Chronic Alcoholism Decreases Polyunsaturated Fatty Acid Levels in Human Plasma, Erythrocytes, and Platelets – Influence of Chronic Liver Disease

1997 ◽  
Vol 78 (02) ◽  
pp. 808-812 ◽  
Author(s):  
María-Luisa Pita ◽  
José-María Rubio ◽  
María-Luisa Murillo ◽  
Olimpia Carreras ◽  
Mariá-José Delgado

SummaryThe effect of chronic ethanol ingestion on fatty acid composition of plasma, erythrocyte and platelet phospholipids and on plasma 6-keto-PGF1α was studied. Two groups of alcoholic subjects, one of them with chronic liver disease, were studied and compared to a control group of healthy subjects. Linoleic acid was not affected by alcoholism but its larger metabolites arachidonic acid (20:4n6) and docosatetraenoic acid (22: 4n6) tended to be lower in erythrocytes and platelets of both groups of alcoholic patients; the decrease was more marked in the presence of chronic liver disease. Docosahexaenoic acid (22:6n3) was markedly decreased in plasma, erythrocytes and platelets obtained from alcoholic patients with chronic liver disease. Plasma levels of 6-keto-PGF1α, a metabolite of prostacyclin (PGI2), remained unchanged. We conclude that chronic ethanol ingestion induces important changes in long-chain polyunsaturated fatty acids, mainly in platelets, and that these changes are exacerbated when patients suffer from chronic liver disease.

2021 ◽  
Vol 17 (2) ◽  
pp. 174-179
Author(s):  
Muhammad Javaid Iqbal ◽  
Muhammad Usman ◽  
Mubarak Ali Anjum ◽  
Yasir Yaqoob ◽  
Ghulam Mujtaba Nasir ◽  
...  

Objective: To evaluate the role of Immature platelet fraction in patients with chronic liver disease, a marker for evaluating cirrhotic changes. Methodology: This case control study was conducted at department of Pathology, Aziz Fatima Medical and Dental College, Faisalabad, over a period of Seven months from June 2020 to January 2021. A total of 126 participants were included in the study consisting of 63 patients with chronic liver disease in group A and 63 participants without any known disease in group B as control. The IPF master program in combination with XE-2100 multiparameter automatic hematology analyzer was used to measure the immature platelet fraction. Ethylene diamine tetraacetic acid was used to collect the blood sample for IPF measurement and was maintained till analysis on room temperature. Ten repeated analyses, immediately and after 24 hours were done for reproducibility of IPF%. Results: The mean age of liver disease patients was 52.35 ± 13.64 years and in control group the mean age was 51.62 ± 11.27 years. There was no significant (p-value > 0.05) difference between both groups based on age and gender. The hemoglobin level and red cell count was found to be significantly (p-value < 0.05) reduced in cases group. While white blood cells count was comparable in both groups. The mean platelet count was significantly (p-value < 0.05) less in cases group (163.5 ± 90.4 vs 233.4 ± 54.5 (x10*3/µl). The mean value of immature platelet fraction (IPF%) was significantly (p-value < 0.05) raised in cases group (5.62 ± 2.92 vs 3.06 ± 1.87). The multivariate discriminant analysis (MDA) score showed a significant (p-value < 0.05) association with chronic hepatis as compared to other liver related diseases. Conclusions: In chronic liver disease patients, there is an inverse relationship between platelet count and IPF% with decreased platelet count and increased IPF%. The proposed MDA function can be used to identify the cirrhotic changes in liver disease patients.


Children ◽  
2021 ◽  
Vol 8 (8) ◽  
pp. 675
Author(s):  
Tobias Laue ◽  
Zeynep Demir ◽  
Dominique Debray ◽  
Mara Cananzi ◽  
Paola Gaio ◽  
...  

Infection is a serious concern in the short and long term after pediatric liver transplantation. Vaccination represents an easy and cheap opportunity to reduce morbidity and mortality due to vaccine-preventable infection. This retrospective, observational, multi-center study examines the immunization status in pediatric liver transplant candidates at the time of transplantation and compares it to a control group of children with acute liver disease. Findings show only 80% were vaccinated age-appropriately, defined as having received the recommended number of vaccination doses for their age prior to transplantation; for DTP-PV-Hib, less than 75% for Hepatitis B and two-thirds for pneumococcal conjugate vaccine in children with chronic liver disease. Vaccination coverage for live vaccines is better compared to the acute control group with 81% versus 62% for measles, mumps and rubella (p = 0.003) and 65% versus 55% for varicella (p = 0.171). Nevertheless, a country-specific comparison with national reference data suggests a lower vaccination coverage in children with chronic liver disease. Our study reveals an under-vaccination in this high-risk group prior to transplantation and underlines the need to improve vaccination.


2020 ◽  
Vol 21 (10) ◽  
pp. 3558
Author(s):  
Asad Mehmood Raja ◽  
Ester Ciociola ◽  
Imran Nazir Ahmad ◽  
Faisal Saud Dar ◽  
Syed Muhammad Saqlan Naqvi ◽  
...  

Chronic liver disease, with viral or non-viral etiology, is endemic in many countries and is a growing burden in Asia. Among the Asian countries, Pakistan has the highest prevalence of chronic liver disease. Despite this, the genetic susceptibility to chronic liver disease in this country has not been investigated. We performed a comprehensive analysis of the most robustly associated common genetic variants influencing chronic liver disease in a cohort of individuals from Pakistan. A total of 587 subjects with chronic liver disease and 68 healthy control individuals were genotyped for the HSD17B13 rs7261356, MBOAT7 rs641738, GCKR rs1260326, PNPLA3 rs738409, TM6SF2 rs58542926 and PPP1R3B rs4841132 variants. The variants distribution between case and control group and their association with chronic liver disease were tested by chi-square and binary logistic analysis, respectively. We report for the first time that HSD17B13 variant results in a 50% reduced risk for chronic liver disease; while MBOAT7; GCKR and PNPLA3 variants increase this risk by more than 35% in Pakistani individuals. Our genetic analysis extends the protective role of the HSD17B13 variant against chronic liver disease and disease risk conferred by the MBOAT7; GCKR and PNPLA3 variants in the Pakistani population.


1970 ◽  
Vol 5 (2) ◽  
pp. 175-176
Author(s):  
T. Sakamaki ◽  
Y. Sawada ◽  
A. Yoshioka

Healthcare ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 550
Author(s):  
Liliana Vecerzan ◽  
Ariela Olteanu ◽  
Ionela Maniu ◽  
Adrian Boicean ◽  
Călin Remus Cipăian ◽  
...  

The knowledge about coagulation disorders in patients with chronic liver disease changed in the last decade. The aim of this study was to analyze the parameters of thrombin generation in patients with chronic liver disease, as they are the most appropriate biomarkers to explore coagulation. (1) Background: The knowledge about coagulation disorders in patients with chronic liver disease changed in the last decade. The study of thrombin generation in patients with chronic liver disease provides a much more accurate assessment of the coagulation cascade; (2) Methods: This study is a prospective observational pilot study on hospitalized patients with chronic liver diseases that analyzed thrombin generation performed from their platelet-poor plasma versus that of control subjects. We analyzed a group of 59 patients with chronic liver disease and 62 control subjects; (3) Results: Thrombin generation was lower in hepatitis and cirrhosis patients compared to controls and decreases as the disease progressed. Lag time was higher in ethanolic etiology compared to the control group. Peak thrombin and endogenous thrombin potential were shorter in all etiologies when compared to the control group. The velocity index was significantly lower in HCV hepatopathies, ethanolic, and mixed etiology when compared with normal individuals; (4) Conclusions: Given the variability of thrombin generation in patients with chronic liver disease, its assay could serve to identify patients with high thrombotic and hemorrhagic risk and establish personalized conduct toward them.


1986 ◽  
Vol 3 (1) ◽  
pp. 104-110 ◽  
Author(s):  
M. Merli ◽  
S. Iapichino ◽  
A. Bolognese ◽  
A. Bruni ◽  
A. Cantafora ◽  
...  

2019 ◽  
Vol 8 (2) ◽  
pp. 15-20
Author(s):  
Rishab Shrestha ◽  
Alisha Rajbhandari ◽  
Pradip Chaudhary ◽  
Kausal Sigdel

Background: Alcohol is widely consumed socially accepted recreational beverage, that is toxic and affects directly or indirectly almost every organ. Spectrum of alcoholic liver disease ranges from fatty liver to cirrhosis. One of the complications of the later spectrum is portal hypertension, around 50% develops varices and bleeding depends on the size of the varices. Predicting varices without endoscopic is difficult but few non-invasive parameters are available. Materials and Methods: It was a prospective cross-sectional study done in Nobel Medical College Teaching Hospital, Biratnagar, Nepal from September 2018 to August 2019. Approval was acquired from Institutional Review Committee. Patients with chronic ethanol ingestion and features suggestive of chronic liver disease clinically and investigation wise were enrolled in the study. History, physical examinations along with platelet count, prothrombin time was taken and ultrasonography abdomen and upper gastrointestinal endoscopy was done to see the splenic diameter, and varices. Results: Esophageal varices were present in 53%. Mean platelet count with variceswas 122566 ± 36024.8 /mm3, splenic diameter was 133.1 ± 21.3 mm, prothrombintime (PT) time was 19.3 ± 5.0 sec andratio of platelet per spleen diameter was 930.2 ± 259.4 /mm3/mm.Platelet count < 163500/mm3 has sensitivity and specificity 83.0% and 83.0% respectively. Ratio of platelet per splenic diameter ratio cutoff 1293.7 has 88.7% sensitivity and 85.1% specificity for predicting varices. Conclusion: In chronic alcoholic liver disease patients low platelet count, increased splenicdiameter, low platelet per splenic diameter ratio are useful in predicting presence of esophageal varices.


2020 ◽  
Author(s):  
SeyedAli Jafari ◽  
Aramesh Rezaeian ◽  
Zahra Nomjuo ◽  
Majid Ghayour-Mobarhan ◽  
Zahra ghaneifar

Abstract Background: Liver disease leads to complex pathophysiological injuries that affect digestion, absorption, distribution, storage and use of food. The effect that chronic liver disease has on the nutritional status and health of the child is determined by the cause and severity of liver disease and the age of onset of liver disease. As liver disease progresses, so do the symptoms and complications of the disease. The aim of this study was to determine the effect of specific nutrition adjustment program on specific liver findings in children with chronic liver disease.Methods: In this clinical trial study, 75 children with chronic liver disease were randomly divided into two groups (45 in the intervention group and 30 in the control group). At the beginning of the study, the necessary experiments were taken from two groups. The intervention group received a nutritional adjustment program during 6 sessions of the workshop. After 12 weeks of follow-up, bilirubin level (total, direct), albumin level, PT, INR, transaminases (AST, ALT) were measured in both groups. Data analysis was performed using SPSS software version 16 and Wilcoxon and Mann-Whitney tests.Results: At the beginning of the study, both groups were homogeneous in terms of demographic variables. In the post-intervention stage compared to the pre-intervention stage in the intervention group, the mean scores of prothrombin time (P = 0/040), albumin (P = 0/007), aspartate transaminase and alanine transaminase (p˂0/001)were statistically significant:. But the mean score of total bilirubin (P = 0/063) in the post-intervention stage compared to before the intervention in the intervention group was not statistically significant.Conclusion: Nutrition education and encouragement of patients with chronic liver disease to follow a special diet can be an important factor in feeling healthy and preventing the progression of the disease.Trial registration: Name of registry: Zahra NamjouIRCT registration number: IRCT2015091424019N1 Registration date: 2016-01-30 Registration timing: retrospective


2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e15033-e15033
Author(s):  
Hasmukh J. Prajapati ◽  
James R. Spivey ◽  
Bassel F. El-Rayes ◽  
John S. Kauh ◽  
Hyun Sik Kim

e15033 Background: To investigate the prognostic factors (PFs) associated with survival after DEB TACE in patients (pts) with at least > 5cm sized index HCC (iHCC). Methods: Consecutive pts with at least > 5cm sized iHCC, who received DEB TACE over last 82 months, were studied. Median overall survivals (mOSs) were analyzed according to different parameters from 1st DEB TACE. Kaplan Meier estimator by log rank test and Cox proportional Hazard model (for MVA) were used survival analyses using v20 SPSS. Results: 332 DEB TACEs (mean 3, medium 2) were performed in 112 pts (mean 62.1 years, SD 12), who had at least >5cm sized iHCC (mean 9.5 cm, SD 3.7). MOS from diagnosis and DEB TACE were 14.3 months (m) and 9.4 m respectively. MOS were 31.9 m, 11.1 m and 2.8 m in pts who received > 4, 2-4 and a 1 DEB TACEs respectively (p<0.001). Etiological factors for HCC were hepatitis C virus (54.4%), hepatitis B virus (12.5%), chronic alcoholism (7.1%), other causes of chronic liver disease (17%) and unknown with no chronic liver disease (9%); mOS were 8.8 m, 4.4 m, 5.8 m, 27 m, and 9.4 m respectively (p=0.01). MOS in pts with Child-Pugh Class A (58.9%), B (34.8%) and C (6.3%) were 17.2 m, 5.8 m and 1.6 m respectively (p<0.001). MOS in pts with BCLC stage B (17%), C (69.6%) and D (13.4%) were 20.9 m, 9.4 m, and 3.4 m respectively (p=0.003). 46.4% of pts had portal vein thrombosis (PVT) with mOS of 5.4 m vs. 17.1m in pts without PVT (p=0.006). Pts with serum alfa feto protein (sAFP) level>400 ng/dl (43.7%) had mOS of 5.4 m vs. 16.6 m in pts with sAFP<400ng/dl (p=0.008). 32.1% of pts received sorafenib systemic chemotherapy; mOS were 13.3m vs. 7.6m who did not receive the sorafenib (p=0.2). Pts with >5 HCCs (20.5%) had mOS of 5.4m vs. 13m in pts who had <5 HCCs (p=0.009). The following variables were independent significant PFs of survival on MVA: Child-Pugh class, etiology, number (no) of DEB TACEs, presence of vascular invasion and ECOG PS. Conclusions: Higher number of DEB TACE treatments correlates independently to improved OS in patients with at least >5cm sized index HCC. Other independent PFs of survival were etiology, Child-Pugh class, no of HCC tumors, ECOG PS and PVT.


2016 ◽  
Vol 23 (1) ◽  
pp. 72-77 ◽  
Author(s):  
Aida Saray ◽  
Rusmir Mesihovic ◽  
Nenad Vanis ◽  
Mehmedović Amila

There is accumulating evidence that the coagulation system is involved in the process of fibrogenesis in chronic liver disease. Recent studies postulated a possible connection between plasmatic hypercoagulability and progression of fibrosis. The aim of the study was to investigate disorders of the coagulation system in patients with chronic hepatitis C having different extent of hepatic fibrosis well defined by liver histology. A total of 62 patients with chronic hepatitis C were recruited and categorized into 2 groups according to their histological fibrosis stage : mild/moderate fibrosis group (F0-F3 group, n = 30) and extensive fibrosis/cirrhosis group (F4-F6 group, n = 32). The control group consisted of 31 healthy individuals. The following hemostatic assays were evaluated: antithrombin III (AT), protein C (PC) activity, activated partial thromboplastin time, prothrombin time, plasma fibrinogen as well as conventional liver function test. The PC level exhibited a significant reduction in both patient groups when compared to the normal control group (89.25% ± 10.05% and 48.33% ± 15.86% vs 111.86 ± 10.90; P < .001 and P < .001). The PC was found to be the strongest associated factor to histological fibrosis stage ( r = –.834; P < .0001). Univariate and multivariate analysis showed that AT ( P = .003) and PC ( P = .0001) were the most important factors associated with advanced fibrosis. The PC ( P = .001) was found to be the only predictor of mild fibrosis. In conclusion, PC deficiency occurs in an early stage of liver fibrosis. The severity of deficiency is proportional to extent of fibrosis. The PC may have a key role in linking hypercoagulability with hepatic fibrogenesis in chronic liver disease.


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