We read with great interest the paper of Choe and colleagues who
investigated possible relationships between H. pylori infection with iron
deficiency anaemia (IDA) and subnormal growth at puberty.[1] They
concluded that H. pylori infection and related IDA, rather than bacterial
infection per se, might cause delayed pubertal growth. We believe that
Choe et al’s results need some considerations.
We read with great interest the paper of Choe and colleagues who
investigated possible relationships between H. pylori infection with iron
deficiency anaemia (IDA) and subnormal growth at puberty.[1] They
concluded that H. pylori infection and related IDA, rather than bacterial
infection per se, might cause delayed pubertal growth. We believe that
Choe et al’s results need some considerations.
H. pylori infection may cause IDA in different ways
(a) the bacterium
causes a decrease in the gastric juice of the concentration of ascorbic
acid,[2] that is the best promoter of non-heme iron absorption
(b) H. pylori may increase iron demand because iron is an essential bacterial
growth factor
(c) H. pylori contains a 19.6 kDA protein resembling ferritin
with a binding activity for heme iron in erythrocytes[3]
(d) acute or
chronic blood loss and IDA are obviously related to typical H. pylori-
related gastroduodenal lesions.
In Choe et al’s study the treatment of
H. pylori infection with antibiotics (but also with proton pump inhibitors (PPI)) was probably
associated with a more rapid response to oral iron replacement also for
the effects of PPI in healing some of these lesions.
However, IDA, failure to thrive and delayed pubertal growth are important
features of subclinical and silent coeliac disease. Therefore, coeliac
disease should be suspected everywhere in children or adolescents with
these signs, especially when IDA is refractory to oral iron replacement.
In a recent study,[4] both in children and in adults IDA appeared to be
the most frequent extra-intestinal marker of coeliac disease, followed by
short stature for children. Thus, it appears mandatory to screen
paediatric and juvenile populations with IDA and/or failure to thrive
and/or delayed pubertal growth by means of determination of coeliac
related antibodies (anti-endomysial, anti-transglutaminase, anti-gliadin)
in order to identify coeliac patients who need life-long gluten withdrawal
for recover of iron metabolism and growth.
Finally, it is reasonable that H. pylori infection may concur and worsen
iron deficiency in coeliac patients and subsequently impair the growth in
paediatric ages who need a great amount of this essential element.
Lucio Cuoco, MD Giovanni Cammarota, MD Regina Anna Jorizzo, MD Rossella Cianci, MD Giovanni Gasbarrini, MD
Corresponding author: Dr L Cuoco Università Cattolica del Sacro
Cuore, Policlinico “A.Gemelli” Istituto di Medicina Interna e Geriatria Largo A.Gemelli, 8 - 00168 Roma, Italia
Fax: +39 06 35502775
email: gcammarota@libero.it
References
(1) Choe YH, Kim SK, Hong YC. Helicobacter pylori infection with iron
deficiency anaemia and subnormal growth at puberty. Arch Dis Child
2000;82:136-40.
(2) Banerjee S, Hawksby C, Miller S, Dahill S, Beattie AD, McColl KE.
Effect of Helicobacter pylori and its eradication on gastric juice
ascorbic acid. Gut 1994;35:317-22.
(3) Doig P, Austin JW, Trust TJ. The Helicobacter pylori 19.6-
kilodalton protein is an iron-containing protein resembling ferritin. J
Bacteriol 1993;175:557-60.
(4) Bottaro G, Cataldo F, Rotolo N, Spina M, Corazza GR. The clinical
pattern of subclinical/silent coeliac disease: an analysis on 1026
consecutive cases. Dig Dis Sci 1999;94:691-6.
This article tells us that over the last 30 years the US youth
has shown a decrease in total energy consumed, as well as the percentage
of energy from fat and in particular saturated fats. So what are the
conclusions of the article? That "these trends .... may compromise the
health of future US populations". In the discussion section worries are
expressed about low iron and fibre intakes: despite the fact th...
This article tells us that over the last 30 years the US youth
has shown a decrease in total energy consumed, as well as the percentage
of energy from fat and in particular saturated fats. So what are the
conclusions of the article? That "these trends .... may compromise the
health of future US populations". In the discussion section worries are
expressed about low iron and fibre intakes: despite the fact that both
have risen steadily in the past 30 years. Concern is also expressed about
falling calcium intake, due to a decrease in consumption of dairy
products. US milk intake has always been exceptionally high, and being
rich in saturated fat a reduction was probably desirable. However, the
current lower intake still supplies levels of calcium much higher than
those for children in other developed countries.
There seems little doubt that US children are growing fatter, but I
am at a loss to see in what way their dietary intake explains this.
Presumably the reduction in energy intake is offset by an even greater
reduction in activity, but the effect is that the diet of today's
adolescents, though supplying more energy than required for current levels
of activity, in composition terms appears to be healthier than it has ever
been.
The old fashioned disciplinarian mother used to shout to her children
in the next room "whatever you're doing: stop it!". This appears to
still be our attitude to young people as a group. It is sad to see a
scientific article falling back onto the accepted paradigm that the youth
of today are decadent and unhealthy. Could they not have had the
imagination to actually explore the meaning of these results and even dare to suggest that some things might be improving instead of getting worse?
Garner, Panpanich and Logan (Arch Dis Child 2000;82:197-201) presented a much needed review of growth monitoring. This is a
component of primary health care on which so much finance and health
workers' time has and is being expended. No doubt this review will
stimulate more necessary trials.
However, they did not touch on one important aspect of growth
monitoring, that is whether health work...
Garner, Panpanich and Logan (Arch Dis Child 2000;82:197-201) presented a much needed review of growth monitoring. This is a
component of primary health care on which so much finance and health
workers' time has and is being expended. No doubt this review will
stimulate more necessary trials.
However, they did not touch on one important aspect of growth
monitoring, that is whether health workers making use of growth charts
comprehend the weight-for-age graph.
Piaget (1896-1980) considered the line graph to be one of
the more difficult subjects to teach. Graphic representation of number
is not taught in primary schools in developing countries and colleagues
with knowledge of primary education suggest that primary school teachers
would
not be able to teach it. Experience with post graduate doctors in the
1970s suggested that a proportion could not complete a weight chart and
even more would have problems in interpreting it (Morley 1984). A similar
problem has arisen with midwives in the use and interpretation of the
partograph to plot the progress of labour.
Fortunately, an alternative method of weighing may overcome this
difficulty. This involves weighing in or near the home, not in the clinic,
with a Direct Recording Scale. With this the mother sees a large spring
stretching up her child's chart, located in the scale, as she releases her
child's weight into the weighing trousers below the scale. She then with a
ball pen creates the next point on her child's growth curve through a hole
in the pointer at the top of the spring. In this way even unschooled
mothers can themselves create their child's growth curve This in time
leads them, the grandmother and their older daughters to understand the
weight for age curve. (Meegan 1988, Meegan 1999). In one study
among the pastoral Maasai in Kenya they took action when faltering occurred
giving such children an additional drink of milk (Meegan 1999).
Anyone interested in this new approach to Growth Monitoring or who want copies of the above papers and details of the Direct Recording
Scale should contact TALC on: talcuk@btinternet.com
or by post to TALC, POB 49 St Albans AL1
5TX, UK
References
Morley DC. Will growth monitoring continue to be part of primary health care? S Afr Med J 1994;84(suppl):25-16.
Meegan M, Morley D, et al. Child weighing by the
unschooled; a report of a controlled study of growth monitoring over 12
months of Maasai children using a Direct Recording Scale. Trans R Soc Med Hyg 1994;88:635-637.
Meegan M, Morley D. Growth Monitoring: Family
Participation: Effective Community Development Tropical Doctor 1999;29;23-27.
Seizures in infancy and early childhood responsive
to pyridoxine are well recognised but rare. Baxter (1)
has recently observed that "almost a third of neonatal
cases of pyridoxine dependency present with
apparent birth asphyxia and/or suspected
hypoxic-ischaemic encephalopathy" and recommended
that, because of the high proportion of atypical cases,
"all children with early onset (younger than 3 years
ol...
Seizures in infancy and early childhood responsive
to pyridoxine are well recognised but rare. Baxter (1)
has recently observed that "almost a third of neonatal
cases of pyridoxine dependency present with
apparent birth asphyxia and/or suspected
hypoxic-ischaemic encephalopathy" and recommended
that, because of the high proportion of atypical cases,
"all children with early onset (younger than 3 years
old) intractable seizures or status should receive a
trial of pyridoxine whatever the suspected cause".
Following this recommendation can be of remarkable
benefit.
Case Report
A Caucasian boy was born at term in a state of
unexpected collapse requiring intubation and
resuscitation. He developed tonic seizures within hours
of birth and was treated with phenobarbitone,
phenytoin and clonazepam. At 48 hours an EEG showed
a burst suppression pattern. There was biochemical
evidence of multi-organ damage. He was extubated on
day 5 and discharged on day 16 on phenobarbitone.
He continued to have frequent myoclonic seizures. At 6
months phenobarbitone was substituted with sodium
valproate with some initial benefit. By 7 months he was
having focal motor seizures affecting his right arm
upto 40 times a day and additional atypical absences
and tonic seizures. He also had signs of an emerging
spastic quadraparesis. EEG showed right sided spike
and wave discharge with a frontal emphasis. At 8
months a trial of oral pyridoxine (30mg/kg/day) was
given. No seizures have been observed since pyridoxine
was started. He is now 16 months of age. He is
maintained on pyridoxine 15 mg/kg/day and is weaning
off his valproate. The EEG no longer shows spike and
wave activity. The signs of spastic quadraparesis
remain.
We have reviewed the notes of children attending
The David Lewis Centre, a residential school for
children with severe epilepsy. Children at The David
Lewis Centre are referred from all over the country -
their early epilepsy management has therefore been
undertaken at many different centres. 31 children with
intractable cryptogenic epilepsies of onset prior to 3
years of age were identified (dates of birth 1979 -
1992). Only one of these children was recorded as
having received a trial of pyridoxine early in the
evolution of their epilepsies.
The true prevalence of pyridoxine responsive
epilepsy is difficult to assess if the recommendations
of Baxter are seldom applied. Giving pyridoxine can be
diagnostic and therapeutic - not giving a trial of
pyridoxine is common and can leave a treatable cause
of difficult epilepsy unrecognised and inadequately
treated.
Dr Daniel Hindley Consultant Paediatrician Fairfield
General Hospital, Bury, UK
Dr Margaret Huyton Associate Specialist The David Lewis Centre, Alderley Edge, Cheshire, UK
1. Baxter P. Epidemiology of pyridoxine dependent and
pyridoxine responsive seizures in the UK. Arch Dis Child
1999;81:431-3.
In reply to the comments by Yim Yee Chan and R Lakshman in which they
ask if all patients truely suffered from appendicitis in our study group.
The answer is that histopathological investigation confirmed the diagnosis
appendicitis in all cases.
Yours sincerely,
VC Cappendijk, MD and FWJ Hazebroek, MD, PhD
Department of Paediatric Surgery, Sophia Children's Hospital...
In reply to the comments by Yim Yee Chan and R Lakshman in which they
ask if all patients truely suffered from appendicitis in our study group.
The answer is that histopathological investigation confirmed the diagnosis
appendicitis in all cases.
Yours sincerely,
VC Cappendijk, MD and FWJ Hazebroek, MD, PhD
Department of Paediatric Surgery, Sophia Children's Hospital University
Hospital Rotterdam The Netherlands
The paper by Cappendijk and Hazebroek[1] successfully demonstrates
the problems with diagnosis of appendicitis in the young child.
It makes the important point that diarrhoea may be a feature of
appendicitis and lead to misdiagnosis. In addition, children can have
coexisting pathologies leading to delayed diagnosis. We have seen a cystic
fibrosis child with DIOS (distal intestinal obstruction...
The paper by Cappendijk and Hazebroek[1] successfully demonstrates
the problems with diagnosis of appendicitis in the young child.
It makes the important point that diarrhoea may be a feature of
appendicitis and lead to misdiagnosis. In addition, children can have
coexisting pathologies leading to delayed diagnosis. We have seen a cystic
fibrosis child with DIOS (distal intestinal obstruction syndrome) and
appendicitis. Urinary tract infection and appendicitis can also occur
together.
Children with communication problems and learning difficulties are
another high risk group for delay in diagnosis.
The differential diagnosis of appendicitis is large[2] and a child
who presented with abdominal pain and subsequently had appendectomy need
not necessarily have suffered from appendicitis. We would be interested to
know whether the histopathological results were in agreement with clinical
diagnosis.
References
1. Cappendijk VC, Hazebroek FWJ. The impact of diagnostic delay on
the course of acute appendicitis. Arch Dis Child 2000;83:64-6
2. Hutson JM, Woodward AA and Beasley SW. Jones' Clinical Paediatric
Surgery - Diagnosis and management. Blackwell Science Asia publications.
Fifth Edition. 1999;Chapter 20:page 142.
Poor postnatal weight gain was a significant factor in the
multivariate analysis despite controlling for low birthweight,
prematurity, neonatal problems, poor socio-economic status and many other
potential confounding factors and remained significant when further highly
predictive covariates of SIDS such as infants put down prone, infants
found with head covered and tobacco exposure were added...
Poor postnatal weight gain was a significant factor in the
multivariate analysis despite controlling for low birthweight,
prematurity, neonatal problems, poor socio-economic status and many other
potential confounding factors and remained significant when further highly
predictive covariates of SIDS such as infants put down prone, infants
found with head covered and tobacco exposure were added to the model. In
this sense postnatal weight gain was independently associated with an
increased risk of SIDS. We also found the difference in weight gain
between the two groups measured from birthweight to the last known weight
was equally apparent if measured from birth to the 6 week assessment. We
therefore stand by our conclusion in the abstract that poor postnatal
weight gain ‘was independently associated with an increased risk of SIDS’
and also that poor postnatal weight gain ‘could be identified at the
routine six week assessment’.
We find it difficult to understand how this conclusion advocates an
intervention campaign on the basis of these two statements and disagree
with Logan and colleagues that our discussion on this matter was
circumspect. We point out clearly that poor weight gain itself is not a
sensitive marker and that it ‘should be seen as a thread in a web of
factors that render an infant vulnerable to SIDS and is both a consequence
of adverse health and social conditions’.
We agree that absolute risks must be used for targeted prevention
campaigns but do not advocate such a campaign based on our solitary
finding. Preliminary analysis of risk scoring on the first two years of
our dataset, tested on the third year show that 42% of SIDS families can
be identified from 8% of the population using just a few prenatal factors.
Incorporating postnatal factors such as weight gain may improve the
specificity and sensitivity of such a scoring system.
To our knowledge the “Back to Sleep” campaign initiated in October
1991 has not been evaluated in an appropriately controlled study yet the
SIDS rate in England & Wales more than halved from 1.7 deaths per 1000
livebirths in 1990 to 0.77 deaths in 1992.[1] Findings from our study have
helped build upon the advice regarding safe sleeping practices, parents
are now advised not only to avoid placing infants in the prone position
but also the side position, bed-sharing under certain circumstances,
sharing a sofa to sleep and to avoid head covering by placing the feet of
the infant at the foot of the cot. In 1998 the SIDS rate fell a further
25% in England & Wales to 0.45 deaths per 1000 livebirths.[2] There is
no direct evidence that these recommendations and fall in SIDS rates are
linked although the dramatic fall in the prevalence of parents placing
their infant in the prone position to sleep (57% before the campaign[3] to
3% after the campaign[4]) suggest many parents take up such
recommendations.
A targeted population intervention would perhaps be inappropriate
given the reduced number of SIDS deaths in this country but risk scoring
systems could be used to identify and study ‘high risk’ families to both
increase our understanding of the risks associated with the infant
sleeping environment and improve the advice we give parents in the hope
that the number of SIDS deaths reduces still further.
Peter S Blair*
Peter J Fleming*
Martin Ward Platt#
*FSID Research Unit, Dept Child Health,
Royal Hospital for Children, St Michael’s Hill, Bristol BS2 8BJ, UK
# Newcastle Neonatal Service, Ward 35,
Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP, UK
2. ONS Health Statistics Quarterly 05 Spring 2000. The Stationery Office: 10.
3. Fleming PJ, Gilbert R, Azaz Y et al. Interaction between bedding and sleeping position in the sudden infant death syndrome: a population based case-control study. BMJ 1990;301:85-9.
4. Fleming PJ, Blair PS, Bacon C et al. Environment of infants during sleep and risk of the sudden infant death syndrome: results from 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy BMJ 1996;313:191-5.
I thank doctors Lakshman and Finn for their kind reply, and
recognise that my use of the word "hospital" has given rise
to a misunderstanding. My letter was based on the analysis
the authors have made, not in the ADC article,[1] but in
their eLetter to BMJ.[2]
They wrote:
(1) immunisation with any vaccine in any child
always carries a risk of potentially fatal anaphylaxis...
I thank doctors Lakshman and Finn for their kind reply, and
recognise that my use of the word "hospital" has given rise
to a misunderstanding. My letter was based on the analysis
the authors have made, not in the ADC article,[1] but in
their eLetter to BMJ.[2]
They wrote:
(1) immunisation with any vaccine in any child
always carries a risk of potentially fatal anaphylaxis
(2)
and must always be carried out in settings where personnel
equipped to recognise and manage it are present (3) annual
updates in recognition and management of anaphylaxis for
personnel involved in immunisation are desirable (4)
essential equipment - adrenaline, airway, Ambu bag with
masks and a telephone to call for emergency help should
always be to hand and regularly checked (5) infants and
children must be observed for at least 30 minutes after the
injection to confirm that they are completely well before
they leave the premises".
According to my interpretation, all these prerequisites are
rarely to be found in the offices of paediatricians.
(1) I do not know how many paediatricians are equipped to
recognise and manage anaphylaxis, considering that they
usually operate not in "settings", but in their offices
(2) How many paediatricians are expert in the treatment of
such reactions, and have adrenaline ready in the same tray
as the vaccine?
(3) annual updates for paediatricians are helpful, however
the authors prefer annual updates for personnel involved in
immunisation, but I do not know in which specific place they
are to be held, according to the authors
(4) paediatricians' offices are rarely equipped with Ambu
masks, they are not reanimators or expert in resuscitation
manoeuvres, in addition, adrenaline should also be kept in a
refrigerator, and is no longer valid after 24-36 months;
from an economical point of view, it is not convenient to
store drugs used perhaps once in a year
(5) observation of vaccinated infants and children for at
least 30 minutes is the easiest procedure to follow in a
paediatrician's office.
Can the "settings where personnel equipped, etc",
be paediatricians' offices? or can the "settings" be
interpreted as "hospital-like premises", where annual
discussions are to be held, where adrenaline is used
continuously, and personnel with Ambu masks are operating?
No such precautions were applied during MMR vaccinations in
egg-allergic children made by us, and as far as I know, in
the rest of about 1800 children previously cited by me.[3]
I repeat, such precautions are valid only with children with
severe reactions to egg documented with challenge tests.
However to extend these recommendations[2] to all children
subjected to MMR vaccine appears to be not practical as it
would eliminate all programs in which vaccination is performed by nurses without doctors in attendance, as occurs in most Developing World countries and in almost all public
health clinics First World countries.[3]
References
1. Lakshman R, Finn A. MMR vaccine and allergy. Arch Dis
Child 2000;82:93-5
2. Lakshman R, Finn A. MMR Vaccine and Egg Allergy. BMJ
[eLetter] 31 March 2000
3. Cantani A, Serra A, Arcese G, Lucenti P. Allergic
reactions to MMR vaccines in egg- and not-egg-sensitive
children: a continuing controversy. Pediatr
Asthma Allergy Immunol 1995;9:7-14
Masters et al describe how a modified endotracheal tube can
be used as a nasopharyngeal airway in infants with Pierre Robin syndrome.[1]
We describe further modifications made to overcome some problems which we
encountered in using the technique in one of our patients.
In the original description the protruding part of the airway is cut
into four strands and the upper one cut off. We found t...
Masters et al describe how a modified endotracheal tube can
be used as a nasopharyngeal airway in infants with Pierre Robin syndrome.[1]
We describe further modifications made to overcome some problems which we
encountered in using the technique in one of our patients.
In the original description the protruding part of the airway is cut
into four strands and the upper one cut off. We found the remaining
strands rather thick, so cut them to half the width. We found that
leucoplast tape was the only tape that held the stands in place with no
additional benefit resulting from the use of Tinc Benz. The strands
rubbed badly where they curved over the edge of the nostril. To overcome
this a piece of suction catheter (8F) of just sufficient length to extend
over the lateral and medial walls of the nostril is tied transversely
across the tube with a 3/O silk tie, figure. This lifts the three stands
off the edge of the nostril and prevents any rubbing.
In our patient blockage of the airway occurred after formula but not
breast milk feeds. It is therefore advisable to suction the airway after
each feed. We used a suction catheter with graduation marks enabling
insertion no further than the tip of the airway. If inserted further the
pharyngeal stimulation usually caused vomiting.
If a nasogastric tube is also required this can be taped to one of
the strands rather than the face. The airway was changed every 4-6 days,
immediately before a feed and alternating between nostrils. Using 1%
lignocaine drops and smearing the tube with lignocaine jelly reduced
crying time after insertion.
Compared to the use of an unmodified tube with a large connector
attached to the end, we feel that the technique described by Masters et al
is far superior as it enables the child to lie prone and is less liable to
get knocked or blocked through kinking. We suggest that the modifications
we have described will further improve the acceptability of the technique.
Maria Galogavrou, Keith Foote
Department Paediatrics, Royal Hampshire County Hospital
Winchester, Hampshire SO22 5DG, UK
Reference
1. Masters IB, Chang A B, Harris M, O’Neil M C. Modified
nasopharyngeal tube for upper airway obstruction. Arch Dis Child 1999;186-7.
Maria Galogavrou
Keith Foote
Department Paediatrics,
Royal Hampshire County Hospital,
Winchester, Hampshire, SO22 5DG
Professor Cantani's[1] experience is very similar to what we found
in our review[2] - that egg allergic children do not appear to be at any
greater risk to severe allergic reactions with MMR vaccine.
In our review, we do not advocate hospitalisation of children with
egg allergy for MMR immunisation; on the contrary we suggest that all
children (including
children with egg allergy) can be immu...
Professor Cantani's[1] experience is very similar to what we found
in our review[2] - that egg allergic children do not appear to be at any
greater risk to severe allergic reactions with MMR vaccine.
In our review, we do not advocate hospitalisation of children with
egg allergy for MMR immunisation; on the contrary we suggest that all
children (including
children with egg allergy) can be immunised with MMR vaccine in the
community.
Since anaphylaxis is an extremely rare and unpredictable
consequence of any vaccination, we suggested in our review that all
children (not just children with egg allergy) must receive all
vaccinations (not just MMR) in a place which is equipped to deal with
anaphylaxis- by this we did not mean a hospital - and they must be
observed for sufficient time after the injection to make sure they are
well.
As Professor Cantani mentions, many of the reactions to the MMR may be
due to the gelatin or neomycin. It is generally agreed that MMR vaccine
is contraindicated
in children who have had severe systemic reactions to either gelatin or
neomycin.
References
1. Cantani A, Serra A, Arcese G, Lucenti P. Allergic reactions to MMR
vaccines in egg- and not-egg-sensitive children: a continuing
controversy. Pediatr Asthma Allergy Immunol 1995;9:7-14.
2 Lakshman R, Finn A. MMR vaccine and allergy. Arch Dis Child
2000;82:93-5
Dear Editor
We read with great interest the paper of Choe and colleagues who investigated possible relationships between H. pylori infection with iron deficiency anaemia (IDA) and subnormal growth at puberty.[1] They concluded that H. pylori infection and related IDA, rather than bacterial infection per se, might cause delayed pubertal growth. We believe that Choe et al’s results need some considerations.
...
This article tells us that over the last 30 years the US youth has shown a decrease in total energy consumed, as well as the percentage of energy from fat and in particular saturated fats. So what are the conclusions of the article? That "these trends .... may compromise the health of future US populations". In the discussion section worries are expressed about low iron and fibre intakes: despite the fact th...
Garner, Panpanich and Logan (Arch Dis Child 2000;82:197-201) presented a much needed review of growth monitoring. This is a component of primary health care on which so much finance and health workers' time has and is being expended. No doubt this review will stimulate more necessary trials.
However, they did not touch on one important aspect of growth monitoring, that is whether health work...
Dear Editor
Seizures in infancy and early childhood responsive to pyridoxine are well recognised but rare. Baxter (1) has recently observed that "almost a third of neonatal cases of pyridoxine dependency present with apparent birth asphyxia and/or suspected hypoxic-ischaemic encephalopathy" and recommended that, because of the high proportion of atypical cases, "all children with early onset (younger than 3 years ol...
Dear Editor
In reply to the comments by Yim Yee Chan and R Lakshman in which they ask if all patients truely suffered from appendicitis in our study group. The answer is that histopathological investigation confirmed the diagnosis appendicitis in all cases.
Yours sincerely,
VC Cappendijk, MD and FWJ Hazebroek, MD, PhD
Department of Paediatric Surgery, Sophia Children's Hospital...
Dear Editor
The paper by Cappendijk and Hazebroek[1] successfully demonstrates the problems with diagnosis of appendicitis in the young child.
It makes the important point that diarrhoea may be a feature of appendicitis and lead to misdiagnosis. In addition, children can have coexisting pathologies leading to delayed diagnosis. We have seen a cystic fibrosis child with DIOS (distal intestinal obstruction...
Authors response
Poor postnatal weight gain was a significant factor in the multivariate analysis despite controlling for low birthweight, prematurity, neonatal problems, poor socio-economic status and many other potential confounding factors and remained significant when further highly predictive covariates of SIDS such as infants put down prone, infants found with head covered and tobacco exposure were added...
Dear Editor
I thank doctors Lakshman and Finn for their kind reply, and recognise that my use of the word "hospital" has given rise to a misunderstanding. My letter was based on the analysis the authors have made, not in the ADC article,[1] but in their eLetter to BMJ.[2]
They wrote:
(1) immunisation with any vaccine in any child always carries a risk of potentially fatal anaphylaxis...
Dear Editor:
Masters et al describe how a modified endotracheal tube can be used as a nasopharyngeal airway in infants with Pierre Robin syndrome.[1] We describe further modifications made to overcome some problems which we encountered in using the technique in one of our patients.
In the original description the protruding part of the airway is cut into four strands and the upper one cut off. We found t...
Dear Editor
Professor Cantani's[1] experience is very similar to what we found in our review[2] - that egg allergic children do not appear to be at any greater risk to severe allergic reactions with MMR vaccine.
In our review, we do not advocate hospitalisation of children with egg allergy for MMR immunisation; on the contrary we suggest that all children (including children with egg allergy) can be immu...
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