. TIPS diverts partial blood supply from the liver, aggravates liver impairment, and shunts ammonia-rich blood from the intestine into the systemic circulation. These may be the mechanisms leading to hepatic encephalopathy caused by molecular targeted drugs following TIPS. When clinicians choose molecular targeted therapy as the second or third targeted therapy for patients who have undergone TIPS, the consequence of drug-induced hepatic encephalopathy should also be considered.