Growth Hormone Secretagog Receptor 1a

One month after initial diagnosis, the patient remains well on a tapering course of corticosteroids

One month after initial diagnosis, the patient remains well on a tapering course of corticosteroids. Recently, some cases of AIH that developed after COVID-19 vaccination have been reported [3,4]. analytical development. Some recent reports have been suggested that COVID-19 vaccination can lead to the development of autoimmune diseases. It is speculated that this vaccine can disturb self-tolerance and trigger autoimmune responses through cross-reactivity with host cells. Therefore, healthcare providers must TAK-960 remain vigilant during mass COVID-19 vaccination. strong class=”kwd-title” Keywords: COVID-19 vaccine, Moderna mRNA vaccine, Autoimmune hepatitis There have been some concerns regarding the possibility of COVID-19 vaccine-induced autoimmunity [1]. Molecular mimicry was suggested as a potential mechanism for this association. Indeed, antibodies against the spike protein S1 of SARS-CoV-2 experienced a high affinity against some human tissue proteins [2]. As vaccine mRNA codes the same viral protein, they can trigger autoimmune diseases in predisposed patients. We statement the case of a 65-year-old woman, with JAK2 V617F-positive polycythemia vera diagnosed in 2006, under pegylated interferon since 2019. Her routine medication also included acetylsalicylic acid 100?mg/day, sertraline 25?mg/day and esomeprazole 20?mg/day for over two years. She experienced no history of liver disease and was known to have normal routine liver assessments (AST 28U/L, ALT 24U/L, GGT 24U/L, ALP 108U/L, total bilirubin 0.72?mg/dL). Moreover, she experienced no personal or family history of autoimmune disease. After receiving the first dose of Moderna-COVID-19 vaccine, the patient presented mild abdominal pain. Two weeks later, routine liver function tests showed AST 1056U/L, ALT 1092U/L, GGT 329U/L, ALP 24U/L, total bilirubin 1.14?mg/dL. Total blood cell count and international normalized ratio were normal. She denied recent changes in drug therapy. The serology for hepatitis A computer virus, human immunodeficiency computer virus, cytomegalovirus, Epstein-Barr computer virus and herpes simplex virus type 1 and 2 were all unfavorable. Polymerase chain reaction for hepatitis B, C and TAK-960 E viruses were also unfavorable. Ceruloplasmin, alpha-1 antitrypsin and iron assessments were normal, as well as thyroid function. Antinuclear antibody was positive (1:100, speckled pattern), detected by indirect immunofluorescence assay on HEP-20-10?cells/monkey liver (initial dilution 1/100; final dilution 1/1000). Anti-mitochondrial, anti-smooth muscle mass, anti-liver-kidney microsomal, anti-soluble liver antigen and antineutrophil cytoplasmic antibodies were all negative. At this point, serum IgA, IgM and IgG levels were normal. Abdominal Doppler ultrasound showed hepatomegaly without cirrhotic morphology, and no biliary dilation or thrombosis. Five weeks after vaccination, the patient presented with jaundice and choluria. Liver profile was worsening and IgG levels were now elevated (Fig. 1 ). The patient was admitted for clinical management. A percutaneous liver biopsy was performed, exposing a marked growth of the portal tracts due to dense inflammatory infiltrate, with aggregates of plasma cells; severe interface hepatitis and multiple confluent foci of lobular necrosis were also observed TAK-960 (Fig. 2 ). Open in a separate windows Fig. 1 C Development of liver function assessments (A), total bilirubin (B) and total IgG levels (C) over time. AST – aspartate aminotransferase, ALT – alanine aminotransferase, GGT – gamma-glutamyl transferase, ALP – alkaline phosphatase, IgG – Immunoglobulin G. Open in a separate windows Fig. 2 Liver biopsy findings C (A) Marked portal tract inflammation with intense lymphoplasmacytic infiltrate and interface hepatitis (HE, 30x). The TAK-960 inflammation is made up primarily of lymphocytes and aggregates of plasma cells, with few eosinophils. (B) Intense lobular activity associated with centrilobular necrosis (HE 20x). The score of simplified diagnostic criteria of the International Autoimmune Hepatitis Group was 8 [definite diagnosis of autoimmune hepatitis (AIH)]. Treatment with prednisolone 60?mg/day was started with a quick improvement of liver function assessments and normalization of Rabbit polyclonal to HA tag IgG levels. One month after initial diagnosis, the patient remains well on a tapering course of corticosteroids. Recently, some cases of AIH that developed after COVID-19 vaccination have been reported [3,4]. There are some similarities between the previously explained cases and the present case, such as a short interval between vaccination and symptoms onset [3]. Although our patient received the Moderna mRNA vaccine, there are already other reports of AIH induced by the Pfizer-BioNTech and Oxford-AstraZeneca vaccines, supporting the idea that this COVID-19 vaccine triggers autoimmune phenomena regardless of its mechanism of action [4]. In contrast to other cases, our individual did not have confounding factors such as pregnancy or autoimmune conditions [3,4]. However, she was under treatment with pegylated interferon for polycythemia vera. In fact, this drug has been linked to induction of autoimmune conditions, including AIH [5]. Nevertheless, this side effect usually occurs within 1C2 months of starting therapy and our patient had already started pegylated interferon for over two years. In addition, the timing of the liver injury, the considerable exclusion of other causes of hepatic disease and the normalization of liver function assessments and IgG levels after treatment, make it very.