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Acute liver injury is most frequently generated by paracetamol intoxication,hepatotropic viruses or drug-induced liver injury (DILI).
A 68-year-old male patient was admitted to the emergency department for clinical symptoms of 15 days of evolution with asthenia, adynamia, anorexia, generalized weakness, myalgia, jaundice in skin and mucous membranes. On admission the vital signs were stable, the physical examination showed only jaundice on skin and mucous membranes (+++), the rest of the examination was unaltered. Laboratory tests showed hyperbilirubinemia, hypertransaminasemia, hyperazoemia, INR 2.0; PT 21.5 sec; monocytes 13.8%; the rest of the tests were normal. Anti-HAV IgM, Anti-HAV IgG, HBsAg and anti-HBc IgM negative, Anti-HCV and HIV non-reactive, autoimmune hepatitis panel (Anti DNA, Anti ANA, AMA, ASMA, LKM1) negative and awaiting PCR results for non-hepatotropic viruses (EBV, Parvovirus B19,
cytomegalovirus). Spleno-portal Doppler ultrasound did not report portal venous thrombosis or in suprahepatic veins, ruling out Budd-Chiari syndrome. The diagnosis on admission was severe acute liver injury and acute kidney injury KDIGO 1.
Patient evolved with increased jaundice, deterioration of liver function, coagulopathy, and azoemia [image 1,2]. He received treatment with N-acetyl cysteine according to protocol to limit oxidative stress and albumin at 1mg/kg for the management of acute kidney injury in the context of liver injury. Decreased platelets and increased bilirubin values were evidenced, this alteration is described as a cause of perpetuation of liver injury and persistence of the inflammatory response. Due to the deterioration of the hepatic and renal function and in order to limit the inflammatory response regardless of the cause and as a bridge therapy until recovery, DPMAS modality Liver Support Therapy was performed. Five sessions were performed with clinical and analytical improvement (decrease of more than 50% of total
bilirubin) [image 1,2,3]. A few days later a positive PCR for CMV was reported, the fundus report shows CMV findings in the retina, liver biopsy with findings compatible with CMV viral infection and eosinophilic infiltrate that may be related to an adaptive response, indicating a good prognosis [image 4].
In relation to the confirmation of viral disease, treatment with Valganciclovir and low dose corticosteroids was started. Once hepatic support and specific antiviral treatment were completed, outpatient follow-up was performed.
Acute liver injury is a serious disease characterized by hepatic and systemic inflammatory response. Management focuses on limiting complications and specific treatment according to the etiology and when an adequate response is not achieved, extracorporeal liver support is advised to limit the inflammatory response and limit the perpetuation of damage, as a bridge to recovery of function. liver and in those with unfavorable evolution as a bridge to transplant.
No conflict of interest.