Volume 174 Issue 4

Research Iron deficiency in Australian-born children of Arabic background in central Sydney Margaret A Karr, Michael Mira, Garth Alperstein, Samia Labib Boyd H Webster, Ahti T Lammi and Patricia Beal MJA 2001; 174: 165-168 For editorial comment, see Couper and Simmer Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Public and environmental health Abstract Objectives: To determine the prevalence of iron depletion and deficiency, and iron-deficiency anaemia, along with risk factors for iron depletion, in Australian-born children aged 12-36 months of Arabic-speaking background. Design: Community-based survey. Setting: Central Sydney Area Health Service (CSAHS), NSW, April to August, 1997. Participants: All children born at five Sydney hospitals between 1 May 1994 and 30 April 1996, whose mothers gave an Arabic-speaking country of birth and resided in the area served by the CSAHS. Main outcome measures: Full blood count (haemoglobin, mean corpuscular haemoglobin, mean corpuscular volume), plasma ferritin concentration, haemoglobin electrophoresis, potential risk factors for iron depletion. Results: Families of 641 of the 1161 eligible children were able to be contacted, and 403 agreed to testing (response rate, 62.9% among those contacted). Overall, 6% of children had iron-deficiency anaemia, another 9% were iron deficient without anaemia, and 23% were iron depleted. Multiple logistic regression analysis showed three significant independent risk factors for iron depletion: < 37 weeks' gestation (odds ratio [OR], 5.88, P = 0.001); mother resident in Australia for less than the median time of 8.5 years (OR, 1.96, P = 0.016); and daily intake of > 600 mL cows' milk (OR, 3.89, P = < 0.001). Conclusion: Impaired iron status is common among children of Arabic background, and targeted screening is recommended for this group. Numerous studies have documented the adverse health effects of iron deficiency in infants and preschool children, including growth retardation,1,2 gastrointestinal changes,3 impaired immune function,4 impaired behavioural and mental development5,6 and decline in psychomotor development.7,8 In 1992-1994, a study of Sydney children aged 9-62 months found that 1.1% had iron-deficiency anaemia, while 2.8% were iron deficient without anaemia and another 10.5% were iron depleted.9 The prevalence of iron-deficiency anaemia appeared to be higher among children of Arabic-speaking background, but the small number of these children prevented firm conclusions, and the reasons for any difference were not clear. The most important determinants of iron status in infants are growth rate relative to iron endowment at birth, dietary iron content and bioavailability and gastrointestinal blood loss.10 Risk factors for iron deficiency in infancy and childhood include prematurity, low birth weight,11,12 exclusive breastfeeding beyond six months of age,13 introduction of whole cows' milk before 12 months of age,14 and high intake of cows' milk.15 We examined the prevalence of impaired iron status in a large group of Australian-born children of Arabic-speaking background and evaluated their risk factors for iron depletion. Methods The study was a community-based survey undertaken between April and August 1997. Participants Children were identified from the medical records of five Sydney hospitals, which, according to the Midwives Data Base, account for 92% of deliveries to mothers born in an Arabic-speaking country and residing in the area served by the Central Sydney Area Health Service (CSAHS).16 Eligibility criteria were: birthdate between 1 May 1994 and 30 April 1996; mother gave an Arabic-speaking country of birth on admission; postcode of mother's place of residence was in the area served by the CSAHS. Hospitals were asked to exclude stillbirths and neonatal deaths. Contact details were obtained from the medical records. Survey Parents of all eligible children were sent a letter about the study in both Arabic and English. Five days later, they were telephoned to discuss queries and to invite their child's participation. If they agreed, an appointment was made at a convenient early childhood health centre, or a home visit was arranged. Parents were asked to bring the child's Personal Health Record for assessment of birth weight and gestation. Demographic data were obtained using a structured questionnaire administered by an Arabic-speaking research assistant (S L). Questions were also asked about the child's feeding habits since birth and whether the child had had a fever in the two weeks before the blood test, as fever can elevate plasma ferritin concentration.17 Investigations About 0.75 mL of blood was collected by fingerprick and tested at the Royal Alexandra Hospital for Children (RAHC), Sydney, NSW. Haematological investigations (using a Coulter S+IV, Fullerton, Cal, USA) included measurement of haemoglobin and red cell indices. Plasma ferritin concentration was measured by immunoradiometric assay (Biorad, Hercules, Cal, USA). Haemoglobin electrophoresis was performed on all samples to detect haemoglobinopathies. Definitions of impaired iron status are shown in Box 1. All parents were notified of their children's results. Children with poor iron status or haemoglobinopathy were referred to their general practitioners (GPs). A copy of the laboratory report was sent to the GP and to the parents, if they so requested. Statistical analyses Children found to have a haemoglobinopathy were excluded from the analyses, which were performed using Stata (version 5).21 Statistical tests were performed after adjustment for possible cluster effects both within hospitals and within families (as some families contributed more than one child to the study). Confidence intervals were similarly adjusted. Adjusted χ2 tests were used to examine relationships between iron depletion and demographic and risk factors. Variables found to be significantly associated with iron depletion were then entered into a multivariate logistic regression model. Prevalence of impaired iron status was compared with prevalence in children from the general population of central Sydney assessed in 1992-1994.9 Data from that study were re-examined for children aged 12-38 months, using a ferritin level < 10 µg/L to define iron depletion. To test the representativeness of our sample group, demographic characteristics of the mothers were compared with those of all women who in the 1996 census gave an Arabic-speaking country of birth, resided in the area served by the CSAHS, were aged 15-45 years and had children aged 12-38 months. These data were obtained from the Australian Bureau of Statistics. Ethical approval for all components of this study was obtained from the CSAHS Ethics Review Committee. All participating parents gave informed written consent. Results We were able to contact families of 641 of the 1161 eligible children and tested 403 of these children (63% response rate among those able to be contacted). Haematological testing identified a haemoglobinopathy in 21 children, who were therefore excluded from analysis, although two had other haematological parameters consistent with iron depletion. This left 382 children with a plasma ferritin result, and 315 with complete haematological results (blood volume was insufficient for a complete examination in the other 67). Median age of the 382 children at the time of data collection was 25 months (range, 12-38 months). Age distribution was 12-23 months (149 children), 24-35 months (204), and 36-38 months (29). Just over half the children (53%) were male. Prevalence of impaired iron status Prevalence of impaired iron status is shown in Box 2. Overall, 38% of children with an Arabic background had impaired iron status, comprising 6% with iron-deficiency anaemia, a further 9% with iron deficiency without anaemia and a further 23% with iron depletion. The Box also shows prevalences found in 1992-1994 among children the same age in the general population of central Sydney.9 The proportion of children with impaired iron status was substantially higher among Australian-born children of Arabic-speaking background in 1997 than among children of the same age in the general community in 1992-1994. Among the children of Arabic background, those who were reported as having a fever in the two weeks before the blood test were statistically less likely to fulfil the criteria for iron depletion (19/122 versus 68/260; F1,339 = 5.07; P = 0.025). However, they did not differ significantly in rates of iron deficiency (11/108 versus 16/207; F1,282 = 0.49; P = 0.48) or iron-deficiency anaemia (8/108 versus 12/207; F1,282 = 0.31; P = 0.58). The rate of iron depletion among the 260 children reported not to have had a fever in the two weeks before the blood test was 26% (95% CI, 21%-32%). There were no significant differences in iron status between the sexes or between age groups. Risk-factor analysis Potential risk factors among the 382 children are shown in Box 3. Univariate analysis revealed that prematurity, mother resident in Australia less than the median time of 8.5 years, mother born in a country other than Lebanon, and daily intake of more than 600 mL of cows' milk were significantly associated with iron depletion (Box 4). None of the other variables tested, including age of introduction of cows' milk, were significantly associated with iron depletion. Multivariate logistic regression analysis determined that prematurity, mother resident in Australia less than the median time of 8.5 years, and daily intake of more than 600 mL of cows' milk, but not mother born in a country other than Lebanon, were independently associated with iron depletion (Box 4). Children who had been born prematurely were almost six times more likely to be iron depleted, while those who drank more than 600 mL cows' milk per day were almost four times as likely and those whose mothers had been in Australia less than the median time (8.5 years) were almost twice as likely. Representativeness of sample We compared post-secondary education and time in Australia between the sample group and all women who in the 1996 census gave an Arabic-speaking country of birth, resided in the area served by the CSAHS, were aged 15-45 years and had children aged 12-38 months. In the sample group, 29% (116/403) had post-secondary qualifications (95% CI, 24%-33%), compared with 30.2% in the census group (421/1392). Similarly, 30% (121/401) of our sample had been in Australia for six to 10 years (95% CI, 26%-35%), while the corresponding figure for the census group was 26.4% (368/1392). The 238 parents who declined a blood test for their child were questioned by telephone about the age and sex of the child and the volume of cows' milk consumed daily; 180 parents (76%) responded. There were no significant differences between their children and those who had blood tests in age (P = 0.7), sex (P = 0.6) or reported volume of cows' milk consumed daily (P = 0.17). Among the 382 children tested for iron depletion, 67 had moved place of residence since birth and 315 had not moved. The proportion with iron depletion did not differ between these two groups (OR, 1.31; 95% CI, 0.73-2.36). Nor did it differ between the 67 children who had only ferritin level estimated and the 315 who gave sufficient blood for a full haematological examination (OR, 1.03; 95% CI, 0.53-2.01). Discussion These results indicate a public health problem in Australian-born children of Arabic-speaking background in central Sydney that could indicate a nationwide problem. More than a third of these children had impaired iron status, including 6% with iron-deficiency anaemia and another 9% with iron deficiency without anaemia. These prevalences are higher than those found in children the same age in the general population of central Sydney in 1992-1994.9There are several potential sources of bias in this study. The first was the use of retrospective records and consequent failure to contact about 45% of mothers. This is a common problem in such retrospective studies.22,23 However, the mothers of the children studied did not differ significantly from all women in the 1996 census who were aged 15-45 years with children in the target age range, gave an Arabic-speaking country of birth and resided in the CSAHS, while prevalence of iron depletion did not differ between children who had moved residence since birth and those who had not. It is unlikely that our sample differed substantially from the total study population. A second potential source of bias was non-response. However, children whose parents refused a blood test did not differ significantly from those who had a blood test in age, sex and proportion who drank more than 600 mL cows' milk daily. Finally, children whose blood samples were insufficient for full haematological assessment did not differ significantly in prevalence of iron depletion from those who had a full assessment. In the group of children reported to have had a fever in the two weeks before the blood test, a significantly lower proportion fulfilled the criteria for iron depletion. Therefore, the rate of iron depletion reported may be an underestimate. The definition of iron deficiency used in this study was particularly stringent, requiring abnormal values for three laboratory indicators of iron status. Criteria used by the United States Third National Health and Nutrition Examination Survey were less stringent: individuals were diagnosed as iron-deficient if they had abnormal values for two of three laboratory indicators (serum ferritin, free erythrocyte protoporphyrin or transferrin saturation).18 Nevertheless, that survey found rates of iron deficiency and iron-deficiency anaemia among children aged one to two years less than half the rates found in our study (3% versus 6% in our study). The US rate was similar to the rate found in children in the general population of central Sydney in 1992-1994. Risk of iron depletion in our study was greater in children whose mothers had been in Australia for less than the median time of 8.5 years. About 79% of these mothers spoke Arabic, or mainly Arabic, in the home. Early childhood health centres in central Sydney have specific days on which an Arabic interpreter is present, but anecdotal reports suggest that many mothers do not avail themselves of this service. Newly arrived mothers should be targeted in hospital, immediately postpartum, and given information as to which days an Arabic interpreter will be at their local centre and strongly encouraged to attend on a regular basis. Prematurity is well documented as a risk factor for iron deficiency, and this should be kept in mind by GPs and other healthcare providers. Of particular interest is the risk associated with the volume of cows' milk consumed daily. The National Health and Medical Research Council recommends that children aged under 12 months should not receive cows' milk as the main source of milk, while those aged over 12 months should not receive more than 600 mL per day.24 In the multiple logistic regression model, children who consumed more than 600 mL per day were almost four times as likely to have iron depletion, and targeted screening is strongly indicated based on this dietary history. Cows' milk is a poor source of iron, displaces foods with greater available iron and may also increase gastrointestinal occult blood loss. GPs should be aware of the importance of a dietary history for children of Arabic-speaking background and should enquire particularly about the volume of cows' milk consumed per day after 12 months of age. Acknowledgements We wish to thank the parents and children who participated in this study, the haematology laboratory staff at the Royal Alexandra Hospital for Children, Sydney, and the nurses of the participating Early Childhood Health Centres. The blood collection skills of Mrs Rhonda Dryden were invaluable to this study. The study was funded by the National Health and Medical Research Council Public Health Research Development Committee, Grant No: 97-417-7. References Aukett MA, Parks YA, Scott PH, Wharton BA. Treatment with iron increases weight gain and psychomotor development. Arch Dis Child 1986; 61: 849-857. Prasad AN, Prasad C. Iron deficiency; non-hematological manifestations. Prog Food Nutr Sci 1991; 15: 255-283. Berant M, Khourie M, Menzies IS. Effect of iron deficiency on small intestinal permeability in infants and young children. J Pediatr Gastroenterol Nutr 1992; 14: 17-20. Thibault H, Galtn P, Selz F, et al. The immune response in iron-deficient young children: effect of iron supplementation on cell-mediated immunity. Eur J Pediatr 1993; 152: 120-124. Oski FA, Honig AS, Helu B, Howanitz P. Effect of iron therapy on behavior performance in nonanemic, iron-deficient infants. Pediatrics 1983; 71: 877-880. Lozoff B, Jiminez E, Wolf AW. Long-term developmental outcome of infants with iron deficiency. N Engl J Med 1991; 325: 687-694. Williams J, Wolff A, Daly A, et al. Iron supplemented formula milk related to reduction in psychomotor decline in infants from inner city areas: randomised study. BMJ 1999; 318: 693-697. Walter T, De Andraca I, Chadud P, Perales CG. Iron deficiency anemia: adverse effects on infant psychomotor development. Pediatrics 1989; 84: 7-17. Karr M, Alperstein G, Causer J, et al. Iron status and anaemia in preschool children in Sydney. Aust N Z J Public Health 1996; 20: 618-622. Dallman PR, Siimes MA, Stekel A. Iron deficiency in infancy and childhood [review]. Am J Clin Nutr 1980; 33: 86-118. Gorten MK, Cross ER. Iron metabolism in premature infants: 2. Prevention of iron deficiency. J Pediatr 1964; 64: 509-520. Friel JK, Andrews WL, Matthew JD, et al. Iron status of very-low-birth-weight infants during the first 15 months of infancy. CMAJ 1990; 143: 733-737. Calvo EB, Galindo AC, Aspres NB. Iron status in exclusively breast-fed infants. Pediatrics 1992; 90: 375-379. Penrod JC, Anderson K, Acosta PB. Impact on iron status of introducing cow's milk in the second six months of life. J Pediatr Gastroenterol Nutr 1990; 10: 462-467. Mills AF. Surveillance for anaemia: risk factors in patterns of milk intake. Arch Dis Child 1990; 65: 428-431. NSW Department of Health, NSW Midwives Data Collection, 1994. Sydney: NSW Department of Health, 1995. Elin RJ, Wolff SM, Finch CA. Effect of induced fever on serum iron and ferritin concentrations in man. Blood 1977; 49: 147-153. Looker AC, Dallman PR, Carroll MD, et al. Prevalence of iron deficiency in the United States. JAMA 1997; 277: 973-976. Dallman PR, Siimes MA. Percentile curves for hemoglobin and red cell volume in infancy and childhood. J Pediatr 1979; 94: 26-31. Dallman PR, Looker AC, Johnson CL, Carroll M. Influence of age on laboratory criteria for the diagnosis of iron deficiency anaemia and iron deficiency in infants and children. In: Hallberg L, Asp N-G, editors. Iron nutrition in health and disease. London: J Libbey, 1996: 64-74. Stata statistical software release 5.0 [computer program]. College Station, Texas: Stata Corporation, 1997. McBride WG, Black BP, English BJ. Blood lead levels and behaviour of 400 preschool children. Med J Aust 1982; 2: 26-29. Ranmuthugala G, Karr M, Mira M, et al. Opportunistic sampling from early childhood centres: a substitute for random sampling to determine lead and iron status of pre-school children? Aust N Z J Public Health 1998; 22: 512-514. National Health and Medical Research Council. Dietary guidelines for children and adolescents. Canberra: AGPS, 1995. (Received 2 Mar, accepted 1 Sep, 2000) Authors' details Central Sydney Area Health Service, Sydney, NSW. Margaret A Karr, MPH, MSc(Med), Senior Research Officer, Division of General Practice; Michael Mira, MB BS, PhD, Clinical Professor, Department of General Practice, University of Sydney; Garth Alperstein, FRACP, Paediatrician and Clinical Senior Lecturer, University of Sydney, and Conjoint Senior Lecturer, University of New South Wales, Sydney, NSW; Samia Labib, BA, MEd(Health), Senior Interpreter, Health Interpreter Service. Department of Haematology, Royal Alexandra Hospital for Children, Sydney, NSW. Boyd H Webster, FRCPA, Senior Staff Specialist; Ahti T Lammi, FRACP, FRCPA, Senior Staff Specialist; Patricia Beal, MSc, Senior Hospital Scientist. Reprints will not be available from the authors. Correspondence: Professor M Mira, General Practice Casualty, Balmain Hospital, Booth Street, Balmain, NSW 2041. michaelmira_auATyahoo.co.uk 1: Definitions of impaired iron status used in the survey of children of Arabic background Iron depletion18 Plasma ferritin level Iron deficiency19 Iron depletion plus Mean corpuscular volume plus Mean corpuscular haemoglobin Iron-deficiency anaemia20 Iron deficiency plus Haemoglobin level Back to text 2: Prevalence of impaired iron status among children aged 12-38 months of Arabic background in central Sydney in 1997 Arabic background General population9 Iron status* Number % (95% CI) Number % (95% CI) Iron depletion Iron deficiency Iron-deficiency anaemia 87/382 27/315 20/315 23% (19%-27%) 9% (5%-12%) 6% (4%-9%) 36/381 14/329 5/329 9% (7%-12%) 4% (2%-7%) 2% (0-3%) *Definitions of iron status in children of Arabic background are shown in Box 1. The same definitions were used for children in the general population, except that iron deficiency was defined as iron depletion plus mean corpuscular volume < 70fL (age, 12-23 months) or < 73fL (age, 24-38 months), or red cell zinc protoporphyrin level > 80µmol/mol haem. Back to text 3: Potential risk factors for iron depletion among 382 children aged 12-38 months of Arabic background in central Sydney, 1997 Children with Children without Potential risk factors iron depletion iron depletion P* Born before 37 weeks' gestation 12/87 (14%) 10/295 (3%) 0.001 Birth weight 7/86 (8%) 8/293 (3%) 0.05 Breastfed initially 70/87 (81%) 245/295 (83%) 0.59 Breastfed at time of data collection 4/87 (5%) 9/295 (3%) 0.49 Cows' milk introduced before age of 12 months 32/87 (37%) 76/295 (26%) 0.06 Cows' milk introduced before age of 9 months 15/87 (17%) 36/295 (12%) 0.20 Consume >600mL cows' milk per day 54/83 (65%) 109/287 (38%) Consume ≥1L cows' milk per day 23/83 (28%) 30/287 (11%) Iron-fortified cereal as first solid 38/87 (44%) 149/295 (51%) 0.27 Consume meat 42/87 (48%) 122/295 (41%) 0.26 Receiving vitamin supplement 3/87 (3%) 11/295 (4%) 0.90 Receiving iron-containing supplement 1/87 (1%) 4/295 (1%) 0.88 Mother not born in Lebanon 26/87 (30%) 49/295 (17%) 0.01 Arabic or mainly Arabic spoken at home 58/87 (67%) 180/293 (61%) 0.39 Mother resident in Australia less than median time (8.5 years) 53/86 (62%) 137/294 (47%) 0.02 *By adjusted χ2 test. Back to text 4: Risk factors significantly associated with iron depletion among children aged 12-38 months of Arabic background in central Sydney, 1997 Univariate analysis Multivariate analysis Risk factor Odds ratio (95% CI) P Odds ratio (95% CI) P Gestation ≥37 weeks 1.00 1.00 4.55 (1.70-12.50) 0.003 5.88 (2.22-20.0) 0.001 Years mother in Australia ≥8.5 years 1.00 1.00 1.82 (1.10-3.03) 0.02 1.96 (1.36-3.33) 0.016 Cows' milk consumed daily ≤600mL 1.00 1.00 >600mL 3.04 (1.80-5.13) 3.89 (2.22-6.80) Country of birth Lebanon 1.00 Country other than Lebanon 2.14 (1.18-3.88) 0.01 NS NS=Not significant. Back to text

Margaret A Karr · Michael Mira · Garth Alperstein · Samia Labib · Boyd H Webster · Ahti T Lammi · Patricia Beal

Transmission of hepatitis C virus (HCV) occurs primarily through blood-to-blood contact, with injecting drug use reported as the predominant risk factor for infection.1 Epidemiological studies have implicated tattooing as a risk factor for HCV infection.2-7 Possible transmission of hepatitis C virus by tattooing has rarely been reported in the literature,8-10 and none of the three previous reports has documented HCV seroconversion. HCV infection is highly prevalent in correctional facilities, and inmates commonly report behaviours associated with blood-to-blood contact.9,11,12 Despite high levels of HCV seroprevalence among prison inmates, reports of HCV transmission in the prison setting are uncommon.11,13,14 We report a well-defined case of acute HCV infection and subsequent viral clearance in a prisoner after tattooing. Clinical record In April 1999, a 25-year-old man who had been continuously imprisoned since 1997 presented with symptoms of jaundice, dark urine, malaise, nausea, anorexia, sweats and headache. Liver function tests showed biochemical hepatitis (see Figure), and he was hospitalised. The patient had never been tattooed before entering prison, but was tattooed on four occasions inside prison (December 1997, September and December 1998, and early April 1999). The two most recent episodes were within the recognised incubation period for hepatitis C virus infection of 3-20 weeks.1 On both occasions fellow inmates tattooed him with sewing needles. The needle used for the December 1998 episode of tattooing was soaked in a 1% bleach solution for one hour, and then wiped and rinsed with water before use. The patient was unsure if the needle was used to tattoo another prisoner before him. He reported that the needle used in the most recent episode (in April 1999) had not been previously used for tattooing. He was unsure if the same stock of pigment had been used to tattoo another prisoner before him on either occasion. The patient denied previous tattooing, injecting drug use, blood transfusion, needlestick injury and sharing of razors or toothbrushes and having sex while inside prison. He took no regular medications. In March 1998 he had been in a fight, in which he sustained lacerations to his lips and knuckles. He admitted to using drugs, including cocaine, marijuana and ecstasy, before his imprisonment, but only via non-injecting routes of administration. During imprisonment he admitted to smoking marijuana, and had lost visiting privileges when three random urine tests detected marijuana. His prison medical record had no reference to injecting drug use. Several healthcare workers, including a drug and alcohol counsellor, had interviewed him over a two-year period and all had recorded a similar history of non-injecting drug use only. Physical examination five months after presentation, in November 1999, showed no stigmata of chronic liver disease, a normal liver span and no splenomegaly. There were three tattoos and no evidence of injection scars in the cubital fossae or elsewhere. Testing showed seroconversion to HCV in samples collected longitudinally between 1997 and 1999 (see Figure). HCV viraemia was detected by polymerase chain reaction on two occasions in the acute phase of the illness. Serological testing for alternative causes of hepatitis showed no evidence of recent infection with hepatitis A, B or E, human immunodeficiency virus, syphilis or cytomegalovirus. Immunoglobulin G (IgG) antibodies against Epstein-Barr virus, human herpes virus type 6 and Toxoplasma gondii were detected at the first sampling point, indicating prior exposure. To corroborate the inmate's self-report and medical interviews, a 5 cm scalp hair sample was taken and tested for injectable drugs. The sample represented hair growth from July to November 1999, a period after the onset of hepatitis, during which the inmate had been prescribed a combination oral analgesic containing codeine. This sample was tested by gas chromatography and mass spectrometry for cocaine, amphetamines, methadone, codeine, morphine and 6-monoacetyl morphine (a heroin metabolite). The analysis showed the presence of codeine and morphine; a quantitative analysis was not possible. Discussion This report describes a case of HCV transmission in prison in which tattooing was the most likely route of transmission -- there were two episodes of tattooing during the recognised incubation period of HCV infection, with subsequent symptomatic hepatitis, seroconversion and viraemia. Previous reports have not demonstrated seroconversion, leaving uncertainty as to the association between the tattooing, hepatitis and HCV infection.8-10 Nor have they attempted to exclude injecting drug use as a confounding risk for HCV acquisition. In this patient, the presence of morphine in the hair may relate to prescribed codeine analgesia or indicate undisclosed drug use in the period after the onset of the illness (the period represented by the hair sample). This was unable to be resolved with further interviews as the inmate was lost to follow-up. Thus, the possibility of undisclosed injecting drug use cannot be completely discounted as the route of transmission. It is very unlikely that the patient acquired HCV through blood-to-blood contact during the reported fight, as the clinical illness occurred more than one year after this event. Although tattooing represents a biologically plausible means for the transmission of HCV, this case illustrates that undisclosed injecting drug use may be a confounder in studies where tattooing is the only acknowledged risk factor for transmission of HCV. Indeed, in one study of recently released New South Wales prison inmates, injecting drug users were more likely to report receiving a tattoo in prison than non-injecting drug users.12 Previously reported modes of transmission of HCV in prisons include sharing drug injecting equipment, fights between inmates, barbers shears11 and a blood splash to the eye.14 Clinically apparent cases are likely to represent a small proportion of new HCV infections in prisons. Clinically apparent hepatitis is uncommon in primary HCV infection,1 occurring in only one case in every five. Prison inmates report boredom as a common motivation for tattooing inside prison.15 As tattooing is likely to continue among prison inmates despite being banned, allowing access to licensed tattooists (or trained prisoners), with effective infection control procedures, may reduce the risk of HCV transmission in prisons. In conclusion, large, prospective studies with meticulous assessment of confounding risk factors are required to effectively assess the potential association between tattooing and primary HCV infection. References MacDonald M, Crofts N, Kaldor J. Transmission of hepatitis C virus: rates, routes, and cofactors. Epidemiol Rev 1996; 18: 137-148. Balasekaran R, Bulterys M, Jamal MM, et al. A case-control study of risk factors for sporadic hepatitis C virus infection in the southwestern United States. Am J Gastroenterol 1999; 94: 1341-1346. Ko YC, Ho MS, Chiang TA, et al. Tattooing as a risk of hepatitis C virus infection. J Med Virol 1992; 38: 288-291. Holsen DS, Harthug S, Myrmel H. Prevalence of antibodies to hepatitis C virus and association with intravenous drug abuse and tattooing in a national prison in Norway. Eur J Clin Micro Infect Dis 1993; 12: 673-676. Kaldor JM, Archer GT, Buring ML, et al. Risk factors for hepatitis C virus infection in blood donors: a case-control study. Med J Aust 1992; 157: 227-230. Neal KR, Jones DA, Killey D, James V. Risk factors for hepatitis C virus infection. A case-control study of blood donors in the Trent Region (UK). Epidemiol Infect 1994; 112: 595-601. Sun CA, Chen HC, Lu CF, et al. Transmission of hepatitis C virus in Taiwan: prevalence and risk factors based on a nationwide survey. J Med Virol 1999; 59: 290-296. Abildgaard N, Peterslund NA. Hepatitis C virus transmitted by tattooing needle. Lancet 1991; 338: 460. Thompson SC, Hernberger F, Wale E, Crofts N. Hepatitis C transmission through tattooing: a case report. Aust N Z J Pub Health 1996; 20: 317-318. Sun DX, Zhang FG, Geng YQ, Xi DS. Hepatitis C transmission by cosmetic tattooing in women [letter]. Lancet 1996; 347: 541. Haber PS, Parsons SJ, Harper SE, et al. Transmission of hepatitis C within Australian prisons. Med J Aust 1999; 171: 31-33. Dolan KA, Wodak AD, Hall WD. A bleach program for inmates in NSW: an HIV prevention strategy. Aust N Z J Pub Health 1998; 22: 838-840. Vlahov D, Nelson KE, Quinn TC, Kendig N. Prevalence and incidence of hepatitis C virus infection among male prison inmates in Maryland. Eur J Epidemiol 1993; 9: 566-569. Rosen HR. Acquisition of hepatitis C by a conjunctival splash. Am J Infect Control 1997; 25: 242-247. Crofts N, Thompson S, Wale E, Hernberger F. Risk behaviours for blood-borne viruses in a Victorian prison. Aust N Z J Criminol 1996; 29: 20-28. (Received 26 Jul, accepted 3 Oct, 2000) Authors' details University of NSW, Sydney, NSW. Jeffrey J Post, MB BS(Hons), FRACP, NHMRC Scholar; Andrew R Lloyd, MD, FRACP, Associate Professor, Inflammation Research Unit, School of Pathology; Kate A Dolan, PhD, Senior Lecturer, National Drug and Alcohol Research Centre. Prince of Wales Hospital, Sydney, NSW. L Ross Whybin, BSc, MASM, Senior Hospital Scientist, SEALS Area Serology Laboratory; Ian W J Carter, MSc, Senior Hospital Scientist, Virology Diagnostic Laboratory, Microbiology Department. Drug and Alcohol Department, Royal Prince Alfred Hospital, Sydney, NSW. Paul S Haber, MD, FRACP, Staff Specialist. Reprints will not be available from the authors. Correspondence: Dr J J Post, Inflammation Research Unit, School of Pathology, University of NSW, Sydney, NSW, 2052. j.postATunsw.edu.au Seroconversion to hepatitis C virus antibodies (anti-HCV) occurred after tattooing, in association with clinical hepatitis and HCV viraemia. Subsequent clearance of viraemia and resolution of biochemical hepatitis are illustrated. ELISA=Enzyme linked immunosorbent assay for anti-HCV. ELISA 1 and 2 represent two different commercial assays (Murex anti-HCV version III, Murex Biotech, South Africa; and Innotest HCV Ab III, Innogenetics, Belgium). HCV PCR=qualitative HCV RNA in serum by polymerase chain reaction (Roche Amplicor HCV version 1.0, Roche Diagnostics, USA). Upper limit of normal range for alanine aminotransferase, 35U/L. Back to text

Jeffrey J Post · Kate A Dolan · Paul S Haber · Andrew R Lloyd

EBM in Action Does drinking carrot juice affect cancer of the prostate? MJA 2001; 174: 197 Clinical question - Search question - Search - Summary of findings - Outcome - References - - More articles on Men's health Clinical question "Does drinking carrot juice have any effect on prostate cancer?" A general practitioner asked this question after her patient, a 77-year-old man who had been diagnosed with invasive prostate cancer, commenced drinking four glasses of carrot juice a day. Information about the exact staging of the cancer was not available. Search question The search question was refined to "What effect does the consumption of beta-carotene have on prostate cancer? Are there any adverse effects, and if so, at what quantity of consumption do they occur?". Ideally, a randomised controlled trial of men recently diagnosed with prostate cancer, comparing a high intake of beta-carotene with no beta-carotene intake, would be the appropriate clinical study design to answer this question. The outcomes assessed would be the appearance of metastases, patient morbidity and mortality, and any adverse effects of the beta-carotene. Search The search terms "beta-carotene", "prostate" and "cancer" were combined to identify appropriate trials. We searched databases including Cochrane Library and SUMSearch (<http://sumsearch.uthscsa.edu/searchform4.htm>), which searches for systematic reviews and original research, and links to PubMed Clinical Queries. Our search yielded five relevant studies. Summary of findings The best evidence identified was a large randomised controlled trial of 29 133 healthy men who were cigarette smokers.1 The men receiving beta-carotene (20 mg) daily had an increased incidence of prostate cancer compared with those receiving placebo (138 v 112 men with prostate cancer). Further analysis of the results showed prostate cancer incidence to be 23% higher (95% CI, -4% to 59%) and mortality 15% higher (95% CI, -30% to 89%) in men who received beta-carotene compared with those who did not, but this trend was not significant.2 A prospective cohort study found no evidence of either protection or harm associated with dietary beta-carotene.3 Two case-control studies, one involving beta-carotene supplements and the other dietary beta-carotene, found a protective effect of high levels of beta-carotene intake.4,5 One of these studies reported a significant protective effect of high levels of dietary beta-carotene (relative risk of prostate cancer [RR], 0.60; 95% CI, 0.37 to 0.99), particularly in men younger than 68 years (RR, 0.30; 95% CI, 0.13 to 0.66).5We were unable to find any studies evaluating the influence of beta-carotene in patients with established prostate cancer. Outcome Although two observational studies suggested that high levels of beta-carotene intake reduced the risk of prostate cancer, the best evidence found that beta-carotene increased the incidence of prostate cancer. The GP discussed this information with her patient, who nevertheless elected to continue to drink lots of carrot juice! Christopher B Del Mar Professor Paul P Glasziou Associate Professor Anneliese B Spinks Research Officer Sharon L Sanders Research Officer Centre for General Practice Medical School, University of Queensland, Herston, QLD c.delmarATcgp.uq.edu.au References Albanes D, Heinonen OP, Huttunen JK, et al. Effects of alpha-tocopherol and beta-carotene supplements on cancer incidence in the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study. Am J Clin Nutr 1995; 62 (6 Suppl): 1427S-1430S. Heinonen OP, Albanes D, Virtamo J, et al. Prostate cancer and supplementation with alpha-tocopherol and beta-carotene: incidence and mortality in a controlled trial. J Natl Cancer Inst 1998; 90: 440-446. Daviglus ML, Dyer AR, Persky V, et al. Dietary beta-carotene, vitamin C, and risk of prostate cancer: results from the Western Electric Study. Epidemiology 1996; 7: 472-477. Gann PH, Ma J, Giovannucci E, et al. Lower prostate cancer risk in men with elevated plasma lycopene levels: results of a prospective analysis. Cancer Res 1999; 59: 1225-1230. Mettlin C, Selenskas S, Natarajan N, Huben R. Beta-carotene and animal fats and their relationship to prostate cancer risks. A case-control study. Cancer 1989; 64: 605-612.

Paul P Glasziou · Anneliese B Spinks · Sharon L Sanders