Asploro Journal of Biomedical and Clinical Case Reports

Asploro Journal of Biomedical and Clinical Case Reports

Tahani Aljuhani^1*
1Prince Sultan Ibn Abd Al Aziz Rd, Al Madinah, Saudi Arabia

Corresponding Author: Tahani Aljuhani
Address: Prince Sultan Ibn Abd Al Aziz Rd, Al Madinah, Saudi Arabia.
Received date: 29 March 2023; Accepted date: 11 April 2023; Published date: 17 April 2023

Citation: Aljuhani T. Vogt-Koyanagi-Harada Syndrome in a Pregnant Patient with Azathioprine-Induced Hepatitis and Cholestasis. Asp Biomed Clin Case Rep. 2023 Apr 17;6(2):76-78.

Copyright © 2023 Aljuhani T. This is an open-access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium provided the original work is properly cited.

Keywords: Vogt-Koyanagi-Harada Syndrome, Azathioprine-Induced Hepatitis, Cholestasis, Pregnancy, Hepatotoxicity, Prednisolone, Fetal Death

Vogt-Koyanagi-Harada disease (VKH) is a central nervous system condition that specifically affects vision and hearing. Descriptions of this disease date back to the 12th century, but the disease is named after three 20th-century physicians who described the collective manifestations of this disease. Alfred Vogt initially described bilateral iridocyclitis and eyebrow depigmentation in 1906, followed by Yoshizo Koyanagi’s 1926 description of bilateral serous detachments in association with cerebrospinal fluid (CSF) pleocytosis. Einosuke Harada identified the integumentary symptoms of the condition shortly thereafter. The disease presents with signs and symptoms of a loss of immune tolerance to melanocytes within the meninges, eyes, skin, hair, and ears [1]. The exact etiology of VKH is not firmly established, but current theories posit that patients develop T cell-mediated immunity against melanocytes following recovery from an inciting viral environmental factor [2]. Recent genetic studies have implicated the presence of human leukocyte antigen (HLA) cell surface markers HLA-DRB4, HLA-DRB1-04*05, and HLA-DRB-04*01, as well as non-HLA genes involving lymphocyte regulations in IL-12 production and IL-17 production [3,4]. Downregulation of microRNA in the production of interleukins and changes in non-coding RNA may also play a role in this condition [5].