- Email: [email protected]
Tropheryma whippelii DNA in saliva of healthy people
Mean (range) room entries/h Mean (range) contacts/h Mean (range) duration of interaction (min)
Patients in contact isolation
Controls
p
3·9 (0–8) 2·1 (0–6) 4·5 (0·08–30)
7·9 (1–26) 4·2 (1–13) 2·8 (0·08–18)
0·06 0·03 0·6
2
3
Table 2: Frequency and duration of contact between health-care workers and patients
4
hands: they washed either before or after two (17%) of 12 patient contacts, compared with non-physicians, who washed before or after 67 (64%) of 105 contacts (p=0·003). Handwashing compliance was significantly higher among health-care workers who cared for patients in contact isolation than among those who cared for controls. However, almost all handwashing by health-care workers caring for patients in contact isolation occurred after the encounter; handwashing occurred before care of a patient in contact isolation only twice (table 1). Compliance with the use of gowns and gloves in the care of patients in contact isolation was 90%. In addition, health-care workers wore gloves during 38 (43%) of 88 encounters with controls. These workers were twice as likely to wash their hands as those who did not wear gloves (relative risk 2·1 [95% CI 1·3–3·3]). Health-care workers who treated patients in contact isolation entered their rooms less frequently, and had signficantly less direct contact with them, than those caring for controls. The mean length of time spent in a patient’s room did not differ significantly between the groups (table 2). Our observations suggest that policies requiring the use of gowns and gloves in caring for patients in contact isolation increase the frequency of handwashing by health-care workers, but decrease the likelihood of contact between health-care workers and patients. The costs of using gowns and gloves as a way of prompting health-care workers to wash their hands are high. In our study, the average length of hospital stay for patients in contact isolation was 46 days. Assuming 90% compliance with contact-isolation policies, we estimate that 2070 disposable gowns and 4140 latex gloves are used during the average hospital stay for a patient in contact isolation within the intensive care unit; the estimated cost is US$1627 per patient. Moreover, the timing of the extra handwashing associated with contact isolation (after care of the patient) is not ideal. Handwashing before contact with patients is clearly beneficial in preventing the nosocomial spread of organisms to the patient. In our study, however, handwashing occurred before contact with patients only 15 times in 117 encounters. The observed tendency of health-care workers to wash after rather than before contact with patients suggests that they may perceive handwashing more as an act of personal protection than as a way to prevent spread of nosocomial pathogens to patients. Our finding that health-care workers were about two times less likely to enter the rooms of patients in contact isolation supports suggestions made by other investigators that patients in isolation receive less frequent care, and may even suffer psychologically.3–5 Particularly in an intensive-care unit, where the number of interactions between health-care workers and patients should be determined by the severity and complexity of illness, less frequent hands-on contact could have a negative impact on disease outcome. Our study raises concerns that contact isolation may have negative consequences for patients. We conclude that contact isolation should not be accepted as a substitute for handwashing. Moreover, until there is convincing evidence that the routine use of contact isolation adds to the efficacy of handwashing alone in controlling the spread of endemic resistant organisms, its routine use (outside an outbreak setting) should be reconsidered.
5
We thank Daniel J Sexton for his critical review of the paper. 1 Garner JS, Hospital Infection Control Practices Advisory Committee.
1178
Guideline for isolation precautions in hospitals. Infect Control Hosp Epidemiol 1996; 17: 54–80. Hospital Infection Control Practices Advisory Committee. Recommendations for preventing the spread of vancomycin resistance. Infect Control Hosp Epidemiol 1995; 16: 105–13. Teare EL, Barrett SP. Stop the ritual of tracing colonised people. BMJ 1997; 314: 665–66. Peel RK, Stolarek I, Elder AT. Is it time to stop searching for MRSA? Isolating patients with MRSA can have long term implications. BMJ 1997; 315: 58. Knowles HE. The experience of infectious patients in isolation. Nursing Times 1993; 89: 53–56.
Department of Medicine, Duke University Medical Center (K B Kirkland MD) and Duke University (J M Weinstein BSc), Durham, NC, USA Correspondence to: Dr Kathryn B Kirkland, Department of Medicine, Dartmouth-Hitchcock Medical Center, 1 Medical Center Drive, Lebanon, NH 03756, USA
Tropheryma whippelii DNA in saliva of healthy people Sara Street, Helen D Donoghue, G H Neild In a random sample of 40 healthy people, 35% showed evidence of Tropheryma whippelii DNA in their saliva. Consistent detection of T whippelii DNA on repeated sampling suggests that this organism can be an oral commensal.
Tropheryma whippelii is the putative pathogen in Whipple’s disease. It has not been cultured, but has been propagated in deactivated macrophages. On the basis of its 16S ribosomal RNA (rRNA) gene sequence, it is related to the group B actinomycetes and the family Cellulomonadaceae. With PCR a heterogeneous group of multisystem diseases were reported in which T whippelii DNA was found in blood and various organs that were both clinically involved and uninvolved.1 While investigating the presence of T whippelii in peripheral blood, the chance finding was made of the presence of T whippeliispecific DNA in saliva. We have now examined the saliva of 40 healthy people. 2 mL of saliva was centrifuged at 2000 g for 15 min, and the pellet resuspended in 3 mL of Cell Lysis Solution (PureGene kit, Flowgen Instruments Ltd, Lichfield, UK). DNA was extracted according to the PureGene protocol with additional steps of cell lysis with Proteinase K and further lysis with guanidinium thiocyanate. 2 PCR was done with 45 cycles, with primers W3AF and W4AR3 that are based on the 16S rRNA gene of T whippelii and yield a specific product of 160 bp. Specimens from 14 people (35%) were positive. One was from a 22-year-old Indian woman, the remainder were white aged 16–58, and nine were male. Further samples were obtained from six of those initially positive and were again positive on one or more occasions. 26 specimens were negative from 14 men and 12 women, aged 22–52 years, of whom three were African, four Oriental, two Indo-Asian, and the remainder white. Six PCR products (amplicons) were sequenced, commercially, from both the 5⬘ and 3⬘ ends with the same nucleotide sequence as the primers. The sequences were aligned with GenBank/EMBL sequences with accession numbers X99636, M87484, M77832, AJ242539. All showed 100% sequence homology for 16S rRNA T whippelii. We have found that a third of a random sample of healthy people had T whippelii DNA in their saliva, which suggests that T whippelii can be an oral commensal organism. This finding is consistent with reports that T whippelii DNA was recorded in 25 out of 38 waste-water samples obtained from five different sewage treatment plants in Southwest Germany, 4 and in 13·3% of either duodenal biopsy specimens or gastric juice of 105 patients having elective gastroscopy, with no clinical signs of Whipple’s disease.5 T whippelii has been regarded as a
THE LANCET • Vol 354 • October 2, 1999
mysterious and remote organism. We suggest that T whippelii is another environmental or commensal organism that is ubiquitous and generally not pathogenic. The project was funded by The Special Trustees of the Middlesex Hospital and UCH and UCL Medical School. 1
Misbah SA, Ozols B, Franks A, Mapstone N. Whipple’s disease without malabsorption: new atypical features. Quart J Med 1997; 90: 765–72. 2 Boom R, Sol CJ, Salimans MM, Jansen CL, Wertheim-van DP, van-der Noordaa J. Rapid and simple method for purification of nucleic acids. J Clin Microbiol 1990; 28: 495–503. 3 Ramzan NN, Loftus E, Burgart LJ, et al. Diagnosis and monitoring of Whipple disease by polymerase chain reaction. Ann Intern Med 1997; 126: 520–27. 4 Maiwald M, Schuhmacher F, Ditton HJ, von Herbay A. Environmental occurrence of the Whipple’s disease bacterium (Tropheryma whippelii). Appl Environ Microbiol 1998; 64: 760–62. 5 Ehrbar H-U, Bauerfeind P, Dutley F, Koelz H-R, Altwegg M. PCRpositive tests for Tropheryma whippelii in patients without Whipple’s disease. Lancet 1999; 353: 2214.
Department of Bacteriology, Windeyer Institute, University College of London, London W1P 6DB, UK (S Street BSc, H D Donoghue PhD, Prof G H Neild FRCPath) Correspondence to: Prof G H Neild (e-mail: [email protected])
Incidence of paediatric Crohn’s disease in Stockholm, Sweden Johan Askling, Lena Grahnquist, Anders Ekbom, Yigael Finkel We report an increase in the incidence of Crohn’s disease in northern Stockholm, Sweden.
Reports from Wales, Scotland, and Canada during the past decade have shown an increasing incidence of Crohn’s disease among children and adolescents.1–3 So far, no such increase has been reported from Scandinavia. On the contrary, reports have consistently shown a stable incidence in the 1980s and 1990s.4,5 However, during the past few years we have noticed an increasing number of new patients with Crohn’s disease in northern Stockholm. All children with inflammatory bowel disease in Stockholm are referred to and treated by paediatric gastroenterologists, with uniform diagnostic investigations and criteria, and the primary catchment area is well defined. This system provides a good opportunity to accurately assess the incidence. The aim of this study was to study the incidence of paediatric inflammatory bowel disease to assess the incidence of Crohn’s disease. All cases of Crohn’s disease and ulcerative or indeterminate colitis diagnosed from 1990 to 1998 in individuals below 17 years of age and resident in the northern part of Stockholm County were identified. Case records were sought from the three hospitals in the study area and from the remaining two hospitals in Stockholm County as well as from adult gastroenterology departments. All patients were diagnosed on the basis of endoscopy, histopathology, and small-bowel enema. Data on the background population by sex, single-year age groups, and calendar year were obtained from Statistics Sweden. In total, 91 cases of inflammatory bowel disease were diagnosed during the study period (table). The mean incidence (per 100 000) was 6·9 (95% CI 5·7–8·5) for all inflammatory bowel disease, 3·8 (2·8–5·0) for Crohn’s disease, 2·1 (1·4–3·0) for ulcerative colitis, and 1·1 (0·6–1·8) for indeterminate colitis. The incidence of Crohn’s disease increased from 2·4 (1·0–4·7) in the period 1990–92 to 2·9 (1·5–5·0) in 1993–95 and 5·4 (3·6–7·7, p=0·027 compared with 1990–92) in 1996–98. The corresponding incidence of ulcerative and indeterminate colitis, however, remained unchanged: 3·9 (2·1–6·6), 2·6 (1·3–4·7), and 3·0 (1·8–4·9).
THE LANCET • Vol 354 • October 2, 1999
Annual incidence
Crohn’s disease (n=50)
Ulcerative colitis (n=27)
Unspecified colitis (n=14)
1990 1991 1992 1993 1994 1995 1996 1997 1998
0·0 (0·0–3·3) 2·7 (0·6–7·8) 4·4 (1·4–10) 1·7 (0·2–6·2) 4·2 (1·4–9·8) 2·7 (0·9–6·3) 4·3 (1(9–8·5) 5·9 (2·9–11) 5·9 (2·9–11)
0·9 (0·0–5·0) 3·6 (1·0–9·1) 4·4 (1·4–10·2) 0·9 (0·0–4·8) 2·5 (0·5–7·4) 1·6 (0·3–4·8) 2·7 (0·9–6·3) 2·1 (0·6–5·5) 0·5 (0·0–3·0)
0·9 (0·0–5·0) 1·8 (0·2–6·4) 0·0 (0·0–3·2) 1·7 (0·2–6·2) 1·7 (0·2–6·1) 0·0 (0·0–2·0) 1·6 (0·3–4·7) 1·6 (0·3–4·7) 0·5 (0·0–3·0)
Incidence (per 100 000, 95% CI) of inflammatory bowel disease among individuals below 17 years of age in northern Stockholm, Sweden, 1990–98
Four children were diagnosed with Crohn’s disease at or below 5 years of age. Three of these were diagnosed in 1996–98. Six children with Crohn’s disease developed fistulae, four of whom were diagnosed in 1997–98. In conclusion, after more than a decade of stable incidence of paediatric inflammatory bowel disease in Scandinavia, we report a recent increase in the incidence of Crohn’s disease, which is not related to a reciprocal decrease in ulcerative or indeterminate colitis. The increasing incidence is in accordance with reports from other parts of the world.1–3 In fact, the 1997–98 incidence of Crohn’s disease in Stockholm is even higher than that previously reported.1,2 The difference in comparison with previous Scandinavian studies4,5 may reflect how recent the increase is or indicate important differences in study-population characteristics. The additional findings of an increasing number of Crohn’s disease in the very young and fistulating disease also indicate a change in disease appearance. 1 2 3
4
5
Cosgrove M, Al-Atia RF, Jenkins HR. The epidemiology of paediatric inflammatory bowel disease. Arch Dis Child 1996; 74: 460–61. Armitage E, Drummond H, Ghosh S, Ferguson A. Incidence of juvenile-onset Crohn’s disease in Scotland. Lancet 1999; 353: 1496–97. Seidman EG, Weber AM, Morin CL, Roy CC. Inflammatory bowel disease in childhood. In: Freeman HJ, ed. Inflammatory bowel disease. Vol 2. Boca Raton: CRC Press 1989: 217–27. Lindberg E, Hildebrand H, Holmquist L, Lindquist B. Paediatric inflammatory bowel disease in Sweden 1984–1995. J Ped Gastroenterol Nutr 1998; 26: 554 (abstr). Langholz E, Munkholm P, Kraslinikoff A, Binder V. Inflammatory bowel diseases with onset in childhood. Scand J Gastroenterol 1997; 32: 139–47.
Department of Medical Epidemiology, Karolinska Institute, S-171 77 Stockholm, Sweden (J Askling MD, A Ekbom MD); Department of Women and Child Health, Paediatric Unit, Karolinska Institute and Astrid Lindgren Children’s Hospital, Karolinska Sjukhuset, Stockholm, Sweden (L Grahnquist MD, Y Finkel MD); and Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA (A Ekbom) Correspondence to: Dr Johan Askling (e-mail: [email protected])
Oxaliplatin-induced haemolytic anaemia J Desrame, H Broustet, P Darodes de Tailly, D Girard, J M Saissy A case of haemolytic anaemia after therapy with oxaliplatin, an anticancer chemotherapeutic agent, was investigated. Haemolytic anaemia has been associated with cisplatin and carboplatin, two related drugs, but not with oxaliplatin.
Oxaliplatin, a new third-generation platinium complex, is active in the treatment of advanced colorectal cancer and has shown a very good safety profile both as monotherapy and in combination with fluorouracil and folinic acid.1 We report a case of fatal acute haemolysis after therapy with oxaliplatin.
1179
Patients in contact isolation
Controls
p
3·9 (0–8) 2·1 (0–6) 4·5 (0·08–30)
7·9 (1–26) 4·2 (1–13) 2·8 (0·08–18)
0·06 0·03 0·6
2
3
Table 2: Frequency and duration of contact between health-care workers and patients
4
hands: they washed either before or after two (17%) of 12 patient contacts, compared with non-physicians, who washed before or after 67 (64%) of 105 contacts (p=0·003). Handwashing compliance was significantly higher among health-care workers who cared for patients in contact isolation than among those who cared for controls. However, almost all handwashing by health-care workers caring for patients in contact isolation occurred after the encounter; handwashing occurred before care of a patient in contact isolation only twice (table 1). Compliance with the use of gowns and gloves in the care of patients in contact isolation was 90%. In addition, health-care workers wore gloves during 38 (43%) of 88 encounters with controls. These workers were twice as likely to wash their hands as those who did not wear gloves (relative risk 2·1 [95% CI 1·3–3·3]). Health-care workers who treated patients in contact isolation entered their rooms less frequently, and had signficantly less direct contact with them, than those caring for controls. The mean length of time spent in a patient’s room did not differ significantly between the groups (table 2). Our observations suggest that policies requiring the use of gowns and gloves in caring for patients in contact isolation increase the frequency of handwashing by health-care workers, but decrease the likelihood of contact between health-care workers and patients. The costs of using gowns and gloves as a way of prompting health-care workers to wash their hands are high. In our study, the average length of hospital stay for patients in contact isolation was 46 days. Assuming 90% compliance with contact-isolation policies, we estimate that 2070 disposable gowns and 4140 latex gloves are used during the average hospital stay for a patient in contact isolation within the intensive care unit; the estimated cost is US$1627 per patient. Moreover, the timing of the extra handwashing associated with contact isolation (after care of the patient) is not ideal. Handwashing before contact with patients is clearly beneficial in preventing the nosocomial spread of organisms to the patient. In our study, however, handwashing occurred before contact with patients only 15 times in 117 encounters. The observed tendency of health-care workers to wash after rather than before contact with patients suggests that they may perceive handwashing more as an act of personal protection than as a way to prevent spread of nosocomial pathogens to patients. Our finding that health-care workers were about two times less likely to enter the rooms of patients in contact isolation supports suggestions made by other investigators that patients in isolation receive less frequent care, and may even suffer psychologically.3–5 Particularly in an intensive-care unit, where the number of interactions between health-care workers and patients should be determined by the severity and complexity of illness, less frequent hands-on contact could have a negative impact on disease outcome. Our study raises concerns that contact isolation may have negative consequences for patients. We conclude that contact isolation should not be accepted as a substitute for handwashing. Moreover, until there is convincing evidence that the routine use of contact isolation adds to the efficacy of handwashing alone in controlling the spread of endemic resistant organisms, its routine use (outside an outbreak setting) should be reconsidered.
5
We thank Daniel J Sexton for his critical review of the paper. 1 Garner JS, Hospital Infection Control Practices Advisory Committee.
1178
Guideline for isolation precautions in hospitals. Infect Control Hosp Epidemiol 1996; 17: 54–80. Hospital Infection Control Practices Advisory Committee. Recommendations for preventing the spread of vancomycin resistance. Infect Control Hosp Epidemiol 1995; 16: 105–13. Teare EL, Barrett SP. Stop the ritual of tracing colonised people. BMJ 1997; 314: 665–66. Peel RK, Stolarek I, Elder AT. Is it time to stop searching for MRSA? Isolating patients with MRSA can have long term implications. BMJ 1997; 315: 58. Knowles HE. The experience of infectious patients in isolation. Nursing Times 1993; 89: 53–56.
Department of Medicine, Duke University Medical Center (K B Kirkland MD) and Duke University (J M Weinstein BSc), Durham, NC, USA Correspondence to: Dr Kathryn B Kirkland, Department of Medicine, Dartmouth-Hitchcock Medical Center, 1 Medical Center Drive, Lebanon, NH 03756, USA
Tropheryma whippelii DNA in saliva of healthy people Sara Street, Helen D Donoghue, G H Neild In a random sample of 40 healthy people, 35% showed evidence of Tropheryma whippelii DNA in their saliva. Consistent detection of T whippelii DNA on repeated sampling suggests that this organism can be an oral commensal.
Tropheryma whippelii is the putative pathogen in Whipple’s disease. It has not been cultured, but has been propagated in deactivated macrophages. On the basis of its 16S ribosomal RNA (rRNA) gene sequence, it is related to the group B actinomycetes and the family Cellulomonadaceae. With PCR a heterogeneous group of multisystem diseases were reported in which T whippelii DNA was found in blood and various organs that were both clinically involved and uninvolved.1 While investigating the presence of T whippelii in peripheral blood, the chance finding was made of the presence of T whippeliispecific DNA in saliva. We have now examined the saliva of 40 healthy people. 2 mL of saliva was centrifuged at 2000 g for 15 min, and the pellet resuspended in 3 mL of Cell Lysis Solution (PureGene kit, Flowgen Instruments Ltd, Lichfield, UK). DNA was extracted according to the PureGene protocol with additional steps of cell lysis with Proteinase K and further lysis with guanidinium thiocyanate. 2 PCR was done with 45 cycles, with primers W3AF and W4AR3 that are based on the 16S rRNA gene of T whippelii and yield a specific product of 160 bp. Specimens from 14 people (35%) were positive. One was from a 22-year-old Indian woman, the remainder were white aged 16–58, and nine were male. Further samples were obtained from six of those initially positive and were again positive on one or more occasions. 26 specimens were negative from 14 men and 12 women, aged 22–52 years, of whom three were African, four Oriental, two Indo-Asian, and the remainder white. Six PCR products (amplicons) were sequenced, commercially, from both the 5⬘ and 3⬘ ends with the same nucleotide sequence as the primers. The sequences were aligned with GenBank/EMBL sequences with accession numbers X99636, M87484, M77832, AJ242539. All showed 100% sequence homology for 16S rRNA T whippelii. We have found that a third of a random sample of healthy people had T whippelii DNA in their saliva, which suggests that T whippelii can be an oral commensal organism. This finding is consistent with reports that T whippelii DNA was recorded in 25 out of 38 waste-water samples obtained from five different sewage treatment plants in Southwest Germany, 4 and in 13·3% of either duodenal biopsy specimens or gastric juice of 105 patients having elective gastroscopy, with no clinical signs of Whipple’s disease.5 T whippelii has been regarded as a
THE LANCET • Vol 354 • October 2, 1999
mysterious and remote organism. We suggest that T whippelii is another environmental or commensal organism that is ubiquitous and generally not pathogenic. The project was funded by The Special Trustees of the Middlesex Hospital and UCH and UCL Medical School. 1
Misbah SA, Ozols B, Franks A, Mapstone N. Whipple’s disease without malabsorption: new atypical features. Quart J Med 1997; 90: 765–72. 2 Boom R, Sol CJ, Salimans MM, Jansen CL, Wertheim-van DP, van-der Noordaa J. Rapid and simple method for purification of nucleic acids. J Clin Microbiol 1990; 28: 495–503. 3 Ramzan NN, Loftus E, Burgart LJ, et al. Diagnosis and monitoring of Whipple disease by polymerase chain reaction. Ann Intern Med 1997; 126: 520–27. 4 Maiwald M, Schuhmacher F, Ditton HJ, von Herbay A. Environmental occurrence of the Whipple’s disease bacterium (Tropheryma whippelii). Appl Environ Microbiol 1998; 64: 760–62. 5 Ehrbar H-U, Bauerfeind P, Dutley F, Koelz H-R, Altwegg M. PCRpositive tests for Tropheryma whippelii in patients without Whipple’s disease. Lancet 1999; 353: 2214.
Department of Bacteriology, Windeyer Institute, University College of London, London W1P 6DB, UK (S Street BSc, H D Donoghue PhD, Prof G H Neild FRCPath) Correspondence to: Prof G H Neild (e-mail: [email protected])
Incidence of paediatric Crohn’s disease in Stockholm, Sweden Johan Askling, Lena Grahnquist, Anders Ekbom, Yigael Finkel We report an increase in the incidence of Crohn’s disease in northern Stockholm, Sweden.
Reports from Wales, Scotland, and Canada during the past decade have shown an increasing incidence of Crohn’s disease among children and adolescents.1–3 So far, no such increase has been reported from Scandinavia. On the contrary, reports have consistently shown a stable incidence in the 1980s and 1990s.4,5 However, during the past few years we have noticed an increasing number of new patients with Crohn’s disease in northern Stockholm. All children with inflammatory bowel disease in Stockholm are referred to and treated by paediatric gastroenterologists, with uniform diagnostic investigations and criteria, and the primary catchment area is well defined. This system provides a good opportunity to accurately assess the incidence. The aim of this study was to study the incidence of paediatric inflammatory bowel disease to assess the incidence of Crohn’s disease. All cases of Crohn’s disease and ulcerative or indeterminate colitis diagnosed from 1990 to 1998 in individuals below 17 years of age and resident in the northern part of Stockholm County were identified. Case records were sought from the three hospitals in the study area and from the remaining two hospitals in Stockholm County as well as from adult gastroenterology departments. All patients were diagnosed on the basis of endoscopy, histopathology, and small-bowel enema. Data on the background population by sex, single-year age groups, and calendar year were obtained from Statistics Sweden. In total, 91 cases of inflammatory bowel disease were diagnosed during the study period (table). The mean incidence (per 100 000) was 6·9 (95% CI 5·7–8·5) for all inflammatory bowel disease, 3·8 (2·8–5·0) for Crohn’s disease, 2·1 (1·4–3·0) for ulcerative colitis, and 1·1 (0·6–1·8) for indeterminate colitis. The incidence of Crohn’s disease increased from 2·4 (1·0–4·7) in the period 1990–92 to 2·9 (1·5–5·0) in 1993–95 and 5·4 (3·6–7·7, p=0·027 compared with 1990–92) in 1996–98. The corresponding incidence of ulcerative and indeterminate colitis, however, remained unchanged: 3·9 (2·1–6·6), 2·6 (1·3–4·7), and 3·0 (1·8–4·9).
THE LANCET • Vol 354 • October 2, 1999
Annual incidence
Crohn’s disease (n=50)
Ulcerative colitis (n=27)
Unspecified colitis (n=14)
1990 1991 1992 1993 1994 1995 1996 1997 1998
0·0 (0·0–3·3) 2·7 (0·6–7·8) 4·4 (1·4–10) 1·7 (0·2–6·2) 4·2 (1·4–9·8) 2·7 (0·9–6·3) 4·3 (1(9–8·5) 5·9 (2·9–11) 5·9 (2·9–11)
0·9 (0·0–5·0) 3·6 (1·0–9·1) 4·4 (1·4–10·2) 0·9 (0·0–4·8) 2·5 (0·5–7·4) 1·6 (0·3–4·8) 2·7 (0·9–6·3) 2·1 (0·6–5·5) 0·5 (0·0–3·0)
0·9 (0·0–5·0) 1·8 (0·2–6·4) 0·0 (0·0–3·2) 1·7 (0·2–6·2) 1·7 (0·2–6·1) 0·0 (0·0–2·0) 1·6 (0·3–4·7) 1·6 (0·3–4·7) 0·5 (0·0–3·0)
Incidence (per 100 000, 95% CI) of inflammatory bowel disease among individuals below 17 years of age in northern Stockholm, Sweden, 1990–98
Four children were diagnosed with Crohn’s disease at or below 5 years of age. Three of these were diagnosed in 1996–98. Six children with Crohn’s disease developed fistulae, four of whom were diagnosed in 1997–98. In conclusion, after more than a decade of stable incidence of paediatric inflammatory bowel disease in Scandinavia, we report a recent increase in the incidence of Crohn’s disease, which is not related to a reciprocal decrease in ulcerative or indeterminate colitis. The increasing incidence is in accordance with reports from other parts of the world.1–3 In fact, the 1997–98 incidence of Crohn’s disease in Stockholm is even higher than that previously reported.1,2 The difference in comparison with previous Scandinavian studies4,5 may reflect how recent the increase is or indicate important differences in study-population characteristics. The additional findings of an increasing number of Crohn’s disease in the very young and fistulating disease also indicate a change in disease appearance. 1 2 3
4
5
Cosgrove M, Al-Atia RF, Jenkins HR. The epidemiology of paediatric inflammatory bowel disease. Arch Dis Child 1996; 74: 460–61. Armitage E, Drummond H, Ghosh S, Ferguson A. Incidence of juvenile-onset Crohn’s disease in Scotland. Lancet 1999; 353: 1496–97. Seidman EG, Weber AM, Morin CL, Roy CC. Inflammatory bowel disease in childhood. In: Freeman HJ, ed. Inflammatory bowel disease. Vol 2. Boca Raton: CRC Press 1989: 217–27. Lindberg E, Hildebrand H, Holmquist L, Lindquist B. Paediatric inflammatory bowel disease in Sweden 1984–1995. J Ped Gastroenterol Nutr 1998; 26: 554 (abstr). Langholz E, Munkholm P, Kraslinikoff A, Binder V. Inflammatory bowel diseases with onset in childhood. Scand J Gastroenterol 1997; 32: 139–47.
Department of Medical Epidemiology, Karolinska Institute, S-171 77 Stockholm, Sweden (J Askling MD, A Ekbom MD); Department of Women and Child Health, Paediatric Unit, Karolinska Institute and Astrid Lindgren Children’s Hospital, Karolinska Sjukhuset, Stockholm, Sweden (L Grahnquist MD, Y Finkel MD); and Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA (A Ekbom) Correspondence to: Dr Johan Askling (e-mail: [email protected])
Oxaliplatin-induced haemolytic anaemia J Desrame, H Broustet, P Darodes de Tailly, D Girard, J M Saissy A case of haemolytic anaemia after therapy with oxaliplatin, an anticancer chemotherapeutic agent, was investigated. Haemolytic anaemia has been associated with cisplatin and carboplatin, two related drugs, but not with oxaliplatin.
Oxaliplatin, a new third-generation platinium complex, is active in the treatment of advanced colorectal cancer and has shown a very good safety profile both as monotherapy and in combination with fluorouracil and folinic acid.1 We report a case of fatal acute haemolysis after therapy with oxaliplatin.
1179