Bile Duct Necrosis Research Articles

Doppler ultrasonography blood flow changes of the hepatic artery in liver transplants complicated with cholangitis

Cholangitis after liver transplantation may lead to bile duct necrosis. Early diagnosis is essential to prevent graft loss. We aimed to investigate cholangitis related hepatic arterial Doppler ultrasonography findings in liver transplants. Patients complicated with biopsy proven cholangitis in grafts were prospectively evaluated. Vascular complications were excluded. Doppler ultrasonography parameters including hepatic arterial diameter, resistive index, volume flow, and portal vein maximum velocity were measured twice: first during cholangitis and after full recovery. Data of two groups were compared using paired samples t test and Mann-Whitney U test. The mean hepatic arterial volume flow, resistive index, and diameter of 33 patients complicated with cholangitis was observed to decrease after recovery from 0.356 to 0.273 L/min (p = 0.007), from 0.64 to 0.60 (p < 0.001) and from 4.9 to 4.4 mm (p < 0.001), respectively. Portal vein maximum velocity alteration was not statistically significant (p = 0.6). Ultrasound follow-ups after liver transplantation can give us the clue of cholangitis initiation through some altering hepatic arterial Doppler parameters. Even though these are nonspecific findings that can also be observed in vascular complications, baseline Doppler data should be saved for future comparison and considered to prevent biliary associated graft loss.

Selective Androgen Receptor Modulators: An Emerging Liver Toxin.

Selective androgen receptor modulators (SARMs) are a class of nonsteroidal drugs that are favored over anabolic androgenic steroids (AASs) for their tissue-selectivity and improved side-effect profile. These drugs have been evaluated for treatment of various diseases including muscle-wasting disorders, osteoporosis, and breast cancer. Despite lacking approval for therapeutic use, SARMs are widely used recreationally as performance enhancing drugs by bodybuilders and athletes. In recent years, cases of drug-induced liver injury (DILI) secondary to SARMs have begun to emerge, but little is known regarding their hepatotoxicity. In this review, we provide current knowledge regarding DILI from SARMs. A literature search was conducted regarding SARMs and liver injury to evaluate relevant cases and information. SARMs have been associated with a cholestatic syndrome congruent with that of DILI from AASs, and it consists of a bland cholestasis in which there is minimal bile duct injury, inflammation, or necrosis. Patients present with an insidious onset of jaundice with marked hyperbilirubinemia and mild hepatic enzyme elevations. No clear treatment exists, although patients typically show improvement with cessation of the offending SARM. Given the novelty of these drugs, further study is necessary to understand diagnosis, management, and complications of SARM-related DILI.

Liver-restricted deletion of the biliary atresia candidate gene Pkd1l1 causes bile duct dysmorphogenesis and ciliopathy.

A recent multicenter genetic exploration of the biliary atresia splenic malformation syndrome identified mutations in the ciliary gene PKD1L1 as candidate etiologic contributors. We hypothesized that deletion of Pkd1l1 in developing hepatoblasts would lead to cholangiopathy in mice. CRISPR-based genome editing inserted loxP sites flanking exon 8 of the murine Pkd1l1 gene. Pkd1l1Fl/Fl cross-bred with alpha-fetoprotein-Cre expressing mice to generate a liver-specific intrahepatic Pkd1l1 -deficient model (LKO). From embryonic day 18 through week 30, control ( Fl/Fl ) and LKO mice were evaluated with standard serum chemistries and liver histology. At select ages, tissues were analyzed using RNA sequencing, immunofluorescence, and electron microscopy with a focus on biliary structures, peribiliary inflammation, and fibrosis. Bile duct ligation for 5 days of Fl/Fl and LKO mice was followed by standard serum and liver analytics. Histological analyses from perinatal ages revealed delayed biliary maturation and reduced primary cilia, with progressive cholangiocyte proliferation, peribiliary fibroinflammation, and arterial hypertrophy evident in 7- to 16-week-old LKO versus Fl/Fl livers. Following bile duct ligation, cholangiocyte proliferation, peribiliary fibroinflammation, and necrosis were increased in LKO compared with Fl/Fl livers. Bile duct ligation of the Pkd1l1 -deficient mouse model mirrors several aspects of the intrahepatic pathophysiology of biliary atresia in humans including bile duct dysmorphogenesis, peribiliary fibroinflammation, hepatic arteriopathy, and ciliopathy. This first genetically linked model of biliary atresia, the Pkd1l1 LKO mouse, may allow researchers a means to develop a deeper understanding of the pathophysiology of this serious and perplexing disorder, including the opportunity to identify rational therapeutic targets.

Pathological lesions associated with Vibrio infection in Atlantic horse mackerel (Trachurus trachurus L., 1758) from the western coast of Tripoli, Libya.

Vibrios are aquatic bacteria causing Vibriosis in humans and aquatic animals. Vibriosis is a significant disease of cultured and wild fish. The present study aimed to address the impact of Vibrios on the health status of Trachurus trachurus inhabiting the coastal area of Tripoli. A total of 100 samples of (T. trachurus) were collected randomly from the Western Coast of Tripoli and Bab Al-Baher market, throughout the period from spring 2019 to summer 2019. All the sampled fish were examined externally and internally and lesions were recorded. Bacterial isolation from the liver and kidney was carried out using the appropriate culture media. Tissue samples were taken from the liver, kidney, and spleen in 10% neutral buffered formalin for a histopathology examination. The tissue sections were stained with hematoxylin and eosin to assess morphologically and Perl's Prussian blue for the demonstration of ferric iron. On average 69% of the infected fish exhibited at least one pathological lesion. Vibrios were recovered from 90% of the examined fish. The histopathological changes of the liver showed severe congestion of blood vessels (BVs), mononuclear cell infiltration surrounding a bile duct, granular degeneration and coagulative necrosis of hepatocytes in the centrilobular area, marked vacuolar degeneration of hepatocytes, activation of melano-macrophage centers (MMCs), multiple cysts of nematode in hepatic tissue (incidental finding). The histopathological alterations of the kidney showed severe congestion of BVs, vacuolar degeneration of the renal tubular epithelium, severe interstitial mononuclear cell infiltration, and marked activation of MMCs in the kidney. Moreover, congestion of BVs and marked activation of melano-macrophages (MMCs) were found in the spleen. The MMCs of most of the sampled tissues showed a strong positive reaction for ferric iron. The polluted aquatic environment by sewage at Tripoli Coast is an essential factor for triggering the pathogenicity and invasion of Vibrios to vulnerable Atlantic horse mackerel. Also, this study is a preliminary step to give a baseline for further future studies on epidemiology and control of Vibrio infection in Libyan fish.

Extrahepatic Bile Duct Necrosis: An Exceedingly Rare Complication in Severe Acute Pancreatitis

Extrahepatic Bile Duct Necrosis: An Exceedingly Rare Complication in Severe Acute Pancreatitis

Detecting Aquatic Pollution Using Histological Investigations of the Gills, Liver, Kidney, and Muscles of Oreochromis niloticus.

The present study aimed to determine the degree of changes in the histological architecture of the liver, gills, kidneys, and muscles of fish Oreochromis niloticus collected from different polluted river sites. Fish samples collected from the Faisalabad Fish Hatchery and upstream of Chakbandi drain acted as a control. Necrosis, hemorrhage, and epithelial hyperplasia were observed in the gills of fish inhabiting the river downstream of the Chakbandi drain entrance. Liver tissues were found to be affected by vacuolated cytoplasm, bile duct proliferation, melanomacrophages, and necrosis. In kidney tissues, shrinkage of the renal cortex, necrosis, and destructive renal tubules were observed. Histopathology of muscles indicates the presence of hypertrophy and swollen myofibers. In contrast, upstream specimens of fish exhibited mild tissue alterations. Histopathology of gills tissue showed vacuolization. Liver tissues indicated the presence of hypertrophy and more frequent Kupffer cells than usual. The vacuolation was also observed in kidney tissues. Muscle tissues expressed splitting of muscle fibres and degeneration in muscle bundles. However, sections of tissues collected from farmed fish have normal morphology and no anomalies. The histopathological assessment indicated various cellular, biochemical, and histological changes in response to the contamination in the vicinity of the fish.

Peribiliary Intravascular Fibrin Occlusions and Bile Duct Necrosis in DCD Livers During Ex Situ Perfusion: Prevention With Tissue Plasminogen Activator and Fresh Frozen Plasma.

We have observed epithelial loss from the luminal surface of the bile ducts, often in conjunction with underlying stromal necrosis, in livers donated after circulatory death (DCD) undergoing ex situ normothermic machine perfusion (NMP).1 On occasion, the overlying epithelium has been intact but the underlying stroma necrotic, suggesting a vascular occlusive process as opposed to an intraluminal cause. With Research Ethics Committee approval (14/EE/0137), we perfused 5 DCD livers for at least 4 h using the metra (OrganOx, Oxford, United Kingdom). Livers were then formalin-fixed, and the extrahepatic biliary tree and major septal ducts dissected out and cross-sections examined, noting stromal necrosis on hematoxylin and eosin staining, intravascular fibrin deposition with Martius Scarlet Blue (MSB) stain, and vessel density with CD31 stain. Histological appearances were normal in 1 liver; 4 had stromal necrosis affecting hilar and septal ducts involving between 25% and 100% of the circumference. Fibrin/erythrocyte plugs were visible on MSB in between 25 and 50% of vessels where there was stromal necrosis, but not in its absence (Figure 1A and B are typical examples). In total, 26 duct profiles were reviewed in the 4 affected livers, and 24 exhibited necrosis/fibrin plugs. A second series of 5 liver perfusions were performed with 50 mg tissue plasminogen activator (TPA, Alteplase, Boehringer Ingelheim, Germany) and 250 mL fresh frozen plasma (FFP) infused into the perfusate; no intravascular fibrin and no septal duct necrosis was observed in any liver (Figure 1C and D). Lastly, TPA alone was added to 2 livers with similar appearances to the no-TPA group.FIGURE 1.: Hematoxylin and eosin (H&E) and Martius Scarlet Blue (MSB) stained sections of bile ducts. A, H&E stained section showing widespread stromal necrosis and epithelial loss in an intrahepatic bile duct. Eosinophilic inclusions are present in the subendothelial vessels (arrowed in the magnified panels). B, Corresponding MSB stained section showing that the same subendothelial areas are intravascular aggregates of fibrin and erythrocytes (also arrowed in the panels). These stain red and yellow; collagen stains blue with MSB. C, H&E section of intrahepatic bile duct from a liver treated with fresh frozen plasma (FFP) and tissue plasminogen activator (TPA). The stroma is viable with no subepithelial eosinophilic inclusions. D, Corresponding MSB stained section of the same liver showing no fibrin/erythrocyte intravascular aggregates.Intravascular deposition of fibrin has been noted to occur de novo after NMP in peripheral biopsies of DCD livers and kidneys.2,3 These observations, coupled with observations from our small series of perfusions, need further and more detailed investigation, with clinical evaluation, but have prompted us to suggest the following hypotheses/observations: Bile duct stromal infarcts occur secondary to occlusion of peribiliary vessels with fibrin/erythrocyte plugs. The fibrin/erythrocyte plugs develop after reperfusion as a consequence of ischemia, which is more profound in DCD livers. Stromal infarcts seen to occur during ex situ perfusion may correspond to nonanastomotic biliary strictures (NAS) in transplanted livers. FFP provides an exogenous source of plasminogen enabling TPA to generate sufficient plasmin to clear fibrin deposits in peribiliary vessels. Ex situ treatment of livers undergoing NMP with the combination of FFP and TPA appears to prevent the occurrence of stromal infarcts and may therefore prevent nonanastomotic biliary strictures. NAS have long been thought to be related to bile duct ischemia and occur even where donor heparinization before withdrawal of treatment is routine, suggesting that intravascular thrombosis per se is not a perimortem event. Administration of TPA into the hepatic artery during implantation is reported to reduce NAS, albeit with an increase in intraoperative bleeding due to its widespread fibrinolytic effect.4 This beneficial effect in vivo may be achievable ex situ without the associated intraoperative bleeding since the TPA half-life is very short (5 min) and the liver flushed before implantation.

Hepatoprotective effects of Lactobacillus plantarum 299v supplemented via drinking water against aflatoxin-induced liver damage

ABSTRACT The aim of this study was to examine the impact of intake of a lactic acid bacterium, Lactobacillus plantarum 299v (Lp299v) on aflatoxin-induced hepatotoxicity in broilers. For this, broilers were intoxicated with dietary aflatoxins and simultaneously treated with live Lp299v in drinking water. One-day-old male broilers were divided into eight groups (n = 10/group) as follows. Aflatoxin groups fed basal diet contaminated with aflatoxins (200 or 2000 ppb). The probiotic groups received drinking water enriched with live (Lp299v) (108 CFU/ml). A group of birds was given a commercial mycotoxin binder (2.5 g/kg feed). Control groups received basal diet without probiotic or aflatoxin binder. The growth performance was calculated for the entire period (0–42 days), and blood and liver specimens were processed for histology and determination of liver damage markers. Results showed extensive damage including bile duct hyperplasia, hepatocellular ballooning, and necrosis in chickens fed aflatoxin alone. However, liver lesions were limited to lobular inflammation and pyknosis in broilers treated with aflatoxins along with Lp299v. The histology of the liver tissues from the birds on aflatoxin-free diet + probiotic appeared to be normal when compared to the respective controls. Histopathological indices in different experimental groups were corroborated with the liver damage markers namely, serum ALT, AST, LD, and γ-GT. It is concluded that the improvement in the growth performance and prevention of aflatoxin-related liver lesions could be mainly assigned to the probiotic therapy for the entire period of breeding, although the aflatoxin-binding ability of the Lp299v in inactivation of aflatoxins cannot be ruled out. RESEARCH HIGHLIGHTS Aflatoxin-related liver damage progression was inhibited by probiotics in broilers. Aflatoxin inactivation by probiotics can be assessed by liver histopathology. Growth performance in broilers was improved following the intake of probiotics.

Recombinant Ax21 protein is a promising subunit vaccine candidate against Stenotrophomonas maltophilia in a murine infection model

Stenotrophomonas maltophilia is an emerging pathogen that can cause several disease manifestations such as bacteremia, meningitis, respiratory tract infections and others. More seriously, this pathogen has a highly evolving antibiotic resistance profile. Antibiotic misuse is further aggravating the situation by inducing the development of multi- and even pan-resistance. Thus, employing diverse strategies to overcome this increasing antibiotic resistance is of paramount importance. In general, vaccination is one of these strategies that prevents the onset of infection, provides long term protection against infection, and most importantly diminishes the antibiotic consumption, thus, resulting in controlling resistance. Unfortunately, vaccine research concerning S. maltophilia is very scarce in the literature. Ax21 protein is an outer membrane protein implicated in several virulence mechanisms of S. maltophilia such as quorum sensing, biofilm formation, and antibiotic resistance. Our computational analysis of Ax21 revealed its potential immunogenicity. In the current study, Ax21 protein of S. maltophilia was cloned and heterologously expressed in Escherichia coli. Mice were immunized with the purified recombinant antigen using Bacillus Calmette-Guérin(BCG) and incomplete Freund’s adjuvant (IFA) as immune-adjuvants. Enzyme-linked immunosorbent assay (ELISA) revealed significant antigen-specific IgG1, IgG2a and total IgG levels in immunized mice which reflected successful immune stimulation. Immunized mice that were challenged with S. maltophilia showed a substantialreduction in bacterial bioburden in lungs, liver, kidneys, and heart. In addition, liver histological examination demonstrated a remarkable decrease in pathological signs such as necrosis, vacuolation, bile duct fibrosis and necrosis, infiltration of inflammatory cells, and hemorrhage. Whole cell ELISA and opsonophagocytic assay confirmed the ability of serum antibodies from immunized mice to bind and facilitate phagocytosis of S. maltophilia, respectively. To our knowledge, this is the first report to demonstrate the vaccine protective efficacy of Ax21 outer membrane protein against S. maltophilia infection.

Effective Microorganisms (EM) Improve Internal Organ Morphology, Intestinal Morphometry and Serum Biochemical Activity in Japanese Quails under Clostridium perfringens Challenge.

The effect of effective microorganisms (EM) on internal organ morphology, intestinal morphometry, and serum biochemical activity in Japanese quails under Clostridium perfringens challenge was determined. After 30 days of EM addition, one group of quails was orally inoculated with Clostridium perfringens. The second group did not receive EM and was inoculated with C. perfringens. In the gut, EM supplementation reduced the number of lesions, enhanced gut health, and protected the mucosa from pathogenic bacteria. EM showed an anti-inflammatory effect and fewer necrotic lesions in villi. In the internal organs, EM showed a protective effect against a typical lesion of C. perfringens infection. Necrosis and degeneration of the hepatocytes, necrosis of bile ducts, and bile duct proliferation were more severe in the infected group without EM. Morphometric evaluation showed significantly higher villi in the jejunum after EM addition. A greater crypt depth was observed in the C. perfringens group. Biochemical analysis of the blood indicated lower cholesterol on the 12th day of the experiment and between-group differences in total protein, lactate dehydrogenase (LDH), and albumin levels in the EM group. Further studies are needed to improve EM activity against pathologic bacteria as a potential alternative to antibiotics and to develop future natural production systems.

Transcatheter arterial chemoembolization-induced bile duct necrosis with hemobilia in hepatocellular carcinoma: endoscopic visualization and repair.

Transcatheter arterial chemoembolization-induced bile duct necrosis with hemobilia in hepatocellular carcinoma: endoscopic visualization and repair.

Pathophysiology and Imaging Findings of Bile Duct Necrosis: A Rare but Serious Complication of Transarterial Therapy for Liver Tumors.

Simple SummaryBile duct necrosis (BDN) is rare but serious complication of transarterial therapy for liver tumors. During development of BDN, ischemia of the peribiliary vascular plexus (PBP) induces the disruption of the bile duct epithelial protection mechanism, causing necrosis of the surrounding tissue by the detergent action of exuded bile acids, and eventually a biloma forms. Once BDN starts, persistent tissue damage to the surrounding bile duct is induced by imbibed bile acids, and portal vein thrombosis may also be observed. On CT images, BDN shows similar findings to intrahepatic bile duct dilatation, and, therefore, it is sometimes misdiagnosed. Clinicians should be aware that although BDN and biloma can usually be treated conservatively, in the presence of symptoms such as moderate or severe infection or interval growth of the biloma, prompt treatment is essential to avoid lethal abscess formation and sepsis.Bile duct necrosis (BDN) with biloma formation is a type of ischemic bile duct injury that is one of the serious complications associated with transarterial therapies, such as transcatheter chemoembolization therapy (TACE), and radioembolization for hepatocellular carcinoma (HCC) and hepatic arterial infusion chemotherapy (HAIC) for metastatic liver cancer from colorectal carcinoma. In terms of the occurrence of BDN and subsequent biloma formation, ischemic injury to the peribiliary vascular plexus (PBP), the supporting vessel of bile duct epithelium, is thought to be intimately associated. In this paper, we first describe the anatomy, blood supply, and function of the intrahepatic bile duct, and then illustrate the pathophysiology of BDN, and finally present the imaging findings of BDN. Under the process of BDN formation, ischemia of the PBP induces the disruption of the bile duct epithelial protection mechanism that causes coagulation and fibrinoid necrosis of the surrounding tissue by the detergent action of exuded bile acids, and eventually a biloma forms. Once BDN occurs, persistent tissue damage to the surrounding bile duct is induced by imbibed bile acids, and portal vein thrombosis may also be observed. On pre-contrast and contrast-enhanced computed tomography (CT), BDN shows similar findings to intrahepatic bile duct dilatation, and, therefore, it is sometimes misdiagnosed. Differentiation of imaging findings on CT and ultrasound (US)/magnetic resonance (MR) imaging/MR cholangiopancreatography (MRCP) is important for correct diagnosis of BDN.

&lt;p&gt;Pathological studies on &lt;em&gt;Pteris cretica&lt;/em&gt; (L.) fern-Bovine Papilloma Virus infection in Syrian Golden Hamsters (&lt;em&gt;Mesocricetus auratus&lt;/em&gt;)&lt;/p&gt;

Pteris cretica (L.) commonly known as Cretan brake is widely distributed in nature and considered as potential environmental carcinogen. However, only limited literature is available on this fern commonly taken by cattle while grazing. It is known that in cattle Bovine papilloma virus (BPV) induced benign tumours are converted into malignant with interaction of ptaquiloside (Pta) present in ferns. In the present investigation, we evaluated the pathological effects of P. cretica (PC)-BPV infection in laboratory model hamster. Though toxic principle Pta was detected in fern samples but quercetin could not be found. Tumours were successfully induced in hamsters by cutaneous wart suspension and histopathologically diagnosed as fibroma and lipofibroma. Histopathologically, hamsters showed mild to moderate vascular changes in vital organs, multiple cysts, degenerative changes, bile duct hyperplasia and necrosis in liver, haemorrhages and haemosiderosis in spleen, hypersecretory activity and prominent Peyer’s patches in ileum, degenerative changes and presence of eosinophilic casts in renal tubules. Ultrastructural study revealed apoptosis in hepatocytes, abundance of variable shaped mitochondria in renal tubular lining epithelial cells and enterocytes showed abundance of mitochondria and cytoplasmolysis in the fern fed groups. Almost all the hamsters from BPV, fern and virus infection (PC+BPV) groups developed similar type of tumorous growths. The visible growths in the hamsters of these groups were either single or double large sized except multiple tumorous growths in one hamster from PC+BPV group. However, multiple palpable subcutaneous nodules were developed at the site of scarification in all the hamsters of BPV and PC+BPV groups. Our findings suggest that the Pta containing P. cretica feeding induced hepatotoxic and nephrotoxic lesions in hamsters, but effects of P. cretica -BPV infection were found negligible.

Gallbladder and Bile Duct Necrosis after Surgery for Stanford Type A Aortic Dissection Finally Performed Choledohojejunostomy—A Case Report—

Gallbladder and Bile Duct Necrosis after Surgery for Stanford Type A Aortic Dissection Finally Performed Choledohojejunostomy—A Case Report—

Evaluation of histologic changes in the livers of patients with early and late hepatic artery thrombosis

Hepatic artery thrombosis (HAT) following orthotopic liver transplantation (OLT) can cause hepatic parenchymal necrosis and ischemic cholangiopathy. This study investigates additional histologic features that may suggest HAT in post-OLT liver specimens. For 94 liver specimens (explanted allografts and biopsies) from patients with a clinical or pathologic diagnosis of HAT, we recorded length of time between OLT and procedure, categorizing cases into early HAT (;≤30 days since OLT) and late HAT (>30 days since OLT). Common histologic findings in HAT included lobular necrosis (60 cases, 64%), portal inflammation (68 cases, 72%), ductular reaction (73 cases, 78%), lobular cholestasis (70 cases, 74%), and bile-tinged macrophages (40 cases, 43%). Ductular cholestasis was seen in 30 cases (32%); 10 of those patients were clinically septic. Bile in veins was seen in 16 (17%) cases and arteritis in 6 (6%) cases. Findings more common in resection than biopsy specimens included lobular necrosis (P < .0001), hemorrhage (P = .0044), ductular cholestasis (P = .0003), and bile-tinged macrophages (P < .0001). Lobular necrosis was more common in early HAT (P = .0002), and ductular reaction (P = .006) and bile in veins (P = .03) were more common in late HAT. Histologic changes in HAT vary based on specimen type and whether HAT is early or late. In late HAT, biliary injury might occur after a prolonged period of ischemia, with subsequent bile duct necrosis, bile in veins, and remodeling (eg, ductular reaction). Bile in veins is an unusual finding that may occur in HAT, although it can be seen in bile infarcts from other causes.

Bile duct necrosis at hepatic hilum: description of two cases and role of transhepatic drainage

Bile duct necrosis at hepatic hilum: description of two cases and role of transhepatic drainage

Bile duct necrosis at hepatic hilum: description of two cases and role of transhepatic drainage

Bile duct necrosis at hepatic hilum: description of two cases and role of transhepatic drainage

Seasonal development of the coccidian parasite Goussia bayae and hepatobiliary histopathology in white perch Morone americana from Chesapeake Bay.

The coccidium Goussia bayae infects the gallbladder and bile ducts of white perch Morone americana from Chesapeake Bay, USA. Seasonal changes in coccidian infections were analyzed from bile specimens of 1588 fish from the Choptank River during 2016-2018 using wet mount preparations with a Sedgwick-Rafter counting chamber. Histopathology of the gallbladder and liver was analyzed from a subset (n = 480) of these fish. Maximum parasite prevalence (100%) and intensities in the gallbladder occurred during the fish spawning season in March and April. Asynchronous coccidian development and prevalence of infections in fish increased gradually during autumn and winter, but coccidian intensity increased sharply 2-4 wk prior to the onset of fish spawning activity and decreased after spawning activity concluded. Sporulation was internal, and the gallbladder was the primary reservoir for oocysts. Two previously undescribed species of coccidia were observed in the intestine. Lesions in the gallbladder were rare and included cholecystitis and epithelial necrosis. Intrahepatic bile duct lesions were more common and included distension, cholangitis, epithelial erosion and necrosis, cholestasis, hyperplasia, and neoplasia. Cholangitis and necrosis of intrahepatic bile ducts were significantly associated with coccidial infections, while plasmodia of a myxosporean (spore morphology consistent with the genera Myxidium and Zschokella) were significantly associated with bile duct hyperplasia. Biliary neoplasia included cholangiomas (5% prevalence) and cholangiocarcinomas (1% prevalence). No association was detected between G. bayae and biliary neoplasms, but an association may exist between these lesions and the myxosporean plasmodia.

Observations on the ex situ perfusion of livers for transplantation.

Normothermic ex situ liver perfusion might allow viability assessment of livers before transplantation. Perfusion characteristics were studied in 47 liver perfusions, of which 22 resulted in transplants. Hepatocellular damage was reflected in the perfusate transaminase concentrations, which correlated with posttransplant peak transaminase levels. Lactate clearance occurred within 3 hours in 46 of 47 perfusions, and glucose rose initially during perfusion in 44. Three livers required higher levels of bicarbonate support to maintain physiological pH, including one developing primary nonfunction. Bile production did not correlate with viability or cholangiopathy, but bile pH, measured in 16 of the 22 transplanted livers, identified three livers that developed cholangiopathy (peak pH < 7.4) from those that did not (pH > 7.5). In the 11 research livers where it could be studied, bile pH > 7.5 discriminated between the 6 livers exhibiting >50% circumferential stromal necrosis of septal bile ducts and 4 without necrosis; one liver with 25‐50% necrosis had a maximum pH 7.46. Liver viability during normothermic perfusion can be assessed using a combination of transaminase release, glucose metabolism, lactate clearance, and maintenance of acid‐base balance. Evaluation of bile pH may offer a valuable insight into bile duct integrity and risk of posttransplant ischemic cholangiopathy.

Inflammatory and Ischemic Post Liver Transplant Complications Mimic Malignancy on 18F-FDG PET/CT.

A 65-year-old male patient with a one year history of liver transplantation was referred for an 18F-fluoro-2-deoxy-D-glucose (18F-FDG) positron emission tomography/computed tomography (PET/CT) to rule out post transplant lymphoproliferative disease. Multiple foci of intense abnormal 18F-FDG uptake were seen in the transplanted liver which were concerning for malignancy. Explantation of the liver approximately 1 month following the PET/CT revealed multiple inflammatory and ischemic changes including large bile duct necrosis, acute cholangitis, bile duct obstruction changes and periportal fibrosis, with no evidence of malignancy. We present the 18F-FDG PET/CT image findings of this case.