Reduction in neutrophil count during hepatitis C treatment: drug toxicity or predictor of good response?
BACKGROUND
Bone marrow suppression is a well-recognized toxicity of the treatment of hepatitis C virus (HCV). Reduction of the peginterferon dose because of neutropenia is common in clinical practice. However, reduction of peginterferon dose during the first weeks of HCV treatment is associated with failure to achieve sustained virological response.


OBJECTIVE
The objective of this study is to investigate whether the fall of neutrophil count during hepatitis C treatment is associated with achieving sustained virological response.


METHODS
We performed an observational study of patients who completed peginterferon and ribavirin treatment in an Infectious Diseases Department in Manchester, UK.


RESULTS
Of the 74 patients included in the analysis, 78% had genotype 2 or 3 hepatitis C and 15% had liver cirrhosis. Sustained virological response was achieved in 78% of patients. On univariate analysis, factors related to achieving sustained virological response were younger age, genotype 2 or 3, baseline neutrophil count, and fall of neutrophil count during treatment. Multivariate analysis showed baseline neutrophil count >3.5 x 10(3) cells/mm(3) [odds ratio (OR) 5.7; 95% confidence interval (CI) 1.24-26.3] and a reduction of neutrophil count >60% (OR 4.5; 95% CI 1.03-19.9) to be independently associated with achieving sustained virological response. Neutropenia was not associated with an increased risk of infections.


CONCLUSIONS
In this observational study, higher baseline neutrophil count and fall of neutrophil count during the treatment of hepatitis C was associated with achieving sustained virological response. These findings could have important implications for the monitoring and management of HCV treatment with peginterferon if they are confirmed in other studies.
Alvarez-Uria
Gerardo
G
Department of Infectious Diseases, North Manchester General Hospital, Manchester, UK. gerardouria@gmail.com
Day
Jeremy N
JN
Nasir
Anisa J
AJ
Russell
Susan K
SK
Vilar
F Javier
FJ
D000328:Adult; D000998:Antiviral Agents / Q000009:adverse effects* / Q000627:therapeutic use; D015331:Cohort Studies; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D004359:Drug Therapy, Combination; D005260:Female; D005500:Follow-Up Studies; D016174:Hepacivirus / Q000187:drug effects / Q000302:isolation & purification; D006526:Hepatitis C / Q000175:diagnosis / Q000188:drug therapy*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000009:adverse effects* / Q000627:therapeutic use; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009503:Neutropenia / Q000139:chemically induced* / Q000453:epidemiology; D009504:Neutrophils; D011092:Polyethylene Glycols / Q000009:adverse effects* / Q000627:therapeutic use; D011237:Predictive Value of Tests; D012367:RNA, Viral / Q000097:blood; D011994:Recombinant Proteins; D012254:Ribavirin / Q000009:adverse effects* / Q000627:therapeutic use; D018570:Risk Assessment; D018709:Statistics, Nonparametric; D016896:Treatment Outcome; D019562:Viral Load / Q000187:drug effects
D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; C100416:peginterferon alfa-2a