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Leucocyte interferon‐α retreatment for chronic hepatitis C patients previously intolerant to other interferons
Author(s) -
Cacopardo B.,
Benanti F.,
Brancati G.,
Romano F.,
Nunnari A.
Publication year - 1998
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1046/j.1365-2893.1998.00113.x
Subject(s) - medicine , tolerability , adverse effect , gastroenterology , headaches , immunology , interferon , alpha interferon , serology , lymphoblast , hepatitis , surgery , antibody , biology , genetics , cell culture
The activity and tolerability of a retreatment cycle with leucocyte interferon‐α (IFN‐α) (6 million units (MU) three times weekly for 12 months) was evaluated in a group of 22 hepatitis C patients who had been intolerant to a previous course of lymphoblastoid IFN‐α. Seven patients (31%) discontinued the new therapy owing to either a lack of response (six patients) or to severe leucopenia (one patient). Fifteen patients (68%) completed the 12‐month treatment: all had a biochemical response and 10 (45%) also had disappearance of serum HCV RNA (complete response). Mild adverse reactions (fever, headaches and diarrhoea) were seen in these patients during retreatment. After 12 months of follow‐up, 11 patients (50%) still maintained the biochemical response (long‐term response); seven of these patients (32%) were also negative for serum HCV RNA. Biochemical and complete responses, at the end of both treatment and follow‐up, were similar to those seen with lymphoblastoid IFN‐α. The full dose of leucocyte IFN‐α, when used in patients previously intolerant to the same dosage of lymphoblastoid IFN‐α, was better tolerated: only one of the 15 patients who completed the 12‐month treatment had a severe adverse event leading to withdrawal vs 22 of 68 patients treated with lymphoblastoid IFN‐α. Furthermore, there were no manifestations of serological or clinical autoimmunity caused by leucocyte IFN‐α, even in patients with autoantibodies associated with previous IFN therapy.