The review of Guillain-Barre Syndrome (GBS) (Arch Dis Child Educ
Pract Ed 2007; 92: ep161-ep168) was clear and comprehensive and will be of
practical value to all who manage these children, whether or not they are
admitted to an intensive care unit. The authors appropriately address the
important issue of communication and emphasise that this may be very
difficult if not impossible for the child and young person who is
c...
The review of Guillain-Barre Syndrome (GBS) (Arch Dis Child Educ
Pract Ed 2007; 92: ep161-ep168) was clear and comprehensive and will be of
practical value to all who manage these children, whether or not they are
admitted to an intensive care unit. The authors appropriately address the
important issue of communication and emphasise that this may be very
difficult if not impossible for the child and young person who is
conscious but unable to speak or move. Readers my find it interesting and
useful to learn about the often ingenious ways that a number of these
young people have used to ‘communicate’ in this situation, and it is often
not until later that these methods, together with other thoughts, can be
articulated 1,2.
At the Royal Liverpool Children’s Hospital (Alder Hey) we have
designed a single Integrated Care Pathway document which has replaced the
child’s medial case notes and is used by all medical, nursing and therapy
professionals involved in the management of patients with GBS wherever the
child is seen within the hospital (submitted for publication). One of the
main advantages of this single care pathway document is that it has
facilitated communication and knowledge-sharing between the many
disciplines involved with these children. A future version of this GBS
pathway will include a communication sheet for the family and, where
appropriate, the child.
(No conflict of interest)
References
1. Smith M, Appleton RE. (2001) Guillain-Barré syndrome; a patient’s
experience. Dev Med Child Neurol 43: 69-70.
2. Mistry T. Experiencing Guillain Barre: a mother and daughter
perspective. Arch Dis Child 2007; 92: 462-463.
R E Appleton
Consultant Paediatric Neurologist
Roald Dahl EEG Unit
Paediatric Neurosciences Foundation.
Royal Liverpool Children’s Hospital (Alder Hey)
Liverpool L12 2AP
Richard.Appleton@rlc.nhs.uk
Although examples of interstitial lung disease such as diffuse alveolar
haemorrhage and interstitial fibrosis were the only ones acknowledged to
be associated with Henoch-Schonlein purpura(HSP) in a recent review(1),
the association of HSP and pan-acinar emphysema attributable to alpha-1
antitrypsin(AAT) deficiency also deserves mention(2), especially in view
of the speculative relationship between anti neutrophil cytosp...
Although examples of interstitial lung disease such as diffuse alveolar
haemorrhage and interstitial fibrosis were the only ones acknowledged to
be associated with Henoch-Schonlein purpura(HSP) in a recent review(1),
the association of HSP and pan-acinar emphysema attributable to alpha-1
antitrypsin(AAT) deficiency also deserves mention(2), especially in view
of the speculative relationship between anti neutrophil cytosplasmic
antibodies(ANCA) and AAT deficiency, on the one hand(2), and ANCA vs HSP
on the other(3)(4). Although the precise pathogenic basis of the
association of AAT deficiency and the vasculitides is unclear, according
to a recent evaluation a major role of alpha-1 antitrypsin(AAT) is to
inhibit the destructive capabilities of proteinase-3(PR3), the serine
protease released from neutrophils and monocytes at local sites of
inflammation and tissue injury. Deficiency of AAT results in an increase
in blood levels of free and active PR3 which, in turn generate further
tissue injury and also generate an antibody response in the form of ANCA.
ANCA, in turn, compounds PR3-related vascular injury by generating a
cascade which includes activation of tumour necrosis factor(TNF)-primed
neutrophils, accelaration of apoptosis of TNF-primed neutrophils, and
secondary necrosis of the TNF-primed neutrophils themselves. The premature
release of the toxic contents of the apoptopic cells is a further episode
in the catalogue of ANCA-related tissue destruction.(2). In the clinical
context a literature review revealed six cases of the association of AAT
deficiency and HSP, one being a child aged 1.8 years when first reported,
and the other five being adults aged 27-82. In the paediatric case there
was no documentation of lung disease, and, in that instance, chronic renal
disease was the significant complication of AAT deficiency. Among the five
adults, four had documented pan-lobular emphysema, with co-existing
chronic renal disease in three of those four. The one adult in whom
pulmonary status had not been documented did also have chronic renal
disease but the fourth adult with pan-lobular emphysema only experienced
transient proteinuria and transient haematuria(2). In the latter instance,
HSP was associated with ANCA of the Immunoglobulin G(IgG) subtype(5)
whereas, among the three adults in whom pan-lobular emphysema co-existed
with chronic renal disease, the one patient with ANCA was characterised
by the IgA subtype of ANCA(2). In all, ANCA was present in only two of
the 6 patients characterised by the association of AAT deficiency and
HSP(2). Both had pan-lobular emphysema, but only one had chronic renal
disease. ANCA of the IgA subclass was a feature of the patient with
chronic renal disease(2), and ANCA of the IgG subclass charcterised the
patient who was free of chronic renal disease(5). Although IgA ANCA has
been identified in as many as 82.3% of 35 chidren aged 3-16 in the acute
phase of HSP(3), among 28 consecutive adult HSP patients who presented
predominantly with abdominal symptoms, the prevalence of ANCA(subtype not
stated) was only 32.1%(4). In the former, no relationship was found
between severity of HSP and IgA ANCA(3), but in the latter HSP patients
with ANCA had significantly(p=0.02) higher clinical scores, significantly
higher(p=0.01)serum creatinine levels, and significantly(p=0.03)higher 24
hour urinary protein excretion than their ANCA negative counterparts(4)
However, given the variability in prevalence of ANCA in HSP patients free
of AAT deficiency(3)(4), and the low prevalence of ANCA when HSP is
associated with AAT(2), the role of ANCA, though speculative, nevertheless
remains intriguing, especially in view of the theoretical considerations
evaluated by Patterson et al(2).
References
(1) Tizard EJ., Hamilton-Ayres MJJ
Henoch-Schonlein purpura
Archives of Disease in Childhood 2008:93:1-8
(2)Patterson CC., Ross P., Pope-Harman AL., Knight DA., Magro CM
Alpha-1 anti-trypsin deficiency and Henoch-Schonlein purpura associated
with anti-neutrophil cytoplasmic and anti-endothelial cell antibodies of
immunoglobulin-A isotype
Journal of Cutaneous Pathology 2005:32:300-6
(3) Ozaltin F., Bakkaloglu A., Ozen S et al
The significance of IgA class of antineutrophil cytoplasmic
antibodies(ANCA) in childhood Henoch-Schonlein purpura
Clinical Rheumatology 2004:23:426-9
(4) Zhang Y., Wu Y-K., Ciorba MA., Ouyang Q
Significance of antineutrophil cytoplasmic antibody in adult patients with
Henoch-Schonlein purpura presenting mainly with gastrointestinal symptoms
World Journal of Gastroenterology 2008:14:622-6
(5) Meier P., Dayer E., Lemoine R., Blanc E
Henoch-Schonlein purpura with IgG PR3-ANCA in a PiZZ alpha 1- antitrypsin
deficient patient
Nephrology Dialysis Transplantation 2001:16:1932-5
We found Lio’s paper on alopecia in children (Arch. Dis. Child. Ed.
Pract., December issue) very interesting, but noticed that the author does
not mention celiac disease among the autoimmune diseases associated with
alopecia areata.
Both thyroid dysfunction and alopecia may point to celiac disease
even in the absence of gastrointestinal complaints.[1, 2] Alopecia areata
is in fact significantly associated to cel...
We found Lio’s paper on alopecia in children (Arch. Dis. Child. Ed.
Pract., December issue) very interesting, but noticed that the author does
not mention celiac disease among the autoimmune diseases associated with
alopecia areata.
Both thyroid dysfunction and alopecia may point to celiac disease
even in the absence of gastrointestinal complaints.[1, 2] Alopecia areata
is in fact significantly associated to celiac disease in children as well
as in adults; it might even be its only manifestation, as reported in
several papers.[1, 3, 4] In these cases full recovery with hair re-growth
may be achieved on a gluten free diet. [3, 4] Moreover, we have previously
demonstrated that when associated to celiac disease, alopecia is one of
the autoimmune disorders apparently related to the duration of exposure to
gluten.[5]
We are therefore convinced that all children with alopecia areata
should be screened for celiac disease, particularly (but not exclusively)
if thyroid dysfunction is present.
1 Tursi A, Giorgetti G, Brandimarte G, et al. Prevalence and clinical
presentation of subclinical/silent celiac disease in adults: analysis on
12-yerar observation. Hepatogastroenterology 2001;48:462-4.
2 Berti I, Della Vedova R, Paduano R, et al. Coeliac disease in
primary care: evaluation of a case-finding strategy. Dig Liver Dis
2006;38:461-7.
3. Corazza GR, Andreani ML, Venturo N, et al. Celiac disease and
alopecia areata: report of a new association. Gastroenterology
1995;109:1333-7.
4. Naveh Y, Rosenthal E, Ben-Arieh Y, et al. Celiac disease-
associated alopecia in childhood. J Pediatr 1999;134:362-4.
5. Ventura A, Magazzù G, Greco L. Duration of exposure to gluten and
risk for autoimmune disorders in patients with celiac disease.
Gastroenterology 1999;117:297-303.
We read with great interest the paper by Shaw “Osteoporosis in
pediatrics” (Arch. Dis. Child. Ed. Pract., December issue).
The author doesn’t cite celiac disease as a specific cause of osteoporosis
in children, although he correctly recommends celiac screening in case of
suspected secondary osteoporosis.
A diminished bone mineral density with z score lower than -1.0
standard deviation (SD) can be found in up to...
We read with great interest the paper by Shaw “Osteoporosis in
pediatrics” (Arch. Dis. Child. Ed. Pract., December issue).
The author doesn’t cite celiac disease as a specific cause of osteoporosis
in children, although he correctly recommends celiac screening in case of
suspected secondary osteoporosis.
A diminished bone mineral density with z score lower than -1.0
standard deviation (SD) can be found in up to 50% of children with celiac
disease; more severe reduction of mineral density with z score lower than
-2.5 SD is generally observed only in newly diagnosed children or in
adults.[1] Moreover, celiac patients, including children, are at increased
risk of hip fractures and fractures of any type.[2]
Osteoporosis in celiac disease may be due not only to malabsorption,
but also to abnormalities in cytokine levels.[3] Increased levels of
osteoclast-triggering cytokines, such as IL-1, IL-6 and TNFalfa, have in
fact been found in untreated CD patients, while the level of inhibitory
cytokines such as IL-18 and IL-12 may be lowered. Normalization of
cytokines levels with a gluten-free diet may explain the increased bone
mineral density observed in osteopenic celiac children, particularly under
4 years, while this effect is not so obvious in adults. [1, 4] As bone
mineral density can be reduced both in symptomatic and in silent celiac
disease, early diagnosis is important not only in order to achieve a
normal bone mineral density, but also to prevent the onset of autoimmune
conditions associated to celiac disease.[5]
In conclusion, osteopenia and osteoporosis may be the only
manifestation of silent/latent celiac disease, leading to an increased
risk of fractures. Given the high prevalence of celiac disease, and the
effectiveness of a gluten-free diet in treating and preventing its
complications, it is relevant to consider celiac disease in the
differential diagnosis of osteoporosis in pediatrics.
References
1 Kalayci AG, Kansu A, Girgin N, et al. Bone mineral density and
importance of a gluten free diet in patients with celiac disease in
childhood. Pediatrics 2001;108:E89.
2 Ludvigsson JF, Michaelsson K, Ekbom A, et al. Coeliac disease and
the risk of fractures – a general population based cohort study. Aliment
Pharmacol Ther 2007;25:273-85.
3 Bernstein CN, Leslie WD. The pathophysiology of bone disease in
gastrointestinal disease. Eur J Gastroenterol Hepatol 2003;15:857-64.
4 Tau C, Mautalen C, De Rosa S, et al. Bone mineral density in
children with celiac disease. Effect of a gluten free diet. Eur J Clin
Nutr 2006;60:358-63.
5 Hill ID, Dirks MH, Liptak GS, et al. Guideline for the diagnosis
and treatment of celiac disease in chldren: recommendations of the North
American Society for Pediatric Gastroenterology, Hepatology and Nutrition.
J Pediatr Gastroenterol Nutr 2005;40:1-19.
Alopecia may also be attributable to the use of hair relaxants such
as sodium hydroxide and guanidine hydroxide, respectively(1) or other
products containing sodium, potassium, or guanine sulfites or
thioglycolates(2) to straighten or "relax" tightly curly(spiral) black
hair of the type found among South African blacks(1) or African-
Americans(2). These products work by rearranging the cysteine disulfide
bonds of the hai...
Alopecia may also be attributable to the use of hair relaxants such
as sodium hydroxide and guanidine hydroxide, respectively(1) or other
products containing sodium, potassium, or guanine sulfites or
thioglycolates(2) to straighten or "relax" tightly curly(spiral) black
hair of the type found among South African blacks(1) or African-
Americans(2). These products work by rearranging the cysteine disulfide
bonds of the hair, but an undesirable consequence is to damage the hair
shaft and to decrease its tensile strenghth(3). In one South African study
in which the definitive analysis comprised 1020 subjects aged 6-21,
alopecia was significantly(p < 0.0001) more prevalent among those with
"relaxed" hair than among those with "natural" hair(1). In an American
study, as many as 95% of 464 patients suffered hair breakage and hair loss
after using a hair relaxant(4) which was subsequently withdrawn after
intervention by the United States FDA. Chemical relaxants can also cause
scarring alopecia, exemplified by 5 subjects in whom the initial symptom
was onset of head discomfort within minutes of the application of the hair
relaxant. The vertex of the head was involved, and it healed with
scarring(5). Given the fact that hair relaxants have been used on children
as young as six(1), hair relaxant-related alopecia should enter into the
differential diagnosis of alopecia in children of African descent.
References
(1) Khumalo NP., Jessop S., Gumedze F., Ehrlich R
Hairdressing is associated with scalp disease in African schoolchildren
British Journal,of Dermatology 2007:157:106-110
(2) McMichael AJ
Hair breakage in normal and weathered hair:focus on the black patient
Journal of Investigative Dermatology Symposium Proceedings 2007:12:6-9
(3) Khalil EN
Cosmetic and hair treatments for the black consumer
Cosmetic Toiletries 1986:101:51-8
(4)Swee W., Klontz KC., Lambert LA
A nationwide outbreak of alopecia associated with the use of a hair-
relaxing formulation
Archives of Dermatology 2000:36:1104-8
(5)Khumalo NP., Pillay K., Ngwanya RM
Acute "relaxer"-associated scarring alopecia: a report of five cases
British Journal of Dermatology 2007:156:1394-6
Dr Roberts questions the point of treating warts and molluscum which
are benign and will often spontaneously resolve, and expresses concern
about discussing these methods of treatment at all. In terms of the
former, I regret that I did not more explicitly state that the so-called
"tincture of time" is, by far, the preferred method of treating these
lesions. The focus of the review is on those cas...
Dr Roberts questions the point of treating warts and molluscum which
are benign and will often spontaneously resolve, and expresses concern
about discussing these methods of treatment at all. In terms of the
former, I regret that I did not more explicitly state that the so-called
"tincture of time" is, by far, the preferred method of treating these
lesions. The focus of the review is on those cases where there is a
compelling reason to seek further treatment, with emphasis on sorting
through the vast (and often anecdotal) literature on these treatments.
As Dr Roberts notes, the consultant dermatologists carry a heavy load
in the UK, and this is perhaps equally true in the US.[1] Ironically, it
was the tremendous number of "emergency" consultations that are referred
to our practice for warts and molluscum that prompted me to write this
article. Many patients are referred by their pediatricians for warts and
molluscum that have persisted or are spreading, causing a great deal of
anxiety and frustration for all parties. Importantly, many of these
patients express anger towards their pediatrician and frequently feel
marginalized because they were told the lesions would go away without
treatment. Sometimes, the children are ostracized from school, public
pools or sporting events, adding psychological stress to the entire
family.[2]
Much more concerning, however, is when doctors or the patients
themselves feel compelled to treat these lesions and do so in ways that
may cause harm. I specifically cautioned against using imiquimod for
molluscum, for example, as I have seen many adverse effects when used for
this purpose. I have seen patients apply powerful acids and create
painful ulcers which scar, and have seen children traumatized by curettage
without anesthesia of any sort. The secondary purpose of the paper, then,
is to discuss these methods openly and without bias, so that if treatment
is deemed necessary, there is some context and experience for choosing an
appropriate treatment in a manner that is safe for the patient.
Drs Goodyear and Taibjee raise concern that I impugn evidence-based
medicine (EBM). In fact, in my five-page paper with almost 50 references
from the peer-reviewed literature including heavy reliance on the Cochrane
Database, I sought to explore the area where there is not yet enough
evidence to make easy rational choices about treatment of these skin
diseases. Indeed, on the British Association of Dermatologists website,
the only treatments that were given the strength of evidence D ("There is
fair evidence to support the rejection of the use of the procedure") were
oral cimetidine and homeopathy.[3] There were no treatments given
strength of evidence E ("There is good evidence to support the rejection
of the use of the prodedure"). In fact, two of the treatments I discussed
(imiquidmod and heat treatment/balneotherapy) were deemed to have
insufficient evidence at this time. As a strong proponent of EBM, I try
to remain vigilant for the fallacy of argumentum ad ignorantiam in all its
forms, which in this case might be best put: "absence of evidence is not
evidence of absence."
In sum, I overwhelmingly agree with the comments of Drs Goodyear,
Taibjee, and Roberts and appreciate the opportunity to put the review in a
proper light.
References:
1. Tsang MW, Resneck JS Jr. Even patients with changing moles face long
dermatology appointment wait-times: a study of simulated patient calls to
dermatologists. J Am Acad Dermatol 2006;55(1):54-8.
2. Braue A, Ross G, Varigos G, et al. Epidemiology and impact of
childhood molluscum contagiosum: a case series and critical review of the
literature. Pediatr Dermatol 2005;22:287–94.
The August edition of ADC Education and Practice supplement
prominently displays on the front cover an infant receiving treatment for
molluscum lesions on the thigh. The associated article on the management
of warts and molluscum contagiosum explores available treatment options
and the differential diagnosis of these benign skin infections.
What messages are conveyed in this review of Nort...
The August edition of ADC Education and Practice supplement
prominently displays on the front cover an infant receiving treatment for
molluscum lesions on the thigh. The associated article on the management
of warts and molluscum contagiosum explores available treatment options
and the differential diagnosis of these benign skin infections.
What messages are conveyed in this review of North American practice
to Paediatricians and General Practitioners in the UK? The high prevalence
of these conditions in school age children is well known, as is the
natural history for them to spontaneously resolve without medical
intervention. Are we now expected to routinely offer treatment advice or
even refer affected children to dermatology clinics? It would be helpful
to know if the recommendations contained in Dr Lio’s guide had the general
support of the British Association of Dermatologists. (2.)
The questionable benefits to the child of removing warts and
molluscum have to be balanced with the disadvantages of discomfort,
psychological trauma and the possibility of permanent scarring. Most
children prefer not to undergo such procedures if given the choice even
though their parents may wish us to adopt a more active cosmetic approach.
In support of the no treatment option, we should also consider the
practicalities of providing a clinical service for inessential treatments.
Consultant Dermatologists in the UK already carry a heavy patient load and
their expertise should perhaps be restricted to the assessment of lesions
which cause occasional diagnostic difficulty. Inflamed and irritated
lesions are best managed by treatment of the associated eczematisation
which can usually be achieved in primary care. Hospital paediatric
services do not normally have staff who are trained in minor skin surgery
or dermatological procedures so that patients referred for such treatments
would perhaps languish on a waiting list for several months until their
lesions spontaneously resolved.
Several helpful information leaflets are in general circulation to
guide parents and their doctors with general advice on benign
dermatological conditions in children. (2.3.4.) this should be the first
stage and often the only stage required in management.
Yours sincerely
Dr S Roberts
Consultant Paediatrician
University Hospital of South Manchester NHS Foundation Trust
Manchester M23 9LT
We welcome the Education and Debate article on Toxic Shock
Syndrome(1), which helps improve the profile of this potentially
devastating disease and enhances diagnostic recognition.
It is however important to highlight some specific areas in
prevention, diagnosis and therapy which are not fully discussed within
this review.
As the authors state, early diagnosis can be difficult but...
We welcome the Education and Debate article on Toxic Shock
Syndrome(1), which helps improve the profile of this potentially
devastating disease and enhances diagnostic recognition.
It is however important to highlight some specific areas in
prevention, diagnosis and therapy which are not fully discussed within
this review.
As the authors state, early diagnosis can be difficult but is crucial
to improving prompt intervention and therapy. Case definitions are
complex but are well established and importantly differentiate
staphylococcal from streptococcal toxic shock (2). It is important to
realise that streptococcal toxic shock does not always present with a
rash, nor is pyrexia included within the case definition, although
isolation of GAS is required. Rash is therefore not an essential
diagnostic criteria when assessing children initially before the results
of cultures are known.
Prevention is important and there was little expansion on the role of
prophylactic antibiotics in burns which has gathering evidence for
efficacy in the prevention of toxic shock syndrome(8,9).
The authors state that effective antitoxin therapy is considered an
essential part of management, but describe only the potential for
antitoxin blocking antibody. There is however a growing literature on the
specific antitoxin effect of antibiotics such as clindamycin,
aminoglycosides and linezolid which have been shown to reduce TSST 1 and
streptococcal exotoxin A (3,4,5). Clindamycin is now an accepted and
recommended adjunctive therapy for both staphylococcal and streptococcal
toxic shock (2-5).
Inhibition of T cell activation by blocking or inactivating
staphylococcal and streptococcal superantigens is theoretically attractive
(6). Its use in streptococcal toxic shock has suggested benefit,
(statistically significant results perhaps prevented by early termination
of this study because of slow recruitment) (7), but there have been no
such studies with FFP, which the authors suggest is useful. Although
specific anti-toxin antibody may be detected in FFP, the level of this
antibody is likely to be significantly lower than in IVIG and hence
passive immunity may not be achieved. There is no other evidence base for
FFP apart from the authors’ experience, and although it may well have been
successful for the authors is not consistent with other accepted
guidelines (2).
Management guidelines for Toxic shock are specifically outlined by
the American Academy of Pediatrics (2) as follows:
• Fluid management to maintain adequate venous return and cardiac filling
pressures to prevent end organ damage.
• Anticipatory management of multi system organ failure.
• Parental antimicrobial therapy at maximal doses for age.
o Kill organism with bactericidal cell wall inhibitor (e.g. beta-lactamase
resistant antistaphylococcal antimicrobials).
o Stop enzyme, toxin, or cytokine production with protein synthesis
inhibitor (e.g. clindamycin).
• Intravenous immune globulin may be considered for an infection
refractory to several hours of aggressive therapy, in the presence of an
undrainable focus, or where there is persistent oliguria with pulmonary
oedema.
The guidelines for the management of toxic shock syndrome should
include Clindamycin as an adjunctive treatment and IVIG where necessary.
FFP should not be used as a specific anti-toxin (without an evidence base)
but may be useful as part of volume expansion management.
References:
1. A Young, K Thornton. Toxic shock syndrome in burns: diagnosis and
management. Arch Dis Child Educ Pract Ed 2007;92:ep97-ep100.
2. American Academy of Pediatrics [Toxic Shock Syndrome]. In: Pickering
LK,ed. 2000 Red Book: Report of the Committee on Infectious Diseases. 25th
edition. Elk Grove Village, IL: American Academy of Pediatrics;2000:p580.
3. Chuang et al. Toxic shock syndrome in children epidemiologic,
pathogenis, and management. Pediatric drugs. 2005;7(1):11-25.
4. Coyle E.A, Cha R, Rybak M J. Influences of linezolid, penicillin and
clindamycin alone and in combination on streptococcal pyrogenic ExotoxinA
release. Antimicrobial Agents and Chemotherapy. 2003;47(5);1752-1755.
5. Annane D, Clair B, Salomon J. Managing toxic shock syndrome with
antibiotics. Expert Opin. Pharmacother. 2004;5(8):1701-1709.
6. Darenberg J et al. Differences in potency of Intravenous polyspecific
immunoglobulin G against streptococcal and staphylococcal superantigens:
implications for therapy of toxic shock syndrome. CID. 2004:38:836-842.
7. Darenberg J et al. Intravenous immunoglobulin G therapy and
streptococcal toxic shock syndrome. CID. 2003;37:333-40.
8. Abid Rashid, Alastair P. Brown, Khalid Khan. On the use of
prophylactic antibiotics in prevention of toxic shock syndrome. Burns 31
(2005) 981–985.
9. Edwards-Jones V, Dawson MM, Childs C. A survey into toxic shock
syndrome (TSS) in UK burns units. Burns 26 (2000) :323–33.
We read this article with concern. Incorrect and potentially harmful
messages may be relayed to paediatricians, especially to those in training
and other healthcare professionals.
Dr Lio asserts that Evidence-based Medicine (EBM) leads to stagnation
in medicine and therapeutic nihilism, and expresses his concerns of EBM as
a “philosophy in treating actual human beings”. Unfortunately this is
rath...
We read this article with concern. Incorrect and potentially harmful
messages may be relayed to paediatricians, especially to those in training
and other healthcare professionals.
Dr Lio asserts that Evidence-based Medicine (EBM) leads to stagnation
in medicine and therapeutic nihilism, and expresses his concerns of EBM as
a “philosophy in treating actual human beings”. Unfortunately this is
rather missing the point. The cornerstone of EBM is reviewing the wealth
of data and applying this to the individual patient.
In 2006 there were comprehensive Cochrane reviews of treatment of
warts and molluscum in otherwise healthy individuals.[1,2] These had
simple and easy-to-understand recommendations; firstly, awaiting
spontaneous resolution of molluscum and secondly, topical preparations
containing salicylic acid are safe and effective for warts. No randomised
controlled trials address physical destructive methods for molluscum.
Cantharidin causes pain and blistering with multiple treatments often
required.[3] Regarding warts, cryotherapy appears to be no more effective
than simple topical preparations.[1] Balneotherapy is potentially
dangerous due to risk of burns. Up to 85% children using imiquimod have
side effects.[4] Doctors registered with the General Medical Council have
a duty to provide effective treatments based on best available
evidence.[5] In the absence of a clearly demonstrable superior efficacy of
a given treatment compared to placebo or no treatment we should not
persist with such treatments.
Additionally to physical side effects, we should consider that for a
child distressing treatments may lead to longlasting phobias and distrust
of healthcare professionals and hospitals. Treatment of molluscum and
warts is appropriate when clearly troubling or impairing the child, and in
the child’s best interests. However, the front cover picture of August
2007 Education and Practice depicting cantharidin treatment in infants is
worrisome. Doctors may feel pressured to offer treatment based on parental
anxiety and expectations but frequently all that is required is simple
reassurance for common, asymptomatic and self-limiting conditions.
References:
1.Gibbs S, Harvey I. Topical treatments for cutaneous warts. Cochrane Database of Syst Rev 2006:3:CD001781.
2.Van Dr Wouden JC, Menke J, Gajadin S et al. Interventions for cutaneous molluscum contagiosum. Cochrane Database of Syst Rev 2006;2:CD004767.
3.Hanna D, Hatami A, Powell J et al. A prospective randomised trial compating the efficacy and adverse effects of four recognised treatments of molluscum contagiosum in children. Pediatr Dermatol 2006;23:574-9.
4.Bayerl C, Feller G, Goerdt S. Experience in treating molluscum contagiosum in children with imiquimod 5% cream. Br J Dermatol 2003;149:25-8.
5.The General Medical Council. Good Medical Practice. London, GMC 2006.
Dr Helen M Goodyear
Consultant Paediatrician Heart of England NHS
Foundation Trust Bordesley Green East Birmingham B9 5SS
Keady S (1) provides some updated guidelines on the drug treatment of
gastro-oesophageal reflux (GOR) and gastro-oesophageal reflux disease
(GORD).
However, in order to give clear management guidelines, we believe that the
review should have first addressed the definition of GOR (ie,
physiological) versus GORD (ie, pathological). In fact, the results of a
recent survey on the knowledge, attitudes a...
Keady S (1) provides some updated guidelines on the drug treatment of
gastro-oesophageal reflux (GOR) and gastro-oesophageal reflux disease
(GORD).
However, in order to give clear management guidelines, we believe that the
review should have first addressed the definition of GOR (ie,
physiological) versus GORD (ie, pathological). In fact, the results of a
recent survey on the knowledge, attitudes and practice styles of North
American Pediatricians regarding GOR show that still many infants are
inappropriately treated for GORD when all they have is physiological GOR
(2). The first important goal of future educational efforts should be
therefore directed to avoid overtreatment of “happy spitters” (ie, GOR).
Second, in his conclusions Keaty correctly underlines that “the majority
of drugs used have limited robust data supporting their use”. However,
some evidence from randomised controlled trials (RCTs) is now available
but it is not clearly reflected by the practice guidelines Keaty
suggested. An example of this is the use of prokinetic drugs (domperidone
or erythromycin), in association with an appropriate acid suppressant,
recommended for the treatment of moderate o severe GORD. A recent
systematic review of RCTs showed that, even if from the limited evidence
available (the 4 RCTs named by the same Keaty), domperidone does not
appear to be more effective than placebo in reducing symptoms of GOR and
GORD (3). Given the usually benign nature of GOR, the widespread use of
prokinetic drugs is therefore not indicated. In severe cases of GORD,
where medical management is required, available evidence suggest that
domperidone is yet not indicated. Its use may be re-considered if further
data was to provide robust evidence of a favourable benefit-risk profile.
The overall variability in practice style and lack of conformity to
Naspghan GORD guidelines (4) merit further efforts in education and in
terms of guideline availability based on the results of good clinical
trials with relevant outcome measures.
Federico Marchetti, Jenny Bua, Alessandro Ventura
Department of Paediatrics, Institute of Child Health, IRCCS Burlo
Garofolo, Trieste, Italy
e-mail: fedemarche@tin.it
Competing interests: None declared
References:
1.Keady S. Update on drugs for gastro-oesophageal reflux disease.
Arch Dis Child Educ Pract 2007;92:ep114-ep118
2.Diaz DM, Winter HS, Colletti RB, Ferry GD, Rudolph CD, Czinn SJ,
Cochran W, Gold BD; NASPGHAN/CDHNF Scientific Advisory Board. Knowledge,
attitudes and practice styles of North American pediatricians regarding
gastroesophageal reflux disease. J Pediatr Gastroenterol Nutr
2007;45(1):56-64.
3.Pritchard DS, Baber N, Stephenson T. Should domperidone be used for
the treatment of gastro-oesophageal reflux in children? Systematic review
of randomized controlled trials in children aged 1 month to 11 years old.
Br J Clin pharmacol 2005;59(6):725-9
4.Rudolph CD, Mazur LJ, Liptak GS, et al. Guidelines for evaluation
and treatment of gastroesophageal reflux in infants and children.
Recommendations of the North American Society for Pediatric
Gastroenterology and Nutrition. J Pediatr Gastroenterol Nutr 2001;32
(Suppl 2) :S1–S31
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