I read this article with great interest. It has been a long time
since a PICU data from England and Wales has been published in the
Archives of Diseases in Childhood.
Interestingly, I noted that although the admission in 1-4 yr age
group was lesser (7.54 & 7.22%) than other age groups (more than 10%)
amongst male and female South Asians respectively, the 0–4 yr standardised
admission (incident) rate amongst...
I read this article with great interest. It has been a long time
since a PICU data from England and Wales has been published in the
Archives of Diseases in Childhood.
Interestingly, I noted that although the admission in 1-4 yr age
group was lesser (7.54 & 7.22%) than other age groups (more than 10%)
amongst male and female South Asians respectively, the 0–4 yr standardised
admission (incident) rate amongst South Asian males [351 (336 to 367
95%CI)] and females [264 (250 to 278 95% CI)] is significantly more than
non-South Asian males and females [252 (248 to 256 95% CI)] and [195 (192
to 199 95% CI)] respectively. This presumably reflects that less South
Asian babies are born per 100,000 South Asian population in the U.K.
compared to non-South Asian babies per 100,000 non-South Asians. But is
that really so?
Secondly, I wonder what the standardised incidence rate is for South
Asian and non-South Asian infants less than 1 years of age; and moreover
what proportion of this figure comprises of congenital heart defects,
chromosomal abnormalities, respiratory tract infections and NAIs
(suspected or proven).
Since 95% CI of Odds Ratio of death in all Townsend categories lie on
both sides of 1, the data does not reliably suggest that chance of a
paediatric patient’s death is higher if he/she comes from a less deprived
community, in contrary to author’s statement.
It was also interesting to note that the risk of a paediatric
patient’s death generally increases given that a surgical procedure took
place; irrespective of sex, ethnic origin or Townsend category of the
patient.
I could not locate any data mentioning the impact of PIM index on
admission on the actual standardised (proportional population adjusted)
mortality rates in South Asians and non-South Asians respectively. This
parameter would in my opinion open up the very debatable and controversial
grey area of possibility of any treatment bias which we may have in
treating non-South Asian and South Asian subsets of PICU patients (the
bias originating from their ethnic origins).
This paper clearly states that South Asian children are at greater
risk of dying compared to their non-South Asian counterparts when admitted
in PICU setting in the given geographical area studied: England and Wales.
I believe such a statement would automatically raise issue of quality of
medical service provided to the South Asian children when they are treated
in the PICU. Putting this rather boldly, I mean: Is the PICU staff in
England and Wales really intolerant to racial discrimination while
treating their patients? Will this study lead to a modification in PIM
scoring to a higher mortality prediction score for a South Asian child
admitted in PICU in future?
The Authors have probed into some reasons that could explain this
phenomenon, including higher infant mortality in South Asians in general,
possibility of effect of consanguineous marriages in Pakistani population
leading to chromosomal disorders. They acknowledged that their study could
not identify children with congenital abnormalities in their collected
data. I would be more interested to know if PIM index of South Asian and
non-South Asian children really reflected their actual population adjusted
mortality rates. If it does, then it would reflect PICU staff’s good
medical and ethical (of intolerance to racial discrimination) practice.
However, if it does not, then unfortunately it might open up, I am afraid,
the unwanted floodgate of debate on racial discrimination in paediatric
practice until proven otherwise
I read this article with interest and was pleased by the emphasis
given to Medical Education in this journal(1, 2). There is necessity for
more literature on Medical Education in frontline journals like this.
Reading the RCPCH document for Level 2 competency for Core Highest
Specialist Training in Paediatrics(3), I was disappointed that Best
Evidence Medical Education (BEME)was not included.
I read this article with interest and was pleased by the emphasis
given to Medical Education in this journal(1, 2). There is necessity for
more literature on Medical Education in frontline journals like this.
Reading the RCPCH document for Level 2 competency for Core Highest
Specialist Training in Paediatrics(3), I was disappointed that Best
Evidence Medical Education (BEME)was not included.
It is necessary to move from opinion-based education to evidence-
based education. Since its introduction, the implementation of BEME has
been slow due to lack of awareness. We hardly read literature on
education, or more appropriately, are not even aware that such literature
exists(4).
Whereas it was once assumed that a competent basic or clinical
scientist would naturally be an effective teacher, it is now acknowledged
that preparation for teaching is essential. In a review of this topic,
authors conclude that the very nature of being professional in today's
social and fiscal context demands that medical educators provide evidence
of effectiveness and efficiency of their programs(5).
Fortunately we live in a time where ubiquitous acceptance of Evidence
Based Medicine (EBM) has made the concept of Evidence- based practise
irrefutable. All that is needed now is to lead Trainees into applying the
equivalent principles of seeking evidence and implementing appropriate
change based on the best available evidence to engender the thought
process of Evidence –based education.
Specialist Trainee curriculum should therefore encompass guidance on
how BEME can be applied. This may include:
1.encouraging reflection on teaching methods allowing the trainees to
identify the gaps in their teaching practice
2.encouragement to seek feedback from students and the opportunity to
discuss the feedback with experienced teachers to decide on the required
strategy for improvement
3.facilitating the process by providing information about database
such as the Campbell Collaboration (www.campbell.gse.upenn.edu) and Best
Evidence Medical Education collaboration (www.bemecollaboration.org)
These are suggestions for creating a paradigm shift to encourage
young doctors to look at teaching activities in the light of exsisting
best evidence. Emphasis given to Medical Education in high impact journals
will aid in achieving this goal.
Reference:
1.McGraw ME. Delivery of the paediatric curriculum of the Royal College of
Paediatrics and Child Health (RCPCH). Arch Dis Child2009;94(4):254-7.
2.Bindal T, Wall D, Goodyear HM. Specialist registrars’ views on their
teaching role. Arch Dis Child2009;94(4):311-3.
3.A Framework for Competences for Level 2 Training in Paediatrics, 2005
Royal College of Paediatrics and Child Health
4.BEME Guide No. 1: Best Evidence Medical Education. Medical Teacher, 1999
;21 (6): 553 – 562
5.Dauphinee WD, Wood-Dauphinee S.The need for evidence in medical
education: the development of best evidence medical education as an
opportunity to inform, guide, and sustain medical education research. Acad
Med. 2004;79(10):925-30.
Dear Sir,
I appreciate the review of mtDNA depletion provided by Drs Rahman &
Poulton,
and whole-heartedly agree with there opinion that oligo-arrayCGH is not a
first line test for single gene disorders but rather is a follow on test
when sequencing fails to detect 2 causal alleles.
However, in their perspective, they state: “a molecular diagnosis of
dGK deficiency may be regarded as a useful prognostic ind...
Dear Sir,
I appreciate the review of mtDNA depletion provided by Drs Rahman &
Poulton,
and whole-heartedly agree with there opinion that oligo-arrayCGH is not a
first line test for single gene disorders but rather is a follow on test
when sequencing fails to detect 2 causal alleles.
However, in their perspective, they state: “a molecular diagnosis of
dGK deficiency may be regarded as a useful prognostic indicator in
patients in whom liver transplantation is being considered…. molecular
diagnosis of dGK mutation may lead to a decision not to transplant,
particularly if there is evidence of neurological involvement.”
This statement is problematic as in DGUOK deficiency, possibly in
contrast to other disorders such as POLG and MPV17 related depletion,
liver transplantation may be associated with very good long term outcome
and the absence of significant neurological disease. (Dimmock et al Liver
Transplantation 2008 Oct;14(10):1480-5) Since outcome does not correlate
directly with genotype, it is my opinion that molecular diagnosis in
isolation should not be used to make decisions regarding transplantation.
Packman et al. responded to Howell et al.’s article (doi
10.1136/adc.2007.134114) on bilingualism and stuttering. We showed that
speaking two languages in the preschool years increased the chances of
children starting to stutter and decreased the likelihood of recovery from
stuttering relative to speakers who learned English when they started
school.
Packman et al. responded to Howell et al.’s article (doi
10.1136/adc.2007.134114) on bilingualism and stuttering. We showed that
speaking two languages in the preschool years increased the chances of
children starting to stutter and decreased the likelihood of recovery from
stuttering relative to speakers who learned English when they started
school.
We do not consider, as Packman et al. suggest, that studying the
general population of bilinguals would benefit the study of how speaking a
second language affects stuttering. First, statistically speaking,
demonstrating that bilingualism has no effect on stuttering, as the
authors wish to do, is impossible. Also, investigating the general
population of bilinguals is a flawed approach as bilingualism is massively
heterogeneous within and between societies (including the US, Australia
and Canada, where the authors work). Consequently, stringent controls (not
biased sampling) have to be imposed in studies on bilingualism and
stuttering. The controls we imposed excluded children who were brought up
bilingual for social, educational or financial advantage. This reduced the
heterogeneity in the bilingual sample. We compared bilinguals who had to
use an additional language in the home with a matched sample who only
spoke a language other than English in the home. The two groups of
children selected for our study were directly comparable with respect to
socio-economic status etc., and provided an appropriate sample on which to
test the hypothesis of whether deferring learning English as a second
language affected onset of stuttering and whether stuttering recovered.
The same controls are appropriate for selecting similar groups for study
across countries (unlike a sample from the general population of
bilinguals at large).
They go on to state that our cohort is biased, and refer to a
clinical study that followed up children from about age 3 to 8. 1 They say
that the generally accepted age of stuttering onset is 3 years. However,
the authoritative handbook in the area notes that the onset of
developmental stuttering can occur at any age up to 13 years. 2
Consequently, studies that cease examination at age 8 bias estimates of
age of onset to lower ages by excluding cases where onset occurs after age
8. They also incorrectly state that the gender ratio is 1:1 (there was a
higher ratio of males/females in our study). All studies we are aware of
(including the one they cited 1) show more males stutter than females. For
example, the classic study by Andrews and Harris 3 from 2 to teenage
reported a ratio of 2.4:1. A gender ratio of 1:1 suggests they are
including children who do not stutter as stutterers (they have many false
positives) and there is about an equal chance of misdiagnosis for each
gender. The reasons for such misdiagnoses could be because they 4 use
parental nominations for identifying cases and employ symptoms for
diagnosing stuttering (whole word repetitions) that are excluded by
several authorities. 5 6 7 The inclusion of these would lead to fluent
children being classed as stutterers.
Packman et al. suggest that the Lidcombe program of therapy may be
appropriate to treat bilingual children who stutter. However, the study
they cited excluded children who did not have “proficiency in English” and
there is no translation of the procedure into several of the languages
spoken by our participants. In addition to the fact that they may be
treating children who do not stutter, the statistical treatment in the
study they cite has been faulted and long-term follow-up indicates that
some “children [treated by Lidcombe] may start to stutter again”. 8
They state that an epidemiological study is appropriate to determine
whether there is a relationship between stuttering and bilingualism. We
have warned about the problems of grouping together heterogeneous
bilinguals for study, as is necessary in epidemiological work. They
overlook the fact that our work reported on the risk of starting to
stutter and chance of recovery, using longitudinal data through to
teenage. They suggest the onset age is about three years and that most
recovery occurs in the first three years after onset. Conceivably, an
epidemiological study at ages less than 8 could provide information about
risk factors for onset of stuttering. However, it would not be informative
about recovery since 50% of cases still stuttering at age 8 will recover 9
10, and recovery is not resolved until teenage. 3 9 10 Although
epidemiological work does not require a longitudinal dimension, this is
necessary when studying recovery, where results on the same speakers are
needed in order to avoid biases. As in our study, they will need to use
standardized instruments to establish persistence and recovery at teenage.
If they intend to asses the impact bilingualism has on school performance,
they will again need to extend examination to teenage.
In their last paragraph, they state that 4% stutter-like dysfluencies
suggests our children would still be stuttering. Frequencies around this
value have been used to differentiate young children who stutter from
normally fluent speaking peers for English 1 and Dutch. 11 As discussed
earlier, relatively high rates of supposed stuttering events may be due to
inclusion of monosyllabic whole word repetitions, which are a common
feature in fluent children’s and adults’ speech. 12
In summary, we consider our conclusions to be valid. Our experimental
groups were matched appropriately and thoroughly documented with respect
to language background and assessment for stuttering. The authors of the
letter make statements that are contradicted in the literature. There are
major faults in the way the authors of the letter propose to study the
relationship between bilingualism and stuttering.
Acknowledgement
This work was supported by grant 072639 from the Wellcome Trust to Peter
Howell. Address Correspondence to: Peter Howell, Division of Psychology
and Language Sciences, University College London, Gower Street, London
WC1E 6BT, England. Email: p.howell@ucl.ac.uk
References
1Yairi E., Ambrose NG. Early childhood stuttering. Austin, TX: Pro-
Ed, 2005.
2Bloodstein O., Bernstein Ratner N. A handbook on stuttering, 6th ed.
Clifton Park, NY: Thomson, 2007.
3Andrews G., Harris M. The syndrome of stuttering. Clinics in
Developmental medicine (No 17). London: Heinemann, 1964.
4Reilly S., et al. Predicting stuttering onset by the age of 3 years.
Pediatrics, 2009;123:270-277.
6Ryan B. A longitudinal study of articulation, language, rate, and
fluency of 22 preschool children who stutter. Journal of Fluency
Disorders, 2001;26:107-127.
7Wingate ME. Foundations of stuttering. San Diego: Academic; 2002.
8Packman A., Kuhn L. Looking at stuttering through the lens of
complexity. International Journal of Speech-Language Pathology,
2009;11:77– 82.
9Fritzell B. The prognosis of stuttering in schoolchildren: A 10-year
longitudinal study. In Proceedings of the XVI Congress of the
International Society of Logopedics and Phoniatrics, 186-187. Basel:
Karger, 1976.
10Howell P, Davis S, Williams R. Late childhood stuttering. Journal
of Speech Language and Hearing Research, 2008;51:669-687.
11 Boey et al., Characteristics of stuttering-like disfluencies in
Dutch speaking older children, adolescents and adults. Journal of Fluency
Disorders, 2007;32:310-329..
12 Levelt W. Speaking: From intention to articulation. Cambridge, MA:
Bradford Books, 1989.
Peter Howell,
Stephen Davis,
Division of Psychology and Language Sciences, University College
London, United Kingdom
Roberta Williams,
Department of Language and Communication Science, City University
London, United Kingdom
In a recent article published in the journal, Taekema et al.
discussed the use of clinical criteria and laboratory tests to
differentiate between septic arthritis and transient synovitis in
children.2 Distinguishing between these two conditions is crucial to avoid
local and systemic complications (if a joint infection is missed) or
unnecessary hospitalization, surgical interventions, and antibiotic
treatment (if transien...
In a recent article published in the journal, Taekema et al.
discussed the use of clinical criteria and laboratory tests to
differentiate between septic arthritis and transient synovitis in
children.2 Distinguishing between these two conditions is crucial to avoid
local and systemic complications (if a joint infection is missed) or
unnecessary hospitalization, surgical interventions, and antibiotic
treatment (if transient synovitis is misclassified as septic arthritis).
After carefully reviewing available data, the authors concluded that the
presence of fever, refusal to bear weight, and elevated acute-phase
reactants should raise the suspicion of septic arthritis, whereas the
likelihood of transient synovitis increases if these predictors are
absent.2
In recent years, increasing use of blood culture vials for culturing
synovial fluid exudates and nucleic acid amplification techniques have
resulted in the recognition of K. kingae as an emerging pediatric pathogen
and the most common etiology of skeletal system infections below the age
of 3 years.3 Involvement of the hip has been observed in 25 of 116 (22%)
patients with K. kingae arthritis, apyrexia or low-grade fever are common,
and the majority of affected children appear to be only mildly or
moderately ill.3 In addition, the blood white cell count (WCC), C-reactive
protein level, and the erythrocyte sedimentation rate are frequently
within normal limits or only slightly elevated3, and a joint fluid
aspirate WCC <50,000/ml-1 has been found in 11 of 30 (37%) patients
with culture-proven K. kingae arthritis detected in southern Israel since
1987.
Although bacterial arthritis is not considered a self-limited disease,
transient involvement of the joints during an episode of K. kingae
bacteremia has been documented.1, 4 Children with this condition presented
with a body temperature <380C, limping or refusal to walk or bear
weight, but lacked objective signs of osteoarthritis or leukocytosis.
Despite this apparently benign clinical presentation, blood cultures were
obtained, and K. kingae was isolated, usually 3-4 days after collection.
By the time blood cultures became positive, the skeletal complaints had
resolved without antimicrobial therapy, suggesting an abortive joint
infection. Even when no antibiotics were prescribed after the positive
culture results were known, some patients made an uneventful recovery.1
Had blood cultures not been obtained, these children would have been
diagnosed as suffering from transient synovitis, raising the possibility
that patients in which this diagnosis is made have, in fact, hip joint
infections caused by K. kingae. Adding blood cultures to the laboratory
work-up of children with presumptive transient synovitis is strongly
recommended, even in the absence of fever, constitutional symptom, or
elevated acute-phase reactants. If the hip joint is aspirated, the
specimen should be inoculated into a blood culture vial to improve the
recovery of K. kingae.
REFERENCES
1.Lebel E, Rudensky B, Karasik M, Itzchaki M, Schlesinger Y. Kingella
kingae infections in children. J Pediatr Orthop B 2006; 15:289-92.
2.Taekema HC, Landham PR, Maconochie I. Towards evidence based medicine
for paediatricians. Distinguishing between transient synovitis and septic
arthritis in the limping child: how useful are clinical prediction tools?
Arch Dis Child 2009; 94:167-8.
3.Yagupsky P. Kingella kingae: from medical rarity to an emerging
paediatric pathogen. Lancet Infect Dis 2004; 4:358-67.
4.Yagupsky P, Press J. Unsuspected Kingella kingae infections in afebrile
children with mild skeletal symptoms: the importance of blood cultures.
Eur J Pediatr 2004; 163:563-4.
Dear Sir,
Some days ago we received a letter from colleagues in London asking us to
comment on the article of Simeone and coll. reporting a lack of
relationship between chronic constipation (CC) and cow’s milk allergy
(CMA), recently published in ADC (1). Our English Colleagues referred that
they had observed “dramatic cases” of chronic constipation unresponsive to
laxative treatment which fully resolved on CM-free diet a...
Dear Sir,
Some days ago we received a letter from colleagues in London asking us to
comment on the article of Simeone and coll. reporting a lack of
relationship between chronic constipation (CC) and cow’s milk allergy
(CMA), recently published in ADC (1). Our English Colleagues referred that
they had observed “dramatic cases” of chronic constipation unresponsive to
laxative treatment which fully resolved on CM-free diet and as this is
also our experience in many cases (2-5) they asked to “defend this truth”.
However, we think that the study of Simeone and coll. is very different
from our previous studies on CC and CMA. In their article (1) they
investigated for an association between CC and atopic disease and to do
this performed a series of IgE-mediated assays. It is, in part, not
surprising that they did not find a more frequent association of atopy
(positive assays and clinical history) in CC patients than in controls, as
it is well known that the immunologic mechanisms of the majority of
gastrointestinal manifestations of food allergy are not based on IgE-
mediated mechanisms (6) and we ourselves have not found a higher frequency
of positive IgE-based assays in patients with CC due to CMA. Thus, a lack
of association between atopy or IgE-mediated assays and CC was to have
been expected and does not mean that CC cannot be due to CMA. The only
aspect of the Simeone study which could be compared with our and others’
previous studies (7-10), is that they placed eleven CC patients
unresponsive to laxative treatment on CM-free diet. They found that none
of these eleven patients improved on CM-free diet. On the basis of this
very small patient sample they concluded that “the refractory constipation
is not associated with CMA in the general paediatric population”. This
could also be true in the general population, although we do have doubts
about this, but more than eleven patients must be evaluated before a firm
conclusion can be reached.
What is certain is that in a tertiary gastroenterology clinic with
experience in the food allergy-intolerance field – as ours is - the
frequency of CC unresponsive to laxative treatments and due to food
allergy is higher than one third of cases. Probably this high frequency is
biased by the pre-selection of the patients referred to our clinic, but
whatever the real frequency of the relationship between CC and food
allergy may be, many prestigious research groups from England (7), the USA
(10), Finland (11) and other centres world-wide (8,9) have reported
results identical to ours and firmly confirmed that CC can be a
manifestation of food allergy. Furthermore, the CC-CMA association has
also been included in a review published in Gastroenterology (12).
Finally, we recently suggested the possibility that the patients could be
suffering from multiple food allergy and not simply from CM
hypersensitivity. In fact, bowel movements normalised in some patients
unresponsive to CM-free diet when they were placed on a more restricted
oligoantigenic diet (5).
Do paediatricians who first visit a child consider the hypothesis of CMA-
related constipation? We believe they do, but this does not mean that a CM
-free diet should be prescribed for every patient with CC. The first
treatment approach must be a regular diet (water, fibre, etc) and
laxatives. However, if the patient does not improve and especially when
he/she has a previous history or a family history of CMA, the probability
of a CMA diagnosis increases. In these cases a consultation with a
specialist should be suggested and, after further evaluation, an
elimination diet could be prescribed. We do not know how many
paediatricians - or paediatric gastroenterologists - in the world use this
approach, but we think there are too few. Despite the clear evidence,
there are still many paediatricians who do not accept that CMA can be a
cause of CC. The Naples Gastroenterology School is a medical teaching
school which we have learned a great deal from and its members contribute
to form opinions and guidelines in paediatric gastroenterology.
Unfortunately, their experience with CC conflicts with the evidence in the
literature about the relationship between CC and CMA and this certainly
hinders the possibility of a correct treatment for patients with CC due to
CMA. Our role can be to add further data to help better understand the
problem and to offer further evidence of this relationship.
Yours faithfully,
REFERENCES
1) Simeone D, Miele E, Boccia G, Marino A, Troncone R, Staiano A.
Prevalence of atopy in children with chronic constipation. Arch Dis Child
2008;93;1044-1047
2) Iacono G, Carroccio A, Cavataio F, Montalto G, Cantarero MD,
NotarbartoloA. Chronic constipation as a symptom of cow milk allergy. J
Pediatr 1995; 126: 34–9.
3) Iacono G, Cavataio F, Montalto G, et al. Intolerance of cow’s milk and
chronic constipation in children. N Engl J Med 1998; 338: 1100–4.
4) Carroccio A, Scalici C, Maresi M, et al. Chronic constipation and food
intolerance: a model of proctitis causing constipation. Scand J
Gastroenterol 2005; 40: 33–42
5) Iacono G, Bonventre S, Scalici C, et al. Food intolerance and chronic
constipation: manometry and histology study. Eur J Gastroenterol Hepatol
2006; 18: 143–50.
6) Sampson H, Sicherer SH, Birnbaim AH. American Gastroenterological
Association Medical Position Statement: guidelines for the evaluation of
food allergies. Gastroenterology 2001; 120: 1023–5.
7) Shah N, Lindley K, Milla P. Cow’s milk and chronic constipation in
children. N Engl J Med 1999; 340: 891–2.
8) Daher S, Sole` D, de Morais MB. Cow’s milk and chronic constipation in
children. N Engl J Med 1999; 340: 891.
9) Daher S, Tahan S, Sole` D, et al. Cow’s milk protein intolerance and
chronic constipation in children. Pediatr Allergy Immunol 2001; 12:
339–43.
10) Vanderhoof JA, Perry D, Hanner TL, Young RJ. Allergic constipation:
association with infantile milk allergy. Clin Pediatr 2001; 40: 399–402
11) Turunen S, Karttunen TJ, Kokkonen J. Lymphoid nodular hyperplasia and
cow’s milk hypersensitivity in children with chronic constipation. J
Pediatr 2004; 145: 606–11.
12) Bischoff S, Crowe SE. Gastrointestinal food allergy: new insights into
pathophysiology and clinical perspectives. Gastroenterology 2005; 128:
1089–113
Poor weight gain over the first 6-8 weeks is known to be a risk
factor in its own right for developmental delay, which can be demonstrated
not only at school age but, as shown by McDougall et al as early as 4
months.1
McDougall et al suggest that the Child Health Surveillance check at 6
-8 weeks provides the opportunity to identify infants with early weight
faltering; and that future research could ascertain whet...
Poor weight gain over the first 6-8 weeks is known to be a risk
factor in its own right for developmental delay, which can be demonstrated
not only at school age but, as shown by McDougall et al as early as 4
months.1
McDougall et al suggest that the Child Health Surveillance check at 6
-8 weeks provides the opportunity to identify infants with early weight
faltering; and that future research could ascertain whether intervention,
presumably to increase weight gain, would improve later outcomes for
infants. However the first 6-8 weeks are the vulnerable period,
interventions are needed during and not after the completion of this time.
It has already been shown that interventions can be used to encourage
weight gain in both breast and formula fed infants during this early
“window” of opportunity.2 3
UK Health Visitors (and midwives) carry calibrated electronic
weighing scales and see mothers frequently during this important time. If
infants are weighed weekly, then there is the opportunity to detect and
promptly remedy weight faltering thereby reducing the risk of
developmental delay. Also since the effect on later intellectual
development has been shown to be approximately linear over the whole range
of weight velocities, there is the opportunity to help all babies.4
The proposal to omit the first 2 weeks from the WHO2006 breastfed
weight charts (for UK use),5 thereby also removing birth weight from the
chart so that birth centile cannot be identified, may unfortunately limit
the implementation of a cheap worthwhile public health intervention.
Yours sincerely
Dr C A Walshaw
References
1 McDougall P., Drewett R.F., Hungin P, Wright C.M. The detection of
early weight
faltering at the 6-8 week check and its association with family
factors, feeding and
We understand the concerns of doctors Lin and Fu about reverse
causation regarding the protective effect of fish on eczema at one year of
age. We cannot, of course, be sure that reverse causation does not
contribute to our results, but there are reasons that speak in favour of a
real effect.
Firstly, we found no correlation between time of onset of the eczema
and age at introduction of fish....
We understand the concerns of doctors Lin and Fu about reverse
causation regarding the protective effect of fish on eczema at one year of
age. We cannot, of course, be sure that reverse causation does not
contribute to our results, but there are reasons that speak in favour of a
real effect.
Firstly, we found no correlation between time of onset of the eczema
and age at introduction of fish.
Secondly, when excluding infants with food-induced eczema, there was
still a protective effect, as was the case when excluding infants with
food allergy.
Thirdly, when excluding infants with onset of eczema before 4 months
of age, there was still a protective effect in infants with later onset of
eczema. Also, the protective effect was equal between infants with and
without atopic heredity.
Furthermore, we are not the only group that has reported such
effects. In the BAMSE study (1), Kull et al. found that fish consumption
during the first year of life was protective against allergic disease at 4
years. In a Norwegian study (1), Øien et al. found that fish reduced the
risk of having allergic disease at 2 years. Both studies excluded children
with disease before one year of age to avoid reverse causation.
We are at this moment analysing the data from our follow-up when the
children are 4.5 years old, and will hopefully be able to address the
question further.
References:
1. Kull I, Bergström A, Lilja G, Pershagen G, Wickman M. Fish
consumption during the first year of life and development of allergic
diseases during childhood. Allergy. 2006;61:1009-15.
2. Øien T, Storrø O, Johnsen R. Fish and cod liver oil consumption
during pregnancy and the first year of life and allergic diseases at 2
years of age. A prospective birth cohort study. XXVII Congress of the
European Academy of Allergology and Clinical Immunology, Barcelona.
[Abstract]. 2008.
Yours sincerely,
Bernt Alm MD PhD, Nils Åberg MD PhD, Laslo Erdes MD, Per Möllborg MD,
Rolf Pettersson MD, Gunnar Norvenius MD PhD, Emma Goksör MD, and Göran
Wennergren MD PhD.
Most patients presenting to a paediatric department for acute care
will be weighed as part of the nursing assessment especially because
weights are important for drug and fluid prescriptions.
Junior doctors however generally fail to take the next step in this
opportunistic contact to plot these weights. Unless clinically indicated
e.g. as part of body surface area for drug prescriptions, the height is
often not measured,...
Most patients presenting to a paediatric department for acute care
will be weighed as part of the nursing assessment especially because
weights are important for drug and fluid prescriptions.
Junior doctors however generally fail to take the next step in this
opportunistic contact to plot these weights. Unless clinically indicated
e.g. as part of body surface area for drug prescriptions, the height is
often not measured, nor is head circumference routinely measured.
Indeed, this is a reflection of less than best practice and needs to be
highlighted as part of junior doctor induction.
The study by T Sommerfield et al. (1) provides a valuable insight
into the epidemiological trend of infantile hypertrophic pyloric stenosis
(IHPS) in Scotland. It was interesting to note the proposed association
between incidence of IHPS and deprivation.
We have recently reviewed cases of IHPS presenting to our hospital,
which is a medium sized district general hospital serving a deprived
population in the Sou...
The study by T Sommerfield et al. (1) provides a valuable insight
into the epidemiological trend of infantile hypertrophic pyloric stenosis
(IHPS) in Scotland. It was interesting to note the proposed association
between incidence of IHPS and deprivation.
We have recently reviewed cases of IHPS presenting to our hospital,
which is a medium sized district general hospital serving a deprived
population in the South Wales valleys. We were keen to assess the clinical
presentation and our performance in terms of diagnosing and managing
pyloric stenosis. A retrospective case review of all ultrasongraphically
confirmed cases of pyloric stenosis over a seven year period (January 2000
to September 2007) was undertaken. Standards for notekeeping, clinical
assessment,investigations and fluid management were derived from
literature search and textbooks.
We found that majority of patients were term( 95%), first born(
100%), male infants( 90%) presenting between 2 - 10 weeks of life
.Vomiting was the predominant presenting feature at median age of 24 days.
No significant seasonal variation was noted. With a birth rate of about
2200/ year in our hospital the cumulative incidence of IHPS over the last
7 years amounts to 37 cases in 17,500 births which is about 2.1 per 1000
live births. 38% of infants were initially diagnosed to have Gastro
Oesophageal reflux; however the time between initial presentation and
surgical correction ranged from 2 to 3 days. Recovery was uneventful in
92% of the cases. Apart from one infant who had restenosis of the pylorus,
complications in the rest were minor, responding to conventional
treatment.
A study done in early 1980s by A R Webb et al.(2) showed that the
incidence of surgically confirmed IHPS in the South Glamorgan region rose
sharply after 1976 from 1.4/ 1000 live births to 3.6/ 1000 live births.
This seemed to reflect epidemiological trends throughout Wales. Although
there was speculation that this rise could be attributed to a change in
feeding practises at that time (from formula to breast feeding), the data
lacked statistical significance. Studies since exploring the relation
between IHPS and maternal variables like breast feeding have been impeded
by lack of sufficient data and tend to contradict each other (3, 4).
It was also interesting to note the association between IHPS and
deprivation observed by the authors. Others have also suggested a relation
between rural living and pyloric stenosis (5). Census has shown that
Rhondda Cynon Taff suffers from high levels of economic and social
deprivation with 67% of the total population living within the top third
of the most deprived wards in Wales (6). Besides it also has a high
proportion of rural population. Perhaps somewhat surprisingly the
incidence of pyloric stenosis is only marginally different from the
Scottish population. Social deprivation undoubtedly is an important
contributor to the incidence of pyloric stenosis but it is probably just
one of the many environmental variables determining the incidence of this
fascinating condition.
References
1. The changing epidemiology of infantile hypertrophic pyloric
stenosis in Scotland. T. Sommerfield et al. Arch Dis Child 2008; 93:1007-
1011.
2. Infantile hypertrophic pyloric stenosis in South Glamorgan 1970-9.
Effects of changes in feeding practice. A R Webb et al. Arch Dis
Child.1983 August; 58(8): 586–590
3. Breast feeding and hypertrophic pyloric stenosis: population based
case-control study. Alfredo Pisacane et al. BMJ.1996 march; 312:745-746
4. Does Exclusive Breastfeeding Confer Protection Against Infantile
Hypertrophic Pyloric Stenosis? A 30-year Experience in Benin City,
Nigeria. David Osarumwese Osifo and Iyekoretin Evbuomwan.Journal of
Tropical Pediatrics. 2008; 0: fmn094v1-fmn094.
5. Population demographic indicators associated with incidence of
pyloric stenosis. T. To et al.Arch Pediatr Adolesc Med. 2005;159:520-525.
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Most patients presenting to a paediatric department for acute care will be weighed as part of the nursing assessment especially because weights are important for drug and fluid prescriptions. Junior doctors however generally fail to take the next step in this opportunistic contact to plot these weights. Unless clinically indicated e.g. as part of body surface area for drug prescriptions, the height is often not measured,...
The study by T Sommerfield et al. (1) provides a valuable insight into the epidemiological trend of infantile hypertrophic pyloric stenosis (IHPS) in Scotland. It was interesting to note the proposed association between incidence of IHPS and deprivation.
We have recently reviewed cases of IHPS presenting to our hospital, which is a medium sized district general hospital serving a deprived population in the Sou...
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