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Needle-stick exposure in the health care setting: do not forget hepatitis C!
The Netherlands Journal of Medicine 2000;57:4–6
Editorial
Needle-stick exposure in the health care setting: do not forget hepatitis C! Andy I.M. Hoepelman* Eijkman–Winkler Institute, University Medical Center Utrecht, PO Box 85500, 3508 GA Utrecht, The Netherlands Received 21 March 2000; accepted 8 May 2000 Keywords: Needle-stick injury; Hepatitis C; Health care workers
Exposure to blood, either through needle stick or mucosal exposure, often leads to fear and unrest among Health Care Workers (HCW’s) because of the risk of infection with blood-borne pathogens. In most hospitals protocols do exist that focus on exposure to hepatitis B and HIV infected fluids. Hepatitis C (HCV), however, is often forgotten and may be one of the viruses that is sensitive to early therapy. Van der Vlies et al. in this issue of the Netherlands Journal of Medicine describe the case of a health care worker with acute hepatitis C infection who was cured after short term monotherapy with interferona. See p. 30
Health care workers in the USA account for 2 to 4% of acute cases of hepatitis C, and most cases are thought to be a result of accidental needle sticks [1].
*Tel.: 1 31-30-250-6228; fax: 1 31-30-252-3741. E-mail address: [email protected] (A.I.M. Hoepelman)
In the United States, approximately 4 million people have chronic hepatitis C virus infection [2]. In the Netherlands the risk for iatrogenic transmission of HCV has substantially decreased since 1991, due to the introduction of routine HCV antibody screening of blood donors. In our country 0.03 to 0.1% of the healthy donor population has antibodies to HCV [3]. In for instance patients on dialysis the prevalence is considerably higher, 3% [4]. The risk of a blood-borne infection after a needle stick injury with blood from a HbsAg-positive patient is greater (5–40%) than after exposure to HCV-RNA positive blood (2–10%), but again considerably greater than after exposure of HIV-infected blood (0.3%) [5]. Mucous membrane exposures to blood rarely lead to transmission of HCV. A minority of a hepatitis B infections becomes chronic (3–5%), compared to 70–90% for hepatitis C. Moreover, treatment of acute hepatitis C is easier and has a higher success rate than therapy of chronic hepatitis C. After initial exposure, HCV-RNA can be detected in blood in 1–3 weeks. Within an average of 50 days (range: 15–150 days), virtually all patients develop liver cell injury, as shown by elevation of serum alanine aminotransferase (ALAT) [6]. The majority of patients, however, are asymptomatic and anicteric
0300-2977 / 00 / $ – see front matter 2000 Elsevier Science B.V. All rights reserved. PII: S0300-2977( 00 )00042-5
A.I.M. Hoepelman / Acute hepatitis C
[7]. Only 25–35% develops malaise, weakness, or anorexia, and some become icteric, these patients are probably the ones that clear the infection spontaneously and may not need therapy. Fulminant liver failure following HCV infection is rare. Composite analysis of studies into the long-term outcome of acute hepatitis C shows that cirrhosis develops in 20% of patients and hepatocellular carcinoma is rare [6]. HCV infection is self-limited in about 15% of cases [6,7]. Spontaneous disappearance of HCVRNA from blood (usually by 6–9 months) and return of liver enzymes to normal characterize recovery. A variety of tests are available for hepatitis C diagnosis. Antibodies to HCV (anti-HCV) almost invariably become detectable during the course of illness. Anti-HCV can be detected in 50–70% of patients at the onset of symptoms and in approximately 90% of patients 3 months after onset of infection and can therefore not be used to detect very early infection. A single positive assay for HCVRNA by PCR confirms HCV infection; unfortunately, a single negative assay does not prove that the patient is not viremic (depending on the time point the sample was taken) or has recovered from hepatitis C. This probably indicates a follow-up of potential ‘patients’ should be done by clinicians familiar with the interpretation of these assays. Cooreman et al. advise, after proven exposure, to follow-up persons for 6 months. Four-weekly determinations of serum alanine aminotransferase (ALAT) should be performed and if positive HCV-RNA PCR should be done to confirm infection. Since ALAT is not always elevated when HCV-RNA is already present, a practical suggestion might be to test exposed individuals at 0, 1, 3 and 6 months after exposure for ALAT. At 0, 3 and 6 months for anti-HCV and at 3 and 6 months for HCV-RNA, unless ALAT elevation or seroconversion (HCV-RNA determination should then be done earlier). When HCV-RNA becomes positive the person is definitely infected with HCV. Primary prevention (usage of gloves and special containers for used needles) is the most important measure. Up to date no vaccine has been developed and current formulations of immune serum globulin, for usage as post-exposure prophylaxis, are not effective for prevention of HCV. Sustained virologic response after combined
5
therapy with interferon-a and ribavirin in chronic HCV, is seen in about half of the patients, however at least 6–12 months of this expensive and difficult to undergo (side-effects) therapy is needed to achieve these numbers [6]. Although no large prospective randomized studies do exist, meta-analyses of interferon therapy for acute hepatitis do suggest that short-term (6 weeks to 6 months) treatment of acute hepatitis C produces a better long term response than prolonged therapy in chronic HCV [8,9]. As van der Vlies et al. and others indicate the exact duration of therapy needed is unknown [10]. No measures are currently available to prevent all infections with HCV after an exposure. Health care facilities should develop and implement policies to determine the HCV status of all persons involved in exposures. In turn, post-exposure procedures for follow-up of the exposed persons also should be developed and implemented. Furthermore, education of health care workers about the risk and prevention of occupational transmission of all blood-borne pathogens should be emphasized.
References [1] APIC. APIC position paper: Hepatitis C exposure in the health care setting (1998 APIC Guidelines). Am J Infection Control 1999;27:54–5. [2] Alter MJ, Kruszon-Moran D, Nainan AV, McQuillan GM, Gao F, Moyer LA et al. The prevalence of hepatitis C virus infection in the United States, 1988 through 1994. New Engl J Med 1999;341:556–62. [3] van den Poel C, Reesink HW, Mauser Bunschoten EP, Kaufmann RH, Leentvaar Kuypers A, Chamuleau RA et al. Prevalence of anti-HCV antibodies confirmed by recombinant immunoblot in different population subsets in The Netherlands. Vox Sang 1991;61:30–6. [4] Schneeberger PM, Keur I, van den Vliet W et al. Hepatitis C virus infection in dialysis centers in the Netherlands: a national survey by serological and molecular methods. J Clin Microbiol 1998;36:1711–5. [5] Cooreman MP, Weegink C, Reesink HW. Beleid bij acute hepatitis C en bij prikaccidenten met hepatitis-C-viruspositief bloed. Ned Tijdschr Geneeskd 1998;142:2298–300. [6] Rehermann B. Immunopathogenesis of hepatitis C. In: Liang TJ, moderator. Pathogenesis, natural history, treatment, and prevention of hepatitis C. Ann Intern Med 2000;132:297–9. [7] Villano SA, Vlahov D, Nelson KE, Cohn S, Thomas DL.
The Netherlands Journal of Medicine 2000;57:4 – 6
6
A.I.M. Hoepelman / Acute hepatitis C
Persistence of viremia and the importance of long-term follow-up after acute hepatitis C infection. Pathology 1999;29:908–14. [8] Camma C, Almasio P, Craxi A. Interferon as treatment for acute hepatitis C. A meta-analysis. Dig Dis Sci 1996;41:1248–55.
[9] Quin JW. Interferon therapy for acute hepatitis C viral infection – a review by meta-analysis. Aust NZ J Med 1997;27:611–7. [10] Vogel W. Treatment of acute hepatitis C virus infection. J Hepatol 1999;31(suppl 1):189–92.
The Netherlands Journal of Medicine 2000;57:4 – 6
Editorial
Needle-stick exposure in the health care setting: do not forget hepatitis C! Andy I.M. Hoepelman* Eijkman–Winkler Institute, University Medical Center Utrecht, PO Box 85500, 3508 GA Utrecht, The Netherlands Received 21 March 2000; accepted 8 May 2000 Keywords: Needle-stick injury; Hepatitis C; Health care workers
Exposure to blood, either through needle stick or mucosal exposure, often leads to fear and unrest among Health Care Workers (HCW’s) because of the risk of infection with blood-borne pathogens. In most hospitals protocols do exist that focus on exposure to hepatitis B and HIV infected fluids. Hepatitis C (HCV), however, is often forgotten and may be one of the viruses that is sensitive to early therapy. Van der Vlies et al. in this issue of the Netherlands Journal of Medicine describe the case of a health care worker with acute hepatitis C infection who was cured after short term monotherapy with interferona. See p. 30
Health care workers in the USA account for 2 to 4% of acute cases of hepatitis C, and most cases are thought to be a result of accidental needle sticks [1].
*Tel.: 1 31-30-250-6228; fax: 1 31-30-252-3741. E-mail address: [email protected] (A.I.M. Hoepelman)
In the United States, approximately 4 million people have chronic hepatitis C virus infection [2]. In the Netherlands the risk for iatrogenic transmission of HCV has substantially decreased since 1991, due to the introduction of routine HCV antibody screening of blood donors. In our country 0.03 to 0.1% of the healthy donor population has antibodies to HCV [3]. In for instance patients on dialysis the prevalence is considerably higher, 3% [4]. The risk of a blood-borne infection after a needle stick injury with blood from a HbsAg-positive patient is greater (5–40%) than after exposure to HCV-RNA positive blood (2–10%), but again considerably greater than after exposure of HIV-infected blood (0.3%) [5]. Mucous membrane exposures to blood rarely lead to transmission of HCV. A minority of a hepatitis B infections becomes chronic (3–5%), compared to 70–90% for hepatitis C. Moreover, treatment of acute hepatitis C is easier and has a higher success rate than therapy of chronic hepatitis C. After initial exposure, HCV-RNA can be detected in blood in 1–3 weeks. Within an average of 50 days (range: 15–150 days), virtually all patients develop liver cell injury, as shown by elevation of serum alanine aminotransferase (ALAT) [6]. The majority of patients, however, are asymptomatic and anicteric
0300-2977 / 00 / $ – see front matter 2000 Elsevier Science B.V. All rights reserved. PII: S0300-2977( 00 )00042-5
A.I.M. Hoepelman / Acute hepatitis C
[7]. Only 25–35% develops malaise, weakness, or anorexia, and some become icteric, these patients are probably the ones that clear the infection spontaneously and may not need therapy. Fulminant liver failure following HCV infection is rare. Composite analysis of studies into the long-term outcome of acute hepatitis C shows that cirrhosis develops in 20% of patients and hepatocellular carcinoma is rare [6]. HCV infection is self-limited in about 15% of cases [6,7]. Spontaneous disappearance of HCVRNA from blood (usually by 6–9 months) and return of liver enzymes to normal characterize recovery. A variety of tests are available for hepatitis C diagnosis. Antibodies to HCV (anti-HCV) almost invariably become detectable during the course of illness. Anti-HCV can be detected in 50–70% of patients at the onset of symptoms and in approximately 90% of patients 3 months after onset of infection and can therefore not be used to detect very early infection. A single positive assay for HCVRNA by PCR confirms HCV infection; unfortunately, a single negative assay does not prove that the patient is not viremic (depending on the time point the sample was taken) or has recovered from hepatitis C. This probably indicates a follow-up of potential ‘patients’ should be done by clinicians familiar with the interpretation of these assays. Cooreman et al. advise, after proven exposure, to follow-up persons for 6 months. Four-weekly determinations of serum alanine aminotransferase (ALAT) should be performed and if positive HCV-RNA PCR should be done to confirm infection. Since ALAT is not always elevated when HCV-RNA is already present, a practical suggestion might be to test exposed individuals at 0, 1, 3 and 6 months after exposure for ALAT. At 0, 3 and 6 months for anti-HCV and at 3 and 6 months for HCV-RNA, unless ALAT elevation or seroconversion (HCV-RNA determination should then be done earlier). When HCV-RNA becomes positive the person is definitely infected with HCV. Primary prevention (usage of gloves and special containers for used needles) is the most important measure. Up to date no vaccine has been developed and current formulations of immune serum globulin, for usage as post-exposure prophylaxis, are not effective for prevention of HCV. Sustained virologic response after combined
5
therapy with interferon-a and ribavirin in chronic HCV, is seen in about half of the patients, however at least 6–12 months of this expensive and difficult to undergo (side-effects) therapy is needed to achieve these numbers [6]. Although no large prospective randomized studies do exist, meta-analyses of interferon therapy for acute hepatitis do suggest that short-term (6 weeks to 6 months) treatment of acute hepatitis C produces a better long term response than prolonged therapy in chronic HCV [8,9]. As van der Vlies et al. and others indicate the exact duration of therapy needed is unknown [10]. No measures are currently available to prevent all infections with HCV after an exposure. Health care facilities should develop and implement policies to determine the HCV status of all persons involved in exposures. In turn, post-exposure procedures for follow-up of the exposed persons also should be developed and implemented. Furthermore, education of health care workers about the risk and prevention of occupational transmission of all blood-borne pathogens should be emphasized.
References [1] APIC. APIC position paper: Hepatitis C exposure in the health care setting (1998 APIC Guidelines). Am J Infection Control 1999;27:54–5. [2] Alter MJ, Kruszon-Moran D, Nainan AV, McQuillan GM, Gao F, Moyer LA et al. The prevalence of hepatitis C virus infection in the United States, 1988 through 1994. New Engl J Med 1999;341:556–62. [3] van den Poel C, Reesink HW, Mauser Bunschoten EP, Kaufmann RH, Leentvaar Kuypers A, Chamuleau RA et al. Prevalence of anti-HCV antibodies confirmed by recombinant immunoblot in different population subsets in The Netherlands. Vox Sang 1991;61:30–6. [4] Schneeberger PM, Keur I, van den Vliet W et al. Hepatitis C virus infection in dialysis centers in the Netherlands: a national survey by serological and molecular methods. J Clin Microbiol 1998;36:1711–5. [5] Cooreman MP, Weegink C, Reesink HW. Beleid bij acute hepatitis C en bij prikaccidenten met hepatitis-C-viruspositief bloed. Ned Tijdschr Geneeskd 1998;142:2298–300. [6] Rehermann B. Immunopathogenesis of hepatitis C. In: Liang TJ, moderator. Pathogenesis, natural history, treatment, and prevention of hepatitis C. Ann Intern Med 2000;132:297–9. [7] Villano SA, Vlahov D, Nelson KE, Cohn S, Thomas DL.
The Netherlands Journal of Medicine 2000;57:4 – 6
6
A.I.M. Hoepelman / Acute hepatitis C
Persistence of viremia and the importance of long-term follow-up after acute hepatitis C infection. Pathology 1999;29:908–14. [8] Camma C, Almasio P, Craxi A. Interferon as treatment for acute hepatitis C. A meta-analysis. Dig Dis Sci 1996;41:1248–55.
[9] Quin JW. Interferon therapy for acute hepatitis C viral infection – a review by meta-analysis. Aust NZ J Med 1997;27:611–7. [10] Vogel W. Treatment of acute hepatitis C virus infection. J Hepatol 1999;31(suppl 1):189–92.
The Netherlands Journal of Medicine 2000;57:4 – 6