Inflammatory Lesions In Liver Research Articles

ОСОБЕННОСТИ ДИАГНОСТИКИ И ХИРУРГИЧЕСКОЙ ТАКТИКИ В ЛЕЧЕНИИ ПАЦИЕНТОВ ПРИ НЕОПУХОЛЕВЫХ ОБРАЗОВАНИЯХ ПЕЧЕНИ

Abstract. Introduction. Etiology of benign non-neoplastic liver lesions is quite diverse. They are usually represented by both purulent inflammatory and parasitic foci. Non-tumor lesions are characterized by severe course and by difficulties in diagnosing and managing the patients. Aim. The aim of the study was to analyze the characteristics of the diagnostic search and surgical treatment of patients with non-neoplastic liver lesions, based on the experience of our clinic.Materials and Methods. Treatment cases of 34 patients with non-tumor liver foci were analyzed by our team. We studied the steps of diagnosing non-neoplastic liver lesions and the surgical approaches to treatment, based on the etiology and nature of each liver lesion. Results and Discussion. In 79% (n=27) of all cases, focal diseases have been observed over the last three years. Etiologically, liver segment lesions were different. In 53.6% (n=18) of cases, 2-3 segments were affected simultaneously. In 11.7% (n=4) of cases, bilobar liver damages were detected. In liver abscesses, minimally invasive surgical approaches were used predominantly; in 70.9% (n=24) of cases, percutaneous abscess drainage was performed under ultrasound navigation. In 8.8% (n=3) of cases, abscess was redrained with a catheter; in 5.8% (n=2) of cases, abscess cavity was evacuated by puncturing. In cholangiogenic abscesses, the leading purpose was to resolve the hypertension of the bile ducts, followed by the abscess drainage. Smaller cholangiogenic abscesses were managed conservatively. Mortality was 5.8%. (n=2) in all groups of interest. Conclusion. In diagnosing the non-neoplastic liver lesions, an integrated approach is required, considering the present history and laboratory findings. In this case, the diagnosis standard is the use of ultrasound technology and computed tomography scans, while magnetic resonance imaging is indicated for diagnosing pathological factors relating to bile ducts. Surgical approaches are dependent on the nature of the pathological process. Minimally invasive technique under ultrasound navigation is the key technique for treating patients with purulent inflammatory liver lesions.

Molecular Identification, Pathogenesis, and Life Cycle of Sarcocystis cruzi from Cattle (Bos taurus) in New Valley Governorate, Egypt.

Sarcocystis cruzi was identified by molecular methods from an intermediate host, cattle (Bos taurus), in El-Kharga, New Valley Governorate, Egypt, and its life cycle and pathogenicity were studied in the final host, dogs (Canis familiaris). 600 slaughtered cattle aged 6-8 years (480/120 males/females) were included. In addition, three laboratory-bred, coccidian-free puppies aged 2-3 months were fed infected bovine muscles to locate the definitive host and analyze sporogony. 18S rRNA-specific gene primers were used for DNA amplification from esophageal muscles. These polymerase chain reaction (PCR) amplicons were subjected to restriction fragment length polymorphism (RFLP) and molecular sequence analysis. Infection was detected in 78.8% (473/600; 95% CI, 75.56-82.11%). Histopathological examination of esophageal muscles showed oval- to spherical-shaped cysts, 96.7 μm wide by 326.9 μm long; cysts in cardiac muscles were ovoid and smaller. Infected puppies began shedding sporocysts in feces 7 days post-inoculation and showed distorted organ architecture, severe cellular damage, and inflammatory lesions in liver, kidney, esophagus, and stomach. Three oocysts with different shapes and sizes were identified. Partial 18S rRNA gene sequences of isolated New Valley sarcocysts were identical to S. cruzi isolated from different areas, verifying their genetic relatedness. Our analysis suggests that S. cruzi is the most prevalent in slaughtered cattle in New Valley Governorate, Egypt.

Non-invasive alloimmune risk stratification of long-term liver transplant recipients

Management of long-term immunosuppression following liver transplantation (LT) remains empirical. Surveillance liver biopsies in combination with transcriptional profiling could overcome this challenge by identifying recipients with active alloimmune-mediated liver damage despite normal liver tests, but this approach lacks applicability. Our aim was to investigate the utility of non-invasive tools for the stratification of stable long-term survivors of LT, according to their immunological risk and need for immunosuppression. We conducted a cross-sectional multicentre study of 190 adult LT recipients assessed to determine their eligibility to participate in an immunosuppression withdrawal trial. Patients had stable liver allograft function and had been transplanted for non-autoimmune non-replicative viral liver disease >3 years before inclusion. We performed histological, immunogenetic and serological studies and measured the intrahepatic transcript levels of an 11-gene classifier highly specific for T cell-mediated rejection (TCMR). In this cohort, 35.8% of patients harboured clinically silent fibro-inflammatory liver lesions (13.7% had mild damage and 22.1% had moderate-to-severe damage). The severity of liver allograft damage was positively associated with TCMR-related transcripts, class II donor-specific antibodies (DSAs), ALT, AST, and liver stiffness measurement (LSM), and negatively correlated with serum creatinine and tacrolimus trough levels. Liver biopsies were stratified according to their TCMR transcript levels using a cut-off derived from biopsies with clinically significant TCMR. Two multivariable prediction models, integrating ALT+LSM or ALT+class II DSAs, had a high discriminative capacity for classifying patients with or without alloimmune damage. The latter model performed well in an independent cohort of 156 liver biopsies obtained from paediatric liver recipients with similar inclusion/exclusion criteria. ALT, class II DSAs and LSM are valuable tools to non-invasively identify stable LT recipients without significant underlying alloimmunity who could benefit from minimisation of immunosuppression. A large proportion of liver transplant patients with normal liver tests have inflammatory liver lesions, which in 17% of cases are molecularly indistinguishable from those seen at the time of rejection. ALT, class II donor-specific antibodies and liver stiffness are useful in identifying patients with this form of subclinical rejection. We propose these markers as a useful tool to help clinicians determine if the immunosuppression administered is adequate.

Phylogenetic relationships and diversity of bat-associated Leptospira and the histopathological evaluation of these infections in bats from Grenada, West Indies.

Bats can harbor zoonotic pathogens, but their status as reservoir hosts for Leptospira bacteria is unclear. During 2015–2017, kidneys from 47 of 173 bats captured in Grenada, West Indies, tested PCR-positive for Leptospira. Sequence analysis of the Leptospira rpoB gene from 31 of the positive samples showed 87–91% similarity to known Leptospira species. Pairwise and phylogenetic analysis of sequences indicate that bats from Grenada harbor as many as eight undescribed Leptospira genotypes that are most similar to known pathogenic Leptospira, including known zoonotic serovars. Warthin-Starry staining revealed leptospiral organisms colonizing the renal tubules in 70% of the PCR-positive bats examined. Mild inflammatory lesions in liver and kidney observed in some bats were not significantly correlated with renal Leptospira PCR-positivity. Our findings suggest that Grenada bats are asymptomatically infected with novel and diverse Leptospira genotypes phylogenetically related to known pathogenic strains, supporting the hypothesis that bats may be reservoirs for zoonotic Leptospira.

Focal infl ammatory liver lesions

Focal infl ammatory liver lesions

Hemostatic assessment of dogs associated with hepatic parasite load of Leishmania infantum chagasi

Abstract Leishmania infantum chagasi liver parasite load was compared to hemostatic abnormalities, as well as to clinical, laboratorial, and histopathological findings in dogs with visceral leishmaniasis. The liver parasite load of 30 dogs L. infantum chagasi naturally-infected was evaluated by quantitative real- time PCR and the results were compared with serum biochemistry and primary and secondary hemostasis findings. Moreover, hepatic histological lesions were described in these dogs. Prolonged bleeding time, prothrombin time (PT), and activated partial thromboplastin time (APTT), were observed in the group with visceral leishmaniasis. Eleven dogs presented inflammatory liver lesions, with predominance of mild multifocal mononuclear periportal hepatitis. No association between the presence of parasites and abnormalities in screening tests was observed by Spearman’s rank correlation coefficient. The clinical progression in leishmaniasis is associated with the occurrence of hemorrhagic diathesis, which depends not only on the presence of the parasite but also the inflammatory process, compromised immunological response, hepatic and renal failure in symptomatic dogs.

Differential Diagnosis of Arterial Phase Enhanced Hepatic Inflammatory Lesions and Hepatocellular Carcinomas with Contrast-enhanced Ultrasound

We aimed to investigate the enhancement patterns of contrast-enhanced ultrasound (CEUS) with SonoVue and determine the utility of this method for differential diagnosis between hepatic inflammatory lesions with arterial phase enhancement and hepatocellular carcinomas (HCC). Twenty-three patients with arterial-enhanced inflammatory liver lesions and 46 HCC patients were included. These lesions had been subjected to CEUS examination and confirmed by pathologic results or imaging follow-up for at least 1 y. In the arterial phase of CEUS, 65.2% of the inflammatory lesions showed patchy (slight enhancement with poorly defined margins) or centripetal enhancement, whereas 89.1% of the HCC lesions showed homogeneous or heterogeneous enhancement (p < 0.001). Moreover, 82.6% of the inflammatory lesions had poorly defined margins, and 78.3% were irregular in shape at the peak, whereas 87.0% of the HCC lesions had well-defined margins and 76.1% were regular (both p < 0.001). Feeding vessels were more frequently visualized in HCCs (71.7%) than in inflammatory lesions (26.1%, p < 0.001). Additionally, 88.2% of the internal non-perfused areas in inflammatory lesions were regular in shape, while 68.0% of these areas in HCCs had an irregular shape (p < 0.001). CEUS pattern analysis provides important information for differentiating inflammatory liver lesions and HCCs and is helpful for improving diagnostic accuracy.

Imaging findings of mimickers of hepatocellular carcinoma.

Radiological imaging plays a crucial role in the diagnosis of hepatocellular carcinoma (HCC) as the noninvasive diagnosis of HCC in high-risk patients by typical imaging findings alone is widely adopted in major practice guidelines for HCC. While imaging techniques have markedly improved in detecting small liver lesions, they often detect incidental benign liver lesions and non-hepatocellular malignancy that can be misdiagnosed as HCC. The most common mimicker of HCC in cirrhotic liver is nontumorous arterioportal shunts that are seen as focal hypervascular liver lesions on dynamic contrast-enhanced cross-sectional imaging. Rapidly enhancing hemangiomas can be easily misdiagnosed as HCC especially on MR imaging with liver-specific contrast agent. Focal inflammatory liver lesions mimic HCC by demonstrating arterial-phase hypervascularity and subsequent washout on dynamic contrast-enhanced imaging. It is important to recognize the suggestive imaging findings for intrahepatic cholangiocarcinoma (CC) as the management of CC is largely different from that of HCC. There are other benign mimickers of HCC such as angiomyolipomas and focal nodular hyperplasia-like nodules. Recognition of their typical imaging findings can reduce false-positive HCC diagnosis.

Long-term persistence of hepatitis B virus DNA in the serum of children with chronic hepatitis B after hepatitis B e antigen to antibody seroconversion.

To evaluate the prevalence and duration of viremia in relation to the features of liver disease, we investigated hepatitis B virus (HBV) DNA by the polymerase chain reaction in the serum of 39 children with chronic hepatitis B, after hepatitis B e antigen to antibody seroconversion. During a mean observation period of 8.2 +/- 3.8 years after seroconversion, all patients were asymptomatic; 36 had persistently normal alanine aminotransferase levels, and three had occasional mild alterations. Liver histology, checked in 21 patients, showed persistent hepatitis in nine, fibrosis in 10, and cirrhosis in two cases. HBV DNA was always undetectable by dot blot hybridization. Five children eventually cleared hepatitis B surface antigen, including one with cirrhosis who developed liver cancer at 19 years. HBV DNA was detected by polymerase chain reaction in 87% of children within 5 years of follow-up, in 58% of cases 6-10 years after seroconversion (p < 0.001), and in 50% of patients investigated later. Long-term viremia was found in two patients (40%) who cleared HBsAg, including the one who developed liver cancer. The chances of clearing viremia during follow-up were higher in children with acute hepatitis at the onset of illness (86%) than in those with asymptomatic onset (37%; p < 0.05). Our results show that low levels of HBV viremia, probably reflecting low levels of virus replication, persist for several years in children with chronic hepatitis B after hepatitis B e antigen to antibody seroconversion and remission of liver disease, even after the clearance of hepatitis B surface antigen. Persistent replication could support mild biochemical alterations and inflammatory liver lesions. It could allow late reactivation of liver disease and may play a role in the development of carcinoma.

401 TRANSPLACENTALLY INDUCED LIVER INJURY DUE TO LITHOCHOLATE: CANALICULAR Na, K-ACTIVATED ATPase AND MEMBRANE MICROVISCOSITY IN NEWBORNS

Administration of lithocholate (L) to pregnant rats has been shown to induce inflammatory lesions in liver of newborn offspring, progressing to intrahepatic biliary hypoplasia and chronic cholestasis (Gastroenterology 73:1214, 1977). The site of action and mechanism of L toxicity in utero was investigated in newborn rats delivered by dams maintained on standard chow (S) or S+2.5% L throughout pregnancy. Newborns were sacrificed at 1,2, and 5 days after birth, plasma collected, and liver removed for histological examination and isolation of canaliculi-enriched plasma membranes. Membrane Na, K-activated ATPase activity was assayed, and surface microviscosity (mV) determined by fluorescence polarization. Plasma L concentration was 2-3 μmol/L in treated, and was undetectable in untreated newborns. Hepatic changes in L-treated newborns were periportal inflammation, formation of pseudoducts and giant cells. ATPase activity in membranes from L-treated newborns was reduced by 40% compared with normals (2.58±0.30 vs 4.14±0.45 μmol P/hr/mg protein). Canalicular mV (in poises) was increased by 30% in L-treated newborns compared with normals (5.65±0.30 vs 3.99±0.18; p<0.01). Conclusion: Exposure to L in utero is associated with changes in canalicular membrane function and physical properties known to interfere with bile secretion, and may thus initiate a self-perpetuating cholestatic disorder after birth.