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Pseudolipoma, also known as pseudolipoma of the Glisson's capsule, is an encapsulated lesion that contains degenerated fat and is enveloped by the liver capsule. In this report, we discuss a 37-year-old male presenting with dysuria and microscopic hematuria who revealed an incidental finding of a pseudolipoma on a CT scan of the abdomen.

A 57-year-old man presented to the emergency department with severe abdominal pain. Three months prior to presentation, he had sustained blunt trauma to his right side whilst cycling but had not sought medical attention. On admission, a CT scan showed small bowel obstruction and he underwent an emergency laparotomy. Intraoperatively, a subcapsular liver haematoma was identified, with incarcerated, necrotic small bowel within the liver capsule. The patient underwent deroofing of the haematoma with an omental patch and a small bowel resection with primary anastomosis. Small bowel obstruction is a common presentation in A&E and is responsible for half of emergency laparotomies in the UK each year. Although hepatic haematomas are also a relatively common complication of blunt trauma to the abdomen, associated bowel herniation into the liver capsule is very unusual. We believe this is the first time such a case of small bowel obstruction has been reported in the literature and we discuss details of operative management and highlight key learning points.

Background In metabolic associated fatty liver disease (MAFLD) vibration controlled transient elastography (VCTE) by Fibroscan has emerged as a non-invasive diagnostic tool for the measurement of controlled attenuation parameter (CAP) and liver stiffness measurement (LSM), which are surrogate markers for hepatic steatosis and fibrosis, respectively. However, obesity constitutes a limitation in terms of creating unreliable examinations due to increased skin to liver capsule distance. Here, we aimed to investigate the feasibility of VCTE in the evaluation of hepatic steatosis and fibrosis in obese individuals. Methods A total of 126 consecutive obese patients (body mass index ≥30 kg/m2) without a known history of MAFLD enrolled in the study. We performed CAP and LSM measurements and calculated Fibrosis-4 Index for each patient and included data of those patients to the analysis, from whom valid measurements were able to be taken. Results Reliable VCTE measurements were able to be obtained in 122 patients (97%), from those in 34 patients with M and 88 patients in XL probe (median age: 50 [18-75], 45 males and 77 females). In 1 patient VCTE failed to take any measurements and in 3 the measurements were classified as unreliable. The mean CAP value was 323 ± 48 dB/m and the median LSM value 5.3 [1.8-34.3] kPa. Conclusion CAP and LSM assessments by Fibroscan are reliable diagnostic tools for the early diagnosis of hepatic steatosis and fibrosis in obese individuals.

Background The purpose of this study was to determine the utility of some imaging findings in predicting microvascular invasion (MVI) and hepatocellular carcinoma (HCC) recurrence risk after liver transplantation. Method This retrospective study included 123 patients with histopathologically proven HCC at explant. All HCCs were classified as MVI positive (group I) or negative (group II) based on histopathological findings. In each group, multifocality, largest tumor size, bulging (tumor causing liver capsule expansion), beak sign (the acute angle between the tumor and liver parenchyma), and diffusion restriction on diffusion weighted images (DWI) were evaluated. These findings were compared between the groups by Student’s t test. The relation between the parameters and MVI was analyzed by using the Spearman’s correlation test. Results Of the total patients, 30.1% had MVI (group I) and 69.9% (group II) did not have MVI. Presence of beak sign (P ≤ .005), bulging sign (P = .002), and diffusion restriction (P = .045) were significantly more frequent in group I than group II. The beak sign, bulging sign, and diffusion restriction were correlated with presence of MVI. Largest tumor size and multifocality were higher in group I than group II, but the differences were not statistically significant. Conclusion Radiologists and transplant surgeons should be aware of some clue imaging findings, especially beak and bulging signs because these findings may predict the presence of MVI in HCC. These patients might benefit from histologic confirmation of the tumor characteristics through biopsy and subsequent bridging treatment options before liver transplantation to reduce the risk of recurrence.

Aim The assessment of liver fibrosis in patients with hepatitis C is important to predict carcinogenesis. In this study, we evaluated the usefulness of virtual touch quantification (VTQ) for staging liver fibrosis, and investigated factors causing discrepancies between the estimated fibrosis stage using VTQ and the pathological fibrosis stage. Methods Patients with hepatitis C (n = 302) were assessed using VTQ and underwent pathological liver investigation within 1 week before and after VTQ. A receiver operator characteristic (ROC) curve was obtained for VTQ, fibrosis-4 (FIB-4) index, and aspartate aminotransferase-to-platelet ratio index (APRI), and each area under the ROC curve (AUROC) was compared to predict fibrosis stage. We used univariate and multivariate analyses to investigate the factors related to the discrepancy between the estimated fibrosis stage using VTQ and the pathological fibrosis stage. Results At any stage, VTQ was the most accurate for staging liver fibrosis. The VTQ cut-off values were 1.33 m/s (AUROC = 0.822) for ≥F2, 1.51 m/s (AUROC = 0.836) for ≥F3, and 1.92 m/s (AUROC = 0.890) for F4. Skin liver capsule distance (SCD) was the most relevant factor for the discrepancy between the estimated fibrosis stage using VTQ and the pathological fibrosis stage. The SCD cut-off value was 17.5 mm. Conclusions Virtual touch quantification is a non-invasive, simple method that is more accurate for staging liver fibrosis than the FIB-4 index and APRI. However, when the SCD is longer than 17.5 mm, there may be measurement failures.

Background: Since the liver is one of the most important organs of the body that can be injured during trauma, that is, during accidents like car crashes, understanding its mechanical properties is of great interest. Experimental data is needed to address the mechanical properties of the liver to be used for a variety of applications, such as the numerical simulations for medical purposes, including the virtual reality simulators, trauma research, diagnosis objectives, as well as injury biomechanics. However, the data on the mechanical properties of the liver capsule is limited to the animal models or confined to the tensile/compressive loading under single direction. Therefore, this study was aimed at experimentally measuring the axial and transversal mechanical properties of the human liver capsule under both the tensile and compressive loadings. Methods: To do that, 20 human cadavers were autopsied and their liver capsules were excised and histologically analyzed to extract the mean angle of a large fibers population (bundle of the fine collagen fibers). Thereafter, the samples were cut and subjected to a series of axial and transversal tensile/compressive loadings. Results: The results revealed the tensile elastic modulus of 12.16 ± 1.20 (mean ± SD) and 7.17 ± 0.85 kPa under the axial and transversal loadings respectively. Correspondingly, the compressive elastic modulus of 196.54 ± 13.15 and 112.41 ± 8.98 kPa were observed under the axial and transversal loadings respectively. The compressive axial and transversal maximum/failure stress of the capsule were 32.54 and 37.30 times higher than that of the tensile ones respectively. The capsule showed a stiffer behavior under the compressive load compared to the tensile one. In addition, the axial elastic modulus of the capsule was found to be higher than that of the transversal one. Conclusions: The findings of the current study have implications not only for understanding the mechanical properties of the human capsule tissue under tensile/compressive loading, but also for providing unprocessed data for both the doctors and engineers to be used for diagnosis and simulation purposes.

Introduction: Endoscopic retrograde cholangiopancreatography (ERCP) has been proven to be a safe and effective method for diagnosis and treatment of biliary and pancreatic disorders. Major complications of ERCP include pancreatitis, hemorrhage, cholangitis, and duodenal perforation. We report a third case in literature of pneumoperitoneum after ERCP due to rupture of intrahepatic bile ducts and Glisson’s capsule in a peripheral hepatic lesion. Case Report: A 50-year-old male with a history of metastatic pancreatic neuroendocrine tumor and who had a partially covered metallic stent placed in the biliary tree 1 year ago presented to the oncology clinic with fatigue, abdominal pain, and hypotension. He was planned for ERCP for possible cholangitis secondary to obstructed previously placed biliary stent. However, the duodenoscope could not be advanced to the level of the major papilla because of narrowed pylorus and severely strictured duodenal sweep. Forward-view gastroscope was then passed with careful manipulation to the severely narrowed second part of the duodenum where the previously placed metallic stent was visualized. Balloon sweeping of stenting was done. Cholangiography did not show any leak. Following the procedure, the patient underwent CT scan of the abdomen that showed pneumoperitoneum which was communicating with pneumobilia through a loculated air collection in necrotic hepatic metastasis perforating Glisson’s capsule. The patient was managed conservatively. Conclusion: In our case, pneumoperitoneum resulted from rupture of intrahepatic bile ducts and Glisson’s capsule in hepatic metastasis. This case emphasizes the need for close clinical and radiological observation of patients with hepatic masses (primary or metastatic) subjected to ERCP.

Carbon tetrachloride-induced liver injury is a thoroughly studied model for regeneration and fibrosis in rodents. Nevertheless, its pattern of liver fibrosis is frequently misinterpreted as portal type. To clarify this, we show that collagen type IV+ “streets” and α-SMA+ cells accumulate pericentrally and extend to neighbouring central areas of the liver lobule, forming a ‘pseudolobule’. Blood vessels in the center of such pseudolobules are portal veins as indicated by the presence of bile duct cells (CK19+) and the absence of pericentral hepatocytes (glutamine synthetase+). It is critical to correctly describe this pattern of fibrosis, particulary for metabolic zonation studies.

A serious complication of chronic hepatic insufficiency is acute-on-chronic liver failure, a recognized syndrome characterized by acute decompensation of cirrhosis and organ/system failure. We investigated the use of adipose-derived mesenchymal stem cells (AD-MSCs) in an experimental model of acute-on-chronic liver failure, developed by microsurgical extrahepatic cholestasis in rats. Rats undergoing microsurgical extrahepatic cholestasis were treated by intraparenchymal liver injection of human or rat AD-MSCs, undifferentiated or previously differentiated in vitro toward the hepatocyte lineage. The groups treated with rat AD-MSCs showed less ascites, lower hepato- and splenomegaly, less testicular atrophy, and an improvement in serum biochemical hepatic parameters. There was also an improvement in histological liver changes, in which the area of fibrosis and bile duct proliferation were significantly decreased in the group treated with predifferentiated rat AD-MSCs. In conclusion, an isograft of hepatocyte-predifferentiated AD-MSCs injected intraparenchymally 2 weeks after microsurgery in extrahepatic cholestatic rats prevents secondary complications of acute-on-chronic hepatic failure. These data support the potential use of autologous AD-MSCs in the treatment of human cholestasis, and specifically of newborn biliary atresia, which could be beneficial for patients awaiting transplant.

Introduction Liver biopsy is the gold standard in diagnosing, staging and guiding clinical management in liver disease. There are currently no standard guidelines for liver biopsy recovery time. The aims of this project are to study the safety of a one-hour recovery time after percutaneous liver biopsies and to measure the rate of complications and identify risk factors. Methods A total of 500 consecutive subjects who underwent a percutaneous liver biopsy at a single-center teaching institution (Brooke Army Medical Center) were enrolled between December 2016 and October 2018. Biopsies were performed using a 14-gauge Bard® Monopty® core biopsy needle using bedside ultrasound. Complications were defined as: Pain level > 5 out of 10, hospitalizations, emergency department visits, or other. Major complications were defined as: hospitalizations and emergency department visits. Results The only complication that required hospitalization was identified during the first hour of recovery. Liver biopsies of subjects with body mass index (BMI) ≥35 kg/m2 were not associated with more complications when compared to patients less than 30 kg/m2. Using a spinal needle (3.5'') to anesthetize the liver capsule in subjects with excess subcutaneous tissue did not result in more complications when compared to the standard 1.5'' needle. Only 3% of the patients who received lidocaine alone for the biopsy required post-procedure medications. Conclusion Ultrasound-guided percutaneous liver biopsies, using a 14-gauge needle, were overall found to be safe. A one-hour post recovery period is adequate to identify all immediate major complications.

Sometimes, the presentation of some diseases can be fulminating. The authors present the case of a 51-year- old male brought to the emergency department visibly drunk and complaining of abdominal pain. Immediately, the diagnosis of hemorrhagic shock due to an accentuated drop of the hemoglobin level was made. After stabilization, he underwent a computed tomography of the abdomen, revealing a hepatocellular carcinoma with rupture of the Glisson capsule and massive intraperitoneal hemorrhage. With this case, the authors want to bring attention to a rare first presentation of hepatocellular carcinoma with a catastrophic result.

Fitz-Hugh–Curtis syndrome, a rare complication of pelvic inflammatory disease, is an inflammation of the liver capsule (thus called perihepatitis) and the surrounding peritoneum. It occurs extremely rarely in men and is typically characterized by a sudden onset of severe pain in the right upper abdominal quadrant. Ultrasound examination of the liver does not reveal any morphologic changes, and liver function tests are usually normal. Computerized tomography shows the thickening of the perihepatic fat, but definitive diagnosis is only possible by direct visualization by laparoscopy or laparotomy. We present a 33-year-old HIV-positive man with Chlamydia trachomatis proctitis who developed severe right upper abdominal quadrant pain. Abdominal ultrasound did not show any liver pathology, while computerized tomography revealed hepatic capsular thickening. After 21 days of doxycycline therapy, the patient’s symptoms subsided. Based on the clinical presentation and liver computerized tomography examination, the diagnosis of proctitis and the resulting Fitz-Hugh–Curtis syndrome was made. Although it is rarely seen in male patients, it should be a part of differential diagnosis in patients who present with right upper abdominal quadrant pain, especially in men who have sex with other men.

Background/aims Chronic liver disease leads to liver fibrosis, and although the liver does have a certain regenerative capacity, this disease is associated with dysfunction of the liver vessels. C-reactive protein (CRP) is produced in the liver and circulated from there for metabolism. CRP was recently shown to inhibit angiogenesis by inducing endothelial cell dysfunction. The objective of this study was to determine the effect of CRP levels on angiogenesis in a rat model of liver dysfunction induced by bile duct ligation (BDL). Methods The diameter of the hepatic vein was analyzed in rat liver tissues using hematoxylin and eosin (H&E) staining. The expression levels of angiogenic factors, albumin, and CRP were analyzed by real-time PCR and Western blotting. A tube formation assay was performed to confirm the effect of CRP on angiogenesis in human umbilical vein endothelial cells (HUVECs) treated with lithocholic acid (LCA) and siRNA-CRP. Results The diameter of the hepatic portal vein increased significantly with the progression of cirrhosis. The expression levels of angiogenic factors were increased in the cirrhotic liver. In contrast, the expression levels of albumin and CRP were significantly lower in the liver tissue obtained from the BDL rat model than in the normal liver. The CRP level was correlated with the expression of albumin in hepatocytes treated with LCA and siRNA-CRP. Tube formation was significantly decreased in HUVECs when they were treated with LCA or a combination of LCA and siRNA-CRP. Conclusion CRP seems to be involved in the abnormal formation of vessels in hepatic disease, and so it could be a useful diagnostic marker for hepatic disease.

Postoperative liver failure is one of the most critical complications following extensive hepatectomy. Although transplantation of allogeneic hepatocytes is an attractive therapy for posthepatectomy liver failure, transplanting cells via the portal veins typically causes portal vein embolization. The embolization by transplanted cells would be lethal in patients who have undergone massive hepatectomy. Thus, transplant surgeons need to select extrahepatic sites as transplant sites to prevent portal vein embolization. We aimed to investigate the mechanism of how liver cells transplanted into the mesentery protect recipient rats from acute liver failure after massive hepatectomy. We induced posthepatectomy liver failure by 90% hepatectomy in rats. Liver cells harvested from rat livers were transplanted into the mesenteries of hepatectomized rats. Twenty percent of the harvested cells, which consisted of hepatocytes and nonparenchymal cells, were transplanted into each recipient. The survival rate improved significantly in the liver cell transplantation group compared to the control group 7 days after hepatectomy (69 vs. 7%). Histological findings of the transplantation site, in vivo imaging system study findings, quantitative polymerase chain reaction assays of the transplanted cells, and serum albumin measurements of transplanted Nagase analbuminemic rats showed rapid deterioration of viable transplanted cells. Although viable transplanted cells deteriorated in the transplanted site, histological findings and an adenosine-5′-triphosphate (ATP) assay showed that the transplanted cells had a protective effect on the remaining livers. These results indicated that the paracrine effects of transplanted liver cells had therapeutic effects. The same protective effects were observed in the hepatocyte transplantation group, but not in the liver nonparenchymal cell transplantation group. Therefore, this effect on the remnant liver was mainly due to the hepatocytes among the transplanted liver cells. We demonstrated that transplanted liver cells protect the remnant liver from severe damage after massive hepatectomy.

Mesothelial cells (MCs) cover the surface of visceral organs and the parietal walls of cavities, and they synthesize lubricating fluids to create a slippery surface that facilitates movement between organs without friction. Recent studies have indicated that MCs play active roles in liver development, fibrosis, and regeneration. During liver development, the mesoderm produces MCs that form a single epithelial layer of the mesothelium. MCs exhibit an intermediate phenotype between epithelial cells and mesenchymal cells. Lineage tracing studies have indicated that during liver development, MCs act as mesenchymal progenitor cells that produce hepatic stellate cells, fibroblasts around blood vessels, and smooth muscle cells. Upon liver injury, MCs migrate inward from the liver surface and produce hepatic stellate cells or myofibroblast depending on the etiology, suggesting that MCs are the source of myofibroblasts in capsular fibrosis. Similar to the activation of hepatic stellate cells, transforming growth factor β induces the conversion of MCs into myofibroblasts. Further elucidation of the biological and molecular changes involved in MC activation and fibrogenesis will contribute to the development of novel approaches for the prevention and therapy of liver fibrosis.

Mesothelial cells (MCs) form a single layer of the mesothelium and cover the liver surface. A previous study demonstrated that, upon liver injury, MCs migrate inward from the liver surface and give rise to hepatic stellate cells (HSCs) in biliary fibrosis induced by bile duct ligation (BDL) or myofibroblasts in CCl4-induced fibrosis. The present study analyzed the role of transforming growth factor-β (TGF-β) signaling in mesothelial-mesenchymal transition (MMT) and the fate of MCs during liver fibrosis and its regression. Deletion of TGF-β type II receptor ( Tgfbr2) gene in cultured MCs suppressed TGF-β-mediated myofibroblastic conversion. Conditional deletion of Tgfbr2 gene in MCs reduced the differentiation of MCs to HSCs and myofibroblasts in the BDL and CCl4 models, respectively, indicating that the direct TGF-β signaling in MCs is responsible to MMT. After BDL and CCl4 treatment, MC-derived HSCs and myofibroblasts were distributed near the liver surface and the thickness of collagen was increased in Glisson's capsule beneath the liver surface. Fluorescence-activated cell sorting analysis revealed that MC-derived HSCs and myofibroblasts store little vitamin A lipids and have fibrogenic phenotype in the fibrotic livers. MCs contributed to 1.4 and 2.0% of activated HSCs in the BDL and CCl4 models, respectively. During regression of CCl4-induced fibrosis, 20% of MC-derived myofibroblasts survived in the liver and deactivated to vitamin A-poor HSCs. Our data indicate that MCs participate in capsular fibrosis by supplying vitamin A-poor HSCs during a process of liver fibrosis and regression.

Fitz-Hugh–Curtis syndrome is characterized by inflammation of the liver capsule following the spread of a pelvic starting point infection. The most commonly involved germ is Chlamydia trachomatis. The clinical presentation can be misleading and simulate cholecystitis or other cause of pain in the right hypochondrium. In imaging, it results in a contrast enhancement characteristic of the hepatic capsule at portal time.

Background Significance of Glisson's capsule invasion in colorectal liver metastases (CLM) patients undergoing resection has been little investigated. Methods CLM patients (244) with curative resection (2011–2016) were divided into two groups: patients with (Group 1; n = 49 [20%]) and without (Group 2; n = 195 [80%]) histologically-proven Glisson invasion. Eight (16%) Group 1 patients were identified by pre- or intra-operative findings. We compared characteristics between Groups 1 and 2 and determined independent prognosticators. Results Group 1 was more commonly associated with right-sided primary, CLM>5 cm, and R1 resections. Independent factors on reduced OS in entire cohort were pre-surgical chemotherapy [hazard ratio (HR): 2.68, P = 0.001], CLM>5 cm (HR: 4.39, P = 0.002), moderate or poor differentiation (HR: 2.38, P = 0.004), and R1 resection (HR: 1.92, P = 0.035). Conclusions CLM Glisson invasion was significantly associated with R1 resection. Advancements in determining Glisson invasion pre- or intra-operatively might produce benefits for CLM patients undergoing resection by reducing R1 resection.

To demonstrate the utility of ultrasound (US) guidance in improving the safety and efficacy of transjugular liver biopsy (TJLB) by analyzing all the TJLBs performed by us in the last 4 years. Forty-seven patients who underwent TJLB in the last 4 years in our two centers were retrospectively analyzed. US guidance was used for all but for one patient during the two crucial steps of the procedure—for internal jugular vein (IJV) access and during the parenchymal biopsy. Biopsies were obtained under real-time sonographic guidance from the right lobe after confirming an adequate room for needle throw without breaching the liver capsule or any major hilar structures. Post-procedure complications, tissue yield, and histopathological adequacy of samples were analyzed. Overall technical success rate was 100%. No major complications were found where ultrasound-assisted TJLB (uTJLB) was performed. One patient who underwent non-US guided TJLB had an event of a capsular breach and intra-peritoneal hemorrhage requiring coil embolization. Samples were of adequate dimension. Histopathological positivity was 100%. The overall complication rate for uTJLB was 4.7% which was due to minor complications in two patients. Addition of US unit to the angiographic suite is effortless and Interventional Radiologists being already skilled in US can easily implement this simple yet valuable modification to conventional TJLB procedures. Our experience on uTJLB further emphasizes the role of US guidance in improving the procedural success rate, safety profile, and efficacy in the histopathological outcome of TJLB in all patients irrespective of age and disease burden.

After initial evaluation of a cancer patient, the building of a treatment plan is an important step. In the setting of multiple therapeutic modalities, chemotherapy is the most widely used one. The metabolism and clearance of chemotherapy drugs are mostly dependent on normally functioning kidney and liver.

Malignant vascular tumors of the liver are rare. The aim of this study was to investigate the applicability of gray scale and contrast-enhanced ultrasonography in patients with epithelioid hemangioendothelioma (EHE) of the liver and hepatic angiosarcoma (HA) and to describe the clinical presentation.We retrospectively analyzed all patients with epithelioid hemangioendothelioma or hemangiosarcoma of the liver from 1998 to 2011, who underwent ultrasound investigation. We describe the findings in gray scale and contrast-enhanced ultrasound and the clinical course of the disease of seven patients with EHE and five patients with HA.Ultrasound investigation in EHE showed mostly multiple hypoechoic irregular lesions close to the liver capsule and with a halo in some cases. Contrast enhancement revealed inhomogeneously and through all contrast phases vascularized tumors with a rim enhancement in 50%, with or without early wash out. All tumors had avascular parts. HA presented as multiple and irregular hypo-, iso- or hyperechoic lesions. After contrast enhancement, hypervascularization with individual patterns was evident in all patients. Of five, three had liquid parts. Patients with HA were significantly older (58 vs. 37 years, p = 0.014) and presented with lower thrombocyte counts (84 vs. 264, p = 0.0025) and with higher CEA levels (4.6 vs. 1.5, p = 0.03).EHE and HA are inhomogeneous tumors, explaining the high inter-individual variability and heterogeneity in ultrasound examination. The presence of multifocal lesions, heterogeneity and undefined margins may differentiate EHE or HA from hemangioma. A biopsy is essential in the diagnosis of vascular tumors.

This study aimed to elucidate the impact of epithelial regenerative responses and immune cell infiltration on biliary complications after liver transplantation. Bile duct (BD) damage after cold storage was quantified by a BD damage score and correlated with patient outcome in 41 patients. Bacterial infiltration was determined by fluorescence in situ hybridization (FISH). BD samples were analyzed by immunohistochemistry for E-cadherin, cytokeratin, CD56, CD14, CD4, CD8, and double-immunofluorescence for cytokine production and by messenger RNA (mRNA) microarray. Increased mRNA levels of adherens junctions (P

Primary biliary cirrhosis is an autoimmune liver disease characterized by the chronic progressive loss of interlobular bile ducts. An immune-mediated destruction of the bile duct epithelium is thought to mediate its pathogenesis. It is a disease that primarily affects middle-aged women of all races. Histologically, it is characterized by portal inflammation comprising aggregates of lymphoid cells and/or granulomas, which invade and destroy biliary epithelial cells. This causes secondary duct loss, decreased bile secretion, and cholestasis that promotes hepatic fibrosis, cirrhosis, and, eventually, liver failure. Serologically, the diagnostic hallmark finding is antimitochondrial antibody.

It has been estimated that there are about 748,3000 cases of newly diagnosed liver cancer worldwide with a mortality of 695,900 cases each year. More than 80% of hepatocellular carcinoma (HCC) is discovered in sub-Saharan Africa or Asia, while the Western countries have a lower incidence. For example, the annual incidence rate of HCC in the United States is (1.5–4.9)/100,000 people. And according to the prediction by American Cancer Society, the new cases of liver cancer would reach 28,720, with 20,550 deaths in 2013, but it did not belong to the top ten malignant tumors with high incidence. In our country, the annual incidence of liver cancer was 25.7/100,000, and the mortality rate was 23.7/100,000, ranking the third and second the incidence and mortality of malignant tumor, respectively. Among 40,656 cases of hepatobiliary tumor diagnosed in the Department of Pathology, Eastern Hepatobiliary Surgery Hospital (EHBH),the Second Military Medical University during the past 30 years, malignant hepatic tumors account for 80% of all the cases, and the top two are HCC (86%) and intrahepatic cholangiocarcinoma (ICC, 8%). The number of surgical cases of both cancers is still increasing (Fig. 7.1), suggesting the high incidence of liver cancers in our country [1, 2, 3] Open image in new window Fig. 7.1 The proportion of surgical resected HCC/ICC in the EHBH over the 30 years

The liver is rarely involved in female genital diseases or pregnancy. Peripheral hepatic and perihepatic lesions are mainly due to the progression of genital malignancies, usually ovarian cancer. It should be distinguished from other malignant and non-malignant lesions. In all clinical situations, liver involvement is a sign of distant extension or dissemination of female genital diseases. Therefore, accurate detection and characterization of hepatic and perihepatic involvement on imaging is of clinical importance and often changes patient management.

To evaluate on magnetic resonance imaging (MRI) the occurrence rate of temporal perilesional parenchymal enhancement (PPE) associated with hepatic hemangiomas in a large consecutive series and to determine which aspects are associated with this observation. Institutional review board approved this retrospective study. A computerized search of the MRI database was performed for consecutive patients between January 2008 and January 2012. The study population included 513 liver hemangiomas in 224 patients (104 males and 120 females; mean age of 55.2 ± 13.5 years; age range 24–89 years). Two readers independently reviewed the frequency of PPE, size, speed of enhancement and location of each hemangioma. Marginal models with generalized estimating equation were used. Wald test was applied to verify if the model coefficients were significant. 80/513 (15.6%) hemangiomas showed PPE. The incidence of PPE was significantly higher (p

Introduction and aims Shear wave elastography (SWE) is an emerging ultrasound-related technology for assessment of liver fibrosis. The usefulness and reliability of SWE is unclear relative to other markers of liver fibrosis. We compared the clinical usefulness of SWE relative to transient elastography (TE), liver ultrasound and other standard biochemical markers of chronic liver disease in patients with varied liver disorders. Methods SWE assessment was performed using a Toshiba Aplio 500 or Canon Aplio i800 machine, concurrently with liver ultrasound on 421 adult patients. Amongst these patients 227 also had liver transient elastography (TE). Patient age, gender, body mass index (BMI), alcohol history, liver disease diagnosis, and laboratory results were recorded. Associations between SWE, TE and patient factors were sought. Suspected significant liver fibrosis was defined by liver stiffness measurement interpretation of ≥ F2 equivalent using Metavir staging. Results Patients were predominantly male (67.5%). Males and females were matched as regards age and BMI. The indications for SWE included nonalcoholic fatty liver disease (10%), chronic hepatitis B (22%), chronic hepatitis C (38%), alcohol-related liver disease (18%) and others (12%). 23%The mean (standard deviation) age was 53 (14) years, body mass index 27.7 (6.3) kg/m2, ultrasound-measured skin to liver capsule distance 20.0 (7.3)mm, serum ALT 39(27) U/L and AST 48(32) U/L. The median (IQR) liver stiffness was 9.9 (6.4-20.0) kPa with SWE and 9.2 (5.8-20.9) kPa with TE. Patients with suspected significant liver fibrosis determined by SWE, compared with patients not suspected of having significant fibrosis, were significantly older, had higher BMI, skin to liver capsule distance, TE liver stiffness measurement, alcohol consumption, and blood based assessments AST (but not ALT), AST/ALT ratio, AST to platelet ratio index (APRI), Fibrosis-4 index (FIB-4), Hepascore and NAFLD fibrosis score (NFS), but lower platelet count and serum albumin (p Conclusions SWE was found to be a useful test for suspected liver fibrosis in various liver disorders, and results were found to correlate with TE liver stiffness measurement plus clinically relevant anthropometric and laboratory parameters.

Considerable progress has been made in developing antifibrotic agents and other strategies to treat liver fibrosis; however, significant long-term restoration of functional liver mass has not yet been achieved. Therefore, we investigated whether transplanted hepatic stem/progenitor cells can effectively repopulate the liver with advanced fibrosis/cirrhosis. Stem/progenitor cells derived from fetal livers or mature hepatocytes from DPPIV+ F344 rats were transplanted into DPPIV− rats with thioacetamide (TAA)-induced fibrosis/cirrhosis; rats were sacrificed 1, 2, or 4 months later. Liver tissues were analyzed by histochemistry, hydroxyproline determination, reverse-transcription polymerase chain reaction (RT-PCR), and immunohistochemistry. After chronic TAA administration, DPPIV− F344 rats exhibited progressive fibrosis, cirrhosis, and severe hepatocyte damage. Besides stellate cell activation, increased numbers of stem/progenitor cells (Dlk-1+, AFP+, CD133+, Sox-9+, FoxJ1+) were observed. In conjunction with partial hepatectomy (PH), transplanted stem/progenitor cells engrafted, proliferated competitively compared to host hepatocytes, differentiated into hepatocytic and biliary epithelial cells, and generated new liver mass with extensive long-term liver repopulation (40.8 ± 10.3%). Remarkably, more than 20% liver repopulation was achieved in the absence of PH, associated with reduced fibrogenic activity (e.g., expression of alpha smooth muscle actin, platelet-derived growth factor receptor β, desmin, vimentin, tissue inhibitor of metalloproteinase-1) and fibrosis (reduced collagen). Furthermore, hepatocytes can also replace liver mass with advanced fibrosis/cirrhosis, but to a lesser extent than fetal liver stem/progenitor cells. Conclusion: This study is a proof of principle demonstration that transplanted epithelial stem/progenitor cells can restore injured parenchyma in a liver environment with advanced fibrosis/cirrhosis and exhibit antifibrotic effects. (Hepatology 2014;58:284–295)

Although aquaporins (AQPs) in normal hepatobiliary system have been studied, little is known about AQP localization and changes in the hepatic microvascular system including sinusoids in cholestatic liver. The present study aimed to clarify the localization of AQP-1 in the microvessels in normal human liver and in primary biliary cirrhosis (PBC). Human normal liver (control) and PBC liver specimens were obtained. Immunohistochemistry, Western blotting, in situ hybridization (ISH) and electron microscopic examination for AQP-1 were conducted. In control liver and stages I-II PBC liver, AQP-1 immunoreactivity was mainly localized in portal venules, hepatic arterioles and bile ducts in the portal tract, but was hardly detected in the sinusoids. However, AQP-1 expression was enhanced in the proliferated bile ductules in PBC. In stages III-IV PBC liver tissues, AQP-1 was aberrantly expressed in proliferated arterial capillaries opening into the sinusoids at the peripheral edge of regenerating hepatic nodules and in the fibrotic septa. Overexpression of AQP-1 at protein and mRNA levels was demonstrated by Western blot and ISH, respectively. Angiogenetic and fibrotic responses are probably induced by AQP-1, leading to enhanced pouring of arterial blood into the sinusoids; thus, contributing to progression of portal hypertension in PBC.

I will never forget sitting in an Advisory Board meeting and watching a presentation by a well-known colleague (and proponent of one of the many alternatives to liver biopsy for fibrosis staging) showing bedside scenes from a “typical” liver biopsy which appeared as a very bloody mess, and no doubt an impressive undertaking to be avoided if at all possible especially to the non-medical Pharma advisory members. Indeed, liver biopsy always must command respect and never can be taken lightly, requiring preparation both mentally and practically for the rare but true emergency. On the other hand, I have never seen a biopsy look quite like the one portrayed by my colleague, and one needs only to see a few remarkable misses in fibrosis staging by the “non-invasive” tests to second-guess relying on these measures routinely let alone exclusively—this is all the more true when trends become evident, such as chronically over-calling or under-calling (or helter-skelter outright missing) the fibrosis stage—all of which appear evident in various forms of non-invasive staging whether by various forms of elastography or blood profiles of collagen metabolites (anecdotal experience). Sometimes derided as a “silver standard” rather than a “gold standard”, biopsy remains a foundational element of evaluating liver disease.1 So what does liver biopsy bring to the table? The strength of biopsy lies in its long and established history and the diversity of findings in one test especially in diagnosis as well as staging. Diagnostically, things are not always as they may seem and hence the obese, diabetic patient with abnormal liver enzymes may have findings of autoimmune hepatitis (AIH) or both steatohepatitis and AIH (anecdotal experience). Conversely, the treated AIH patient with abnormal liver enzymes could have inadequately treated AIH or with steroid induced weight gain may have transitioned to a form of fatty-liver disease. Other key histological findings, which may not always be expected, include granulomatous inflammation, evidence of bile duct injury, venous congestion, or, in the transplanted patient, evidence of rejection or inclusion bodies. Biopsy is also important in establishing tissue metal content in suspected hemochromatosis or Wilson's disease. What are the limitations of liver biopsy? Inherent limitations have been clearly established. Much has been made of the potential for sampling error especially in fibrosis staging, but also in detection of key histological findings such as cellular ballooning in NASH.2 This underscores the fact that biopsy is seldom a stand-alone test and optimal interpretation requires clinical context including history, laboratory values, and imaging results. It also is a reminder of the importance of technique in providing an adequate specimen. Surgical wedge biopsies, although usually providing an ample amount of tissue, are famously known to over-estimate fibrosis stage due to the proximity of the sample to the fibrous liver capsule. Core biopsies can be optimized by ensuring adequate length (>2 cm) and also the width as narrow biopsies can hamper understanding the relationship between portal tracts and central veins. Usually 15–16-gauge cores are adequate but narrower cores can be problematic. Notably, use of guidance collar on the ultrasound probe for real-time guidance can adversely influence the quality of the tissue sample when used with non-cutting, automated coring devices (such as the Biopence needle), and attention should be paid to avoiding impeding the motion of the device. Complications of liver biopsy are uncommon but must be always vigilantly prepared for.3 Use of ultrasound guidance either as real-time guidance or as site-marking clearly reduces inadvertent puncture of adjacent organs such as gall bladder or lung, but probably does not greatly affect the bleeding risk which depends more on transecting a small artery.4 Serious bleeding is usually apparent in the immediate period following the biopsy. Plans for managing this uncommon complication, such as use of urgent imaging and an interventional contingency should be thought out in advance. So where does biopsy fit into the clinical evaluation nowadays? It is clearly less important in the modern era in very straightforward cases, such as uncomplicated hepatitis C, where non-invasive tests can often serve the clinical need to help guide therapy. However, biopsy stands today where it has always been—at the foundation of clinical Hepatology. Few histological findings are genuinely pathognomonic but placed into the clinical context, the biopsy can provide invaluable information to guide optimal patient care and it serves as an important and, sometimes, definitive adjunct to the ever-growing number of non-invasive tests. It is notable that of the wide-variety of clinical trials aiming at therapeutics for NASH, involving investigators from around the world, essentially all require diagnostic entry biopsy and most require end-of-treatment biopsy for assessments of histological response. Two final questions can be reasonably asked. Who should perform standard percutaneous biopsies and who should interpret the biopsy? These are two important questions especially for the people putting the biopsy results into a clinical context and then acting on the results, and hence also an especially important question for the person who is undergoing the biopsy. It is human nature that the closer one is vested in an outcome, the more likely one is to take a strong interest in the outcome, especially one that can have such pivotal therapeutic implications for the patient. One has to see only a few inadequate specimens which require an “encore biopsy” to realize that the performance of liver biopsy and a more than passing familiarity with interpretation of an adequate specimen are core elements of the practice of Hepatology. Having access to a Pathologist with specialized liver training and experience is highly desirable but not always available, and thus all the more reason that training should continue to emphasize this core element of Hepatology.

Hepatic infarcts or abscesses occur after hepatic artery interruption. We explored the mechanisms of hepatic deprivation-induced acute liver injury and determine whether partial portal vein arterialization attenuated this injury in rats. Male Sprague-Dawley rats underwent either complete hepatic arterial deprivation or partial portal vein arterialization, or both. Hepatic ischemia was evaluated using biochemical analysis, light microscopy, and transmission electron microscopy. Hepatic ATP levels, the expression of hypoxia- and inflammation-associated genes and proteins, and the expression of bile transporter genes were assessed. Complete dearterialization of the liver induced acute liver injury, as evidenced by the histological changes, significantly increased serum biochemical markers, decreased ATP content, increased expression of hypoxia- and inflammation-associated genes and proteins, and decreased expression of bile transporter genes. These detrimental changes were extenuated but not fully reversed by partial portal vein arterialization, which also attenuated ductular reaction and fibrosis in completely dearterialized rat livers. Collectively, complete hepatic deprivation causes severe liver injury, including bile infarcts and biloma formation. Partial portal vein arterialization seems to protect against acute ischemia-hypoxia-induced liver injury.

Introduction: The Fitz-Hugh-Curtis syndrome is a perihepatitis produced by secondary peritonitis the rise of bacteria, as a result of pelvic inflammatory disease. In the chronic stage can be observed adhesions between abdominal wall and the liver surface characterized by the similarity to "violin strings". This image is considered diagnostic criterion. Clinical case: Female 37 years-old, Gesta 7, Births 5, Abortion 1, Cesarean Section 0, who intervenes surgically open to present intermittent pain for gallstone cholecystitis two years of evolution. Normal vital signs; Laboratory test preoperative: erythrocytes 3.40 × 106, hemoglobin 9.9 g/dl, hematocrit 33.8%, lymphocytes 19%, leukocytes 11.86 × 103/mm3, total neutrophil 86%. Glucose 139 mg/dl, BUN 4.35 mg/dl, urea 9.3 mg/dl, SGOT (AST) 80 U/I, SGPT (ALT) 66 U/I, Proteins 6.0 g/dl, serum albumin 3.4 mg/dl. VDRL Neg. Urinalysis: Urobilinogen 2 mg/dl; Leukocyte 15-20 x field and postoperatory pregnancy test (+). It proceeds to open cholecystectomy and during exposure of the gallbladder is located in hepatic parenchyma multiple adhesions and congestive liver. Discussion: The combination of a painful liver without biochemical evidence of hepatitis or biliary obstruction, and menorrhagia raised the suspicion of perihepatitis Fitz-Hugh-Curtis, an inflammatory process of the liver capsule due to pelvic inflammatory disease mostly caused by Chlamydia trachomatis or Neisseria gonorrhoeae. The pathophysiology of perihepatitis FHC is unclear, but direct infection of the liver capsule, hematologic or lymphatic spread as well as an exaggerated immune response has been suggested.

Liver disease contributes to significant morbidity and mortality in cystic fibrosis (CF). Although all patients with CF express the defective CF transmembrane conductance regulator in cholangiocytes, many develop asymptomatic fibrosing liver disease. Only some develop cirrhosis, with pathogenesis remaining enigmatic. Available noninvasive diagnostic tools do not identify patients at risk before development of advanced fibrosis. We conducted a pilot study to identify genes associated with hepatic injury and fibrosis on liver biopsy that may help elucidate determinants of CF-associated liver disease (CFLD).Liver tissue from children with CFLD with various stages of hepatic fibrosis was compared with pediatric controls using cDNA array analysis. Differential expression of genes of interest was then assessed relative to pediatric control liver and non-CF cholestatic disease control liver from patients with biliary atresia, using both real-time reverse transcription-polymerase chain reaction and immunohistochemistry.cDNA array demonstrated differential expression of numerous genes associated with hepatic fibrogenesis including collagens, matrix metalloproteinases, and chemokines in CFLD versus normal controls, particularly decreased expression in tissue remodeling genes including plasminogen activator inhibitor-1 (PAI-1, up to 25-fold) and tissue inhibitor of metalloproteinase-1 (TIMP-1); this was validated by real-time reverse transcription-polymerase chain reaction (PAI-1, P = 0.004; TIMP-1, P = 0.019). No significant decrease in PAI-1 or TIMP-1 mRNA was observed in biliary atresia versus normal control. Immunohistochemistry confirmed the decreased expression of hepatic PAI-1 and TIMP-1 protein in CFLD versus both normal and biliary atresia disease controls.The coordinated differential expression of these genes associated with liver fibrosis provides evidence for a transcriptional basis for the pathogenesis of CFLD and provides avenues for further study. Clarifying the pathogenesis of CFLD will facilitate techniques for early, precirrhotic detection and targeted interventions.

Objectives Pyogenic liver abscess is a rare condition in the general population. The source of infection is most often biliary, and more rarely gastrointestinal via the portal tract, or even hematogenic. Other than in special contexts (scarring after radiofrequency ablation), focal liver lesions are not a usual risk factor for hepatic abscesses in patients with a history of bile duct procedures (sphincterotomy, biliary stenting, biliary enteric anastomosis). Materials and method - results We report four cases of focal liver lesions (two patients with benign lesions of the biliary cyst type and two other patients with lesions due to pancreatic cancer) complicated by a superinfection in patients with a history of bile duct procedures. There were no predisposing factors other than a context of cancer or diabetes. Conclusion Superinfection of a focal liver lesion should be considered when there is a suggestive clinical picture and a change in the appearance of the lesion in patients with a history of bile duct procedures in a context of cancer or diabetes.

Background and Aim: Small-for-size grafts are prone to mechanical injury and a series of chemical injuries that are related to hemodynamic force. Hepatic stellate cells activate and trans-differentiate into contractile myofibroblast-like cells during liver injury. However, the role of hepatic stellate cells on sinusoidal microcirculation is unknown with small-for-size grafts. Methods: Thirty-five percent of small-for-size liver transplantation was performed with rats as donors and recipients. Endothelin-1 levels as well as hepatic stellate cells activation-related protein expression, endothelin-1 receptors, and ultrastructural changes were examined. The cellular localizations of two types of endothelin-1 receptors were detected. Furthermore, liver function and sinusoidal microcirculation were analyzed using two different selective antagonists of endothelin-1 receptor. Results: Intragraft expression of hepatic stellate cells activation-related protein such as desmin, crystallin-B and smooth muscle α-actin was upregulated as well as serum endothelin-1 levels and intragraft expression of the two endothelin receptors. The antagonist to endothelin-1 A receptor not to the endothelin-1 B receptor could attenuate microcirculatory disturbance and improve liver function. Conclusions: Small-for-size liver transplantation displayed increased hepatic stellate cells activation and high level of endothelin-1 binding to upregulation of endothelin-1 A receptor on hepatic stellate cells, which contracted hepatic sinusoid inducing graft injury manifested as reduction of sinusoidal perfusion rate and elevation of sinusoidal blood flow.

Introduction The incidence of small-for-size-liver-syndrome after liver transplantation and extended liver resection may be reduced by portal flow modulation. However, many aspects of the small-for-size-liver-syndrome pathogenesis are still unclear. In this experimental study we evaluated the early effects of portal flow modulation after 80% hepatic resection in rats. Materials and methods Rats were randomised in: sham operation (G1), conventional hepatic resection (G2), splenectomy and hepatic resection (G3), splenic transposition followed by hepatic resection after three weeks (G4). Six hours after operation, oxygen saturation of hepatic vein blood, glutathione, and standard liver markers were measured from hepatic venous blood. Glutathione measurement and histopatological examination were performed in the remnant liver. Results Total bilirubin and liver glutathione did not show differences between groups. Aspartate aminotransferase and alanine aminotransferase significantly increased in G2–G4 groups. Blood glutathione and oxygen saturation of hepatic vein blood were lower in G2 than in other groups. A gradient of micro-vesicular degeneration was more severe in G2 compared with G3 and G4. Apoptosis, hemorrhagic necrosis, mitochondrial damage and leucocyte adhesion were evident in G2. Conclusion The portal flow modulation induced by splenectomy or splenic transposition was effective in limiting early damage after extended liver resection.

Systemic concentrations of interleukin-6 (IL-6) are elevated in patients with liver cirrhosis, and impaired hepatic uptake of IL-6 was suggested to contribute to higher levels in these patients. To test this hypothesis IL-6 was measured in portal venous serum (PVS), hepatic venous serum (HVS) and systemic venous serum (SVS) of 41 patients with liver cirrhosis and four patients with normal liver function. IL-6 was higher in PVS than HVS of all blood donors and about 43% of portal vein derived IL-6 was extracted by the healthy liver, and 6.3% by the cirrhotic liver demonstrating markedly impaired removal of IL-6 by the latter. Whereas in patients with CHILD-PUGH stage A IL-6 in HVS was almost 25% lower than in PVS, in patients with CHILD-PUGH stage C IL-6 was similarly abundant in the two blood compartments. Ascites is a common complication in cirrhotic patients and was associated with higher IL-6 levels in all blood compartments without significant differences in hepatic excretion. Hepatic venous pressure gradient did not correlate with the degree of hepatic IL-6 removal excluding hepatic shunting as the principal cause of impaired IL-6 uptake. Furthermore, patients with alcoholic liver cirrhosis had higher IL-6 in all blood compartments than patients with cryptogenic liver cirrhosis. Aetiology of liver cirrhosis did not affect hepatic removal rate indicating higher IL-6 synthesis in patients with alcoholic liver cirrhosis. In summary, the current data provide evidence that impaired hepatic removal of IL-6 is explained by hepatic shunting and liver dysfunction in patients with liver cirrhosis partly explaining higher systemic levels.

Background Confocal endomicroscopy enables histopathology of the GI lumen to be observed in vivo. Recent prototypes of a confocal miniprobe are thin enough to be introduced through a needle. Objective To evaluate the ability of needle-based confocal laser endomicroscopy to distinguish between normal and cirrhotic liver tissue in vivo in a rat model. Design Feasibility study, nonsurvival animal experiments. Setting Academic research facility. Intervention Three normal control and 4 cirrhotic rats were examined under general anesthesia. The liver was exposed by laparotomy and imaged by using 3 different prototypes of confocal miniprobes, with 0, 50, and 100 μm working distances. Images were acquired on the surface of the liver capsule and through a 19-gauge needle inserted into the liver parenchyma. Real-time sequences were recorded after intravenous injection of fluorescein. Biopsy specimens were taken for standard histopathology. Main Outcome Measurements Confocal microscopic images of the surface and interior of livers in normal and cirrhotic rats. Results Miniprobes with 50 or 100 μm working distances identified cords of hepatocytes radiating toward central venules in normal livers and distorted hepatic architecture in cirrhotic livers when the miniprobes were either placed on the liver capsule or inserted into the parenchyma. The miniprobe with a 0 μm working distance identified a novel reticular pattern on the liver surface that was detected only in cirrhosis. Like the 2 longer-working-distance probes, this probe also identified cords of hepatocytes radiating toward central venules in normal livers and distorted hepatic architecture in cirrhotic livers, but this occurred only when the probe was inserted into the parenchyma. Limitations Data were assessed in an experimental animal setting, confocal imaging was performed invasively during laparotomy, only 1 model of cirrhosis was used, and no noncirrhotic liver diseases were examined. Conclusion Needle-based confocal laser endomicroscopy provides sufficient detail to distinguish normal from cirrhotic livers in a rat model. This innovative, minimally invasive technique has the potential to provide real-time identification of liver histology during EUS or natural-orifice transluminal endoscopic surgery procedures.

We report a case of a 68-year-old Chinese man who presented with Fatigue, anorexia more than half month, the body clear yellow dye for a week, liver function tests with alkaline phosphatase, alanine transferase increased, etc. Abdominal ultrasound showed extrahepatic duct dilatation. Enhanced computed tomography revealed signs of hepatic duct obstruction. Magnetic resonance imaging showed about the confluence of hepatic duct and upper common bile duct wall thickening; cholestasis common bile duct, multiple small stones in the lower; cholecystitis, elevation of the tumor markers CA19-9. At laparotomy, gallbladder, common bile duct, extrahepatic bile duct is clearly dissected out, no tumor, tumor eliminated by histologic examination.

This case involved a 75-year-old woman with obstructive jaundice who was diagnosed with hilar bile duct carcinoma. After endoscopic retrograde biliary drainage, the total bilirubin level was normalized. The indocyanine green test retention rate at 15 min (ICGR15) was 26%. The liver uptake ratio (LHL15) by technetium-99m galactosyl human serum albumin (99mTc-GSA) liver scintigraphy was 0.87. Left hepatectomy was scheduled by CT volumetry. However, biliary drainage was insufficient, and the functional liver volume showed functional deterioration of the left liver. After percutaneous transhepatic biliary drainage, future remnant liver volume by 99mTc-GSA liver scintigraphy changed to 52% from 42%, and ICGR15 and LHL15 were improved to 16% and 0.914, respectively. Scheduled left hepatectomy was performed following the results of functional liver volume. The measurement of functional volume by 99mTc-GSA liver scintigraphy provides useful information with respect to segmental liver function for deciding operative indications., Clinical Journal of Gastroenterology, 3(3), pp.174-178; 2010

Purpose. To review the histological features of 26 circumscribed liver lesions associated with liver capsule retraction and discuss the differential diagnosis while evaluating for the presence of fibrous stromal reaction. Materials and methods. Retrospective study performed between January 2005 and June 2008 including 26 patients: 18 males and 6 females, without history of cancer, aged between 42 and 82 years (mean age: 64.5 years), presenting with liver capsule retraction adjacent to a circumscribed liver lesion detected on CT or MRI. A single lesion was present in 17 patients, and multiple lesions were present in 9 patients. All liver lesions were biopsied with semi-quantitative evaluation of fibrous stromal reaction. Results. Twenty-one patients had benign or malignant liver tumors and 5 patients had confluent hepatic fibrosis. Twenty of 21 liver tumors were malignant (95.2%): 3 intra-hepatic cholangiocarcinoma, 17 cases of metastatic disease including colorectal carcinoma (n=8), bronchogenic carcinoma (n=1), pancreatic carcinoma (n=4), esophageal carcinoma (n=1), breast carcinoma (n=1), gallbladder carcinoma (1) and endocrine neoplasm of the pancreas (n=1), and 1 case of liver sclerosing angioma (n=1). There was no case of hepatoma. Excluding the 5 cases of confluent hepatic fibrosis, fibrous stromal reaction was present in 15 of 21 cases. Conclusion. The presence of capsular retraction next to a circumscribed liver lesion, while non-specific, is suspicious. In keeping with previous reports, metastases were frequently the cause and intrahepatic cholangiocarcinoma was the most frequent primary tumor. In patients with chronic hepatocellular disease, confluent fibrosis was a frequent etiology. The fibrous component of the underlying malignant lesion along with its subcapsular location appear to be determining factors in the development of capsular retraction.

The anatomy of the intrahepatic biliary system was evaluated by means of three-dimensional reconstruction of a portal tract in the liver from a stillborn infant with polycystic disease of the liver. This confirmed that the bile duct system in part had the form of a plate. Based on liver embryology a hypothesis is presented concerning the pathogenesis of polycystic disease of the liver and its relation to congenital hepatic fibrosis.