1073
respiratory-tract infection among low-birthweight babies of 50% or need to identify every case of to treat with antibiotics. In a casein time neonatal pneumonia + chest wall retraction" and of use "cough approach, management "history of rapid breathing + chest wall retraction" as alternatives to "cough + RR 50" would identify pneumonia where there is no cough and where respiration is below 50/min. More flexible criteria are important because non-tachypnoeic neonatal pneumonia carries a much higher risk of death.
so.’ To reduce mortality further
we
who sees a child should ask to see the RTHC. If the mother sees the paediatrician ask for the RTHC at the bedside, and that it is used to reach a diagnosis, she will appreciate its importance. The child health record should be attractive to parents. For instance, at the Victorian Aboriginal Health Service a child health record has been designed which includes a fold-out page for the child’s own family tree.
The introduction of these records and their
correct use
should
improve growth monitoring, the documentation of immunisation, and the involvement of the parents in their children’s health.
Department of Paediatrics, Postgraduate Institute of Medical Education & Research, Chandigarh-160 012, India
SUNIT SINGHI PRATIBHA D. SINGHI
Victorian Aboriginal Health Service, Fitzroy, Victoria 3065, Australia
WENDY HOLMES
1. Batchelor J, Kerslake A. Failure to find failure to thrive. London: 1. Shann F, Hart K, Thomas D. Acute lower respiratory infections in children:
possible
selection of patients for antibiotic therapy and hospital admission. Bull WHO 1984; 62: 749-53. 2. Chenan T, John TJ, Simoes E, Steinhoff MC, John M. Evaluation of simple clinical signs for the diagnosis of acute lower respiratory tract infection. Lancet 1988; ii: 125-28. 3 Campbell H, Byass P, Greenwood BM. Simple clinical signs for diagnosis of acute lower respiratory infection. Lancet 1988; ii. 742-43. 4.Campbell H, Bypass P, Lamont AC, et al. Assessment of clinical criteria for identification of severe lower respiratory infections in children Lancet 1989; i: 297-99. 5. World Health Organisation. Respiratory infections in children: management in small hospitals, a manual for doctors. Geneva: WHO: 1988. 6. Haney PJ, Bohlman M, Sun CCJ. Radiographic Findings in neonatal pneumonia. Am criteria for
J Radiol 1984; 143: 23-26. N, Kumar V, Kumar L, Singhi S. Application of case management to the control of acute lower respiratory infections in low birth weight infants: a feasibility study. Bull WHO 1987; 65: 77-82.
7 Datta
Failure to thrive SIR,-Your Sept 15 editorial on failure to thrive did not discuss a useful device that would enable centile charts to be used more effectively. Parent-held child health records can help to solve the difficulties (poor communication between professionals, lost records, and inaccurate charting) identified by Batchelor and Kerslake,’ which lead to many children with poor weight gain being missed. Most children are weighed several times in their first year when they present for immunisations or when ill, even if they are not brought to the clinic for routine weight checks. At present many weight measurements are wasted, because the weight is plotted incorrectly, the record is lost, or the child is weighed in different places. Several studies,2-4 and my own experience in Zimbabwe, show that few parents lose their child’s health record, and that they will bring the record, especially when they know that they are responsible for it, when they attend with their child. There are several designs of centile chart in use, some with difficult decimal scales. A standardised growth chart, especially one based on David Morley’s international Road to Health Card (RTHC), which has been tested and improved many times, would be easier to use and lead to fewer inaccurate charts. My experience in Zimbabwe, where almost every mother keeps a RTHC for her child, has shown me that it can serve as a useful cue to history taking. Thus a gap of several months without a weight recording might prompt the question "What happened in July?" and elicit the response that the child went to the grandmother in a rural area; or a question about the onset of a period of loss of weight might reveal that the father left at that time. Severe weight loss is usually obvious; however, failure to gain weight over several months is a subtle but important sign, easily missed without a RTHC. The RTHC can often show when the failure of growth began. Parent-held records lead to greater parental involvement in the child’s health, which also improves management. A steady increase on the growth chart gives satisfaction to parents at home, just as it does to doctors and nurses in a premature baby unit. A new personal child health record was launched in Britain in June.s Doctors have been criticised3by parents for not taking an interest in the records, and these parents did not keep the charts. Every time the child is weighed the value should be recorded and the growth curve explained to the mother. Every health professional
2. 3. 4. 5.
Whiting and Birch, 1990. Lakhani AD, Avery A, Gordon A, Tait N. Evaluation of a home based health record booklet. Arch Dis Child 1984; 59: 1076-81. Miller SA St J. A trial of parent held child health records in the armed forces. Br Med J 1990; 300: 1046. O’Flaherty S, Jandera E, Llewelyn J, Wall M. Personal health records: an evaluation. Arch Dis Child 1987; 62: 1152-55. Godlee F. Parent held records arrive. Br Med J 1990; 300: 1608-09.
Endogenous prostaglandins as regulators of cell proliferation SIR,-Dr Levi and colleagues (Oct 6, p 840) show that indomethacin administration delays ulcer healing and reduces cell proliferation in the gastric mucosa and that a prostaglandin E1 analogue partly reversed this effect and accelerated ulcer healing. Our group has previously demonstrated that administration of indomethacin to the rat reduces mitotic activity in the gastric and jejunal epithelium1,2 and affects the distribution of proliferating cells along the oxyntic mucosa.2 Mitosis areas have a cluster-like distribution, leaving extensive areas with low or absent mitotic activity in between. Indomethacin increased the mitosis-free areas and reduced the total number of proliferating cells present in 8 mm mucosa. Exogenous E2 prostaglandins modified the proliferative pattern by producing a more even distribution of mitosis, and by reducing the mitosis-free areas without affecting the total number of proliferating cells.2 Important conclusions from these experiments were that endogenous prostaglandins may have a role as regulators of cell proliferation1,2 and that prostaglandin treatment may increase the capacity of the gastric epithelium to repair, whereas indomethacin has the opposite effect. We are happy that Levi and colleagues’ results confirm our preliminary findings. We strongly believe that their elegant work should have been enriched by discussion of our data as well as important contributions from Konturek et aP and Gérard.4 There is increasing evidence that endogenous prostaglandins may be regulators of the cell kinetics of the gastrointestinal epithelium. In addition, to reduce epithelial cell losses,5 prostaglandins might contribute to the facilitation of a trophic reaction as discussed, and, in certain conditions, they may even influence feed-back mechanisms that inhibit cell proliferation.6 Gl Unit Department of Medicine, Karolinksa Hospital, 10401 Stockholm, Sweden
ANDRÉS URIBE
CATJA JOHANSSON
1. Unbe A, Johansson C, Rubio C. Cell proliferation of the rat gastrointestinal mucosa after treatment with E, prostaglandins and indomethacin. Digestion 1987; 36: 238-45. 2 Uribe A, Rubio C, Johansson C Alternating proliferative capacity m the rat gastrointestinal mucosa: effects of E2 prostaglandins and indomethacin. Scand J Gastroenterol 1988; 23: 163-70. 3. Konturek SJ, Radecki T, Brzozowski T, et al Gastric cytoprotection by epidermal growth factor: role of endogenous prostaglandins and DNA synthesis Gastroenterology 1981; 81: 438-43. 4. Gérard A. Cell regeneration in the gastric mucosa of the dog under the influence of various stimulant and ulcerogenic drugs. Biol Gastro-Entérol 1969; 1: 5-14. 5. Uribe A, Johansson C. Initial kinetic changes of prostaglandin E2-induced hyperplasia of the rat small intestinal epithelium occur in the villous compartments 6.
Gastroenterology 1988; 94: 1335-42. Uribe A, Garberg L Prostaglandin E2-induced hyperplasia of the rat antral epithelium is followed by a secondary inhibition of the mitotic activity. Prostaglandins 1990; 40: 1-11
respiratory-tract infection among low-birthweight babies of 50% or need to identify every case of to treat with antibiotics. In a casein time neonatal pneumonia + chest wall retraction" and of use "cough approach, management "history of rapid breathing + chest wall retraction" as alternatives to "cough + RR 50" would identify pneumonia where there is no cough and where respiration is below 50/min. More flexible criteria are important because non-tachypnoeic neonatal pneumonia carries a much higher risk of death.
so.’ To reduce mortality further
we
who sees a child should ask to see the RTHC. If the mother sees the paediatrician ask for the RTHC at the bedside, and that it is used to reach a diagnosis, she will appreciate its importance. The child health record should be attractive to parents. For instance, at the Victorian Aboriginal Health Service a child health record has been designed which includes a fold-out page for the child’s own family tree.
The introduction of these records and their
correct use
should
improve growth monitoring, the documentation of immunisation, and the involvement of the parents in their children’s health.
Department of Paediatrics, Postgraduate Institute of Medical Education & Research, Chandigarh-160 012, India
SUNIT SINGHI PRATIBHA D. SINGHI
Victorian Aboriginal Health Service, Fitzroy, Victoria 3065, Australia
WENDY HOLMES
1. Batchelor J, Kerslake A. Failure to find failure to thrive. London: 1. Shann F, Hart K, Thomas D. Acute lower respiratory infections in children:
possible
selection of patients for antibiotic therapy and hospital admission. Bull WHO 1984; 62: 749-53. 2. Chenan T, John TJ, Simoes E, Steinhoff MC, John M. Evaluation of simple clinical signs for the diagnosis of acute lower respiratory tract infection. Lancet 1988; ii: 125-28. 3 Campbell H, Byass P, Greenwood BM. Simple clinical signs for diagnosis of acute lower respiratory infection. Lancet 1988; ii. 742-43. 4.Campbell H, Bypass P, Lamont AC, et al. Assessment of clinical criteria for identification of severe lower respiratory infections in children Lancet 1989; i: 297-99. 5. World Health Organisation. Respiratory infections in children: management in small hospitals, a manual for doctors. Geneva: WHO: 1988. 6. Haney PJ, Bohlman M, Sun CCJ. Radiographic Findings in neonatal pneumonia. Am criteria for
J Radiol 1984; 143: 23-26. N, Kumar V, Kumar L, Singhi S. Application of case management to the control of acute lower respiratory infections in low birth weight infants: a feasibility study. Bull WHO 1987; 65: 77-82.
7 Datta
Failure to thrive SIR,-Your Sept 15 editorial on failure to thrive did not discuss a useful device that would enable centile charts to be used more effectively. Parent-held child health records can help to solve the difficulties (poor communication between professionals, lost records, and inaccurate charting) identified by Batchelor and Kerslake,’ which lead to many children with poor weight gain being missed. Most children are weighed several times in their first year when they present for immunisations or when ill, even if they are not brought to the clinic for routine weight checks. At present many weight measurements are wasted, because the weight is plotted incorrectly, the record is lost, or the child is weighed in different places. Several studies,2-4 and my own experience in Zimbabwe, show that few parents lose their child’s health record, and that they will bring the record, especially when they know that they are responsible for it, when they attend with their child. There are several designs of centile chart in use, some with difficult decimal scales. A standardised growth chart, especially one based on David Morley’s international Road to Health Card (RTHC), which has been tested and improved many times, would be easier to use and lead to fewer inaccurate charts. My experience in Zimbabwe, where almost every mother keeps a RTHC for her child, has shown me that it can serve as a useful cue to history taking. Thus a gap of several months without a weight recording might prompt the question "What happened in July?" and elicit the response that the child went to the grandmother in a rural area; or a question about the onset of a period of loss of weight might reveal that the father left at that time. Severe weight loss is usually obvious; however, failure to gain weight over several months is a subtle but important sign, easily missed without a RTHC. The RTHC can often show when the failure of growth began. Parent-held records lead to greater parental involvement in the child’s health, which also improves management. A steady increase on the growth chart gives satisfaction to parents at home, just as it does to doctors and nurses in a premature baby unit. A new personal child health record was launched in Britain in June.s Doctors have been criticised3by parents for not taking an interest in the records, and these parents did not keep the charts. Every time the child is weighed the value should be recorded and the growth curve explained to the mother. Every health professional
2. 3. 4. 5.
Whiting and Birch, 1990. Lakhani AD, Avery A, Gordon A, Tait N. Evaluation of a home based health record booklet. Arch Dis Child 1984; 59: 1076-81. Miller SA St J. A trial of parent held child health records in the armed forces. Br Med J 1990; 300: 1046. O’Flaherty S, Jandera E, Llewelyn J, Wall M. Personal health records: an evaluation. Arch Dis Child 1987; 62: 1152-55. Godlee F. Parent held records arrive. Br Med J 1990; 300: 1608-09.
Endogenous prostaglandins as regulators of cell proliferation SIR,-Dr Levi and colleagues (Oct 6, p 840) show that indomethacin administration delays ulcer healing and reduces cell proliferation in the gastric mucosa and that a prostaglandin E1 analogue partly reversed this effect and accelerated ulcer healing. Our group has previously demonstrated that administration of indomethacin to the rat reduces mitotic activity in the gastric and jejunal epithelium1,2 and affects the distribution of proliferating cells along the oxyntic mucosa.2 Mitosis areas have a cluster-like distribution, leaving extensive areas with low or absent mitotic activity in between. Indomethacin increased the mitosis-free areas and reduced the total number of proliferating cells present in 8 mm mucosa. Exogenous E2 prostaglandins modified the proliferative pattern by producing a more even distribution of mitosis, and by reducing the mitosis-free areas without affecting the total number of proliferating cells.2 Important conclusions from these experiments were that endogenous prostaglandins may have a role as regulators of cell proliferation1,2 and that prostaglandin treatment may increase the capacity of the gastric epithelium to repair, whereas indomethacin has the opposite effect. We are happy that Levi and colleagues’ results confirm our preliminary findings. We strongly believe that their elegant work should have been enriched by discussion of our data as well as important contributions from Konturek et aP and Gérard.4 There is increasing evidence that endogenous prostaglandins may be regulators of the cell kinetics of the gastrointestinal epithelium. In addition, to reduce epithelial cell losses,5 prostaglandins might contribute to the facilitation of a trophic reaction as discussed, and, in certain conditions, they may even influence feed-back mechanisms that inhibit cell proliferation.6 Gl Unit Department of Medicine, Karolinksa Hospital, 10401 Stockholm, Sweden
ANDRÉS URIBE
CATJA JOHANSSON
1. Unbe A, Johansson C, Rubio C. Cell proliferation of the rat gastrointestinal mucosa after treatment with E, prostaglandins and indomethacin. Digestion 1987; 36: 238-45. 2 Uribe A, Rubio C, Johansson C Alternating proliferative capacity m the rat gastrointestinal mucosa: effects of E2 prostaglandins and indomethacin. Scand J Gastroenterol 1988; 23: 163-70. 3. Konturek SJ, Radecki T, Brzozowski T, et al Gastric cytoprotection by epidermal growth factor: role of endogenous prostaglandins and DNA synthesis Gastroenterology 1981; 81: 438-43. 4. Gérard A. Cell regeneration in the gastric mucosa of the dog under the influence of various stimulant and ulcerogenic drugs. Biol Gastro-Entérol 1969; 1: 5-14. 5. Uribe A, Johansson C. Initial kinetic changes of prostaglandin E2-induced hyperplasia of the rat small intestinal epithelium occur in the villous compartments 6.
Gastroenterology 1988; 94: 1335-42. Uribe A, Garberg L Prostaglandin E2-induced hyperplasia of the rat antral epithelium is followed by a secondary inhibition of the mitotic activity. Prostaglandins 1990; 40: 1-11
