Pub Date : 2017-04-22DOI: 10.4172/2167-0889.1000210
M. Usui, H. Wada, S. Mizuno, S. Isaji
Transient thrombocytopenia is a common phenomenon after living donor liver transplantation (LDLT), and severe thrombocytopenia after LDLT is associated with graft loss and poor patient outcomes. The various causes of thrombocytopenia include bone marrow hematopoiesis failure due to decreased thrombopoietin (TPO) production in the injured liver, platelet destruction associated with splenomegaly, and the activation and consumption of platelets due to various forms of thrombosis, including disseminated intravascular coagulation (DIC), thrombotic microangiopathy (TMA), and venous thromboembolism (VTE). The observation of biomarkers such as soluble platelet glycoprotein VI (sGPVI), TPO, von Willebrand factor (VWF), VWF propeptide (VWFpp), and disintegrin-like and metalloproteinase with thrombospondin type-1 motifs member 13 (ADAMTS13) is useful in the evaluation of the mechanisms of thrombocytopenia in patients who undergo LDLT. The presence of these biomarkers, including sGPVI, ADAMTS13, VWF and VWFpp, suggests that platelet activation occurs in the early phase of LDLT and that vascular endothelial cell injury occurs on postoperative days 7-14.
{"title":"Platelets Activation and Liver Transplantation","authors":"M. Usui, H. Wada, S. Mizuno, S. Isaji","doi":"10.4172/2167-0889.1000210","DOIUrl":"https://doi.org/10.4172/2167-0889.1000210","url":null,"abstract":"Transient thrombocytopenia is a common phenomenon after living donor liver transplantation (LDLT), and severe \u0000 thrombocytopenia after LDLT is associated with graft loss and poor patient outcomes. The various causes of \u0000 thrombocytopenia include bone marrow hematopoiesis failure due to decreased thrombopoietin (TPO) production in \u0000 the injured liver, platelet destruction associated with splenomegaly, and the activation and consumption of platelets \u0000 due to various forms of thrombosis, including disseminated intravascular coagulation (DIC), thrombotic \u0000 microangiopathy (TMA), and venous thromboembolism (VTE). \u0000The observation of biomarkers such as soluble platelet glycoprotein VI (sGPVI), TPO, von Willebrand factor \u0000 (VWF), VWF propeptide (VWFpp), and disintegrin-like and metalloproteinase with thrombospondin type-1 motifs \u0000 member 13 (ADAMTS13) is useful in the evaluation of the mechanisms of thrombocytopenia in patients who \u0000 undergo LDLT. The presence of these biomarkers, including sGPVI, ADAMTS13, VWF and VWFpp, suggests that \u0000 platelet activation occurs in the early phase of LDLT and that vascular endothelial cell injury occurs on postoperative \u0000 days 7-14.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"16 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2017-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78676318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-04-22DOI: 10.4172/2167-0889.1000211
Luis Vernaza
The Posterior Reversible Encephalopathy Syndrome (PRES) is a known clinical entity that presents as changes on neurological images (CT/MRI) with concomitant appearance of new onset neurological signs and symptoms. It complicates a diversity of diseases and the use of certain medication, mostly immunosuppressive, that should be taken into account when new clinical manifestations with neuroimaging changes appear on a immunosuppressed patient. Case report: We report a case of a Liver Transplant recipient patient with Tacrolimus as main immunosuppression, that develops new onset neurological focalization signs and diffuse atypical changes on imaging (CT and MRI/MRA) not according to her signs and symptoms, which improve once the calcineurin inhibitors are remove from her medication scheme. Conclusion: In any patient receiving calcineurin inhibitors the presence new onset changes on imaging and neurological manifestations, even if they are not the typical ones, imposes the ruling out of common infectious causes and the rotation of the immunosuppressive medication in expectance of improvement of the clinical picture, which support the diagnoses of PRES.
{"title":"Atypical Posterior Reversible Encephalopathy Syndrome Imaging on Liver Transplant Patients","authors":"Luis Vernaza","doi":"10.4172/2167-0889.1000211","DOIUrl":"https://doi.org/10.4172/2167-0889.1000211","url":null,"abstract":"The Posterior Reversible Encephalopathy Syndrome (PRES) is a known clinical entity that presents as changes on neurological images (CT/MRI) with concomitant appearance of new onset neurological signs and symptoms. It complicates a diversity of diseases and the use of certain medication, mostly immunosuppressive, that should be taken into account when new clinical manifestations with neuroimaging changes appear on a immunosuppressed patient. \u0000Case report: We report a case of a Liver Transplant recipient patient with Tacrolimus as main immunosuppression, that develops new onset neurological focalization signs and diffuse atypical changes on imaging (CT and MRI/MRA) not according to her signs and symptoms, which improve once the calcineurin inhibitors are remove from her medication scheme. \u0000Conclusion: In any patient receiving calcineurin inhibitors the presence new onset changes on imaging and neurological manifestations, even if they are not the typical ones, imposes the ruling out of common infectious causes and the rotation of the immunosuppressive medication in expectance of improvement of the clinical picture, which support the diagnoses of PRES.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"61 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2017-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85961964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-03-15DOI: 10.4172/2167-0889.1000209
D. Gonzalez, A. I. Blanco, Óscar Moreno Domínguez, Isabel Calvo Viñuelas
Introduction Nonalcoholic fatty liver disease (NAFLD) is common among morbid obese (MO) with estimated prevalence of 90%. Weight loss (WL) play a main role in its control. Objective To determine the evolution of NAFLD by means of validated fibrosis scores 12 months after bariatric surgery (BS) and measure its impact. Methods Retrospective observational study which enrolled MO who underwent BS at a University Hospital in Madrid, Spain during 2014 and 2015. Patients features were collected at baseline and compared at 12 months after BS. NAFLD fibrosis and FIB-4 scores were calculated. Results 50 patients (37 women, 74%), mean age 44 ± 12 years. At baseline, mean weight was 124.98 ± 19.88 kg, Body Mass Index (BMI) 45.74 ± 5.93 kg/m2, Basal Glycaemia (BG) 104 ± 25 mg/dL, glycated hemoglobin (HbA1c) 5.9 ± 0.8%, alanine aminotransferase (ALT) 27 (12-125) IU, aspartate aminotransferase (AST) 22 (11-126) IU, gamma glutamyl transpeptidase (GGT) 35 (7-216) IU, alkaline phosphatase (AP) 72 (17-159) IU. NAFLD fibrosis and FIB-4 scores were 1.859 (-1.755-4.631) and 0.72 (0.22-3.05), respectively. In the postoperative period, mean weight was 84.17 ± 15.93 kg, BMI 30.76 ± 4.52 kg/m2, BG 85 ± 12 mg/dL, HbA1c 5.3 ± 0.31%, ALT 20 (9-133) IU, AST 20 (11-80) IU, GGT 18 (6-237) IU, AP 75 (8-183) IU. NAFLD fibrosis and FIB-4 scores were 0.412 (-2.643- 4.661) and 0.78 (0.38-1.79), respectively. Mean WL was 40.75 ± 14.59 kg, mean percentage of excess WL after BS was 73.23 ± 20.79%, and mean percentage of excess BMI loss was 72.92 ± 19.36%. Weight, BMI, BG, HbA1c, ALT, GGT, total cholesterol and triglycerides significantly improved after BS, as well as type 2 diabetes, hypertension and dyslipidemia whose prevalence declined. NAFLD fibrosis score significantly decrease after BS, but FIB-4 did not. These two scores were strongly correlated between them. Conclusions BS is an effective intervention to control the progression of NAFLD evaluated through clinical parameters, analytical values and fibrosis scores, of which NAFLD score is better than FIB-4 index.
{"title":"Impact of Bariatric Surgery on Nonalcoholic Fatty Liver Disease Assessedthrough Validated Fibrosis Scores","authors":"D. Gonzalez, A. I. Blanco, Óscar Moreno Domínguez, Isabel Calvo Viñuelas","doi":"10.4172/2167-0889.1000209","DOIUrl":"https://doi.org/10.4172/2167-0889.1000209","url":null,"abstract":"Introduction Nonalcoholic fatty liver disease (NAFLD) is common among morbid obese (MO) with estimated prevalence of 90%. Weight loss (WL) play a main role in its control. Objective To determine the evolution of NAFLD by means of validated fibrosis scores 12 months after bariatric surgery (BS) and measure its impact. Methods Retrospective observational study which enrolled MO who underwent BS at a University Hospital in Madrid, Spain during 2014 and 2015. Patients features were collected at baseline and compared at 12 months after BS. NAFLD fibrosis and FIB-4 scores were calculated. Results 50 patients (37 women, 74%), mean age 44 ± 12 years. At baseline, mean weight was 124.98 ± 19.88 kg, Body Mass Index (BMI) 45.74 ± 5.93 kg/m2, Basal Glycaemia (BG) 104 ± 25 mg/dL, glycated hemoglobin (HbA1c) 5.9 ± 0.8%, alanine aminotransferase (ALT) 27 (12-125) IU, aspartate aminotransferase (AST) 22 (11-126) IU, gamma glutamyl transpeptidase (GGT) 35 (7-216) IU, alkaline phosphatase (AP) 72 (17-159) IU. NAFLD fibrosis and FIB-4 scores were 1.859 (-1.755-4.631) and 0.72 (0.22-3.05), respectively. In the postoperative period, mean weight was 84.17 ± 15.93 kg, BMI 30.76 ± 4.52 kg/m2, BG 85 ± 12 mg/dL, HbA1c 5.3 ± 0.31%, ALT 20 (9-133) IU, AST 20 (11-80) IU, GGT 18 (6-237) IU, AP 75 (8-183) IU. NAFLD fibrosis and FIB-4 scores were 0.412 (-2.643- 4.661) and 0.78 (0.38-1.79), respectively. Mean WL was 40.75 ± 14.59 kg, mean percentage of excess WL after BS was 73.23 ± 20.79%, and mean percentage of excess BMI loss was 72.92 ± 19.36%. Weight, BMI, BG, HbA1c, ALT, GGT, total cholesterol and triglycerides significantly improved after BS, as well as type 2 diabetes, hypertension and dyslipidemia whose prevalence declined. NAFLD fibrosis score significantly decrease after BS, but FIB-4 did not. These two scores were strongly correlated between them. Conclusions BS is an effective intervention to control the progression of NAFLD evaluated through clinical parameters, analytical values and fibrosis scores, of which NAFLD score is better than FIB-4 index.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"2021 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79205242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-28DOI: 10.4172/2167-0889.1000208
Y. Al-Azzawi, Y. Al-Abboodi, Matthew Fasullo, Joan Kheder
There is an ongoing increment in the incidence of Portal venous thrombosis. Many factors play a role in the pathogenesis of the PVT. In this study, commorbities including cirrhosis, chronic viral hepatitis B and C, alcoholicinduced cirrhosis, acquired immune deficiency syndrome (AIDs), hypertension (HTN), chronic lung diseases, diabetes mellitus (DM) and obesity were examined to see their predictability of developing PVT. Portal venous thrombosis (PVT) is a complete or partial occlusion of the portal vein. The most common etiology behind the development of PVT includes but limited to inherited hyper-coagulopathy disorders, cirrhosis, hepatocellular carcinoma, abdominal infection or inflammation. In this study, comorbidities including liver cirrhosis in general, Hepatitis B, C and alcoholic cirrhosis, AIDs, HTN, DM, obesity were examined to see their predictability of developing PVT. Approximately 4408 patients with portal venous thrombosis and randomly selected 4231 without portal venous thrombosis were identified for the study. After controlling for age, sex and race, People with liver cirrhosis are about 8 times more likely to have portal venous thrombosis than non liver cirrhosis group. We conclude that among cancers, Hepatocelluar carcinoma patients have the highest chance of developing PVT while people with lung cancer and prostate have almost the same risk of non cancer patient for developing PVT.
{"title":"Risk Factors Stratifications for Portal Venous Thrombosis (PVT)","authors":"Y. Al-Azzawi, Y. Al-Abboodi, Matthew Fasullo, Joan Kheder","doi":"10.4172/2167-0889.1000208","DOIUrl":"https://doi.org/10.4172/2167-0889.1000208","url":null,"abstract":"There is an ongoing increment in the incidence of Portal venous thrombosis. Many factors play a role in the pathogenesis of the PVT. In this study, commorbities including cirrhosis, chronic viral hepatitis B and C, alcoholicinduced cirrhosis, acquired immune deficiency syndrome (AIDs), hypertension (HTN), chronic lung diseases, diabetes mellitus (DM) and obesity were examined to see their predictability of developing PVT. \u0000Portal venous thrombosis (PVT) is a complete or partial occlusion of the portal vein. The most common etiology behind the development of PVT includes but limited to inherited hyper-coagulopathy disorders, cirrhosis, hepatocellular carcinoma, abdominal infection or inflammation. In this study, comorbidities including liver cirrhosis in general, Hepatitis B, C and alcoholic cirrhosis, AIDs, HTN, DM, obesity were examined to see their predictability of developing PVT. Approximately 4408 patients with portal venous thrombosis and randomly selected 4231 without portal venous thrombosis were identified for the study. After controlling for age, sex and race, People with liver cirrhosis are about 8 times more likely to have portal venous thrombosis than non liver cirrhosis group. We conclude that among cancers, Hepatocelluar carcinoma patients have the highest chance of developing PVT while people with lung cancer and prostate have almost the same risk of non cancer patient for developing PVT.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"34 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2017-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75172958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-09DOI: 10.4172/2167-0889.1000207
Y. Al-Azzawi, S. Mehta
The incidence of seeding/implantation of hepatocellular carcinoma (HCC) after liver biopsy or radio frequency ablation (RFA) is not well reported but estimated to be low. With the introduction of immunosuppression the risk has been increased and most of the seeding sites are chest wall and abdominal muscles. We report the first case report of HCC seeding after 9 years from the original liver biopsy. A 66 years old gentleman with cirrhosis secondary to hepatitis C virus infection and long history of alcohol abuse found to have a liver lesion during his screening by ultrasound and underwent percutaneous liver biopsy, which revealed hepatocellular carcinoma in 2006 and then the patient had a liver transplantation surgery in 2006 from cardiac death donor. The post transplantation course was uneventful and started on dual immunosuppression including Tacrolimus and Mycophenolate mofetil with acceptable levels through the whole treatment duration. All the follow up routine check ups including CT scan, liver biopsy, liver function tests and cancer screening were unremarkable and alphafetoprotein (AFP) was within acceptable level except slight increase in the AFP early 2015. His increase in AFP raised the concern for recurrence of HCC and his work up for possible recurrence or metastasis was negative including CT scan of the chest, abdomen and pelvis. Later in the 2015, the patient presented to his primary care physician complaining of right upper quadrant pain and swelling for which he underwent excisional biopsy of the skin. The skin nodule been fully resected and was 1.5 cm in diameter and its 10-15 cm from the original HCC. The pathology results of the specimen revealed that its metastatic hepatocellular carcinoma involving the subcutaneous tissue with negative margins, the immunostains were positive for Heppar1 immunestains and equivocal for glypican 3. This represents a local seeding of the original HCC 9 years after the liver biopsy location. This finding also was confirmed upon reviewing the images of the original HCC and the new metastatic HCC that showed it has same track of the liver biopsy in 2006. This case report is to increase the awareness of hepatologist and primary care physicians of the risk of skin HCC implantation and consider a routine check during the clinic visits in addition to the dermatologist skin screening visits. More research needed to investigate the rule of immunosuppression on seeding and implantation of HCC.
{"title":"A Confusing Complication of Liver Biopsy: First Case Report of Seeding/ Implantation of Hepatocellular Carcinoma 9 Years from the Original Liver Biopsy","authors":"Y. Al-Azzawi, S. Mehta","doi":"10.4172/2167-0889.1000207","DOIUrl":"https://doi.org/10.4172/2167-0889.1000207","url":null,"abstract":"The incidence of seeding/implantation of hepatocellular carcinoma (HCC) after liver biopsy or radio frequency ablation (RFA) is not well reported but estimated to be low. With the introduction of immunosuppression the risk has been increased and most of the seeding sites are chest wall and abdominal muscles. We report the first case report of HCC seeding after 9 years from the original liver biopsy. A 66 years old gentleman with cirrhosis secondary to hepatitis C virus infection and long history of alcohol abuse found to have a liver lesion during his screening by ultrasound and underwent percutaneous liver biopsy, which revealed hepatocellular carcinoma in 2006 and then the patient had a liver transplantation surgery in 2006 from cardiac death donor. The post transplantation course was uneventful and started on dual immunosuppression including Tacrolimus and Mycophenolate mofetil with acceptable levels through the whole treatment duration. All the follow up routine check ups including CT scan, liver biopsy, liver function tests and cancer screening were unremarkable and alphafetoprotein (AFP) was within acceptable level except slight increase in the AFP early 2015. His increase in AFP raised the concern for recurrence of HCC and his work up for possible recurrence or metastasis was negative including CT scan of the chest, abdomen and pelvis. Later in the 2015, the patient presented to his primary care physician complaining of right upper quadrant pain and swelling for which he underwent excisional biopsy of the skin. The skin nodule been fully resected and was 1.5 cm in diameter and its 10-15 cm from the original HCC. The pathology results of the specimen revealed that its metastatic hepatocellular carcinoma involving the subcutaneous tissue with negative margins, the immunostains were positive for Heppar1 immunestains and equivocal for glypican 3. This represents a local seeding of the original HCC 9 years after the liver biopsy location. This finding also was confirmed upon reviewing the images of the original HCC and the new metastatic HCC that showed it has same track of the liver biopsy in 2006. This case report is to increase the awareness of hepatologist and primary care physicians of the risk of skin HCC implantation and consider a routine check during the clinic visits in addition to the dermatologist skin screening visits. More research needed to investigate the rule of immunosuppression on seeding and implantation of HCC.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"1 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2017-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86830228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-01DOI: 10.4172/2167-0889.1000212
Satoshi Kotani, Shuichi Sato, N. Kohge, K. Tsukano, Sayaka Ogawa, S. Yamanouchi, R. Kusunoki, Masahito Aimi, Youichi Miyaoka, Hirofumi Fujishiro, Tomohiko Yamamoto, H. Ohnuma
Objective: Liver stiffness measurements using shear wave elastography (SWE) for the non-invasive evaluation of liver fibrosis have been developed in the last few years. However, the usefulness of SWE has not been fully investigated. We aimed to evaluate the diagnostic accuracy of SWE for the assessment of liver fibrosis in patients with liver disease. Methods: A total of 54 consecutive patients who underwent SWE measurement and liver biopsy were included. Receiver-operator characteristic (ROC) curves were constructed to calculate the area under the ROC curve (AUC) for F0-2 versus F3-4 and F0-3 versus F4. Results: Fibrosis scores estimated by SWE were F0 for 9 cases, F1 for 18 cases, F2 for 11 cases, F3 for 9 cases, and F4 for 7 cases. The median shear wave velocity in each type of fibrosis was 1.77 m/s in F0, 1.81 m/s in F1, 1.88 m/s in F2, 2.39 m/s in F3, and 3.11 m/s in F4. AUCs for severe fibrosis (F3 and F4) and cirrhosis (F4) were 0.931 (P<0.001) and 0.916 (P<0.001), respectively. Shear wave velocity correlated significantly with liver fibrosis obtained by liver biopsy (r=0.679, P<0.001). Conclusion: SWE is a useful and non-invasive technology to estimate liver fibrosis in liver disease regardless of etiology.
{"title":"The Accuracy of a Non-Invasive Liver Fibrosis Evaluation Method, Shear WaveElastography: A Retrospective Pilot Study","authors":"Satoshi Kotani, Shuichi Sato, N. Kohge, K. Tsukano, Sayaka Ogawa, S. Yamanouchi, R. Kusunoki, Masahito Aimi, Youichi Miyaoka, Hirofumi Fujishiro, Tomohiko Yamamoto, H. Ohnuma","doi":"10.4172/2167-0889.1000212","DOIUrl":"https://doi.org/10.4172/2167-0889.1000212","url":null,"abstract":"Objective: Liver stiffness measurements using shear wave elastography (SWE) for the non-invasive evaluation of liver fibrosis have been developed in the last few years. However, the usefulness of SWE has not been fully investigated. We aimed to evaluate the diagnostic accuracy of SWE for the assessment of liver fibrosis in patients with liver disease. Methods: A total of 54 consecutive patients who underwent SWE measurement and liver biopsy were included. Receiver-operator characteristic (ROC) curves were constructed to calculate the area under the ROC curve (AUC) for F0-2 versus F3-4 and F0-3 versus F4. Results: Fibrosis scores estimated by SWE were F0 for 9 cases, F1 for 18 cases, F2 for 11 cases, F3 for 9 cases, and F4 for 7 cases. The median shear wave velocity in each type of fibrosis was 1.77 m/s in F0, 1.81 m/s in F1, 1.88 m/s in F2, 2.39 m/s in F3, and 3.11 m/s in F4. AUCs for severe fibrosis (F3 and F4) and cirrhosis (F4) were 0.931 (P<0.001) and 0.916 (P<0.001), respectively. Shear wave velocity correlated significantly with liver fibrosis obtained by liver biopsy (r=0.679, P<0.001). Conclusion: SWE is a useful and non-invasive technology to estimate liver fibrosis in liver disease regardless of etiology.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"65 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74469136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-01DOI: 10.4172/2167-0889.1000205
H. Makun, M. Mwanza, H. Iheanacho, D. Apeh, S. K. Abdulrahim, S. Jamiu, O. Shamsudin, Chiamaka Njeakor, Y. Mohammed
Liver as an organ of metabolism is disposed to toxins deposition and Livestock liver contributes to food security as major source of protein. Aflatoxin M1 (AFM1) is a carcinogenous metabolite aflatoxin B1 resulting from hydroxylation. To elucidate aflatoxin M1 incidence and levels in livestock livers from Minna-Nigeria, 24 hours fresh liver samples (n=122; 72 cow livers and 50 goat livers) were collected from five abattoirs and subjected to standard aflatoxin extractions via column chromatography and quantification by high performance liquid chromatography. Data showed the presence of AFM1 in some livestock livers. However, detected toxin levels in mean percentages and correlation of variation amongst the individual livestock livers was evident, with a 83.3% (60/72) incidence and a mean detection level of 1.464 μg/kg in cattle livers, as compared to 58.0% (29/50) incidence and a mean of 0.425 μg/kg in goats livers. Contamination in some samples; 52% (26/50) of goat liver and 62.5% (45/72) cow liver exceeded the EU, US and FDA limit of 0.05 μg/kg, indicating human exposure to animal liver with high level aflatoxin contamination. Therefore, there is a need to limit the exposure to aflatoxin by enforcing regulatory limits on animal feed.
{"title":"Comparative Study of Aflatoxin M1 in Livestock Livers from Minna, Nigeria","authors":"H. Makun, M. Mwanza, H. Iheanacho, D. Apeh, S. K. Abdulrahim, S. Jamiu, O. Shamsudin, Chiamaka Njeakor, Y. Mohammed","doi":"10.4172/2167-0889.1000205","DOIUrl":"https://doi.org/10.4172/2167-0889.1000205","url":null,"abstract":"Liver as an organ of metabolism is disposed to toxins deposition and Livestock liver contributes to food security as major source of protein. Aflatoxin M1 (AFM1) is a carcinogenous metabolite aflatoxin B1 resulting from hydroxylation. To elucidate aflatoxin M1 incidence and levels in livestock livers from Minna-Nigeria, 24 hours fresh liver samples (n=122; 72 cow livers and 50 goat livers) were collected from five abattoirs and subjected to standard aflatoxin extractions via column chromatography and quantification by high performance liquid chromatography. Data showed the presence of AFM1 in some livestock livers. However, detected toxin levels in mean percentages and correlation of variation amongst the individual livestock livers was evident, with a 83.3% (60/72) incidence and a mean detection level of 1.464 μg/kg in cattle livers, as compared to 58.0% (29/50) incidence and a mean of 0.425 μg/kg in goats livers. Contamination in some samples; 52% (26/50) of goat liver and 62.5% (45/72) cow liver exceeded the EU, US and FDA limit of 0.05 μg/kg, indicating human exposure to animal liver with high level aflatoxin contamination. Therefore, there is a need to limit the exposure to aflatoxin by enforcing regulatory limits on animal feed.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"25 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75180471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-01DOI: 10.4172/2167-0889.1000219
R. Niranjan, D. Paneer, Purushothaman Jumbulingam
Dengue fever (dengue hemorrhagic fever or dengue shock syndrome) is a virus infection and comes under one of the major vector-borne diseases [1,2]. Dengue infection has now become the global health threat [2]. High fever, chills, rash and strong headache are the more common clinical features of this disease [3,4]. In addition to these symptoms, some special clinical manifestations appear in response to severe dengue cases where viremia is high [5]. Liver dysfunction is one of the atypical forms of clinical manifestation in the dengue infection [3]. The clinical feature of hepatic dysfunctions in dengue patients are increased liver size and elevated levels of liver enzymes mainly transaminases [4,6]. The increase in size of gallbladder was also observed as early clinical manifestations in dengue patients [7]. Around 46% of dengue infected patients from Indonesia were diagnosed to have enlarged liver size. [8]. The other atypical clinical symptoms of dengue were nausea and abdominal pain [9]. Some dengue patients also manifest jaundice and hyperbilirubinemia [4,10]. However, the number of patients is still very less having liver dysfunction with dengue infections [3]. A wide number of reports have suggested the role of immune cells and mediators of inflammation in the liver dysfunctions however, the exact mechanism is still not clear [11-13]. In this article, we discuss some facts and role of immune components involved in the dysfunctions of liver in dengue fever [14].
{"title":"Liver Dysfunctions in Dengue Infection: An Update on its Pathogenesis","authors":"R. Niranjan, D. Paneer, Purushothaman Jumbulingam","doi":"10.4172/2167-0889.1000219","DOIUrl":"https://doi.org/10.4172/2167-0889.1000219","url":null,"abstract":"Dengue fever (dengue hemorrhagic fever or dengue shock syndrome) is a virus infection and comes under one of the major vector-borne diseases [1,2]. Dengue infection has now become the global health threat [2]. High fever, chills, rash and strong headache are the more common clinical features of this disease [3,4]. In addition to these symptoms, some special clinical manifestations appear in response to severe dengue cases where viremia is high [5]. Liver dysfunction is one of the atypical forms of clinical manifestation in the dengue infection [3]. The clinical feature of hepatic dysfunctions in dengue patients are increased liver size and elevated levels of liver enzymes mainly transaminases [4,6]. The increase in size of gallbladder was also observed as early clinical manifestations in dengue patients [7]. Around 46% of dengue infected patients from Indonesia were diagnosed to have enlarged liver size. [8]. The other atypical clinical symptoms of dengue were nausea and abdominal pain [9]. Some dengue patients also manifest jaundice and hyperbilirubinemia [4,10]. However, the number of patients is still very less having liver dysfunction with dengue infections [3]. A wide number of reports have suggested the role of immune cells and mediators of inflammation in the liver dysfunctions however, the exact mechanism is still not clear [11-13]. In this article, we discuss some facts and role of immune components involved in the dysfunctions of liver in dengue fever [14].","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"18 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84218799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-01DOI: 10.4172/2167-0889.1000206
I. Shah
Chronic Hepatitis B virus (HBV) infection is a major cause of liver disease leading to cirrhosis and hepatocellular carcinoma. Children are more likely to develop chronic HBV infection. Treatment with Interferon alfa (IFN-α), lamivudine (3TC) or adefovir are recommended in children with chronic active HBV with replicating virus. We present a series of 7 patients treated with combination IFN-α (5-10 million units/m² subcutaneously thrice a week)+3TC (4 mg/kg/day, not exceeding 100 mg/day) for 6 months and additional 3TC for 6 months alone). Of the 7 patients, one patient had complete response and viral load remained suppressed even after 2 years of therapy and remaining 6 patients had partial response (viral load became undetectable, but ‘e’ antigen remained positive). Thus we concluded that the antiviral treatment in children while effective remains partial as the reappearance of HBV DNA at variable time after stopping therapy can still occur.
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