This case was reported in a literature article and described the occurrence of acute liver injury in a 42-year-female patient who received Flu Seasonal QIV Dresden. Co-suspect products included Meningococcal polysaccharide groups A, C, W-135, Y conjugate vaccine and glatiramer acetate for multiple sclerosis. The patient's past medical history included transaminitis ((associated with serologic evidence of prior hepatitis A and hepatitis E virus exposure)), optic neuritis (At the age of 36 year) and optic neuritis (At age of 42 year, recurred). Concurrent medical conditions included multiple sclerosis, injection site pain, fatigue, nausea and constipation. Concomitant products included iron supplements, vitamin D, calcium (Unknown), Vitamin B12, norethindrone acetate and ethinyl estradiol and methylprednisolone. On an unknown date, the patient received Influenza vaccine Quadrivalent at an unknown dose, Meningococcal polysaccharide groups A, C, W-135, Y conjugate vaccine at an unknown dose and glatiramer acetate at an unknown dose and frequency. On an unknown date, less than a month after receiving Influenza vaccine Quadrivalent and Meningococcal polysaccharide groups A, C, W-135, Y conjugate vaccine, the patient experienced acute liver injury (serious criteria GSK medically significant), hepatic necrosis (serious criteria GSK medically significant), nausea, vomiting, exertional dyspnea, anorexia, fatigue, urine discoloration and jaundice. The patient was treated with prednisone. On an unknown date, the outcome of the acute liver injury, nausea, vomiting, exertional dyspnea, anorexia, fatigue, urine discoloration and jaundice were recovered/resolved and the outcome of the hepatic necrosis was unknown. The reporter considered the acute liver injury, hepatic necrosis, nausea, vomiting, exertional dyspnea, anorexia, fatigue, urine discoloration and jaundice to be unlikely related to Influenza vaccine Quadrivalent and Meningococcal polysaccharide groups A, C, W-135, Y conjugate vaccine. Additional information was provided. This case was reported in a literature article and described the occurrence of acute liver injury in a 42-year-old female patient who was vaccinated with unspecified influenza and unspecified meningococcal oligosaccharide vaccines (manufacturer unknown for both). The patient had history of transaminitis, which was attributed to a viral aetiology (associated with serologic evidence of prior hepatitis A and hepatitis E virus exposure), followed by many years of normal liver enzymes. At the age of 36 year, the patient presented with unilateral optic neuritis from which she had recovered. At age of 42, the optic neuritis recurred. Brain magnetic resonance imaging (MRI) showed multiple T2-hyperintense white matter lesions and a gadolinium-diethylenetriamine penta-acetic acid-enhancing lesion. Multiple sclerosis (MS) was diagnosed. The patient was treated with methylprednisolone 1 g/daily intravenous (IV) for 5 days. Concomitant medications included norethindrone/ethinyl estradiol with iron, vitamin D, calcium, and vitamin B12. The patient did not take supplements or abuse alcohol. Approximately 3 weeks late, the patient was started on generic glatiramer acetate (GA). The patient's co-suspect included GA. No information on patient's family history was provided. On an unspecified date, the patient received unspecified influenza and unspecified meningococcal oligosaccharide vaccines (administration site and route unspecified; dosages unknown; batch number not provided for both) at the time she began GA. The age of vaccination was not provided. Because of symptoms of injection pain, fatigue, nausea, and constipation, the patient discontinued GA after 13 daily injections. On an unspecified date at the age of 42 year, an unknown period after vaccination and the following day after GA therapy symptoms, the patient developed worsening nausea with vomiting, dyspnoea with exertion, anorexia, fatigue, dark urine, and jaundice. Liver function tests (panel A) were performed from 17 February 2016 (32 days prior to glatiramer acetate [GA]) to 13 June 2016, (102 days following the start of GA treatment). The patient was found to have elevated liver function tests (aspartate aminotransferase: 1,188 U/L , alanine transaminase: 1,879 U/L, alkaline phosphatase: 177 U/L, and total bilirubin: 3.6 mg/dL) compared with normal values just 1 month prior. The following laboratory values were negative or normal: hepatitis A virus (HAV) IgM, HBsAg, HBcAg IgG, hepatitis C virus ribonucleic acid (HCV RNA), HCV antibody, hepatitis E virus (HEV) IgM, Ebola virus (EBV) IgM, Cytomegalovirus (CMV) IgM, human immunodeficiency virus (HIV), Herpes simplex virus (HSV) polymerase chain reaction (PCR), urine toxicology screen, acetaminophen levels, antinuclear antibody (ANA) and anti-smooth muscle antibody. HAV IgG, HBsAb, HEV IgG, and EBV IgG were positive. 24-hour urine copper (193 ug/24 h) was presumed to be elevated secondary to acute liver injury. On day 20, a liver biopsy showed severe portal, interface and panacinar, lymphocyte-predominant inflammation, with confluent necrosis, numerous apoptotic hepatocytes, and central perivenulitis. The bile ducts were intact, and there was no significant ductular reaction. Steatosis, cholestasis, and fibrosis were not present. The patient was treated with IV corticosteroids followed by a several month taper of prednisone for possible autoimmune hepatitis. The patient's liver function tests normalized within 2 months. The authors commented, "Given our patient's negative autoimmune markers, lack of plasma cells on biopsy, and resolution of liver injury on a rapid prednisone taper, it is unlikely that this patient had autoimmune hepatitis. The administration of influenza and meningococcal vaccines seems unlikely to be contributory because neither vaccine is hepatotoxic".