Subclinical Cognitive Impairment and Listing for Kidney Transplantation.

BACKGROUND AND OBJECTIVES: Cognitive impairment is common in patients with kidney disease and can affect physicians' perception and/or patients' ability to complete the pretransplant evaluation. We examined whether cognitive impairment influences the likelihood for transplant listing and whether patients with cognitive impairment take longer to be listed. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: We conducted a single-center longitudinal cohort study. Patients presenting for their index kidney transplant evaluation were screened for cognitive impairment using the Montreal Cognitive Assessment. A score <26 indicated cognitive impairment. The transplant selection committee was blinded to the scores. Kaplan-Meier analysis assessed time to active listing by level of cognition. A Cox proportional hazards model that included age, sex, race/ethnicity, smoking, coronary artery disease, and diabetes was constructed to evaluate the association between Montreal Cognitive Assessment score and listing for transplant. RESULTS: In total, 349 patients who underwent Montreal Cognitive Assessment testing at their initial visit were included in the analysis. Patients with cognitive impairment were more likely to be older, black, and smokers. The time to listing in patients with cognitive impairment was longer than the time to listing in those with no cognitive impairment (median time, 10.6 versus 6.3 months; log rank test P=0.01). Cognitive impairment was independently associated with a lower likelihood of being listed for transplant (hazard ratio, 0.93 per unit lower Montreal Cognitive Assessment score; 95% confidence interval, 0.88 to 0.99; P=0.02). A lower proportion of patients with cognitive impairment were listed compared with patients without cognitive impairment at 1 month (2% versus 11%), 6 months (17% versus 37%), and 1 year (23% versus 41%), (P<0.001 for all). CONCLUSIONS: Cognitive impairment is associated with a lower likelihood of being listed for kidney transplant, and is associated with longer time to transplant listing.

Mitochondrial protein adducts formation and mitochondrial dysfunction during N-acetyl-m-aminophenol (AMAP)-induced hepatotoxicity in primary human hepatocytes.

3'-Hydroxyacetanilide orN-acetyl-meta-aminophenol (AMAP) is generally regarded as a non-hepatotoxic analog of acetaminophen (APAP). Previous studies demonstrated the absence of toxicity after AMAP in mice, hamsters, primary mouse hepatocytes and several cell lines. In contrast, experiments with liver slices suggested that it may be toxic to human hepatocytes; however, the mechanism of toxicity is unclear. To explore this,we treated primary human hepatocytes (PHH) with AMAP or APAP for up to 48 h and measured several parameters to assess metabolism and injury. Although less toxic than APAP, AMAP dose-dependently triggered cell death in PHH as indicated by alanine aminotransferase (ALT) release and propidium iodide (PI) staining. Similar to APAP, AMAP also significantly depleted glutathione (GSH) in PHH and caused mitochondrial damage as indicated by glutamate dehydrogenase (GDH) release and the JC-1 assay. However, unlike APAP, AMAP treatment did not cause relevant c-jun-N-terminal kinase (JNK) activation in the cytosol or phospho-JNK translocation to mitochondria. To compare, AMAP toxicity was assessed in primary mouse hepatocytes (PMH). No cytotoxicity was observed as indicated by the lack of lactate dehydrogenase release and no PI staining. Furthermore, there was no GSH depletion or mitochondrial dysfunction after AMAP treatment in PMH. Immunoblotting for arylated proteins suggested that AMAP treatment caused extensive mitochondrial protein adduct formation in PHH but not in PMH. In conclusion, AMAP is hepatotoxic in PHH and the mechanism involves the formation of mitochondrial protein adducts and mitochondrial dysfunction.

Lack of Direct Cytotoxicity of Extracellular ATP against Hepatocytes: Role in the Mechanism of Acetaminophen Hepatotoxicity.

BACKGROUND: Acetaminophen (APAP) hepatotoxicity is a major cause of acute liver failure in many countries. Mechanistic studies in mice and humans have implicated formation of a reactive metabolite, mitochondrial dysfunction and oxidant stress as critical events in the pathophysiology of APAP-induced liver cell death. It was recently suggested that ATP released from necrotic cells can directly cause cell death in mouse hepatocytes and in a hepatoma cell line (HepG2). AIM: To assess if ATP can directly cause cell toxicity in hepatocytes and evaluate their relevance in the human system. METHODS: Primary mouse hepatocytes, human HepG2 cells, the metabolically competent human HepaRG cell line and freshly isolated primary human hepatocytes were exposed to 10-100 µM ATP or ATγP in the presence or absence of 5-10 mM APAP for 9-24 h. RESULTS: ATP or ATγP was unable to directly cause cell toxicity in all 4 types of hepatocytes. In addition, ATP did not enhance APAP-induced cell death observed in primary mouse or human hepatocytes, or in HepaRG cells as measured by LDH release and by propidium iodide staining in primary mouse hepatocytes. Furthermore, addition of ATP did not cause mitochondrial dysfunction or enhance APAP-induced mitochondrial dysfunction in primary murine hepatocytes, although ATP did cause cell death in murine RAW macrophages. CONCLUSIONS: It is unlikely that ATP released from necrotic cells can significantly affect cell death in human or mouse liver during APAP hepatotoxicity. RELEVANCE FOR PATIENTS: Understanding the mechanisms of APAP-induced cell injury is critical for identifying novel therapeutic targets to prevent liver injury and acute liver failure in APAP overdose patients.

Lack of direct cytotoxicity of extracellular ATP against hepatocytes: role in the mechanism of acetaminophen hepatotoxicity.

BACKGROUND: Acetaminophen (APAP) hepatotoxicity is a major cause of acute liver failure in many countries. Mechanistic studies in mice and humans have implicated formation of a reactive metabolite, mitochondrial dysfunction and oxidant stress as critical events in the pathophysiology of APAP-induced liver cell death. It was recently suggested that ATP released from necrotic cells can directly cause cell death in mouse hepatocytes and in a hepatoma cell line (HepG2). AIM: To assess if ATP can directly cause cell toxicity in hepatocytes and evaluate their relevance in the human system. METHODS: Primary mouse hepatocytes, human HepG2 cells, the metabolically competent human HepaRG cell line and freshly isolated primary human hepatocytes were exposed to 10-100 µM ATP or ATγPin the presence or absence of 5-10 mM APAP for 9-24 h. RESULTS: ATP or ATγP was unable to directly cause cell toxicity in all 4 types of hepatocytes. In addition, ATP did not enhance APAP-induced cell death observed in primary mouse or human hepatocytes, or in HepaRG cells as measured by LDH release and by propidium iodide staining in primary mouse hepatocytes. Furthermore, addition of ATP did not cause mitochondrial dysfunction or enhance APAP-induced mitochondrial dysfunction in primary murine hepatocytes, although ATP did cause cell death in murine RAW macrophages. CONCLUSIONS: It is unlikely that ATP released from necrotic cells can significantly affect cell death in human or mouse liver during APAP hepatotoxicity. RELEVANCE FOR PATIENTS: Understanding the mechanisms of APAP-induced cell injury is critical for identifying novel therapeutic targets to prevent liver injury and acute liver failure in APAP overdose patients.

Late-onset renal vein thrombosis: A case report and review of the literature.

INTRODUCTION: Renal vein thrombosis, a rare complication of renal transplantation, often causes graft loss. Diagnosis includes ultrasound with Doppler, and it is often treated with anticoagulation or mechanical thrombectomy. Success is improved with early diagnosis and institution of treatment. PRESENTATION OF CASE: We report here the case of a 29 year-old female with sudden development of very late-onset renal vein thrombosis after simultaneous kidney pancreas transplant. This resolved initially with thrombectomy, stenting and anticoagulation, but thrombosis recurred, necessitating operative intervention. Intraoperatively the renal vein was discovered to be compressed by a large ovarian cyst. DISCUSSION: Compression of the renal vein by a lymphocele or hematoma is a known cause of thrombosis, but this is the first documented case of compression and thrombosis due to an ovarian cyst. CONCLUSION: Early detection and treatment of renal vein thrombosis is paramount to restoring renal allograft function. Any woman of childbearing age may have thrombosis due to compression by an ovarian cyst, and screening for this possibility may improve long-term graft function in this population.

Mechanisms of acetaminophen-induced cell death in primary human hepatocytes.

UNLABELLED: Acetaminophen (APAP) overdose is the most prevalent cause of drug-induced liver injury in western countries. Numerous studies have been conducted to investigate the mechanisms of injury after APAP overdose in various animal models; however, the importance of these mechanisms for humans remains unclear. Here we investigated APAP hepatotoxicity using freshly isolated primary human hepatocytes (PHH) from either donor livers or liver resections. PHH were exposed to 5mM, 10mM or 20mM APAP over a period of 48 h and multiple parameters were assessed. APAP dose-dependently induced significant hepatocyte necrosis starting from 24h, which correlated with the clinical onset of human liver injury after APAP overdose. Interestingly, cellular glutathione was depleted rapidly during the first 3h. APAP also resulted in early formation of APAP-protein adducts (measured in whole cell lysate and in mitochondria) and mitochondrial dysfunction, indicated by the loss of mitochondrial membrane potential after 12h. Furthermore, APAP time-dependently triggered c-Jun N-terminal kinase (JNK) activation in the cytosol and translocation of phospho-JNK to the mitochondria. Both co-treatment and post-treatment (3h) with the JNK inhibitor SP600125 reduced JNK activation and significantly attenuated cell death at 24h and 48h after APAP. The clinical antidote N-acetylcysteine offered almost complete protection even if administered 6h after APAP and a partial protection when given at 15 h. CONCLUSION: These data highlight important mechanistic events in APAP toxicity in PHH and indicate a critical role of JNK in the progression of injury after APAP in humans. The JNK pathway may represent a therapeutic target in the clinic.

Hepatolithiasis after Hepaticojejunostomy: Ascaris lumbricoides in the biliary tract.

BACKGROUND: Biliary ascariasis is a common problem in Third World countries and other underdeveloped areas of the world. Ascaris lumbricoides migrates into the biliary tree, where it is apparent commonly on diagnostic imaging. We present a unique case of a patient with chronic right upper quadrant abdominal pain, massive hepatolithiasis, and stricture of a previous hepaticojejunostomy in whom ascariasis was found. METHODS: A 28-year-old female presented to the emergency department with right upper quadrant abdominal pain, syncope, and seizure-like activity. She was found by magnetic resonance cholangiopancreatography to have cholangitis, choledocholithiasis, and bile duct stricture. After multiple radiographic studies, she was taken to the operating room for revision of a hepaticojejunostomy performed 10 years previously. RESULTS: Ascaris lumbricoides was found in the right intrahepatic bile duct, that had not been identified by multiple radiologic modalities. The worm was sent to the pathology department for identification. A Fogarty catheter was passed into the hepatic ducts for successful stone extraction. The hepaticojejunostomy was revised, with catheter placement in the Roux limb to accommodate radiologic stone extraction as necessary. Post-operatively, she was given a single dose of albendazole and discharged on hospital day 19. CONCLUSION: The worm was likely the nidus for the stricture and stone formation. Surgical exploration of the biliary tree was required to diagnose and treat her condition accurately. This case is unique in that typical means of diagnosis failed to identify the causative agent of hepatolithiasis because of the prior Roux-en-Y hepaticojejunostomy.

Impact of stem cell marker expression on recurrence of TACE-treated hepatocellular carcinoma post liver transplantation.

BACKGROUND: Liver transplantation is the most effective therapy for cirrhosis-associated hepatocellular carcinoma (HCC) but its utility is limited by post-transplant tumor recurrence. Use of the Milan, size-based criteria, has reduced recurrence rate to less than 10% but many patients remain ineligible. Reduction of tumor size with local therapies has been used to "downstage" patients to allow them to qualify for transplantation, but the optimal criteria to predict tumor recurrence in these latter patients has not been established. The existence of a progenitor cell population, sometimes called cancer stem cells (CSCs), has been proposed to be one mechanism accounting for the chemotherapy resistance and recurrence of hepatocellular carcinoma. The aim of this study was to determine if transcatheter arterial chemoemolization (TACE) treated tumors have increased CSC marker expression and whether these markers could be used to predict tumor recurrence. METHODS: Formalin fixed specimens were obtained from 39 HCC liver explants (23 with no treatment and 16 after TACE). Immunohistochemical staining was performed for EpCAM, CD44, CD90, and CD133. Staining for each marker was scored 0-3 by evaluating the number and intensity of positive tumor cells in 5 hpf of tumor in each specimen. RESULTS: TACE treated tumors displayed greater necrosis and fibrosis than non-TACE treated samples but there were no differences in morphology between the viable tumor cells of both groups. In TACE treated specimens, the staining of both EpCAM and CD133 was greater than in non-TACE specimens but CD44 and CD90 were the same. In the TACE group, the presence of high EpCAM staining was associated with tumor recurrence. Four of ten EpCAM high patients recurred while 0 of 6 EpCAM low patients recurred (P = 0.040). None of the other markers predicted recurrence. CONCLUSION: High pre-transplant EpCAM staining predicted HCC recurrence. This suggests that the abundance of tumor cells with a CSC phenotype may be a critical factor in the likelihood of tumor recurrence in patients receiving liver transplantation after TACE.

Quantifying increased hepatic arterial flow with test balloon occlusion of the splenic artery in liver transplant recipients with suspected splenic steal syndrome: quantitative digitally subtracted angiography correlation with arterial Doppler parameters.

PURPOSE: The purpose of this study is to quantify hepatic arterial flow (HAF) in liver transplants with splenic steal syndrome (SSS) pre- and post-test balloon occlusion of the splenic artery utilizing Doppler ultrasound (DUS) and quantitative digitally subtracted angiography (Q-DSA). METHODS: A total of 193 liver transplants were evaluated retrospectively. Hepatic arterial velocity (HAV) and HAF were calculated utilizing DUS and Q-DSA (i-flow prototype, Siemens) pre- and post-splenic artery balloon occlusion. The rate of HAF increase, total HAF, and peak contrast density (PKD) by Q-DSA were compared with HAF by DUS. RESULTS: Of all, 4 suspected SSS cases underwent test-balloon occlusion with DUS and Q-DSA. Using DUS, HAV and HAF increased by 1.6- to 1.8-fold and 1.7- to 2.6-fold, respectively. Using Q-DSA, the HAF rate, total HAF, and PKD increased by 1.1 to 12.8, 1.5 to 7.6, and 1.3 to 5.3, respectively. CONCLUSION: Occlusion of the splenic artery in liver transplants with SSS doubles the HAF (+1.7- to 2.6-fold). The Q-DSA parameters correlate qualitatively but overestimate the resultant increased HAF.

Elderly recipients of hepatitis C positive renal allografts can quickly develop liver disease.

Our institution explored using allografts from donors with Hepatitis C virus (HCV) for elderly renal transplantation (RT). Thirteen HCV- elderly recipients were transplanted with HCV+ allografts (eD+/R-) between January 2003 and April 2009. Ninety HCV- elderly recipients of HCV- allografts (eD-/R-), eight HCV+ recipients of HCV+ allografts (D+/R+) and thirteen HCV+ recipients of HCV- allografts (D-/R+) were also transplanted. Median follow-up was 1.5 (range 0.8-5) years. Seven eD+/R- developed a positive HCV viral load and six had elevated liver transaminases with evidence of hepatitis on biopsy. Overall, eD+/R- survival was 46% while the eD-/R- survival was 85% (P = 0.003). Seven eD+/R- died during follow-up. Causes included multi-organ failure and sepsis (n = 4), cancer (n = 1), failure-to-thrive (n = 1) and surgical complications (n = 1). One eD+/R- died from causes directly related to HCV infection. In conclusion, multiple eD+/R- quickly developed HCV-related liver disease and infections were a frequent cause of morbidity and mortality.

Sorafenib therapy for hepatocellular carcinoma prior to liver transplant is associated with increased complications after transplant.

This study compared post-transplant outcomes of patients with hepatocellular carcinoma (HCC) who took sorafenib prior to orthotopic liver transplantation (OLT) with those patients who were not treated with sorafenib. Thirty-three patients with HCC who were listed for liver transplantation were studied: 10 patients were treated with sorafenib prior to transplantation in an attempt to prevent progression of HCC while awaiting transplant. The remaining 23 patients were considered controls. The mean duration of sorafenib use was 19.2 (SD 25.2) weeks. Overall death rates were similar between the sorafenib group and control group (20% vs. 8.7%, respectively, P = 0.56). However, the patients in the sorafenib group had a higher incidence of acute cellular rejection following transplantation (67% vs. 22%, OR = 7.2, 95% CI 1.3-39.6, P = 0.04). The sorafenib group also had a higher rate of early biliary complications (67% vs. 17%, OR = 9.5, 1.6-55.0, P = 0.01). The use of sorafenib was found to be an independent predictor of post-transplant biliary complications (OR 12.6, 1.4-116.2, P = 0.03). Sorafenib administration prior to OLT appears to be associated with an increase in biliary complications and possibly in acute rejection following liver transplantation. Caution should be taken in this setting until larger studies are completed.

Closure of ascites leaks with fibrin glue injection in patients with end-stage liver disease.

BACKGROUND: Ascites leaks (AL) in patients with end-stage liver disease (ESLD) are associated with significant morbidity and mortality regardless if they are medically or surgically managed. PATIENTS AND METHODS: In a pilot study, 14 ESLD patients with AL underwent treatment with fibrin glue injection around the leak after failing conservative therapy. The end point of this study was the cessation of AL in the short term and the maintenance of a leak-free abdomen in the long term, allowing for medical optimization of the patients. RESULTS: Median age of the 10 men and 4 women was 50 (range 26-67) years. Underlying ESLDs were chronic hepatitis C (n=5), alcoholic LD (n=2), cryptogenic cirrhosis (n=2), and miscellaneous (n=5). There were six leaking incisions posthernia repair (three umbilical and three inguinal), two leaking/ruptured umbilical hernias, four leaking paracentesis sites, one leaking Jackson-Pratt (JP) drain canal, and one leaking laparoscopic trocar site. Average AL volume per day was 1000 (range 400-2000) mL. All leaks were immediately resolved with a 3-5 mL fibrin glue injection. Five recurred and required a second injection (four within 24 hours). Mental status improved in 7 patients (West Haven Criteria: grade II to I [n=6], grade III to I [n=1]). Median model of end-stage liver disease scores improved from 23 (range 8-33) to 20 (range 14-26). There were no infections, bleeds, or other injection-related complications. Average follow-up for these patients was 441.6 days (range 2-852). Five patients underwent liver transplant (LT) median 15 (range 4-270) days postinjection; 2 of them died. Another 3 patients died (2 from sepsis and 1 from metastatic cancer). CONCLUSION: Fibrin glue injection for the control of AL is a simple and safe bedside procedure that quickly controls AL, allowing for patient recovery in anticipation of further care.

Endovascular therapy for hepatic artery stenosis and thrombosis following liver transplantation.

PURPOSE: To evaluate the effectiveness of endovascular management of steno-oclusive disease in liver transplants. METHODS: Retrospective review of liver transplant recipients with hepatic artery stenosis (HAS) or thrombosis (HAT) was performed. The HAS group was treated with balloon angioplasty with selective stent placement. The HAT group was treated with catheter-directed thrombolysis. Primary, unassisted, and assisted patency and graft survival rates were calculated. RESULTS: In all, 31 patients were identified (21 males; mean age, 51 years). A total of 25 of 31 (81%) patients had HAS and 6 of 31 (19%) had HAT. Collectively, a total of 35 endovascular procedures were performed to treat HAS in 25 patients. Overall technical success rate was 91%, with 11% major complication rate. Primary-assisted patency rate and graft survival at 6 and 12 months were 87% and 81%, and 76% and 72%, respectively. Only 1 successful thrombolysis of HAT was achieved. CONCLUSION: Endovascular management is effective for HAS but not for HAT.

Liver transplantation for T3 lesions has higher waiting list mortality but similar survival compared to T1 and T2 lesions.

BACKGROUND: Restrictive staging criteria for liver transplant (LT) patients with HCC in the U.S. have resulted in favorable long-term recurrence-free survival, but these criteria exclude a subgroup of patients who, despite tumor size beyond T2 stage, demonstrate an acceptable outcome. The aim of this study was to assess the waiting list and post-transplant mortality of patients with HCC tumors greater than Milan T2 stage. METHODS: The U.S. OPTN standard transplant dataset was analyzed for patients with a diagnosis of HCC who were listed for liver transplantation between February 2002 and 2008. Those patients with Milan T3 stage tumors were compared to patients with T1 and T2 lesions. Multivariate survival models were developed to investigate independent predictors of death or tumor recurrence post-transplant. RESULTS: 7,391 patients with HCC were identified. 351 (4.75%) had T3 lesions. Compared to non-T3 patients, total tumor burden was greater and total alpha-fetoprotein (AFP) was higher in the T3 patients. T3 patients also were more likely to receive pretransplant locoregional therapy. There were no significant differences between T3 patients and non-T3 patients in demographic variables or physiologic MELD score at the time of transplant, waiting time, or donor risk index. Waiting list mortality was increased for T3 patients compared to non-T3 and tumor progression while waiting was higher. Independent predictors of waiting list mortality included physiologic MELD score at the time of listing, total tumor burden, and serum AFP. There was significant regional variation in the utilization of exceptions for T3 patients and UNOS regions 4, 9, and 10 performed a higher percentage of their transplants in T3 patients compared to other regions. There was no difference in post transplant survival between T3 and non-T3 patients. Independent predictors of post-transplant mortality included physiologic MELD score at the time of transplant, recipient age, and donor risk index. In patients with T3 tumors, total tumor burden was not an independent predictor of post transplant survival. CONCLUSIONS: Patients who are listed for liver transplantation with Milan stage T3 HCC have higher waiting list mortality but have similar post-transplant survival compared to patients with T1 and T2 HCC.

Anti-thymocyte globulin for the treatment of acute cellular rejection following liver transplantation.

INTRODUCTION: Acute cellular rejection (ACR) post-liver transplantation (LT) can usually be reversed with pulse dose steroids. Anti-thymocyte globulin (ATG) is used to treat steroid-resistant rejection (SRR). PATIENTS AND METHODS: We report 15 male and five female LT recipients with a median age of 48.3 (range 14.3-71.7) years, who received ATG for biopsy-proven steroid-resistant rejection (n =13), severe rejection (6), and severe rejection/recurrent autoimmune hepatitis (n = 1) median 42 (range 6-2,456) days following LT. RESULTS: Underlying liver diseases included HCV (n = 7), alcoholic cirrhosis (n = 3), NASH (n = 2), HBV (n = 2), autoimmune hepatitis (n =1), PSC (n = 1), miscellaneous (n = 4) including three re LTs. All patients responded to treatment (median AST declined from 172 to 34U/l, median total bilirubin from 9.1 to 1.3 mg/dl; p < 0.001). Three patients developed recurrent ACR, and none chronic rejection. All HCV patients developed recurrence with significant rises in HCV RNA levels. Infections included pneumonia, sepsis, intraabdominal infection, chronic diarrhea, wound infection, EBV, and CMV disease. After a median follow-up of 65.5 (range 4.3-101.7) months post-ATG and median 67.7 (range 9.3-306.3) months post-LT, 17 patients are alive, two died from sepsis/multi-organ failure and one from HCV recurrence. CONCLUSION: ATG effectively reversed severe and SSR; HCV recurrence and infections remain significant complications.

Advanced recipient age (>60 years) alone should not be a contraindication to liver retransplantation.

Advanced age has been shown to be a risk factor for survival in primary liver transplantation. We sought to determine the independent influence of recipient age on retransplantation survival. The UNOS dataset was analyzed for adult, nonstatus 1, liver retransplantations since February 27, 2002. The univariate effect of age on 90-day and 1-year survival was analyzed. Multivariate survival models were used to determine 90-day, 1-year, and overall survival. Recipient age, donor age, model for end-stage liver disease (MELD) score, and hepatitis C status were used to construct multivariable survival models. Some 2141 liver retransplantations were analyzed. Overall, increasing recipient age was independently predictive of increasing mortality after liver retransplantation. In recipients between 18 and 60, there remained a direct relationship between age and mortality. However, in recipients aged over 60, increasing age was not independently associated with 90-day mortality (P = 0.88) and 1-year mortality (P = 0.74), despite adjusting for donor age, MELD score, and viral hepatitis status, suggesting that their original liver condition, their co-morbidities or perioperative condition plays an important role in retransplantation survival. Increasing recipient age up to 60, adversely affects liver retransplantation survival. After 60, there are no additional risks. Advanced age alone should not be an exclusionary factor when considering liver retransplantation; only the overall ability of the patient to tolerate a major surgery should be the determining factor.

Gallbladder cancer and liver transplantation.

Gallbladder cancer is the fifth most common malignancy of the gastrointestinal tract. Gallbladder cancer is found incidentally at the time of cholecystectomy in 0.35% of patients. Two previous isolated case reports of incidentally found gallbladder cancer in hepatectomy specimens following liver transplantation (LT) showed no adverse outcomes. We reviewed the outcome of four patients. Three patients had end-stage liver disease secondary to primary sclerosing cholangitis and one patient had cryptogenic cirrhosis. Gallbladder cancer was removed at cholecystectomy in one patient 11 months prior to transplant. One patient had suspected gallbladder cancer prior to LT by ultrasound and CT imaging, as well as a rising CA 19-9. The other two patients had incidentally identified gallbladder cancer. Median follow-up was 30 months. There has been no evidence of recurrence and patient survival was 100%. Early gallbladder cancer is not a contraindication for LT, however further follow-up is needed.

Pseudomonas aeruginosa pseudoaneurysm of the ascending aorta after coronary artery bypass graft surgery.

Mycotic pseudoaneurysms of the ascending aorta are rare in patients undergoing coronary artery bypass graft surgery and are usually caused by Staphylococcus aureus. We describe a patient with a mycotic pseudoaneurysm of the ascending aorta at the proximal vein graft anastomosis site after coronary artery bypass grafting. Cultures from the saphenous vein harvest site and from the aneurysm sac obtained intraoperatively during repair of the pseudoaneurysm grew Pseudomonas aeruginosa. Treatment included femorofemoral bypass and hypothermic circulatory arrest with in situ patch repair. The patient was given ceftazidime and gentamicin intravenously for 2 weeks, then ceftazidime alone for 6 weeks. Thereafter, he began taking ciprofloxacin orally for chronic suppression. He was doing well at 18-month follow-up.