UNASSIGNED: Olmesartan, an angiotensin II receptor antagonist, is associated with an uncommon complication of enteropathy that presents insidiously, usually months to years after initial commencement of anti-hypertensive therapy which can be dose-dependent. It has a variable spectrum of clinical presentation but commonly presents as a moderate to severe malabsorptive process with potential severe complications related to poor end-organ perfusion. Lymphocytic gastritis and microscopic colitis are often noted in patients presenting with olmesartan-induced enteropathy; however, hepatic involvement has been less frequently observed.
UNASSIGNED: We illustrate a case of a 43-year-old female presenting with 2 weeks of profuse non-bloody diarrhea in the context of olmesartan enteropathy which was complicated by an acute severe ischemic and enteropathic hepatopathy.
UNASSIGNED: Our case prompts clinicians to maintain a high index of suspicion in cases presenting with a seronegative enteropathy and concurrent acute liver injury while on olmesartan therapy. Cessation of olmesartan therapy resulted in prompt resolution of diarrheal symptoms and normalization of the acute transaminitis on subsequent three-week follow-up.

BACKGROUND: Macrophage activation syndrome is a rare disorder leading to unregulated immune activity manifesting with nonspecific constitutional symptoms, laboratory abnormalities, and multiorgan involvement. We report the case of a patient who presented with acute hepatitis secondary to macrophage activation syndrome diagnosed by liver biopsy and successfully treated with intravenous immune globulin, anakinra, and rituximab.
METHODS: A 42-year-old Laotian woman with adult-onset immunodeficiency with anti-interferon gamma antibodies presented with a fever, headache, generalized myalgia, dark urine, and reduced appetite in the setting of family members at home with similar symptoms. Her laboratory workup was notable for evidence of acute hepatitis without acute liver failure. After an unrevealing comprehensive infectious and noninvasive rheumatologic workup was completed, a liver biopsy was performed ultimately revealing the diagnosis of macrophage activation syndrome. She was successfully treated with intravenous immune globulin, anakinra, and rituximab.
CONCLUSIONS: This case highlights the importance of maintaining macrophage activation syndrome on the differential of a patient with acute hepatitis of unknown etiology in the correct clinical context and the value of a liver biopsy in making a diagnosis when noninvasive testing is unrevealing.

OBJECTIVE: A20 haploinsufficiency (HA20) is a recently described autoinflammatory disease that manifests symptoms similar to those of Behçet\'s disease. However, little is known about the involvement of the liver in HA20. Here, we report a case of HA20 complicated by autoimmune hepatitis (AIH).
METHODS: A 33-year-old woman was previously diagnosed with HA20 and chronic thyroiditis, and was treated with prednisolone (PSL; 7.5 mg/day) and levothyroxine sodium hydrate (125 μg/day). She experienced general malaise and jaundice, and biochemical evaluation revealed elevated liver function with an aspartate aminotransferase level of 817 U/L, an alanine aminotransferase level of 833 U/L, and a total bilirubin of 8.3 mg/dL. Pathological evaluation of the liver biopsy revealed interface hepatitis and the patient was diagnosed with acute exacerbation of AIH. Upon increasing the PSL dose to 60 mg/day, the liver enzyme levels rapidly decreased. During tapering of PSL, azathioprine 50 mg/day was added, and there was no relapse of AIH with combination therapy of PSL 7 mg/day and azathioprine 50 mg/day.
CONCLUSIONS: This is the first report of biopsy-proven AIH in an Asian patient with HA20. This case has significant implications for the pathogenesis and treatment of AIH in patients with HA20.

Idiosyncratic drug-induced liver injury (DILI) is an unpredictable reaction of individuals exposed to a certain drug, and drug-induced autoimmune hepatitis (DIAIH) presents a DILI phenotype that mimics idiopathic autoimmune hepatitis (AIH) when considering the clinical, biochemical, serological and histological parameters. We present a case report of a 48-year-old male who was hospitalized due to severe hepatocellular liver injury two months after self-treatment with a muscle-building dietary supplement based on arginine-alpha-ketoglutarate, L-citrulline, L tyrosine, creatine malate and beet extract. His immunology panel was positive with increased IgG levels, and radiologic methods showed no signs of chronic liver disease. He underwent corticosteroid treatment with adequate response. After therapy withdrawal, a clinical relapse occurred. Seven months after the initial presentation, liver MR suggested initial cirrhotic changes in the right liver lobe. A liver biopsy revealed abundant lymphoplasmacytic infiltrate with piecemeal necrosis and grade 2 fibrosis. He responded well to the corticosteroid treatment again, and was further treated with low-dose prednisone without additional relapses. Several years later, further management confirmed the presence of liver cirrhosis with no histological or biochemical signs of disease activity. DIAIH is a DILI phenotype that is difficult to distinguish from idiopathic AIH despite a wide armamentarium of diagnostic methods. It should always be considered among the differential diagnoses in patients presenting with hepatocellular liver injury.

(1) Background: Despite the advantages of COVID-19 vaccination, rare cases of acute hepatitis developing after the administration of the COVID-19 vaccine or the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection have been reported. The aim of the study is to describe a case series of patients who experienced the onset of acute hepatitis, with or without autoimmune features, following SARS-CoV-2 vaccination or infection and to hypothesize a genetic susceptibility in the pathogenesis. (2) Methods: A group of patients with acute onset hepatitis following SARS-CoV-2 vaccination or infection were evaluated in our hepatology outpatient clinic, where they underwent biochemical and autoimmune tests. Hepatitis A (HAV), B (HBV), and C virus (HCV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human immunodeficiency virus (HIV) infections were excluded. Patients with a diagnosis of autoimmune hepatitis (AIH) or drug-induced liver injury (DILI) underwent HLA typing and histological testing. (3) Results: Five patients experienced new-onset AIH after COVID-19 vaccination, one of which developed mild symptoms after vaccination that strongly worsened during subsequent SARS-CoV-2 infection. One patient had AIH relapse after COVID-19 vaccination while on maintenance immunosuppressive treatment. All of them had HLA DRB1 alleles known to confer susceptibility to AIH (HLA DRB1*03,*07,*13,*14), and in three of them, HLA DRB1*11 was also detected. Two patients developed acute hepatitis without autoimmune hallmarks which resolved spontaneously, both positive for HLA DRB1*11. (4) Conclusions: An association between AIH and COVID-19 vaccine or infection can be hypothesized in individuals with a genetic predisposition. In patients without autoimmune features and spontaneous improvement of hypertransaminasemia, the diagnosis of drug-induced liver injury (DILI) is probable. Further studies are needed to determine the presence of an actual association and identify a possible role of HLA DRB1*11 in the pathogenesis of acute liver injury after SARS-CoV2 vaccination or infection.

BACKGROUND: Acute liver injury (ALI) refers to inflammation of the hepatic parenchyma without hepatic encephalopathy that lasts less than 6 mo. When the etiology is unknown, Acute Hepatitis of Unknown Origin (AHUO) can present as a diagnostic and treatment challenge. AHUO in the adult population is unusual and poorly documented. It has an incidence between 11% and 75%. Currently, no treatment guidelines exist. With no identified cause, treatment is often blind, and the wrong treatment plan may have unintended consequences.
METHODS: We present the case of a 58-year-old woman who presented to the emergency room for elevated liver function tests (LFTs). Her symptoms started 10 d prior to admission and included nausea, vomiting, jaundice, decreased appetite, weight loss of 10 lbs, and dark urine. She denied drinking alcohol or taking any hepatotoxic agents, including acetaminophen, statins, vitamins, or supplements. She was admitted to the hospital, and an etiologic work-up was carried out. Her initial bloodwork revealed elevated liver enzymes (alanine aminotransferase 2500 U/L, aspartate aminotransferase 3159 U/L, and alkaline phosphatase 714 U/L) and elevated total bilirubin of 6.4 mg/dL. She tested negative for common infectious etiologies such as hepatotropic viruses A, B, C, and E. Further infective work-up revealed negative serology for cytomegalovirus, Epstein-Barr virus, herpes simplex virus 1 & 2, and human immunodeficiency virus. Her autoantibody test results were negative, including anti-smooth muscle antibody, anti-mitochondrial antibody, and anti-liver kidney microsome 1 antibody. Magnetic resonance cholangiopancreatography ruled out biliary causes of elevated LFTs, and her core liver biopsy proved inconclusive. Over the course of her hospital stay, the patient\'s LFTs improved with supportive care and without steroids.
CONCLUSIONS: Idiopathic hepatitis makes treatment challenging. It can leave patients feeling confused and unfulfilled. Thus, educating the patient thoroughly for shared decision-making and management becomes essential.

BACKGROUND: An important but rare adverse effect of vaccines is their association with autoimmune events, including hepatitis and aplastic anemia (AA). In this paper, we report a case of hepatitis followed by AA that occurred after the COVID-19 vaccine was administered.
METHODS: This paper focuses on a 30-year-old female who presented with acute hepatitis three weeks after receiving the second dose of the coronavirus Pfizer/BioNTech vaccine. After an extensive diagnostic evaluation was conducted that did not discover a specific cause, the Pfizer/BioNTech vaccine was suspected and the patient was treated with corticosteroids. One week after the onset of a liver disorder, the patient presented with gum bleeding and pancytopenia, and the diagnosis of AA was established via laboratory testing and bone marrow biopsy. After the diagnosis, the patient received immunosuppressive therapy using anti-lymphocyte serum (ATGAM) and CYCLOSPORINE A with progressive improvements in cytopenia. The important issue is whether AA is related to acute hepatitis or the coronavirus vaccine.
CONCLUSIONS: Clinicians should be aware of the risk of both the possibility of acute hepatitis, AA, or both after receiving the COVID-19 vaccination. It is very hard to distinguish the cause of AA between vaccine- and hepatitis-related AA. Predicting who develops hepatic or myelo-complications after vaccination is difficult.

COVID-19 associated severe acute liver injury in a young healthy patient has not been reported much in the literature. And currently, there are no standard management guidelines. We want to report a case of acute liver injury of mixed pattern in a young healthy female with asymptomatic COVID-19 infection. She presented with abdominal pain, nausea, vomiting and yellowish discoloration of her skin. Further laboratory investigations revealed mixed pattern liver injury with highly raised liver enzymes. She was managed with N-acetyl cysteine protocol and monitoring of her liver enzymes. Other causes of acute liver injury were ruled out. She remained stable during her hospital stay and follow up. Our aim is to highlight the significance of acute liver injury in COVID 19 patients that may lead to fatal outcomes if not managed and monitored accordingly.

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UNASSIGNED: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), first emerging in December 2019 and continuously evolving, poses a considerable challenge worldwide. It was reported in the literature that neonates had mild upper respiratory symptoms and a better outcome after Omicron SARS-CoV-2 variant infection, but there was insufficient data about complications and prognosis.
UNASSIGNED: In this paper, we present the clinical and laboratory characteristics of four COVID-19 neonate patients with acute hepatitis during the Omicron SARS-CoV-2 variant wave. All patients had a clear history of Omicron exposure and were infected via contact with confirmed caregivers. Low to moderate fever and respiratory symptoms were the primary clinical manifestations, and all patients had a normal liver function at the initial stage of the course. Then, the fever lasted 2 to 4 days, and it was noted that hepatic dysfunction might have occurred 5 to 8 days after the first onset of fever, mainly characterized by moderate ALT and AST elevation (>3 to 10-fold of upper limit). There were no abnormalities in bilirubin levels, blood ammonia, protein synthesis, lipid metabolism, and coagulation. All the patients received hepatoprotective therapy, and transaminase levels gradually decreased to the normal range after 2 to 3 weeks without other complications.
UNASSIGNED: This is the first case series about moderate to severe hepatitis in COVID-19 neonatal patients via horizontal transmission. Besides fever and respiratory symptoms, the clinical doctor should pay much attention to evaluating the risk of liver function injury after SARS-CoV-2 variants infection, which is usually asymptomatic and has a delayed onset.