Etiologies of Liver Cytolysis in the Service of Hepato-Gastroenterology of the Gabriel Toure University Hospital

Aggression to the liver by xenobiotic and endogenous agents essentially results in an increase in serum aminotransferases related to hepatic cytolysis, the diagnosis of which is not always easy due to the diversity of its causes. This was a cross-sectional study from April 2019 to March 2020 that took place in the Department of Hepato-gastroenterology of the Gabriel Touré University Hospital Center. This was a cross-sectional study from April 2019 to March 2020 which took place in the Hepato Gastroenterology department of the Gabriel Touré university hospital whose objective of which was to study the etiology of hepatic cytolysis. We included all patients with hepatic cytolysis resulting in increased aminotransferase alanine at a rate higher than the normal upper limit with or without an increase of aspartate aminotransferase. We collected 199/2800 patients who met our inclusion criteria, i.e., a frequency of 7.1%. The mean age was 44.06 years ± 16.4 years, the sex ratio was 1.73. The most common clinical signs were jaundice, ascites, hepatomegaly, asthenia and anorexia. Biologically, chronic cytolysis was noted with a moderate elevation of aminotransferase alanine in 77.9% and a significant elevation in 15.5% of cases. HBs antigen (HBsAg) was positive in 80 patients (40.2%) and anti-hepatitis C virus (HCV) antibody in 18 patients (9%). Abdominal ultrasound was the first-line morphological examination and hepatomegaly alone or associated with splenomegaly was the most common abnormality. The main causes of acute cytolysis were viral hepatitis B, bile duct obstructions, drug-induced hepatitis and malaria while chronic cytolysis was mainly due to cirrhosis and hepatocellular carcinoma (HCC).

Participation of CD45,NKR-P1A and ANK61 antigen in rat hepatic NK cell(pit cell)-mediated target cell cytotoxicity

AIM Several triggering receptors have beendescribed to be involved in natural killer（NK）cell-mediated target cytotoxicity.In these studies,NKcells derived from blood or spleen were used.Pitcells are liver-specific NK cells that possess ahigher level of natural cytotoxicity and a differentmorphology when compared to blood NK cells.The aim of this study was to characterize the roleof the NK-triggering molecules NKR-P1A,ANK61antigen,and CD45 in pit cell-mediated killing oftarget cells.METHODS 51Cr-release and DNA fragmentationwere used to quantify target cell lysis andapoptosis,respectively.RESULTS Flow cytometric analysis showed thatpit cells expressed CD45,NKR-P1A,and ANK61antigen.Treatment of pit cells with monoclonalantibody（mAb）to CD45（ANK74）not onlyinhibited CC531s or YAC-1 target lysis but alsoapoptosis induced by pit cells.The mAbs to NKR-P1A（3.2.3）and ANK61 antigen（ANK61）had no effect on pit cell-mediated CC531s or YAC-1 targetcytolysis or apoptosis,while they did increase theFcγ receptor positive（FcγR+）P815 cytolysis andapoptosis.This enhanced cytotoxicity could beinhibited by 3,4-dichloroisocoumarin,an inhibitorof granzymes.CONCLUSION These results indicate that CD45participates in pit cell-mediated CC531s and YAC-1target cytolysis and apoptosis.NKR-P1A andANK61 antigen on pit cells function as activationstructures against FcγR+ P815 cells,which wasmediated by the perforin/granzyme pathway.

Liver Damage during Dengue Fever in Ouagadougou

Dengue fever is widespread in all tropical and subtropical areas of the world and is the main public health problem posed by arboviroses. In Burkina Faso, an outbreak of dengue serotype “DENV-2”, which is responsible for severe forms of dengue, has been reported. In this study, we will discuss liver damage during this disease. The aim of this study was to describe the sociodemographic, diagnostic, therapeutic and evolutionary aspects of dengue patients with hepatic cytolysis. Patients and Methods: This was a prospective cross-sectional study of dengue disease in 2 facilities in the city of Ouagadougou. The study was spread over a period of 3 months from August to November 2019. The study population consisted of all patients hospitalised for dengue with a positive AgNS1 and/or IgM rapid diagnostic test (RDT) and presenting signs of liver damage. Results: During our study period we recruited 134 patients with dengue fever of which 93 or 69.4% had at least one elevated transaminase. The sex ratio was 1.90 and the average age was 35 years. Symptoms of liver damage were rare with right hypochondrial pain in 4.30% of cases and jaundice in 1.07% of cases. Dengue haemorrhagic fever was found in 5 patients. IgG was negative in 77.42%. The majority of patients (44% or 47.31%) had at least one transaminase value elevated to the upper limit of normal (ULN);and a minority, 14 patients or 15.06%, had transaminases above 10 ULN. A small proportion of patients had hepatocellular failure 26.92% with a lowered prothrombin level. Ninety-four per cent (94.62%) of the patients received analgesics. Level 1 analgesic (paracetamol) was the most widely administered, particularly in 76 patients (86.36%). More than half of the patients (57.14%) had a length of stay of less than or equal to 3 days and the outcome was favourable in 91.40%. Conclusion: Dengue virus causes alterations in the liver parenchyma. The degree of liver damage is variable. As clinical symptoms are almost non-existent, the measurement of transaminases remains important.