Clinical Response to Celiac Plexus Block Confirms the Neurogenic Etiology of Median Arcuate Ligament Syndrome.

PURPOSE: To evaluate the response of median arcuate ligament syndrome (MALS) symptoms, including postprandial pain, nausea, and vomiting, to celiac plexus block (CPB) and correlate the response with arterial anatomy. MATERIALS AND METHODS: In a single-institution, retrospective cohort of clinically diagnosed MALS patients, 96 patients (female, 75; male, 21; mean age, 27 years) underwent 103 computed tomography‒guided percutaneous CPB procedures. Imaging, procedural, and clinical reports were reviewed. Primary outcomes evaluated were technical success, change in self-reported pain score, and change in nausea and vomiting. RESULTS: Computed tomography imaging before the procedure was available for 81 of 96 patients and demonstrated findings of celiac artery compression in 22 of 81 (27%) patients. Technical success was achieved in 102 of 103 cases. No major adverse events and 1 moderate adverse event were reported. The postprandial pain score decreased in 86 (84%) patients, and the mean score decreased from 6.3 to 0.9 points (P < .001). The prevalence of postprandial nausea decreased from 37.9% to 11.6% (P < .001) and that of vomiting decreased from 15.5% to 4.9% (P = .019). No differences were noted in pain relief after CPB between patients with and without celiac artery compression (P = .745). CONCLUSIONS: In patients with a clinical diagnosis of MALS, a large majority reported pain relief and decreased gastrointestinal symptoms after CPB. Pain relief did not correlate with the presence of celiac arterial abnormalities. This supports neuropathy as the primary etiology of MALS and suggests that the absence of celiac stenosis should not be used as an exclusion criterion.

Phase I Hepatic Immunotherapy for Metastases Study of Intra-Arterial Chimeric Antigen Receptor-Modified T-cell Therapy for CEA+ Liver Metastases.

PURPOSE: Chimeric antigen receptor-modified T cells (CAR-T) have demonstrated encouraging results in early-phase clinical trials. Successful adaptation of CAR-T technology for CEA-expressing adenocarcinoma liver metastases, a major cause of death in patients with gastrointestinal cancers, has yet to be achieved. We sought to test intrahepatic delivery of anti-CEA CAR-T through percutaneous hepatic artery infusions (HAIs). EXPERIMENTAL DESIGN: We conducted a phase I trial to test HAI of CAR-T in patients with CEA(+) liver metastases. Six patients completed the protocol, and 3 received anti-CEA CAR-T HAIs alone in dose-escalation fashion (10(8), 10(9), and 10(10) cells). We treated an additional 3 patients with the maximum planned CAR-T HAI dose (10(10) cells × 3) along with systemic IL2 support. RESULTS: Four patients had more than 10 liver metastases, and patients received a mean of 2.5 lines of conventional systemic therapy before enrollment. No patient suffered a grade 3 or 4 adverse event related to the CAR-T HAIs. One patient remains alive with stable disease at 23 months following CAR-T HAI, and 5 patients died of progressive disease. Among the patients in the cohort that received systemic IL2 support, CEA levels decreased 37% (range, 19%-48%) from baseline. Biopsies demonstrated an increase in liver metastasis necrosis or fibrosis in 4 of 6 patients. Elevated serum IFNγ levels correlated with IL2 administration and CEA decreases. CONCLUSIONS: We have demonstrated the safety of anti-CEA CAR-T HAIs with encouraging signals of clinical activity in a heavily pretreated population with large tumor burdens. Further clinical testing of CAR-T HAIs for liver metastases is warranted.