Prevalence of hepatitis C antibodies in clinical health-care workers

Prevalence of hepatitis C antibodies in clinical health-care workers

Summary Health-care workers are known to be at risk from occupational transmission of blood-borne viruses, including hepatitis C. There may be serious implications following infection with hepatitis C including possible transmission to patients. We determined the prevalence of hepatitis C virus (HCV) antibodies among health-care workers at risk of occupational contact with blood and body fluids and among source patients in reported blood-exposure incidents. Anonymised stored blood samples from health-care workers immunised against hepatitis B virus since 1991 (n=1053) and blood samples from source patients in needlestick injuries (retrospective and prospective) since 1989 (n = 373) were analysed. 3 (0·28%) of the serum samples from health-care workers were found to be anti-HCV-positive. 17 (8 5%) of 200 source patients tested retrospectively between January 1989 and January 1992, and 24 (13 9%) of 173 source patients tested prospectively between January 1992 and June 1993 were anti-HCVpositive. During the second period, 15 (10·6%) of 142 source patients tested for human immunodeficiency virus (HIV) were positive and 7 (3·8%) of 184 source patients tested for hepatitis B surface antigen were positive. 6 of 24 (25%) HCV-infected patients were diagnosed only after the incident; for hepatitis B, 2 (33%) of patients were diagnosed after the incident, and for HIV all patients were previously diagnosed. The seroprevalence of HCV among these health-care workers is no higher than that reported in blood donors. This suggests that there has not been significant occupational transmission of HCV to these health-care workers despite the high prevalence of HCV (often covert) among source patients in reported blood exposure in the same hospital.

Occupational Health Unit (J Zuckerman MD, A Cockcroft FRCP), and Department of Virology, Division of Communicable Disease, Royal Free NHS Trust and Royal Free Hospital School of Medicine, London, UK (G Clewely BSc, Prof P Griffiths MRCPath) Correspondence to: Jane Zuckerman, Occupational Health Unit, Royal Free Hospital of Medicine, 5 Rosslyn Hill, London NW3 5UL, UK 1618

Introduction Health-care workers are at risk of infection by blood-borne viruses through needlestick injuries and other bloodexposures. Transmission of hepatitis virus (HCV) after accidental blood inoculation has been recorded1 and several studies on the occupational risk of HCV infection have been reported.24 Occupational infection with HCV may have serious long-term implications: establishment of a carrier state, chronic liver disease, and possible transmission to patients. Understandably, health-care workers are anxious about the possibility of HCV infection when a needlestick injury occurs. We studied the prevalence of HCV antibodies among health-care workers with direct and indirect clinical contact. In the same hospital, we assessed the potential for occupational transmission of HCV infection by measuring its seroprevalence among patients involved in reported blood-exposure incidents.

Subjects and methods The Occupational Health Unit at The Royal Free NHS Trust Hospital, London, UK, has well-established protocols for hepatitis B (HBV) immunisation of staff and for managing needlestick injuries.6 Staff who are at risk of blood exposures at work (doctors, nurses, and laboratory and ancillary staff) are offered HBV immunisation with subsequent testing of antibody response. Several thousand staff have been immunised and many of these have had frozen serum samples stored. This allowed us to investigate the prevalence of HCV by a second-generation enzyme

immunoassay antibody test (Ortho Diagnostics, High Wycombe, UK) and supplementary tests with Ortho immunoblot assay (RIBA II) on any repeatedly reactive samples. Individuals to be tested were those on a computer database of staff immunised against HBV and tested for response since January 1991, stratified by age (< 24 years, 25 to 39 years, and > 40 years); and two occupational groups, those with direct clinical exposure (medical and nursing staff) and those with indirect clinical exposure (laboratory and ancillary staff). There were 1053 stored serum samples available; aliquots were decanted into unlabelled containers, coded for age group and occupational group, and randomly numbered. These anonymous samples were then tested for HCV antibodies. Aliquots of all available 200 source patients in reported blood-exposure incidents January 1986 to December 1991 with stored serum samples were decanted into unlabelled containers and tested anonymously for hepatitis C antibodies. From January 1992, identified source patients in blood exposure incidents have been routinely asked for consent to be tested for HCV antibodies in addition to our previous practice of requesting testing for HIV antibodies and HBV surface antigen (HBsAg). 245 source patients were identified up to June 1993, of whom 184 were tested for HBsAg, 142 for HIV antibodies, and 173 for antibodies to HCV. If any sample was found to be positive for HCV antibodies, supplementary tests were undertaken and the staff member involved in the incident was offered follow-up tests for serum liver enzymes and hepatitis C antibodies for one year.

Clinical exposure group

Age (years)

Total

Direct

Indirect

40

0/246(0%) 1/186 (0 54%) 0/184(0%)

0/84(0%) 0/174(0%) 2/179 (112%)

Total

1/616 (0 16%)

2/437 (0 46%)

24 25-39

0/330(0%) 1/360 (0 28%) 2/363 (0 55%) 3/1053 (0 28%)

Table 1: Prevalence of hepatitis C antibodies in health-care workers with clinical contact

Results The overall seroprevalence of HCV antibodies amongst 1053 health care workers was 028% (table 1). There appeared to be a trend for hepatitis C antibodies to be found more frequently in older age groups, but the number of positive samples (3) was very small. 17 (8-5%) of the 200 source patients involved in blood exposures from January 1989 to January 1992 were HCV-antibody positive. From January 1992 to June 1993, 24 (13.9%) of 173 source patients tested were HCV-antibody positive (table 2). In addition, 15 (10-6%) of 143 source patients were HIVantibody positive and 6 (3-8%) of 184 source patients were

HBsAg-positive (table 2). Table 2 also shows that all 15 source patients who were HIV-positive had been diagnosed before the needlestick injury. In contrast, 2 of 6 (33%) patients infected with HBV and 6 of 24 (25%) infected with HCV were diagnosed only

after the incident. None of the health-care workers followed up after the 24 HCV antibody-positive blood exposures since January 1992 has seroconverted for HCV, nor have there been any HBV or HIV seroconversions in our hospital following infected blood exposures to date.

procedures.

Discussion An increased

A recent prospective study of hospital employees estimated the risk of HCV transmission to be 4% after needlestick exposure to anti-HCV-positive blood.3 A Japanese study found the risk of transmission from a single needlestick accident with HCV RNA-positive blood to be 10%.4 The apparent difference was most likely due to the use of different markers for HCV infection in the two studies. The present study shows that the seroprevalence of HCV infection among health care workers in potential contact with blood in our hospital is no higher than the 0-3% previously reported in UK blood donors.1s There is presently a seroprevalence rate for HCV of 0-07% in new blood donors in north London16 and our figure of 0-28% is somewhat higher. Nonetheless, seroprevalence amongst staff is low. This is encouraging and suggests that there has not been significant occupational transmission of hepatitis C to these workers in the past. The high seroprevalence of HCV in source patients probably reflects the type of patients in the hospital, which has a large liver unit, and renal dialysis and haemophilia units. Incidents involving patients known to be infected with a blood-borne virus may also be more likely to be reported. Recent guidance concerning occupational exposure to HCV17 states that routine HCV-antibody testing from identifiable source patients of unknown HCV status is presently not justified. However, in this study, 25% of source patients infected with HCV were identified as such only after the blood exposure incident (table 2). Therefore, if the resources are available, we suggest it is appropriate to test-with consent-all source patients of unknown HCV status. In this way, the health-care worker involved in the blood exposure incident can be counselled as early as possible about the risk of transmission and either reassured or given informed advice about follow-up

prevalence of markers

of HBV infection was recognised among health-care workers before widespread immunisation.7 Epidemiological and experimental studies have indicated that HCV can be transmitted by the parenteral route, and it is known that infected blood transfusions are an important route of transmission.8 There have been several reports of HCV transmission following needlestick injuries1,9-11 and one report of transmission by a human bite.12 A study of New York dentists2 found that 2% had antibodies to HCV compared with 0-1% among controls. A study of German hospital staff13 reported a seroprevalence of 058°,% compared with 0.24% among blood-donor controls. In contrast, a UK study of dental surgeons 14 reported that none had antibodies to HCV compared with a 0-3% seroprevalence among local blood donor controls.

The results of this study indicate that there is a continuing risk of exposure to blood-borne viruses from blood exposure incidents in this hospital. The fact that HCV and HBV infection in a number of patients in blood exposure incidents was not known at the time of the incident (see table 2) argues in favour of universal precautions for blood and body fluids,18 which is the policy in our hospital. The HCV seroprevalence among staff should not lead to complacency. Efforts to reduce blood exposures are important as the best way to reduce the risk of occupational transmission of HIV, HBV, and HCV. We thank Toyin Shobande and Chris Gooch for their help with this and the Medical Research Council for financial support.

study,

References 1

Marker

HBsAg HIVAbs HCVAbs

Serological status of patient 2

Tested before incident

Tested afterincident

Total tested

No tested

No positive

No tested

No

No tested

No positive

77 53 54

4 15 18

107 90 119

2 0 6

184 143 173

6 15 24

positive

There are 245 identified source patients in 285 blood exposure incidents reported January 1992 to June 1993. Reasons for not testing source patients after the incident. despite a policy of requesting testing in each patient (unless previously tested), have been descnbed elsewhere.’ HBsAg= hepatitis B surface antigen, HIVAbs= human immunodeficiency virus antibodies, HCVAbs = hepatitis C virus antibodies.

Table 2: Results of testing for blood-borne viruses in identified source patients in reported blood exposure incidents (January 1992-June 1993)

3

4

5

Cariani E, Zonaro A, Primi D, et al. Detection of hepatitis C virus RNA and antibodies after needlestick. Lancet 1991; 337: 850. Klein R, Freeman K, Taylor PE, Stevens CE. Occupational risk factors for hepatitis C virus infection among New York City dentists. Lancet 1991; 338: 1539-42. Kiyosawa K, Sodeyama T, Tanaka E. Hepatitis C in hospital employees with needlestick injuries. Ann Interm Med 1991; 115: 367-69. Mitsui T, Iwano K, Masuko K, et al. Hepatitis C virus infection in medical personnel after needlestick accident. Hepatology 1992; 16: 1109-14. Cockcroft A, Soper P, Insall C, et al. Antibody response after hepatitis B immunisation in a group of health care workers. Br J Indust Med

1990; 47: 199-202. 6

Oakley K, Gooch C, Cockcroft A. Review of management of incidents involving exposure to blood in a London teaching hospital. BMJ 1992; 304: 949-51.

1619

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7

West DJ. Risk of hepatitis B infection in health Am J Med Sci 1984; 287: 26-33.

care

workers in USA.

8

Garson J, Tedder RS, Briggs M, et al. Detection of hepatitis C viral sequence in blood donations by nested PCR and prediction of infectivity. Lancet 1991; 335: : 1419.

9

Schlipkopter U, Roggendorf M, Cholmakow K, Weise A, Deinhardt F. Transmission of hepatitis C virus from a haemodialysis patient to a medical staff member. Scand J Infect Dis 1990; 22: 757. Vaglia A, Nicolin R, Puro V, et al. Needlestick hepatitis C virus

10

seroconversion in 11 Seeff LB. 115: 411.

a

Hepatitis

surgeon. Lancet

13

1990; 336: 1315-16.

C from a needlestick injury. Ann Interbn Med 1991;

12 Dusheiko GM, Smith M, Scheuer PJ. Hepatitis C virus transmitted human bite. Lancet 1990; 336: 503-04.

by

Evolutional changes of cortical

Jochen AB. Occupationally acquired hepatitis C virus infection. Lancet

1992; 339: 304. 14 Herbert A-M, Walker DM, Davies KJ, Bagg J. Occupationally acquired hepatitis C virus infection. Lancet 1992; 339: 304-05. 15 Maclennan S, Barbara JA, Hewitt P, Moore C, Contreras M. Screening blood donations for HCV. Lancet 1992; 339: 131-32. 16 Ryan KE, MacLennan S, Barbara JAJ, Hewitt PE. Follow-up of anti-HCV positive blood donors. Br Med J 1994; 308: 696. 17 Centres for Disease Control. Update: universal precautions for prevention of transmission of human immunodeficiency virus, hepatitis B virus and other blood borne pathogens in health care settings. MMWR 1988; 37: 377-88. 18 PHLS Hepatitis Subcommittee. Hepatitis C virus: guidance on the risks and current management of occupational exposure. Comm Dis Rep 1993; 3: R135-139.

hypometabolism

in West’s

syndrome

Summary The pathophysiological basis of the epileptic encephalopathy West’s syndrome remains unknown. We have done serial positron emission tomography (PET) with fluorine-18-labelled 2-deoxy-3-fluoro-D-glucose (FDG) in twelve patients with newly diagnosed West’s syndrome. Throughout follow-up, PET revealed diffuse or focal cortical hypometabolism in eleven patients, whereas magnetic resonance showed (MRI) imaging morphological abnormalities in only five. At disease onset, PET showed cortical hypometabolism in eight patients (diffuse in three, focal in five). The second PET showed normal metabolism in six of these patients but focal abnormalities in three of the four with normal results on first PET. In all seven patients with normal findings on the second PET, tonic spasms ceased after initial treatment and no epileptic seizure occurred thereafter. In the five patients with cortical hypometabolism on the second PET, tonic spasms persisted or recurred, or partial seizures appeared. However, in two patients PET abnormalities disappeared in accordance with the later resolution of epileptic seizures. All patients with normal MRI and second PET results had normal psychomotor development. Diffuse or focal cortical hypometabolism that cannot be detected by MRI or computed tomography is common in patients with West’s syndrome. However, this anomaly is not permanent and changes with clinical symptoms. These functional abnormalities in the cerebral cortex may be associated with the development of West’s syndrome.

Departments of Pediatrics (N Maeda MD, K Watanabe MD, T Negoro MD, K Aso MD, T Ohki MD) and Radiology (K lto MD, T Kato MD), Nagoya University School of Medicine, Nagoya, Japan

Correspondence to: Dr Norihide Maeda, Department of Pediatrics, Nagoya University School of Medicine, 65 Turuma-cho, Showa-ku, Nagoya 466, Japan 1620

Introduction

syndrome is an age-dependent epileptic encephalopathy characterised by clusters of tonic spasms and hypsarrhythmia on electroencephalography. Despite many studies of this syndrome, the pathophysiological basis remains unknown. Many patients show psychomotor regression, and it is speculated that brain function is greatly impaired in these patients. However, there have been few neuroimaging studies of brain function in West’s syndrome. Cerebral dysfunction has been reported, but its association with the pathophysiology has not been clarified. 1,2 We have previously reported a prospective study in which we used positron emission tomography (PET) to measure fluorine-18-labelled 2-deoxy-2-fluoroD-glucose (FDG) uptake in patients with idiopathic West’s syndrome. We found a high frequency of functional abnormalities in the cerebral cortex, which changed over the clinical course.3 We now report PET in patients with West’s syndrome, including some with symptoms, and assess the association between changes on PET and the West’s

clinical

course.

Subjects and methods Between April, 1991, and December, 1993, we did serial PET examinations with 18F-FDG in fifteen children with West’s syndrome. The studies started at the onset of disease. Twelve of the children have been followed up for at least 1 year since the end of the initial treatment; these children are reported here. All patients were diagnosed, treated, and followed up according to the protocol established in our department.3 The following examinations were done to seek underlying diseases: analysis of blood, urine, and cerebrospinal fluid, neurological examination, fundoscopy, interictal EEG, auditory brainstem responses, and computed tomography. As initial treatment we gave first an antiepileptic drug (valproate or clonazepam), then pyridoxine, thyrotropin-releasing hormone, and corticotropin. After treatment, neurological examination and interictal EEG were done every few months, and psychomotor development was assessed with the Tsumori-Inage developmental quotient. In all patients,