Changes in the acute phase complement component and IL-6 levels in patients with chronic hepatitis C receiving interferon α-2b

Biró, Lajos; Varga, Lilian; Pár, Alajos; Nemesánszky, E; Csepregi, A.; Telegdy, László; Ibrányi, E; Dávid, K; Horváth, Gábor; Szentgyörgyi, L.; Nagy, I.; Dalmi, L.; Abonyi, Margit; Füst, George; Horányi, Margit

doi:10.1016/s0165-2478(00)00183-8

Cited by 15 publications

(7 citation statements)

References 18 publications

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“…They observed elevated complemant proteins (C-9 and C1-INH) subsequent to antiviral therapy for 3 months. Increment in C-9 and C1-INH was strongly correlated with virological response 21. In our study, CRP levels were similar between patients with CHC and healthy control group however decrease in CRP levels between initial evaluation and 4th and 12th week was significant (p=0.005 and p=0.014, respectively).…”

Section: Discussionsupporting

confidence: 55%

“…In contrast to patients with nonA-nonB hepatitis, Atono et al19 determined significantly higher levels of CRP in patients with acute hepatitis A or B. Huang et al20 determined significantly higher high-sensitivity CRP (hsCRP) levels in a study conducted on 95 patients with CHC and 95 healthy controls, and also achieved significant decrease in hsCRP level following to treatment with pegylated IFN and ribavirin. Bíró et al21 examined the effect of IFN-α-2b therapy on APRs. They observed elevated complemant proteins (C-9 and C1-INH) subsequent to antiviral therapy for 3 months.…”

Section: Discussionmentioning

confidence: 99%

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Predictive Role of Acute Phase Reactants in the Response to Therapy in Patients with Chronic Hepatitis C Virus Infection

Oğuz

Atay²,

Tas³

et al. 2013

Gut Liver

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Background/AimsBiochemical parameters and acute-phase proteins (APPs) may provide complementary data in patients with chronic hepatitis C (CHC). We aimed to evaluate the predictive role of APPs in the response to antiviral therapy.MethodsForty-five patients underwent antiviral therapy. Serum ferritin, C-reactive protein (CRP), transferrin, albumin, alpha-1 acid glycoprotein (A1AG), and alpha-2 macroglobulin (A2MG) levels were examined at the initial evaluation and at the 4th, 12th, and 48th weeks. HCV RNA levels were examined at the initial evaluation and at the 12th and 48th weeks.ResultsFerritin, transferrin, A1AG, and A2MG levels were significantly higher in the patient group (p<0.05). CRP, ferritin, A1AG, and A2MG levels were significantly increased from baseline to the 4th week (p<0.05). The responders and nonresponders to antiviral therapy had insignificantly but remarkably different levels of CRP, ferritin, transferrin, A1AG, A2MG, and alanine aminotransferase (ALT) both at the initial evaluation and at the 12th week.ConclusionsVariations in ferritin, A1AG, A2MG, albumin, CRP, and transferrin levels are not alternatives to virological and biochemical parameters for predicting an early response to therapy in patients with CHC. However, the investigation of ALT levels and hepatitis C virus RNA in combination with acute-phase reactants may provide supplementary data for evaluating responses to antiviral therapy.

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Predictive Role of Acute Phase Reactants in the Response to Therapy in Patients with Chronic Hepatitis C Virus Infection

Oğuz

Atay²,

Tas³

et al. 2013

Gut Liver

View full text Add to dashboard Cite

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“…In chronic hepatitis C, levels of some acute-phase protein, such as C5b-9 levels, CH50, specific C4 activity, and CRP were lower than controls. Interestingly, some of these changes were reversible in patients who responded to HCV treatment [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Anti-C-reactive protein antibodies in chronic hepatitis C infection: Correlation with severity and autoimmunity

et al. 2007

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“…The levels of cytokines such as IFN-γ, TNF-α, IL-6 and IL-8 are elevated in individuals with chronic hepatitis C [74][75][76][77][78][79][80][81][82], and some authors have shown that this increase is proportional to the extent of the damage, histologically [26,76,83,84].…”

Section: Cell Response To Hcvmentioning

confidence: 99%

Pathogenesis of hepatitis C: HCV consensus 2007

Viso¹

2007

Braz J Infect Dis

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The chronic hepatitis C virus (HCV) infects approximately 130 million people worldwide [1]. It is estimated that approximately 15% of HCV-infected individuals eliminate the virus spontaneously, that 25% develop a mild form of the disease, and that 60% develop the chronic progressive form [2]. The elimination or persistence of HCV infection depends on the balance between the effectiveness, specificity and rapidity of the innate and adaptive immune responses, as well as on the HCV replication rate [3]. Persistence of HCV can also be caused by infection at privileged (extrahepatic) sites, viral inhibition of antigen presentation, selective immune suppression, negative regulation of HCV gene expression, viral mutations, immune exhaustion of T cells and the incomplete differentiation of memory T cells [4,5].Fibrosis is the principal complication of chronic hepatitis C, and it is estimated that 20% of patients develop cirrhosis over a period of 10, 20 or 30 years [2,6]. The progression of fibrosis increases morbidity and mortality in chronic hepatitis C [7], since it can lead to death due to complications caused by cirrhosis or hepatocarcinoma [2].Various studies have associated the progression of fibrosis in hepatitis C with diverse factors such as: the kinetics and pathogenicity of HCV; host-HCV interaction; intrinsic host factors such as demographic profile, body mass index and diabetes mellitus; host exposure to external factors; and the form of HCV acquisition. Life Cycle and Pathogenicity of HCVBelonging to the Flaviviridae family, HCV is a small enveloped virus [8]. Its genome consists of one RNA molecule that is composed of two terminal regions, 5'-and 3'-untranslated regions, and between these there is a single open reading frame that encodes a polyprotein with approximately 3000 amino acids. This polyprotein cleaves at the N-terminal side of three structural proteins, the nucleocapsid (core), envelope 1 (E1) and envelope 2 (E2), all of which are involved in the architectural organization of HCV. At the carboxylterminal side, the polyprotein cleaves to six nonstructural proteins, NS2, NS3, NS4 (NS4A and NS4B), NS5 (NS5A and NS5B) and NS6, which are responsible for the life cycle of the virus [9].After entering a susceptible host, HCV invades, infects and replicates within the blood stream, repeating the process in various tissues, as well as in peripheral B and T lymphocytes, as it proceeds to the liver by tropism, passing through various tissues such as those of the pancreas, thyroid, adrenal glands, spleen and bone marrow [10][11][12]. Since HCV can also directly infect the lymphatic tissue, its stimulation can lead to the development of B-cell lymphomas [13]. It is known that the liver is the principal site of HCV replication, and various studies have shown that this virus infects approximately 10% of hepatic cells [5]. Infection with HCV at extrahepatic sites can promote the appearance of HCV variants [14,15], thereby decreasing the chance that the immune system will recognize the virus.To enter the host ...

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Changes in the acute phase complement component and IL-6 levels in patients with chronic hepatitis C receiving interferon α-2b

Cited by 15 publications

References 18 publications

Predictive Role of Acute Phase Reactants in the Response to Therapy in Patients with Chronic Hepatitis C Virus Infection

Predictive Role of Acute Phase Reactants in the Response to Therapy in Patients with Chronic Hepatitis C Virus Infection

Anti-C-reactive protein antibodies in chronic hepatitis C infection: Correlation with severity and autoimmunity

Pathogenesis of hepatitis C: HCV consensus 2007

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