A liver fibrosis cocktail? Psoriasis, methotrexate and genetic hemochromatosis
1 Department of Histopathology, Royal Cornwall Hospital, Truro, TR1 3 LJ, UK
2 Research and Development Unit, Royal Cornwall Hospital, Truro, TR1 3 LJ, UK
3 School of Clinical and Laboratory Sciences, University of Newcastle upon Tyne, NE2 4HH, UK
BMC Dermatology 2005, 5:12 doi:10.1186/1471-5945-5-12Published: 29 November 2005
Pathologists are often faced with the dilemma of whether to recommend continuation of methotrexate therapy for psoriasis within the context of an existing pro-fibrogenic risk factor, in this instance, patients with genetic hemochromatosis.
We describe our experience with two male psoriatic patients (A and B) on long term methotrexate therapy (cumulative dose A = 1.56 gms and B = 7.88 gms) with hetero- (A) and homozygous (B) genetic hemochromatosis. These patients liver function were monitored with routine biochemical profiling; apart from mild perivenular fibrosis in one patient (B), significant liver fibrosis was not identified in either patient with multiple interval percutaneous liver biopsies; in the latter instance this patient (B) had an additional risk factor of partiality to alcohol.
We conclude that methotrexate therapy is relatively safe in patients with genetic hemochromatosis, with no other risk factor, but caution that the risk of fibrosis be monitored, preferably by non-invasive techniques, or by liver biopsy.