Granulocyte colony stimulating factor (G-CSF) combined with α-interferon for the treatment of liver allograft recipients with viral hepatitis

Wright, Harlan I.; Gavaler, Judith S.; Baddour, Nahed; H, David; Thiel, Van

doi:10.1016/s0168-8278(94)80262-9

Journal of Hepatology

1994

DOI: 10.1016/s0168-8278(94)80262-9

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Granulocyte colony stimulating factor (G-CSF) combined with α-interferon for the treatment of liver allograft recipients with viral hepatitis

Harlan I. Wright¹,

Judith S. Gavaler²,

Nahed Baddour³

et al.

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Cited by 6 publications

(2 citation statements)

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“…To prevent morbidity and mortality associated with recurrent hepatitis C, many centers have used interferon alfa (IFN-␣) and/or ribavirin (RVN) as either antiviral prophylaxis or treatment of established hepatitis C or hepatitis B. Regimens have ranged from monotherapies with RVN, [8][9][10][11][12][13][14] standard IFN-␣ , 9,[15][16][17][18][19][20][21][22][23][24][25][26][27][28][29] or pegylated IFN [30][31][32] to combination therapies with a standard IFN-␣ and RVN 27,29,[33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][48][49][50][51][52] or pegylated IFN-␣ and RVN. 53 Ho...…”

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confidence: 99%

The clinical and immunologic impact of using interferon and ribavirin in the immunosuppressed host

Braun

Vierling

2003

Liver Transplantation

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C irrhosis caused by chronic hepatitis C virus (HCV) infection is the leading indication for cadaver and living donor liver transplantation. 1 Recurrent HCV infection, which occurs within days in virtually all allografts, is associated with a 10-to 20-fold increase in serum HCV RNA levels because of enhanced replication stimulated by immunosuppression. 2,3 A majority develop acute hepatitis C 1 to 4 months post-orthotopic liver transplantation (OLT) that is characterized by lymphocytic infiltration and hepatocyte apoptosis. Progression to chronic hepatitis C is associated with: (1) decline in HCV RNA levels observed in the acute phase because of effects of HCVspecific CD4 T helper subtype 1 (T H 1) and CD8 cell responses, (2) profibrotic effects of interferon-␥ (IFN-␥), and (3) proapoptotic effects of increased hepatocyte expression of Fas. 3 Progression of chronic hepatitis C is accelerated in immunosuppressed patients post OLT, resulting in a cumulative probability of cirrhosis in 30% by 5 years. 4 In addition, a minority develop severe, usually fatal, cholestatic hepatitis C within the first 6 months after OLT that is characterized by a direct cytopathic effect of excessive intrahepatic replication of HVC, intrahepatic anti-inflammatory T H 2 cytokine expression, and absence of an HCV-specific immune response. 3 Studies of the impact of different immunosuppressive regimens on recurrent hepatitis C also have been performed in an attempt to reduce hepatitis C progression while preventing acute cellular rejection (ACR). 5 Overall, HCV infection significantly reduces graft and patient survival compared with patients who undergo OLT for non-HCV-related indications. 6 Results of re-OLT are poor, 7 and this is an increasingly unrealistic option in view of the shortage of organ donors.To prevent morbidity and mortality associated with recurrent hepatitis C, many centers have used interferon alfa (IFN-␣) and/or ribavirin (RVN) as either antiviral prophylaxis or treatment of established hepatitis C or hepatitis B. Regimens have ranged from

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confidence: 99%

The clinical and immunologic impact of using interferon and ribavirin in the immunosuppressed host

Braun

Vierling

2003

Liver Transplantation

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“…For these reasons, treatment with haematopoietic growth factors (HGFs) is often necessary in patients who are undergoing antiviral therapy, although few studies have evaluated such a combination in routine clinical practice [8][9][10][11][12][13].…”

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confidence: 99%

The Impact of Haematopoietic Growth Factors on the Management and Efficacy of Antiviral Treatment in Patients with Hepatitis C Virus

et al. 2005

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Aim To evaluate the benefits of haematopoietic growth factors (HGFs) during the treatment of chronic hepatitis C virus (HCV) infection with severe haematotoxicity. Methods This was a 1-year retrospective study of HCV-positive patients receiving pegylated interferon and ribavirin. Patients received different HGFs, depending on certain criteria: they received erythropoietin (EPO) when their haemoglobin (Hb) levels were less than 10 g/dl and granulocyte colony-stimulating factor (G-CSF) when their neutrophil count was less than 750 cells/mm3. Haematological data, adherence and virological response were analysed and compared according to HGF use. Results In total, 132 patients were studied and 31 (23.5%) required HGF. Under multivariate analysis, baseline Hb levels of less than 13g/dl or a drop in Hb levels of over 2% per week predicted severe anaemia, and a base-line neutrophil count under 2900/mm3 predicted severe neutropaenia. HGF administration restored Hb values and the neutrophil count to above 10 g/dl and 1500 cells/mm3, respectively, in all 31 patients. Adherence to antiviral treatment was achieved in 25% of patients versus 58% of controls without severe haematotoxicity. The primary and sustained virological response did not differ statistically between HGF support and the control group (61% versus 57% and 32% versus 39%, respectively). Conclusion HGF administration counteracts the severe haematological adverse effects which occur during antiviral therapy and maintains the rate of sustained response.

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Consensus symposium on combined antiviral therapy

et al. 1996

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Granulocyte colony stimulating factor (G-CSF) combined with α-interferon for the treatment of liver allograft recipients with viral hepatitis

Cited by 6 publications

References 13 publications

The clinical and immunologic impact of using interferon and ribavirin in the immunosuppressed host

The clinical and immunologic impact of using interferon and ribavirin in the immunosuppressed host

The Impact of Haematopoietic Growth Factors on the Management and Efficacy of Antiviral Treatment in Patients with Hepatitis C Virus

Consensus symposium on combined antiviral therapy

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