• Parasites, Hosts and Diseases
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• v.54 no.4
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• pp.519-525
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• 2016

To investigate the potential role of transforming growth factor (TGF)-${\beta}1$ in liver fibrosis during Echinococcus granulosus infection, 96 BALB/c mice were randomly divided into 2 groups, experimental group infected by intraperitoneal injection with a metacestode suspension and control group given sterile physiological saline. The liver and blood samples were collected at days 2, 8, 30, 90, 180, and 270 post infection (PI), and the expression of TGF-${\beta}1$ mRNA and protein was determined by real-time quantitative RT-PCR and ELISA, respectively. We also evaluated the pathological changes in the liver during the infection using hematoxylin and eosin (H-E) and Masson staining of the liver sections. Pathological analysis of H-E stained infected liver sections revealed liver cell edema, bile duct proliferation, and structural damages of the liver as evidenced by not clearly visible lobular architecture of the infected liver, degeneration of liver cell vacuoles, and infiltration of lymphocytes at late stages of infection. The liver tissue sections from control mice remained normal. Masson staining showed worsening of liver fibrosis at the end stages of the infection. The levels of TGF-${\beta}1$ did not show significant changes at the early stages of infection, but there were significant increases in the levels of TGF-${\beta}1$ at the middle and late stages of infection (P<0.05). RT-PCR results showed that, when compared with the control group, TGF-${\beta}1$ mRNA was low and comparable with that in control mice at the early stages of infection, and that it was significantly increased at day 30 PI and remained at high levels until day 270 PI (P<0.05). The results of this study suggested that increased expression of TGF-${\beta}1$ during E. granulosus infection may play a significant role in liver fibrosis associated with E. granulosus infection.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.9
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• pp.4953-4960
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• 2013

Primary liver cancer is one of the most common cancers at the global level, accounting for half of all cancers in some undeveloped countries. This disease tends to occur in livers damaged through alcohol abuse, or chronic infection with hepatitis B and C, on a background of cirrhosis. Various cancer-causing substances are associated with primary liver cancer, including certain pesticides and such chemicals as vinyl chloride and arsenic. The strong association between HBV infection and liver cancer is well documented in epidemiological studies. It is generally acknowledged that the virus is involved through long term chronic infection, frequently associated with cirrhosis, suggesting a nonspecific mechanism triggered by the immune response. Chronic inflammation of liver, continuous cell death, abnormal cell growth, would increase the occurrence rate of genetic alterations and risk of disease. However, the statistics indicated that only about one fifth of HBV carries would develop HCC in lifetime, suggesting that individual variation in genome would also influence the susceptibility of HCC. The goal of this review is to highlight present level of knowledge on the role of viral infection and genetic variation in the development of liver cancer.

• Journal of Veterinary Clinics
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• v.21 no.3
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• pp.243-247
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• 2004

This studies was carried out to investigate a process of formation for the granulomatous lesions in the liver and the haematological variation with the lapse of time after infection of Capillaria hepatica in dogs. Twelve crossbred puppies, about 3 months of age and 2-3 kg of body weight, were administered with 2,000 Capillaria hepatica infective eggs. Every four puppies was sacrificed on 1 week, 3 weeks and 5 weeks after infection, respectively. Although no marked clinical sign was noticed, total leukocyte values were increased peak on 1 week, and then reduced gradually on 3 weeks and 5 weeks after infection. Absolute differential counts of neutrophils and lymphocytes were significantly increased on 1, 3 and 5 weeks after infection. Absolute differential counts of monocytes and eosinophils were trend to increase during the experimental periods. On grossly findings, liver congestions were observed in all infected puppies, and a few white specks were scattered under liver capsule in one puppy on 3 weeks and two puppies on 5 weeks after infection. On microscopic findings, many fresh larvae were observed in the liver tissues in one puppy on 1 week after infection. A worm was decayed and only a portion of cuticle was shown in one puppy on 3 weeks after infection. Around the central necrotic material, the layers of thick macrophages with a few giant cells and lymphocytes with fibrous connective tissues were consisted the granulomatous lesions on 5 weeks after infection.

• Parasites, Hosts and Diseases
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• v.53 no.6
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• pp.777-783
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• 2015

The nitric oxide (NO) formation and intrinsic nitrosation may be involved in the possible mechanisms of liver fluke-associated carcinogenesis. We still do not know much about the responses of inducible NO synthase (iNOS) induced by Clonorchis sinensis infection. This study was conducted to explore the pathological lesions and iNOS expressions in the liver of mice with different infection intensity levels of C. sinensis. Extensive periductal inflammatory cell infiltration, bile duct hyperplasia, and fibrosis were commonly observed during the infection. The different pathological responses in liver tissues strongly correlated with the infection intensity of C. sinensis. Massive acute spotty necrosis occurred in the liver parenchyma after a severe infection. The iNOS activity in liver tissues increased, and iNOS-expressing cells with morphological differences were observed after a moderate or severe infection. The iNOS-expressing cells in liver tissues had multiple origins.

• Journal of Korean Neurosurgical Society
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• v.54 no.5
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• pp.441-443
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• 2013

Liver abscess following ventriculoperitoneal (VP) shunting occurs very rarely. We report an unusual case of multiple liver abscesses caused by Staphylococcus capitis in a 50-year-old compromised woman due to a complicating VP shunt infection. We reviewed the nine cases of VP shunt complications reported in the English literature, and speculated that the most likely pathogenetic mechanism in our case is an infected peritoneal tip that migrated to and penetrated the liver, which subsequently caused the formation of multiple liver abscesses. The patient was successfully treated with percutaneous aspiration, drainage of the abscesses, intravenous antibiotics, and shunt revision. Awareness and vigilance of the possibility of liver abscess formation caused by VP shunt infection will help establish an early accurate diagnosis and therapeutic strategy.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.16 no.4
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• pp.225-232
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• 2013

Children with abnormal liver function can often be seen in outpatient clinics or inpatients wards. Most of them have respiratory disease, or gastroenteritis by virus infection, accompanying fever. Occasionally, hepatitis by the viruses causing systemic infection may occur, and screening tests are required. In patients with jaundice, the tests for differential diagnosis and appropriate treatment are important. In the case of a child with hepatitis B virus infection vertically from a hepatitis B surface antigen positive mother, the importance of the recognition of immune clearance can't be overstressed, for the decision of time to begin treatment. Early diagnosis changes the fate of a child with Wilson disease. So, screening test for the disease should not be omitted. Non-alcoholic fatty liver disease, which is mainly discovered in obese children, is a new strong candidate triggering abnormal liver function. Muscular dystrophy is a representative disease mimicking liver dysfunction. Although muscular dystrophy is a progressive disorder, and early diagnosis can't change the fate of patients, it will be better to avoid parent's blame for delayed diagnosis.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.13 no.1
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• pp.43-47
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• 2013

Introduction: ALT/AST enzymes are present inside the cells. AST is found in cardiac and skeletal muscle and red blood cells but the ALT is checked mainly in the liver. In general, the rise of these two indicators shows liver damage. The usual measurements of these enzymes are used in liver function tests, but the levels of AST and ALT do not always reflect liver function. Method and Cases: 17 cases of liver dysfunction transiently were evaluated clinically, biochemically, and imaging study of sonogram in pediatric in-patients for 3 years. Result: Most common causes of transient liver dysfunction were infection, especially viral gastroenteritis, and bacterial infection interfering oral food intake. More often occurred in the children who have infant hyperbilirubinemia, positive history of mitochondrial dysfunction or hypoglycemia. Fasting study in one case of hypoglycemia patient showed reversible liver dysfunction during fasting over 20 hours fasting. Discussion: A significant increase in AST and ALT with normal bilirubin can be observed in clinically healthy people during blunt trauma, viral infection, severe pain, metabolic syndrome, fasting or accidental health screening.

• IMMUNE NETWORK
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• v.15 no.4
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• pp.191-198
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• 2015

Hepatitis B virus (HBV) is responsible for approximately 350 million chronic infections worldwide and is a leading cause of broad-spectrum liver diseases such as hepatitis, cirrhosis and liver cancer. Although it has been well established that adaptive immunity plays a critical role in viral clearance, the pathogenetic mechanisms that cause liver damage during acute and chronic HBV infection remain largely known. This review describes our current knowledge of the immune-mediated pathogenesis of HBV infection and the role of immune cells in the liver injury during hepatitis B.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.19 no.2
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• pp.83-95
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• 2016

Hepatitis C virus (HCV) infection is a major medical challenge affecting around 200 million people worldwide. The main site of HCV replication is the hepatocytes of the liver. HCV is a positive enveloped RNA virus from the flaviviridae family. Six major HCV genotypes are implicated in the human infection. In developed countries the children are infected mainly through vertical transmission during deliveries, while in developing countries it is still due to horizontal transmission from adults. Minimal nonspecific and brief symptoms are initially found in approximately 15% of children. Acute and chronic HCV infection is diagnosed through the recognition of HCV RNA. The main objective for treatment of chronic HCV is to convert detected HCV viremia to below the detection limit. Children with chronic HCV infection are usually asymptomatic and rarely develop severe liver damage. Therefore, the benefits from current therapies, pegylated-Interferon plus ribavirin, must be weighed against their adverse effects. This combined treatment offers a 50-90% chance of clearing HCV infection according to several studies and on different HCV genotype. Recent direct acting antiviral (DAA) drugs which are well established for adults have not yet been approved for children and young adults below 18 years. The most important field for the prevention of HCV infection in children would be the prevention of perinatal and parenteral transmission. There are areas of focus for new lines of research in pediatric HCV-related disease that can be addressed in the near future.

• Parasites, Hosts and Diseases
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• v.25 no.2
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• pp.110-122
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• 1987

The rabbits were infected with Clonorchis sinensis and were treated with praziquantel at the dose of $50{\;}mg/kg{\times}2회{\times}2$ days after 1,2,4,8 weeks and 7 months from the infection. Their livers were observed histopathologically 1, 4 and 12 weeks after treatment. The findings are summarized as below. 1. The changes of the liver in control rabbits were relatively mild until 2 weeks after infection. However, widening and thickening of bile ducts, proliferation of biliary epithelium and periductal fibrosis were moderate after 4 weeks from infection and those changes were severe after 8 weeks and 7 months. Goblet cell metaplasia was found after 8 weeks from infection. 2. The mild changes of 2-week infection group were completely recovered by 4 weeks after the treatment. In the groups of 4 or more weeks after infection, the changes of bile ducts became milder in the degree after the treatment, but were still found 12 weeks after the treatment. As the infection duration was passed, more severe changes were observed after the treatment. In this context, it is concluded that the liver changes of acute clonorchiasis in the early two weeks are reversible by treatment while chronic biliary epithelial changes are irreversible. Therefore, early treatment should be recommended as possible to minimize the remaining histopathological changes of liver in clonorchiasis.