There are few controlled studies of pedagogical devices used in
patient education regarding chronic diseases like type 1 diabetes. As
Briars et al points out, this area is worth further study and we agree
that a critical view is needed with respect to such studies. We therefore
performed this controlled study in a general hospital population following
the previous study in a before-after setting at o...
There are few controlled studies of pedagogical devices used in
patient education regarding chronic diseases like type 1 diabetes. As
Briars et al points out, this area is worth further study and we agree
that a critical view is needed with respect to such studies. We therefore
performed this controlled study in a general hospital population following
the previous study in a before-after setting at our University hospital.
Measurement of self-reported outcomes such as severe hypoglycaemia is
rather difficult. In the present study we controlled for many potential
flaws by using a randomised controlled design. It is a weakness, however,
that the primary outcome of severe hypoglycaemia was reported only
retrospectively.
Participants in intervention and control groups were given short and
identical blinded information about the study, their education material
and the related postal questionnaires at baseline, 12 and 24 months. Using
identical questions in both groups, those surveys covered treatment
variables and the patient’s use and perceived benefit of the earlier
posted materials. Questions regarding events of severe hypoglycaemia were
embedded in a series of different questions without highlighting any
particular one. We therefore cannot see any source of bias in the
information about the study design.
As described in the paper, the reduction of reported severe
hypoglycaemia during the first 12 months after intervention was
statistically significant. Considering only those patients responding to
all questionnaires confirmed the reduction. Thus we found less than a 4%
chance that random effects explained this reduction. Taking confidence
intervals into account, we concluded that these data suggest a clinical
effect from the intervention. A larger sample would be needed to show a
significant difference in case of a smaller effect.
Moreover, the related secondary outcomes showed high frequencies of
use and significantly greater perceived usefulness and learning in the
intervention group, especially among those who had reported severe
hypoglycaemia. We interpret this as being in favour of positive effects
from the intervention.
Interestingly, after 24 months, preliminary data showed a persistent
reduction of severe hypoglycaemia in the intervention group, while no
reduction was seen in the control and traditional treatment groups
(manuscript in preparation). We interpret these preliminary data as
favouring the conclusion.
Having said that, we of course agree with Briars et al that there is
a chance that random variation or some kind of measurement bias could
possibly explain the reduction or at least part of it. Some doubt remains
from a scientific point of view and as always, new findings should be
tested in independent studies. The expressed interest in this paper holds
promise for further investigations in this understudied area.
Reference
Nordfeldt S, Johansson C, Carlsson E, Hammersjo JA. Prevention of
severe hypoglycaemia in type I diabetes: a randomised controlled
population study. Arch Dis Child. 2003;88:240-245.
Briars GL et al. Randomised controlled trial of educational video [electronic response to Nordfeldt et al. Prevention of
severe hypoglycaemia in type I diabetes: a randomised controlled
population study] archdischild.com 2003http://adc.bmjjournals.com/cgi/eletters/archdischild;88/3/240#567
We read with interest the paper by Clark and Reid [1] describing the
potential benefits of recombinant surfactant protein D therapy.
The
authors give a range of potential disease targets for surfactant protein D
based therapy including neonatal chronic lung disease, cystic fibrosis,
lung infections, emphysema and asthma. The authors do not however mention
the potential use of surfactant protein D...
We read with interest the paper by Clark and Reid [1] describing the
potential benefits of recombinant surfactant protein D therapy.
The
authors give a range of potential disease targets for surfactant protein D
based therapy including neonatal chronic lung disease, cystic fibrosis,
lung infections, emphysema and asthma. The authors do not however mention
the potential use of surfactant protein D therapy in acute respiratory
distress syndrome (ARDS) where the anti-inflammatory, immune modulation
and antioxidant properties of surfactant protein D may be of benefit.
The pathologic hallmark of ARDS is diffuse alveolar damage, which
results in loss of the alveolar-capillary barrier, transudation of protein
-rich fluid, pulmonary oedema and hypoxemia due to intrapulmonary
shunting. The mechanisms resulting are thought to be mediated by oxygen
radicals, proteolytic enzymes, cytokines and complement. The most common
predisposing conditions for ARDS are infection; including pneumonia and
systemic sepsis, trauma, aspiration of gastric contents, near drowning and
toxic inhalation.
Changes in the surfactant system in ARDS include qualitative and
quantitative changes with reductions of surfactant phospholipids and
increases in non-surfactant phospholipids. There is also inactivation of
surfactant by leakage of various plasma proteins into the lungs.[2]
Beneficial effects of increased oxygenation and decreased mortality
due to endotracheal surfactant administration in ARDS were shown by
Gregory et al.[3] Similarly bronchoscopically administered surfactant has
been also demonstrated to improve oxygenation in case studies.[4,5] The
optimum route of administration and dosing schedule remains uncertain and
surfactant is most commonly used as a rescue therapy in severe ARDS.
Acute respiratory distress syndrome is an important potential target
for surfactant protein D based therapy.
References
(1) Clark H, Reid K. The potential of recombinant surfactant protein D
therapy to reduce inflammation in neonatal chronic lung disease, cystic
fibrosis and emphysema. Arch Dis Child 2003; 88:981- 4
(2) Greise M. Pulmonary surfactant in health and human lung diseases:
state of the art. Eur Respir J 1999; 13:1455-76
(3) Gregory TJ, Steinberg KP, Spragg R, et al. Bovine surfactant
therapy for patients with acute respiratory distress syndrome. Am J Respir
Crit Care Med 1997; 155:1309-15
(4) Spragg RG, Gilliard N, Richman P, et al. Acute effects of a single
dose of porcine surfactant on patients with the adult respiratory distress
syndrome. Chest 1994;105:195-202
(5) Walmrath D, Gunther A, Ghofrani HA, et al. Bronchoscopic
surfactant administration in patients with severe adult respiratory
distress syndrome and sepsis. Am J Respir Crit Care Med 1996; 154:57-62.
It is encouraging that the Royal College supports the notion that
"the general paediatrician remains core to the resuscitation and
stabilisation of the critically ill child" and "exposure to critically ill
patients is an essential part of training", and I am glad they seek to
challenge the solutions proposed. However, to dismiss them as simply
unrealistic fails to heed their own goal of more imaginative...
It is encouraging that the Royal College supports the notion that
"the general paediatrician remains core to the resuscitation and
stabilisation of the critically ill child" and "exposure to critically ill
patients is an essential part of training", and I am glad they seek to
challenge the solutions proposed. However, to dismiss them as simply
unrealistic fails to heed their own goal of more imaginative teaching.
Whilst I can understand the comment, "all specialists feel theirs is
essential", what is their basis for distinguishing the need for neonatal
intensive care as compulsory and paediatric intensive care as not,
especially now that learning opportunities for dealing with critically ill
children have been so diminished by the centralization of critical care
facilities? It also is somewhat paradoxical that they support the General
Paediatrician as core to the resuscitation and stabilization of critically
ill children, and feel a two day course is sufficient training, but demand
a clinical attachment in community medicine?
I also am pleased that they support the use of simulation technology
and agree that it is imperfect and expensive. It is, however, of
sufficient functionality that it has a role as has been demonstrated in
other countries, and hope that their comment indicating they should press
for more funding is translated into action. Simulations use in addressing
human factor error control is, of itself a way to deal with the
exponential rise in legal costs the health service is facing, a major
cause for which is human error. This alone could justify the Government
providing additional funds for the proposed system. Its use to develop
safer systems of operation is as useful as its use in managing the
difficult airway in financial and human terms.
I applaud the attempts to introduce competence based education rather
than time based, but will be interested to see how they will both define
and assess these competencies. I look forward to seeing the development
the Royal Colleges promise, and hope that they will be supportive when
colleagues answer their call to provide inventive ways in which to deal
with the training dilemma rather than dismissive.
I would like to comment on the paper by de San Lazaro et al.[1]
The authors of this paper demonstrated that violent rocking of a baby
chair could produce acceleration/decelaration forces similar as those seen
when violenty shaking a child and that could result in similar lesions as
those seen in a true shaken baby syndrome.
I recently encoutered a similar case where a 2 month old baby was p...
I would like to comment on the paper by de San Lazaro et al.[1]
The authors of this paper demonstrated that violent rocking of a baby
chair could produce acceleration/decelaration forces similar as those seen
when violenty shaking a child and that could result in similar lesions as
those seen in a true shaken baby syndrome.
I recently encoutered a similar case where a 2 month old baby was placed
in a maxi-cosi chair in the car. The chair was incorrectly installed (too
vertically) in a manner that the child was sitting almost in an upright
position. Because of warm weather, the maxi-cosy was covered with a
blanket so that there was no visual control over the child during the
driving. There was a car ride of 2 km with repeated acceleration and
deceleration. Several hours later the child became apathic and refused to
drink his milk. The child finally became comatous. On admission in the
hospital, the child demonstrated all classic symptoms of a shaken baby
syndrome: subdural haemorrhage with interhemisheric component, bilateral
retinal haemorrhage and no external lesions. Clinical progression was
infaust with development of cystic encephalopathy. One month after the
initial trauma the child died of an intractible seizure. It was the this
author's expert opinion that the cause of death was accidental shaking and
there was no criminal prosecution.
This case demonstrates that violent shaking may be inflicted to a child
by incorrect installation of a child seat in a car. This may lead to false
accusations of child abuse. Therefore, it is important that paediatricians
and forensic physicians have knowledge of the prior circumstances that led
to the admission of a child in hopital (or death) so that accidental
causes of "shaking" can be excluded. Furthermore accidental shaking by
misuse or wrongful use of child seating equipment appears to be a true
cause of a shaken baby-like syndrome that may simulate non-accidental
injury.
Although the child's safety should be the first concern of every doctor,
false accusations of child abuse may have a profound impact on parents and
relatives.
Reference
(1) C de San Lazaro, R Harvey, and A Ogden. Shaking infant trauma induced by misuse of a baby chair. Arch Dis Child 2003; 88: 632-634.
I read the article by Allen et al. with interest. I am interested in a potential
systemic effect of pimecrolimus that doesn't seem to have been addressed.
I understand that the cream achieves its desired effect by
surpressing the white cells in the affected area. I understand that the
population of white cells migrating into the eczematous area is in
continuous flux, and that these cells...
I read the article by Allen et al. with interest. I am interested in a potential
systemic effect of pimecrolimus that doesn't seem to have been addressed.
I understand that the cream achieves its desired effect by
surpressing the white cells in the affected area. I understand that the
population of white cells migrating into the eczematous area is in
continuous flux, and that these cells can re-enter the systemic
circulation. I was wondering if the immune surpressive effects of
pimecrolimus are lifelong for the individual white cells, and if so, why
haven't there been any studies of white cell function distant from the
application site, to look not for distant concentrations of the drug, but
for damaged/surpressed white cells that may decrease overall immune
function. As many cells are quite long lived, theoretically the effects of
an application of the drug could also be long lived, and there may be
systemic immune effects caused by these surpressed cells re-entering the
circulation.
I ask the authors - Are you aware of any data addressing these issues?
I have read C. Gilberg’s paper[1] with interest but also with concern
because there to my knowledge is no scientific valid paper about children
with DAMP (deficits in attention, motor control, and perception).
The term DAMP was first introduced by C. Gilberg in 1986 [2] and based on a
study of 6 years old children in Gothenburg, Sweden.[3] The main aim of
this study was to construct a screening i...
I have read C. Gilberg’s paper[1] with interest but also with concern
because there to my knowledge is no scientific valid paper about children
with DAMP (deficits in attention, motor control, and perception).
The term DAMP was first introduced by C. Gilberg in 1986 [2] and based on a
study of 6 years old children in Gothenburg, Sweden.[3] The main aim of
this study was to construct a screening instrument in order to detect MBD
(minimal brain dysfunction) in Swedish public preschool children and
analyse different aspects of the concept of MBD from a psychiatric point
of view.
Unfortunately the Swedish studies by G. Gilberg have great methodological
problems. In the study a non-validated questionnaire for preschool
teachers was used from which the children were classified in a high load
or low load index group. In the groups an unpublished number of children
were included which did not have ”attention deficit” but ”conduct
problems” (involving conduct problems in the definition of MBD and later
DAMP the boarderline between DAMP and conduct disorder became unclear).
In the final investigation, partly by selfmade non-validated tests, the 22
children from the ”high-load” group and 60 children from the low-index
group (66 boys and 16 girls) were compared with a random control group,
which finally consisted of 59 children (29 boys and 30 girls). Of these
141 children 42 were diagnosed as having MBD, 40 were found in the index
groups, 2 in the control group, of whom one had no preschool qustionnaire
”symptoms” at all. Futhermore 3 children in the index group were diagnosed
as having mental retardation, 8 of the children had psychotic behaviour to
a marked degree (one of the boys was already diagnosed as having infantile
autism) and two children were considered to suffer from marked depressive
syndrome.[4] So 10 of 14 children diagnosed as suffering from severe MBD,
had severe psychiatric disorders which one could consider the primary
diagnosis and MBD a secondary diagnosis. It could also explain the reason
why children with socalled severe MBD/DAMP, autistic features were
extremely common.
It was the above mentioned group of 42 children who in 1986 swiched name
to children with DAMP and followed till they were 22 years old.
The above mentioned methodological problems also lead to a very high
prevalence of DAMP, estimated to 18%,[1] page 112 , and in one of the later
studies from 2000 where C. Gilberg et co-workers suggest a new school
screening examination 5 based on the earlier studies the result of the 11
factors of WISC-III the curve for control children and children with
socalled DAMP is completely parallel which means that it is children with
generalized developmental problems and not specific problems that is found
by the new screening test.
So the term DAMP is based on studies with very great methodological
problems and thereby not a valid diagnosis.
In spite of this C. Gilberg now suggests a revival of the DAMP term and
shifts to a new definition by combining ADHD and DCD. I would suggest that
instead of confusing futher investigation one should concentrate on the
ADHD diagnosis and perhaps examine if there are important subgroups e.g.
children with ADHD who also have problems with motor control, of which
there already are several studies.[6,7].
References
(1) Gillberg C. Deficits in attention, motor control, and perception: a
brief review. Arch Dis Child 2003;88:904-10.
(2) Gillberg C. Attention deficit disorder: Diagnosis, prevalence,
management and outcome. Pediatrician 1986;13:108-18.
(3) Gillberg C, Rasmussen P, Carlstrøm G et al. Perceptual, motor and
attentional deficits in six-year-old children. Epidemiological aspects. J
Child Psychol Psychiatry 1982;23:131-44.
(4) Gilberg, C. Perceptual, motor- and attentional deficit in Swedish
primary schoolchildren. Some psychiatric aspects. J Child Psychol Psyciat
1983;24;377-403.
(5) Landgren M, Kjellman B, Gillberg C. Deficits in attention, motor control
and perception (DAMP): A simplified school entry examination. Acta Pediatr
Scand 2000;89:302-9.
(6) Pitcher TM, Piek JP, Hay DA. Fine and gross motor ability in males with
ADHD. Dev Med Child Neurol 2003;45:525-535.
(7) Kalff AC, de Sonneville LM, Hurks PP et al. Low- and high-level
controlled processing in executive motor control tasks in 5-6 year-old
children at risk of ADHD. J Child Psychol Psychiatry. 2003;44:1049-57.
I agree with Dr Spencer that the incidence of the Paediatric Empyema is
on
the increase and the management of this age-old disease is dependent upon
provider-based experiences. Secondly, there is no clear evidence that one
modality of management is superior to the other. Therefore giving rise to
controversies in the management of this disease.
The pathogenesis of the disease (Empyema) is largely ignored w...
I agree with Dr Spencer that the incidence of the Paediatric Empyema is
on
the increase and the management of this age-old disease is dependent upon
provider-based experiences. Secondly, there is no clear evidence that one
modality of management is superior to the other. Therefore giving rise to
controversies in the management of this disease.
The pathogenesis of the disease (Empyema) is largely ignored while
choosing
a particular modality of the surgical intervention. As we know that when
the
disease advances more and more fibrous tissue gets deposited within the
purulent exudate giving rise to pleural rinds. This pleural rinds
restricts
the lung expansion, this process starts after fibro-purulent phase when
fibrinous and not fibrous adhesions exists causing loculations. While in
later phase (the organizational phase) of the empyema fibrosis occurs
restricting the lung expansion.
The objection I have is the use of the word early decortication. I think
what author means is early debridement of the pyogenic material from the
empyema cavity in the fibro-purulent phase. Some reports mentions the use
Video-assisted thoracoscopic (VAT) and early decortication in the
management
of empyema. It is impossible to perform VAT decortication of pleural
rinds,
It requires formal thoracotomy to do real decortication. There is usually
very little plane between firm to hard fibrous tissue restricting the lung
to pass a thoracoscope. The inflamed tissue bleeds heavily hampering the
vision. It is not question of experience, as we have done a number of
early
VAT which is definitely the way forward in reducing morbidity, risk of
developing chronic empyema and hospital stay in these children. Again I
feel
that Fibrinolytics fail in some children because it is used late in the
developing empyema process when fibrosis has commenced. Fibrinolytics is
only useful in early in exudative and early fibro-purulent phases. So in
essence there could be a place for all the surgical interventions only if
applied to the appropriate stage of empyema. The aim of any therapy should
be early intervention, that results in adequate drainage and complte
expansion of lung, thus avoiding Decortication that is the excision of the
pleural rinds which carries high morbidity and even mortality.
Congratulations to Bland et al.[1] for a well-done study, well analyzed and well written up on an issue that needed to be studied the way they did it. I agree with most of their conclusions, particularly their warning that studies linking postnatal HIV transmission to feeding practices need to use more exacting methods to document the latter than most studies have used to date.
Congratulations to Bland et al.[1] for a well-done study, well analyzed and well written up on an issue that needed to be studied the way they did it. I agree with most of their conclusions, particularly their warning that studies linking postnatal HIV transmission to feeding practices need to use more exacting methods to document the latter than most studies have used to date.
I would add to this another point: the "standardised WHO definitions" that they refer to were developed as a way of ensuring that household survey results are comparable and are not necessarily appropriate for studying the relationships between feeding patterns and certain types of morbidity. Thus the fact that the WHO definition "allows" "drops or syrups consisting of vitamins, mineral supplements, or prescribed medicines" should not be accepted unthinkingly. All of these can be provided in a contaminated or outdated form and all contain additional substances that are used as preservatives, fillers, binders, etc. While this may not matter much when studying for example the relationship between feeding patterns and concurrent patterns of diarrhea or growth, it may make a big difference when relating feeding patterns to such outcomes as allergy, micronutrient absorption--and HIV transmission.
The population Bland et al. studied is likely fairly representative of feeding patterns in wealthier rural African settings. However, in other settings their findings are less likely to hold. More importantly, their population was probably not the right one in which to compare the various measurement methods they used. The main reason for this is that there was too little variability in the duration of exclusive breastfeeding in their population. Only 17% were still exclusively breastfeeding after two weeks of age and thus able to switch category. That is, after this age so few infants change categories that high levels of sensitivity and specificity in the tools used to measure it were in a sense unavoidable. This is not to fault their study, but to point out that it needs to be repeated in other settings before generalizing from their findings.
Finally, that mothers tended to exaggerate the duration of EBF when recalling it several months later could in part be an artefact of the slightly different method of operationalizing the definition of EBF that was used in the long-term recall. Water was the only non-milk fluid used and the extent to which other fluids (or fluids mothers did not define as "water" such as “glucose”) were given before water could be partially explanatory.
Reference
(1) RM Bland, NC Rollins, G Solarsh, J Van den Broeck, and HM Coovadia. Maternal recall of exclusive breast feeding duration. Arch Dis Child 2003; 88: 778-783 .
We were pleased to receive the comments from John Craig with which we
largely agree.[1] The audit we published was a retrospective one of reports
received between 1997-2001. This was before many Senior House Officers (SHOs) began shift patterns
of working which has become the norm in recent times. We agree that this
change necessitates a different approach to education and training and we
fully support...
We were pleased to receive the comments from John Craig with which we
largely agree.[1] The audit we published was a retrospective one of reports
received between 1997-2001. This was before many Senior House Officers (SHOs) began shift patterns
of working which has become the norm in recent times. We agree that this
change necessitates a different approach to education and training and we
fully support the suggestions made in 'Liberating Learning'. To help
tutors develop these ideas further, Janet Anderson (on behalf of the
College) organised a workshop for tutors last June and another has been
arranged in December.
We have also altered the 'Essential Features of an SHO Training
Programme' which can be found in the new RCPCH Paediatric Training
Handbook (published September 2003). Paragraph 10 now reads 'There should
be three hours per week dedicated to education and training. The
department should demonstrate its commitment to ongoing teaching. The
format can include: tutorials, lectures, ward-based teaching and
attendance in outpatients for structured teaching and feedback.
Departmental meetings should be arranged so that the majority of SHOs can
attend, i.e. at shift overlap times, including early morning meetings and
lunch times. The educational content should be directed towards the career
aims of the SHOs and sessions should be interactive whenever possible.
Educational sessions should be bleep free and it should be possible to
attend >70% of sessions (ie an average minimum of two hours per week)'.
In summary, we agree with John Craig's comments and the College is
doing its best to support those who are delivering education and training
around the UK.
Reference
(1) Craig JS and Tubman TRJ. Re education and training in the paediatric senior house officer grade
[electronic response to Smith and Anderson; Education and training in the paediatric senior house officer grade: analysis of RCPCH hospital/child health visits reports, 1997–2001] archdischild.com 2003http://adc.bmjjournals.com/cgi/eletters/archdischild;88/5/450#554
Nordfeldt et al[1] conclude from their randomised controlled study that
severe hypoglycaemia incidence can be reduced in type 1 diabetes patients
who study good quality educational videos. Examination of the premise
that patient education reduces morbidity is worthy of study, both in the
current setting of type 1 diabetes and in paediatric disease in general.
Nordfeldt et al[1] conclude from their randomised controlled study that
severe hypoglycaemia incidence can be reduced in type 1 diabetes patients
who study good quality educational videos. Examination of the premise
that patient education reduces morbidity is worthy of study, both in the
current setting of type 1 diabetes and in paediatric disease in general.
The current study relies on their patient’s recall of severe
hypoglycaemic episodes at annual postal survey for its primary outcome
measure. Patient recall might be affected by their understanding of the
study design and might potentially introduce a reporting bias that
suggests a beneficial effect of the educational video. In assessing such a
bias it would be helpful to know what information the participants were
given about their study on consenting to enter.
Despite this potential bias their data show no significant
differences in hypoglycaemia incidence between their experimental groups.
The author’s claimed reduction in hypoglycaemia incidence in the
intervention group from 42 to 27% is therefore most logically accounted
for by a fortuitously higher random incidence of hypoglycaemia in the pre-
video period in the intervention group. Unfortunately no comparative data
were presented for their no video control group.
There are inherent difficulties in subjecting this educational
intervention to a randomised controlled study with potential biasses both
in favour and against the study hypothesis. Even if the study were to have
shown a clear short term effect on hypoglycaemic incidence, one would be
wise to exercise caution before diverting healthcare funding to
production of such video material until longer term benefit had been
demonstrated. Experience dictates that educational messages are subject to
a degree of decay with the passage of time. In contrast to the author’s
claim that their study shows that “severe hypoglycaemia can be reduced
with good quality education materials”, we interpret their data as having
shown no effect of their educational material on the incidence of severe
hypoglycaemia even before the waning of an educational effect, despite
potential bias in favour of accepting the study hypothesis.
Reference
(1) S Nordfeldt, C Johansson, E Carlsson, and J-Å Hammersjö. Prevention of severe hypoglycaemia in type I diabetes: a randomised controlled population study. Arch Dis Child 2003; 88: 240-245.
Dear Editor
There are few controlled studies of pedagogical devices used in patient education regarding chronic diseases like type 1 diabetes. As Briars et al points out, this area is worth further study and we agree that a critical view is needed with respect to such studies. We therefore performed this controlled study in a general hospital population following the previous study in a before-after setting at o...
Dear Editor
We read with interest the paper by Clark and Reid [1] describing the potential benefits of recombinant surfactant protein D therapy.
The authors give a range of potential disease targets for surfactant protein D based therapy including neonatal chronic lung disease, cystic fibrosis, lung infections, emphysema and asthma. The authors do not however mention the potential use of surfactant protein D...
Dear Editor
It is encouraging that the Royal College supports the notion that "the general paediatrician remains core to the resuscitation and stabilisation of the critically ill child" and "exposure to critically ill patients is an essential part of training", and I am glad they seek to challenge the solutions proposed. However, to dismiss them as simply unrealistic fails to heed their own goal of more imaginative...
Dear Editor
I would like to comment on the paper by de San Lazaro et al.[1]
The authors of this paper demonstrated that violent rocking of a baby chair could produce acceleration/decelaration forces similar as those seen when violenty shaking a child and that could result in similar lesions as those seen in a true shaken baby syndrome. I recently encoutered a similar case where a 2 month old baby was p...
Dear Editor
I read the article by Allen et al. with interest. I am interested in a potential systemic effect of pimecrolimus that doesn't seem to have been addressed.
I understand that the cream achieves its desired effect by surpressing the white cells in the affected area. I understand that the population of white cells migrating into the eczematous area is in continuous flux, and that these cells...
Dear Editor
I have read C. Gilberg’s paper[1] with interest but also with concern because there to my knowledge is no scientific valid paper about children with DAMP (deficits in attention, motor control, and perception).
The term DAMP was first introduced by C. Gilberg in 1986 [2] and based on a study of 6 years old children in Gothenburg, Sweden.[3] The main aim of this study was to construct a screening i...
Dear Editor
I agree with Dr Spencer that the incidence of the Paediatric Empyema is on the increase and the management of this age-old disease is dependent upon provider-based experiences. Secondly, there is no clear evidence that one modality of management is superior to the other. Therefore giving rise to controversies in the management of this disease. The pathogenesis of the disease (Empyema) is largely ignored w...
Dear Editor
Congratulations to Bland et al.[1] for a well-done study, well analyzed and well written up on an issue that needed to be studied the way they did it. I agree with most of their conclusions, particularly their warning that studies linking postnatal HIV transmission to feeding practices need to use more exacting methods to document the latter than most studies have used to date.
I would add to...
Dear Editor
We were pleased to receive the comments from John Craig with which we largely agree.[1] The audit we published was a retrospective one of reports received between 1997-2001. This was before many Senior House Officers (SHOs) began shift patterns of working which has become the norm in recent times. We agree that this change necessitates a different approach to education and training and we fully support...
Dear Editor
Nordfeldt et al[1] conclude from their randomised controlled study that severe hypoglycaemia incidence can be reduced in type 1 diabetes patients who study good quality educational videos. Examination of the premise that patient education reduces morbidity is worthy of study, both in the current setting of type 1 diabetes and in paediatric disease in general.
The current study relies on...
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