Prolonged cholestasis and ductopenia following gold salt therapy

Authors

  • Céline Basset,

    1. Département de Pathologie, Hôpital Henri Mondor, 51 Avenue du Maréchal de Lattre de Tassigny, 94010 Créteil cedex, France,
    Search for more papers by this author
  • Jacqueline Vadrot,

    1. Service d'Anatomie et de Cytologie Pathologiques, Hôpital Gilles de Corbeil, 59 Boulevard Henri Dunant, 91106, Corbeil-Essonnes cedex, France,
    Search for more papers by this author
  • Jacques Denis,

    1. Service d'Hépatologie et de Gastroentérologie, Hôpital Gilles de Corbeil, 59 Boulevard Henri Dunant, 91106, Corbeil-Essonnes cedex, France, and
    Search for more papers by this author
  • Joël Poupon,

    1. Service de Biochimie-Toxicologie, Hôpital Fernand Widal, 200 rue du faubourg Saint Denis 75475 Paris cedex 10, France
    Search for more papers by this author
  • Elie Serge Zafrani

    1. Département de Pathologie, Hôpital Henri Mondor, 51 Avenue du Maréchal de Lattre de Tassigny, 94010 Créteil cedex, France,
    Search for more papers by this author

Elie Serge Zafrani, Département de Pathologie, Hôpital Henri Mondor, Assistance Publique-Hôpitaux de Paris, Université Paris 12-Val de Marne, 51 Avenue du Maréchal de Lattre de Tassigny, 94010 Créteil cedex, France.
Tel: 33 1 49 81 27 32. Fax: 33 1 49 81 27 33.
e-mail: elie-serge.zafrani@hmn.ap-hop-paris.fr

Abstract

Abstract: Hepatotoxicity, predominantly cholestatic, is a rare adverse effect of gold salt therapy, which usually completely resolves within a few months. We report the case of a female patient treated for rheumatoid arthritis, who had gold salt overdose, and in whom acute cholestatic hepatitis occurred three weeks after beginning of therapy. Evolution of gold concentration was followed in plasma and urine, as well as in cutaneous and liver dry tissue. Liver biopsy showed marked inflammatory changes of interlobular bile ducts that evolved towards ductopenia, which was responsible for prolonged cholestasis still present 15 months later. In addition, sialadenitis with sicca syndrome was noted six months after onset of the disease. The mechanism of hepatotoxicity was probably immunoallergic since liver lesions were associated with hypersensitivity syndrome including dermatitis and blood and tissue eosinophilia. This is the first report of gold salt hepatotoxicity with histological demonstration of cholangitis followed by ductopenia.

Ancillary