Fleming, Chad J.

Abstract Importance and Objective Pancreatic cancer can lead to severe stenosis of the portomesenteric venous (PV/SMV) confluence due to extrinsic compression or direct invasion. This can result in venous hypertension associated with post-prandial abdominal pain, gastrointestinal bleeding, and ascites. In patients with unresectable tumors, transhepatic PV/SMV stenting has been reported; however, its safety and efficacy are poorly understood. Design, Setting and Participants All unresectable pancreatic cancer patients referred to Interventional Radiology to undergo palliative transhepatic PV/SMV stenting (2011–2024) were collected. Patient demographics, CT scans, transhepatic venograms, and clinical outcomes were reviewed. Intervention, Main Outcomes and Results In total, 129 patients were included; 92% had pancreatic ductal adenocarcinoma. Tumors were unresectable due to unreconstructable vascular involvement, metastatic disease, or poor performance status. Nearly 81% were symptomatic, while the remaining 24 asymptomatic patients presented with significant venous hypertensive varices and collaterals on imaging. Complete venous occlusion was seen in 39% of patients at the PV, the SMV, or the PV/SMV confluence; 97% of procedures were successful, with 4 technical failures at obtaining distal venous wire access. Adverse events occurred in 4 patients. Radiological follow-up was available in 94% of patients. Post-procedural primary stent patency was 80% at a median follow-up time of 20 months. Follow-up was available in 102 of the 105 symptomatic patients, with 85% reporting an improvement in symptoms. Conclusions and Relevance Palliative transhepatic PV/SMV stenting is a technically feasible and safe procedure in well-selected patients. Symptoms improvement can be seen in most patients. High-volume centers should consider this technique for patients with unresectable tumors who present with symptomatic stenosis or short segment occlusion.

Abstract Objectives: Radiologist participation in multidisciplinary tumor board can be time-consuming and demanding, requiring substantial preparation. Anecdotally radiologist participation is felt to help identify discrepancies in previous interpretations; however, there are limited data assessing the actual impact of their tumor board review on patient management. This prospective study aims to evaluate how the reinterpretation of outside imaging and review at hepatobiliary tumor board (HBTB) affects the diagnosis and management of patients with hepatobiliary neoplasms. Methods: This prospective analysis included all patients presented at the weekly HBTB between 6/13/2023 - 6/25/2024. One radiologist reviewed the available reports of outside imaging, the local reinterpretation of outside imaging, the updated local imaging, and documented conclusions from discussion of the case at HBTB. HBTB included 4 radiologists who had reviewed each case. Discrepancies (presence/absence, number, and reasons for) were recorded. When discrepancies occurred, the impact on patient management (5-point Likert scale) was determined by two of the radiologists present at the HBTB in consensus, with input from clinicians if needed. A six-month follow-up was performed to confirm suspected diagnoses. Results: 208 cases (128 males, 104 chronic liver disease patients) were presented at HBTB. Disagreements in the detection or characterization of lesions were found in 59/208 (28.4%) of cases. A change in management occurred in 38/59 (64.6%) of these discrepant cases. In cases with recorded discrepancies in which follow-up confirmation was available, the final interpretation was confirmed in 34/41 (82.9%) of cases. Conclusion: Our study found a discrepant interpretation in nearly one-third of cases presented at a weekly HBTB and a resultant change in management in 65% of those cases. These findings highlight the importance of reinterpretation of prior imaging studies and the presence of radiologists at HBTB to guide optimal patient management.

AbstractObjectiveThe objective of this study was to evaluate the role of adrenal venous sampling (AVS) in guiding the management of patients with corticotropin (ACTH)‐independent glucocorticoid secretory autonomy and bilateral adrenal masses.Design and PatientsA cohort with 25 patients underwent AVS and surgical management.MeasurementsCortisol was measured from the adrenal veins (AVs) and inferior vena cava (IVC). AV/IVC cortisol ratio and cortisol lateralization ratio (CLR) (dominant AV cortisol concentration divided by the nondominant AV cortisol concentration) were calculated. Posthoc receiver‐operating characteristic curves were generated to determine the specificity of revised AV/IVC cortisol ratio and CLR in differentiating unilateral from bilateral disease.ResultsPatients underwent unilateral (n = 21) or bilateral (n = 4) adrenalectomy. The mean AV/IVC cortisol ratio for unilateral adrenalectomy was 12.1 ± 9.6 (dominant) and 4.7 ± 3.8 (contralateral) with a mean CLR of 3.6 ± 3.5. The mean AV/IVC cortisol ratio for bilateral adrenalectomy was 7.5 ± 2.1, with a mean CLR of 1.1 ± 0.6. At a mean follow‐up of 22 months, one patient who underwent unilateral adrenalectomy for the predicted bilateral disease developed recurrent mild autonomous cortisol secretion. Posthoc analyses demonstrated a specificity of 95%–100% for unilateral disease with AV/IVC cortisol ratio >9 for one side, <2.0 for the opposite side and a CLR > 2.3. The specificity was 80%–90% for bilateral disease with AV/IVC cortisol ratio >5.1 bilaterally and a CLR < 1.1.ConclusionsAmong patients with bilateral adrenal masses and ACTH‐independent autonomous cortisol secretion, AVS can distinguish between unilateral and bilateral disease with high specificity and may guide surgical management.

Prostate‐specific membrane antigen (PSMA) is a validated target for molecular diagnostics and targeted radionuclide therapy. Our purpose was to evaluate PSMA expression in hepatocellular carcinoma (HCC), cholangiocarcinoma (CCA), and hepatic adenoma (HCA); investigate the genetic pathways in HCC associated with PSMA expression; and evaluate HCC detection rate with 68Ga‐PSMA‐11 positron emission tomography (PET). In phase 1, PSMA immunohistochemistry (IHC) on HCC (n = 148), CCA (n = 111), and HCA (n = 78) was scored. In a subset (n = 30), messenger RNA (mRNA) data from the Cancer Genome Atlas HCC RNA sequencing were correlated with PSMA expression. In phase 2, 68Ga‐PSMA‐11 PET was prospectively performed in patients with treatment‐naïve HCC on a digital PET scanner using cyclotron‐produced 68Ga. Uptake was graded qualitatively and semi‐quantitatively using standard metrics. On IHC, PSMA expression was significantly higher in HCC compared with CCA and HCA (P < 0.0001); 91% of HCCs (n = 134) expressed PSMA, which principally localized to tumor‐associated neovasculature. Higher tumor grade was associated with PSMA expression (P = 0.012) but there was no association with tumor size (P = 0.14), fibrosis (P = 0.35), cirrhosis (P = 0.74), hepatitis B virus (P = 0.31), or hepatitis C virus (P = 0.15). Overall survival tended to be longer in patients without versus with PSMA expression (median overall survival: 4.2 vs. 1.9 years; P = 0.273). FGF14 (fibroblast growth factor 14) mRNA expression correlated positively (rho = 0.70; P = 1.70 × 10‐5) and MAD1L1 (Mitotic spindle assembly checkpoint protein MAD1) correlated negatively with PSMA expression (rho = −0.753; P = 1.58 × 10‐6). Of the 190 patients who met the eligibility criteria, 31 patients with 39 HCC lesions completed PET; 64% (n = 25) lesions had pronounced 68Ga‐PSMA‐11 standardized uptake value: SUVmax (median [range] 9.2 [4.9‐28.4]), SUVmean 4.7 (2.4‐12.7), and tumor‐to‐liver background ratio 2 (1.1‐11). Conclusion: Ex vivo expression of PSMA in neovasculature of HCC translates to marked tumor avidity on 68Ga‐PSMA‐11 PET, which suggests that PSMA has the potential as a theranostic target in patients with HCC.

Abstract Context Insulinoma is a pancreatic neuroendocrine tumor that causes hyperinsulinemic hypoglycemia. Symptomatic hypoglycemia related to hepatic insulinoma metastases may be addressed with liver-directed therapies such as hepatic artery embolization. Objective This work aimed to determine the safety and effectiveness of bland hepatic artery embolization (HAE) for palliation of symptomatic hypoglycemia in patients with hepatic insulinoma metastases refractory to medical management. Methods An institutional review board–approved retrospective review was undertaken of all patients with a tissue (n = 18) or imaging (n = 2) diagnosis of hepatic insulinoma metastases and symptomatic hyperinsulinemic hypoglycemia refractory to medical management who underwent bland HAE at a single center between January 1, 1998 and November 1, 2020. Twenty patients (10 women, 10 men; mean age, 56 years; range, 18-84 years) were identified who individually underwent 1 (n = 7), 2 (n = 5), 3 (n = 5), 4 (n = 2), or 5 (n = 1) HAEs, for an overall total of 45 HAEs. Post-HAE hypoglycemia recurrence was defined as onset of adrenergic symptoms (eg, sweating, weakness, tremor), neuroglycopenic symptoms (eg, confusion, loss of consciousness), and/or documented serum glucose of less than 50 mg/dL, in the absence of an alternative explanation. Median time to first hypoglycemia recurrence, hypoglycemia-free survival (HFS), and overall survival (OS) were calculated using Kaplan-Meier method. Results Before HAE, all patients experienced adrenergic or neuroglycopenic symptoms alleviated by glucose intake, and 60% (n = 12) of patients had documented serum glucose of less than 50 mg/dL within 1 week of the first treatment. Median post-HAE follow-up was 9.4 months (mean, 26 months; range, 0.1-190 months). Postprocedural hypoglycemic symptom relief after the first HAE was reported in 100% (n = 20) of patients before discharge or at follow-up. Post-HAE hypoglycemia recurrence occurred in 60% (n = 12) of patients with a median time to first hypoglycemia recurrence of 2 months (mean, 14 months; range, 0.2-60 months). After the first HAE, median HFS was 14.5 months, and median OS was 16 months. One patient experienced labile postprocedure blood glucose levels requiring intensive care unit admission for intravenous dextrose. Otherwise, no major procedure-related complications occurred. Conclusion Bland HAE is a safe, effective, and repeatable procedure for palliation of symptomatic hypoglycemia in patients with hepatic insulinoma metastases refractory to medical management.

AbstractLearning Objectives:After completing this course, the reader will be able to:Identify the components of the “postembolization syndrome”: elevated liver function tests, right upper quadrant pain, nausea and vomiting, and fever.Distinguish the postembolization syndrome from rare complications of embolization that would merit an extended hospitalization.CME This article is available for continuing medical education credit at CME.TheOncologist.comBackground.There is scant evidence to guide the management of patients after hepatic artery embolization (HAE). We examined length of stay (LOS), laboratory patterns, medication usage, morbidity, and mortality of patients hospitalized after HAE for metastatic neuroendocrine tumors.Methods.Data were abstracted retrospectively from electronic medical records on LOS, liver function tests (LFTs), i.v. antibiotics, analgesia, peak temperature, bacteremia, hepatic abscess formation, carcinoid crisis, and metastatic burden on cross-sectional imaging.Results.In 2005–2009, 72 patients underwent 174 HAEs for carcinoid and islet cell tumors. The median LOS was 4 days (range, 1–8 days). There was no correlation between peak LFTs and tumor burden. Declines in LFTs were not uniform before hospital discharge; 25%, 37%, 30%, 53%, and 67% of patients were discharged before their respective aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and total and direct bilirubin levels began to decline, with no readmissions for acute hepatic failure. The median i.v. analgesia dose was 60 mg oral morphine equivalents (range, 3–1,961 mg). Pre-HAE i.v. antibiotics were administered in 99% of cases; post-HAE fever occurred in 37% of patients, with no documented bacteremia. One patient developed a hepatic abscess after HAE. There were two carcinoid crises. The single in-hospital death was associated with air in the portal veins.Conclusions.The duration and intensity of in-hospital care following HAE should be managed on an individual basis. A downward trend in LFTs is not required before discharge. Modest use of i.v. analgesia suggests that many patients could exclusively receive oral analgesics. Given the rarity of serious complications, hospital stays could be shortened, thereby reducing costs and nosocomial risks.