The authors appreciate the comments of Dr Giovannoni and fully
recognize the ongoing efforts of the London group in evaluating antibasal
ganglia antibodies (ABGA) in poststreptococcal movement conditions.
Nevertheless, readers must recognize that there are significant
discrepancies between results reported in the article by Church et al.,
[1] and other investigators [2,3].
The authors appreciate the comments of Dr Giovannoni and fully
recognize the ongoing efforts of the London group in evaluating antibasal
ganglia antibodies (ABGA) in poststreptococcal movement conditions.
Nevertheless, readers must recognize that there are significant
discrepancies between results reported in the article by Church et al.,
[1] and other investigators [2,3].
In order to objectively assess methods for measuring ABGA (i.e.,
enzyme-linked immunosorbent assays (ELISA), indirect immunofluorescence,
and Western immunoblotting), we have compared the effects of serum or IgG,
condition of tissue (fresh or frozen), method of tissue preparation (with
or without removal of lipids), and the method of Western immunoblotting
detection (electrochemiluminescent, ECL, or colorimetric detection) on
laboratory results. More specifically, our data indicate that improved
results can be obtained using fresh postmortem tissue homogenates for
Western immunoblots and ELISA and support the use of ECL detection for
Western immunoblots. Our results have also been confirmed in studies
using a fetal neuronal cell line. We concur that there are a variety of
methodologies available to eliminate bands, but question the intent when
one is screening for unknown antigens. Giovannoni does raise an important
issue, that of the precise localization of bands. More specifically, we
have found that purchased molecular weight standards vary in accuracy.
Since I fully doubt that readers of this letter are interested in
methodological discussions, I will conclude by stating that our detailed
comparison manuscript is currently under review.
A second point for emphasis is that before accepting pathogenic
relevance for a monoclonal antibody, readers must demand confirmation
concerning regional and neuronal specificity, evidence of cross-reactivity
with streptococcal proteins, and documentation of passive transfer of the
disorder. As stated in our commentary, we remain concerned that
hypotheses claiming an association between antibodies against epitopes at
98, 60, 45, and 40 kDa and a variety of clinical findings remain unproven.
Giovannoni cites Huntington chorea (HC) as an example of a disorder with a
single etiology and a variety of possible clinical symptoms. While
correct, as compared to controversial clinical disorders like PANDAS [4],
HC also has a typical phenotype, classical neuroradiographic findings, a
well-defined neuropathology, and an established molecular genetic
abnormality
In summary, we believe that the proposal of an autoimmune ABGA
mechanism for poststreptococcal neurological disorders deserves careful
study, but emphasize that final conclusions are currently premature. We
look forward with great anticipation to participating in a double-blind
protocol with investigators on the other side of the pond.
References
(1). Church AJ, Dale RC, Giovannoni G. Anti-basal ganglia antibodies: a
possible diagnostic utility in idiopathic movement disorders? Arch Dis
Child., 89:611-614, 2004.
(2). Singer HS, Loiselle CR, Lee O, Minzer K, Swedo S, Grus FH. Anti-
basal ganglia
antibodies in PANDAS. Mov Disord, 19:406-415, 2004.
(3). Singer HS, Loiselle CR, Lee O, Garvey M, Grus FH. Anti-basal
ganglia antibody
abnormalities in Sydenham’s chorea. J Neuroimmunology, 136:154-161, 2003.
(4). Singer HS, Loiselle C. PANDAS: a commentary. J Psychosomatic
Res., 55:31-39,
2003.
I have read with great interest the article titled “Presentation of
vitamin D deficiency” by Ladhani et al in the in the August 2004 issue of
Archives of Disease in Childhood. [1] The article was excellent, however,
I would like to point out a mistake in the legend of Figure 1 which
states:
"Figure 1 (A) Radiograph of patient aged 1 year with severe rickets.
(B) Radiograph of pati...
I have read with great interest the article titled “Presentation of
vitamin D deficiency” by Ladhani et al in the in the August 2004 issue of
Archives of Disease in Childhood. [1] The article was excellent, however,
I would like to point out a mistake in the legend of Figure 1 which
states:
"Figure 1 (A) Radiograph of patient aged 1 year with severe rickets.
(B) Radiograph of patient aged 11 years presenting with hypocalcaemic
symptoms and no radiological evidence of rickets"
The radiograph in (A) is clearly a normal radiograph of some one who
is definitely not a 1 year old. I think the description in radiograph (A)
fits to radiograph (B) and vice versa.
With kind regards
Reference
(1). Ladhani S, Srinivasan L, Buchanan C, Allgrove J. Presentation of
vitamin D deficiency. Arch Dis Child. 2004;89:781-784.
Dr Mather in her article, Community Child Health in Crisis, states
that in her opinion, the distinction between acute and community
paediatrics needs to disappear. She is not alone in this view. I suspect
very many paediatricians will agree with her.
We all need a good basic training in paediatric medicine as a foundation
for our work and for any special interest. There is already much o...
Dr Mather in her article, Community Child Health in Crisis, states
that in her opinion, the distinction between acute and community
paediatrics needs to disappear. She is not alone in this view. I suspect
very many paediatricians will agree with her.
We all need a good basic training in paediatric medicine as a foundation
for our work and for any special interest. There is already much overlap
between hospital and community based programmes. The term “community” is
ambiguous and means different things to different people.
Many hospital-
based paediatricians do outreach clinics or are involved with care of
children in the community, whilst many community-based paediatricians do
some general paediatrics or have on-call duties in the hospital. We are
all involved in some way with child welfare, development, disability,
child protection, and support for the family.
It may be right that demand for services outside hospital is rising at a
time when the number of community paediatricians is falling.
Part of this
increase stems from the fact that many children are now looked after at
home when previously they would have been in hospital. Recent developments
in paediatric training programmes and the European Working Time Directive
have also caused acute pressures within our hospitals. Consultant
workload has increased and in acute paediatrics consultants are finding
themselves more exposed.
There is an urgent need for consultant
recruitment in many areas. We all need to work much closer together to
deliver the service in the future.
With the new contract for general practitioners it is also time to review
the primary/secondary care interface. We need to understand the
developing concept of Children’s Trusts and how they will fit in with
present Child Health Services. We need to work closely with Primary Care
Trusts to encourage development in line with the new National Service
Framework for Children.
We are in a time of great change and this brings with it great
opportunities.
I agree we have to base the future on the needs of
children and not on our own career aspirations. We should accept the
challenge and all move forward together.
I thank Dr Fenton for his interest and insightful comment. It seems
that there has been a printing mistake. The criteria for diagnosis of
urinary tract infection was >100,000 bacteria per ml in mid stream
urine specimen, and not, >100 bacteria per ml, as was mistakenly
published.
The criteria for diagnosis of UTI was any bacteria in suprapubic
aspirate (as per AAP guidelines[1]), an...
I thank Dr Fenton for his interest and insightful comment. It seems
that there has been a printing mistake. The criteria for diagnosis of
urinary tract infection was >100,000 bacteria per ml in mid stream
urine specimen, and not, >100 bacteria per ml, as was mistakenly
published.
The criteria for diagnosis of UTI was any bacteria in suprapubic
aspirate (as per AAP guidelines[1]), and any bacteria in in-out
catheterization. Urine obtained by transurethral catheterization of the
urinary bladder for urine culture has a sensitivity of 95% and a
specificity of 99% compared with that obtained by SPA [2], and when the
culture growth shows bacteria consistent with UTI (such as gram negative
rods) we considered it to be a UTI even if there were less then 1,000
colonies per ML.
However, following your letter, a revision of the data was made. All
catheter samples were found to be >1,000 cfu/ml, and all but two were
>10,000 cfu/ml (these two patient had a normal renal ultrasound and
normal VCUG).
The renal pelvic diameters accepted as normal were grade 1, echo
contrast in only the ureter; grade 2, echo contrast in the pelvicaliceal
system with no dilatation; grade 3, mild to moderate dilatation of the
pelvicaliceal system; grade 4, moderate to severe dilatation of the
pelvicaliceal system; and grade 5, gross dilatation of the pelvicaliceal
system with total or partial atrophy [3,4].
References
(1). Practice parameter: the diagnosis, treatment, and evaluation of
the initial urinary tract infection in febrile infants and young children.
American Academy of Pediatrics. Committee on Quality Improvement.
Subcommittee on Urinary Tract Infection.
Pediatrics. 1999 Apr;103(4 Pt 1):843-52. Erratum in: 2000 Jan;105(1 Pt
1):141. Pediatrics 1999 May;103(5 Pt 1):1052, 1999 Jul;104(1 Pt 1):118.
(2). Leong YY, Tan KW Bladder aspiration for diagnosis of urinary tract
infection in infants and young children. J Singapore Paediatr Soc. 1976;
18:43-47
(3). Mittelstaedt CA, Vincent LM. In: Abdominal ultrasound. Newyork,
NY: churchill livingstone; 1987:252.
(4). Lebowitz RL, Olbing H, Parkkulainen Kv, Smellie JM, Tamminen-
Moebius TE. International system of radiographic grading of vesicoureteric
reflux. International Reflux Study in Children. Pediatr Radiol.
1985;15:105-9.
Dr Mather’s and Dr Bannon’s articles are timely reminders of the
crisis facing community paediatrics today.
When I am asked what I do as a community paediatrician I say that “I
generally endeavour to manage children with physical, behavioural and
emotional difficulties in their locality rather than them having to come
to see me in a hospital.” If then Dr Bannon’s layperson wants a sentence
or two m...
Dr Mather’s and Dr Bannon’s articles are timely reminders of the
crisis facing community paediatrics today.
When I am asked what I do as a community paediatrician I say that “I
generally endeavour to manage children with physical, behavioural and
emotional difficulties in their locality rather than them having to come
to see me in a hospital.” If then Dr Bannon’s layperson wants a sentence
or two more, I mention physical disability, learning difficulty including
autism and epilepsy as well as a role and duty in management of child
abuse and coordinating childhood immunisations.
As well as a poor image, the spectre of child protection is now the
most significant and growing problem facing community child health.
Most paediatricians, I assume, did not embark upon a career choice
through a wish to sacrifice themselves or their families for the sake of
an abused child or abused children. But this is the stark reality of those
paediatricians who are dealing with child protection. Frankly you’re
damned if you do and damned if you don’t.
It is however a very different matter if you are seeing the occasional
abused child within your clinical practice than routinely seeing suspected
cases as part of your designated role. No one wants for understandable reasons to put themselves in the
firing line.
It is human nature after all to defer or avoid an unpleasant
experience by taking an alternative path. Hence numbers of applicants for
community child health posts are falling and child protection posts remain
unfilled.
This is very bad news indeed for abused children who should be protected.
It is sadly inevitable that this now serious deficiency will contribute to
further child protection tragedies. More child deaths lead to more
enquiries and media driven witch hunts against the “blamed” professionals
involved. All of which exacerbate the situation.
I believe the Government must take responsibility for this problem as it has the final responsibility for the welfare of its citizens. My
feeling is that to deal with this problem it will have to set up some form
of nationally coordinated, local medical child protection panels to
diagnose abuse. It would not necessarily have to include only consultant
community paediatricians, other experienced paediatricians, police
surgeons and child protection nurses could also be included.
Child
protection opinions are given by that panel and the panel takes full
responsibility for the diagnosis rather than a single person. To
constitute and run such panels so that they could deal promptly with
suspected child protection cases would of course cost significant
resources, which perhaps should be directly Government funded thereby
taking pressures off cash strapped PCT’s. Furthermore, it is within the
power of the law, if necessary, to grant the protection of anonymity for
the panel members involved, if child health professionals are going to be
prepared to undertake it.
I believe that community paediatrics is both noble and necessary for
child health. It does of course involve advocacy and social paediatrics
but we delude ourselves that if we trumpet these as our main role which is
within a medical context the assessment, diagnosis and management of
children. It is unlikely ever to be perceived as exciting in the public’s
mind nor would some of us wish it to be.
As a general fact of life, respect is not given, it is earned. Through our
practice and actions we community paediatricians have to both challenge
and alter adverse views regarding our professional work.
I was touched to read the article “From containers to classrooms:
converting capitalism’s swords into ploughshares” and the accompanying
reference: http://www.starfish-initiative.org
There are many noble endeavours in the developing and developed world
like the Starfish Initiative. Another such is the online availability of
BMJ and ADC to paediatricians and doctors in the developing world,...
I was touched to read the article “From containers to classrooms:
converting capitalism’s swords into ploughshares” and the accompanying
reference: http://www.starfish-initiative.org
There are many noble endeavours in the developing and developed world
like the Starfish Initiative. Another such is the online availability of
BMJ and ADC to paediatricians and doctors in the developing world, free of
cost.
I believe that one of the best things that happened in the field of
communications during the last century is the internet and the revolution
in information technology. This technology helps in the Container
Classrooms. It has also helped doctors practicing in remote areas, to keep
in touch with their peers in the rest of the world and with the latest
advances in medicine, through such journals available online. Those who
work in remote areas will probably agree with me that it is very important
not to feel isolated and know that their practice of medicine is not out
of date. It may not always be possible for every institution to subscribe
to international journals.
References
(1). http://www.starfish-initiative.org
(2). N Sellathurai, S Clarke and A N Williams, From containers to classrooms:
converting capitalism’s swords into ploughshares, Archives of Disease in
Childhood 2004;89:410
http://adc.bmjjournals.com/cgi/content/full/89/5/410
The paper by Ladhani et al on vitamin D deficiency reminds us of our wider
duty of care to children in considering background nutrition [1].
Prolonged breast feeding has been recognised as a risk factor for vitamin
D deficiency [2]; it will be interesting to observe whether its incidence
will increase with the international drive to promote exclusive breast
feeding for the first six m...
The paper by Ladhani et al on vitamin D deficiency reminds us of our wider
duty of care to children in considering background nutrition [1].
Prolonged breast feeding has been recognised as a risk factor for vitamin
D deficiency [2]; it will be interesting to observe whether its incidence
will increase with the international drive to promote exclusive breast
feeding for the first six months, and its continuation for two years [3].
The recent United Kingdom Infant Feeding Survey reported an increase in
the initiation of breast feeding, and the length of time providing breast
milk [4]. Whether this trend will continue remains to be seen, but if so,
then vitamin D deficiency may rise.
The use of supplements may prevent this, and has been previously
recommended for at risk children [5,6]. Although not specifically
mentioning vitamin D, the World Health Organisation has suggested that
nutrient supplementation may ensure adequate micronutrients [3] and this
seems increasingly important if their feeding recommendations are to be
embraced. On a local level, although premature infants receive vitamin
supplementation, neither term babies or their breast feeding mothers are
advised to supplement their intake of vitamin D. This is amongst a large,
ethnically diverse, underpriviledged population within the West Midlands.
As the accompanying editorial suggests [7], it may be time to
highlight the preventable morbidity of vitamin D deficiency: whether this
should involve the routine supplementation of vitamin D in breast feeding
infants and their mothers needs further thought if a D for danger is to be
avoided.
References
(1). S Ladhani, L Srinivasan, C Buchanan, and J Allgrove. Presentation
of vitamin D deficiency Arch. Dis. Child. 2004; 89: 781-784
(2). M Z Mughal, H Salama, T Greenaway, I Laing, and E B Mawer. Lesson
of the week: Florid rickets associated with prolonged breast feeding
without vitamin D supplementation
BMJ 1999; 318: 39-40
(3). World Health Organization. Infant and young child nutrition Global
strategy on infant and young child feeding. Geneva: WHO, 2002
(4). Hamlyn B, Brooker S, Oleinikova K, Wands S. Infant Feeding 2000.
London: The Stationery Office, 2002
(5). Department of Health. Dietary reference values for food energy and
nutrients for the United Kingdom. London: HMSO , 1991(Report on health and
social subjects 41.)
(6). N J Shaw and B R Pal Vitamin D deficiency in UK Asian families:
activating a new concern Arch. Dis. Child. 2002; 86: 147-149
We thank Allgrove for drawing attention to the growing problem of
vitamin D deficiency in children [1]. However, we wish to comment on
several of the points raised in the commentary.
As observed by Allgrove, a daily dose of vitamin D less than 10 mcg
(400 IU) does not prevent vitamin D deficiency (serum 25(OH)D <25
nmol/L) in all newborn full-term infants [2]. This evidence conflicts...
We thank Allgrove for drawing attention to the growing problem of
vitamin D deficiency in children [1]. However, we wish to comment on
several of the points raised in the commentary.
As observed by Allgrove, a daily dose of vitamin D less than 10 mcg
(400 IU) does not prevent vitamin D deficiency (serum 25(OH)D <25
nmol/L) in all newborn full-term infants [2]. This evidence conflicts with
the conclusions of the UK Department of Health [3], as well as the US Food
and Nutrition Board (FNB) [4] and the American Academy of Pediatrics [5],
which suggest an ‘adequate intake’ (AI) for infants is 200 IU.
The
guidelines of the Canadian Pediatric Society are more on target [6],
recommending supplementation of at least 400 IU per day for breast-fed
infants (and 800 IU/day for Native infants living at northern latitudes
)[7]. Safety data is scant, but Fomon et al. (1966) reported that infants
receiving daily vitamin D in doses ranging from 7.5 – 54.25 mcg (300 IU –
2170 IU) did not demonstrate differences in linear growth nor serum
calcium concentrations[8] , suggesting doses up to 2000 IU per day are
safe. Further research would likely show that doses of at least 800 IU per
day are advisable for all high-risk infants (e.g., northern latitude, dark
skin, vitamin D-deficient mothers, etc).
Allgrove mentions that single intermittent pulse doses may be useful
for treatment of vitamin D deficiency when adherence is a concern.
However, there is very little evidence that currently guides the selection
of safe and efficacious doses or frequency of intermittent vitamin D
administration in young children, particularly when used as prophylaxis in
infants who do not have clinical features of rickets.
For routine
prophylaxis, the high doses suggested by Allgrove (300 000 – 600 000 IU)
may be unsafe in infants. Markestad et al. (1987) advised against giving
600 000 IU vitamin D2 to German infants, after observing hypercalcemia in
34% of patients studied, and serum 25-hydroxyvitamin D concentrations
above 220 nmol/L [9], which is the upper limit of the physiologic
range [10]. Most of the infants in Markestad’s study had initial 25-
hydroxyvitamin D concentrations in the range of overt vitamin D deficiency
(<20 nmol/L); therefore, infants with rickets may be expected to
experience similar effects. Alternatively, a single oral dose of 100 000
IU vitamin D3 approximately every three months may be a safe and
efficacious means of delivering the equivalent of approximately 900 IU per
day [11] , yet further pharmacokinetic and safety studies are needed before
this regimen can be widely recommended for routine use in infants.
Vieth advises the use of vitamin D3 (cholecalciferol) because
it is more “physiologic”, and notes that the toxicity of vitamin D2
(ergocalciferol) is of greater concern [12] .
We disagree with Allgrove’s statement that “there is probably no
place for universal vitamin D supplementation because of the potential
dangers of hypercalcaemia in a few individuals.” Although the US FNB
states that the tolerable upper intake level of vitamin D is 50 mcg (2000
IU) daily (1000 IU for infants <1 year of age), concerns that intake
above this threshold are harmful are largely unfounded. In the United
Kingdom in the 1950s, after milk and cereals were heavily fortified with
vitamin D, a small number of children who ingested more than 100 mcg (4000
IU) vitamin D per day developed vitamin D intoxication [2]. It has been
suggested that most of these children had features of Williams
syndrome [2]2, which is thought to be associated with abnormally increased
conversion of vitamin D to 25(OH)D.
Although the specific public health approach to improve vitamin D
status in the general population is a subject of ongoing research and
debate, there is good evidence to support the safety and efficacy of
routine vitamin D3 supplementation in the general population with doses
beyond those traditionally considered to be “toxic”. In adults, doses as
high as 4000 IU/day have been shown to be very safe, and effectively raise
the serum 25-hydroxyvitamin D concentration to > 75 nmol/L, widely
considered to be the ideal target range[13] . Heaney et al. demonstrated
that 11 000 IU/day of vitamin D3 for 20 weeks did not lead to elevations
in serum calcium above the upper limits of normal [14].
In French
children aged 10 to 15 years, 100 000 IU vitamin D3 administered orally
every three months during the winter maintained serum 25-hydroxyvitamin D
concentrations and mitigated the wintertime rise in PTH observed in
control participants, without any adverse effects (hypercalcemia, or
changes in urinary serum/creatinine ratio)[15] .
There are high rates of vitamin D insufficiency among health
adolescents in Europe and North America[16,17]. In our recent study of
children and adolescents aged 2 to 16 years in Edmonton (Canada)[18], we
found that the prevalence of vitamin D insufficiency (25-hydroxyvitamin D
<40 nmol/L) at the end of the winter was 34% overall, and 69% among
boys aged 9 to 16 years. Furthermore, we found that 40 % (9/22) of the
children aged 9 to 16 years who consumed at least the recommended 5 mcg
(200 IU)/day had vitamin D insufficiency. Consistent with the findings
described above, none of the participants with dietary vitamin D intakes
greater than 0.45 mcg/kg body weight/day (which approximately corresponds
to an intake of about 900 IU/day for a 50 kg adolescent), demonstrated
vitamin D insufficiency. Therefore, there is now compelling evidence to
suggest that supplementation of the general population, including
children, with 1000 IU/day (or alternatively, 100 000 IU every 3 – 4
months) during the winter is both safe and efficacious for the prevention
of vitamin D insufficiency. Given the high incidence of osteoporosis, this
may prove to be a powerful public health initiative in the long-term.
Current recommendations propose inadequate vitamin D intake, and do
not recognize the growing body of literature that shows that the mere
absence of rickets or osteomalacia does not imply physiologic vitamin D
status[12]12. As Allgrove states, the re-appearance of rickets is likely
the “tip of the iceberg” – alluding to the broader public health
implications of widespread subclinical vitamin D insufficiency that begins
in utero and persists into late adulthood. Illnesses found to be
associated with a state of chronic vitamin D insufficiency are numerous,
and include not only those chronic adult diseases cited by Allgrove, but
also common childhood diseases such as lower respiratory tract
infections[19] and type I diabetes[20]. Further research is clearly
needed to determine the dose, methods of supplementation/fortification,
and specific public health outcomes of ensuring improved vitamin D status
in the general pediatric population.
References
(1). Allgrove J. Is nutritional rickets returning? Arch Dis Child 2004;
89: 699 - 701.
(2). Calikoglu AS, Davenport ML. Prophylactic vitamin D
supplementation. In: Hochberg Z (ed.). Vitamin D and Rickets. Endoc Dev.
Basel, Karger, 2003; 6:233-58.
(3). Subgroup on Bone Health. Department of Health Working Group on the
Nutritional Status of the Population of the Committee on Medical Aspects
of Food and Nutrition Policy. Nutrition and bone health: with particular
reference to calcium and vitamin D. London: HMSO, 1998.
(4). Standing Committee on the Scientific Evaluation of Dietary
Reference Intakes Food and Nutrition Board, Institute of Medicine. DRI:
Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D,
and fluoride. National Academy Press 1999; Washington D.C. (Available at
http://books.nap.edu/html/dri_calcium).
(5). Gartner LM, Greer FR; Section on Breastfeeding and Committee on
Nutrition. American Academy of Pediatrics. Prevention of rickets and
vitamin D deficiency: new guidelines for vitamin D intake. Pediatrics.
2003; 111(4 Pt 1):908-10.
(6). Canadian Paediatric Society, Dietitians of Canada and Health
Canada. Nutrition for Healthy Term Infants. Minister of Public Works and
Government Services. Ottawa: 1998. (Available at http://www.hc-
sc.gc.ca.login.ezproxy.library.ualberta.ca).
(7). Indian and Inuit Health Committee, Canadian Pediatric Society.
Vitamin D supplementation in northern Native communities. Paediatr Child
Health 2002; 7(7):459-63.
(8). Fomon SJ, Younoszai MK, Thomas LN. Influence of vitamin D on
linear growth of normal full-term infants. J Nutr 1966; 88(3):345-50.
(9). Markestad T, Hesse V, Siebenhuner M, Jahreis G, Aksnes L, Plenert
W, Aarskog D. Intermittent high-dose vitamin D prophylaxis during
infancy: effect on vitamin D metabolites, calcium, and phosphorus.
Am J Clin Nutr 1987; 46(4):652-8.
(10). Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D
concentrations, and safety. Am J Clin Nutr 1999; 69:842-56.
(11). Zeghoud F, Ben-Mekhbi H, Djeghri N, Garabedian M. Vitamin D
prophylaxis during infancy: comparison of the long-term effects of three
intermittent doses (15, 5, or 2.5 mg) on 25-hydroxyvitamin D
concentrations. Am J Clin Nutr 1994; 60(3):393-6.
(12). Vieth R, Fraser D. Vitamin D insufficiency: no recommended
dietary allowance exists for this nutrient. CMAJ 2002; 166:1541-1542.
(13). Vieth R, Chan PCR, MacFarlane GD. Efficacy and safety of vitamin
D3 intake exceeding the lowest observed adverse effect level. Am J Clin
Nutr 2001; 73:288-94.
(14). Heaney RP, Davies KM, Chen TC, Holick MF, Barger-Lux MJ. Human
serum 25-hydroxcholecalciferol response to extended oral dosing with
cholecalciferol. Am J Clin Nutr 2003; 77:204-10.
(15). Duhamel JF, Zeghoud F, Sempe M, Boudailliez B, Odievre M, Laurans
M, Garabedian M, Mallet E. Prevention of vitamin D deficiency in
adolescents and pre-adolescents. An interventional multicenter study on
the biological effect of repeated doses of 100,000 IU of vitamin D3
[French]. Arch Pediatr. 2000; 7(2):148-53.
(16). Gordon CM, DePeter KC, Feldman HA, Grace E, Emans SJ. Prevalence
of vitamin D deficiency among healthy adolescents. Arch Pediatr Adolesc
Med 2004; 158(6):531-7.
(17). Lehtonen-Veromaa M, Mottonen T, Irjala K, Karkkainen M, Lamberg-
Allardt C, Hakola P, Viikari J. Vitamin D intake is low and
hypovitaminosis D common in healthy 9- to 15-year-old Finnish girls. Eur J
Clin Nutr. 1999; 53(9):746-51.
(18). Roth DE, Martz P, Yeo R, Prosser C, Bell M, Jones AB. Vitamin D
Insufficiency is Common Among Children and Adolescents in Edmonton,
Alberta. [Manuscript submitted for publication].
(19). Wayse V, Yousafzai A, Mogale K, filteau S. Association of
subclinical vitamin D deficiency with severe acute lower respiratory
infection in Indian children under 5 years. Eur J Clin Nutr 2004; 58:563-
567.
(20). Hypponen E, Laara E, Reunanen A, Jarvelin M-R, Virtanen SM.
Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study.
Lancet 2001; 358:1500-1503.
We read with great interest the a.m. review which comes to the conclusion
that immunosuppressive therapy does not significantly improve the outcome
of children with acute myocarditis. This is in accordance with an
important review concerning the adult age [1]. However,
both reviews show one decisive drawback. They do not take the essential
changes in pathogenetic considerations and diagnostic methods...
We read with great interest the a.m. review which comes to the conclusion
that immunosuppressive therapy does not significantly improve the outcome
of children with acute myocarditis. This is in accordance with an
important review concerning the adult age [1]. However,
both reviews show one decisive drawback. They do not take the essential
changes in pathogenetic considerations and diagnostic methods into
account.
Today it is generally accepted, that virus genomes may persist in
myocardial tissue and may maintain an inflammatory process [2]. In a significant number of patients this results in a loss of
myocytes, degeneration of the contractile apparatus with reactive
myocardial fibrosis up to a dilatation of the heart muscle and myocardial
dysfunc-tion.
At the same time, virus genoma may nowadays be detected by in-situ-
hybridization and PCR even in formaline-fixed endomyocardial specimen.
Enteroviruses, including coxsackievirus B, adenoviruses, human herpes
virus 6, Epstein-Barr virus, human cytomegalovirus, respiratory syncytial
virus and herpes simplex virus can be detected routinely.
As the authors
mention, immunosuppression in the presence of virus genomes may impede
“innate host immune re-sponse to eliminate the virus and this would have
detrimental effects”. The missing diagnostic distinction of patients with
and without virus genomes means that patients with virus-caused chronic
myocaritis and autoreactive myocarditis are not separated. This is the
major disadvantage of all studies analysed. As the studies do not
distinguish between the two causes of the disease, they offer no insight
concerning the effectiveness of different treatments. Therefore, they have
no explanatory value from a clinical point of view.
Already in 1998 we published the design of a multicenter treatment trial,
in which this distinction was made by assess-ment of endomyocardial
biopsies. Only patients with autoreactive myocarditis were treated by
immunosuppression in a randomized manner, while patients with proven virus
genoma were treated by interferone-alpha. Due to the delicate methods,
the diagnostic evaluation is performed centrally by the department of
molecular pathology at the University Hospital of Tuebingen. The study
protocol was approved by several ethical committees in Germany at the
beginning of the study and again this year.
Because of scarce implementation of patients into the study, no
statistically valid conclusions can be drawn at this time. However, we
would like to open the study to departments of pediatric cardiology abroad
and we will be pleased to supply all necessary information.
References
(1). Garg A, Shiau J, Guyatt G: The ineffectiveness of immunosuppressive
therapy in lymphocytic myocarditis. Ann Intern Med 1998; 129: 317-322
Hia CPP, Yip WCL, Zhai BC, Quek SC: Immunosuppressive therapy in acute
myocarditis: an 18 year systematic re-view . Arch Dis Child 2004; 89: 580-
584
(2). Klingel K, Selinka HC, Sauter M: Molecular mechanisms in enterovirus- and
parvovirus B19-associated myocarditis and inflammatory cardiopmyopathy.
Eur Heart J 2002; 4/1:8-12
Dear Editor,
The authors appreciate the comments of Dr Giovannoni and fully recognize the ongoing efforts of the London group in evaluating antibasal ganglia antibodies (ABGA) in poststreptococcal movement conditions. Nevertheless, readers must recognize that there are significant discrepancies between results reported in the article by Church et al., [1] and other investigators [2,3].
In or...
Dear Editor,
I have read with great interest the article titled “Presentation of vitamin D deficiency” by Ladhani et al in the in the August 2004 issue of Archives of Disease in Childhood. [1] The article was excellent, however, I would like to point out a mistake in the legend of Figure 1 which states:
"Figure 1 (A) Radiograph of patient aged 1 year with severe rickets. (B) Radiograph of pati...
Dear Editor,
Forgive me for using this forum to try to re-establish contact with Robin and Sue Ball, but I have no other leads in my quest to do so!
We met in 1986 in Papua New Guinea, stayed in contact for several years but have not corresponded for quite a while.
Please forward this note to Robin if at all possible. With thanks and kind regards.
Dear Editor,
Dr Mather in her article, Community Child Health in Crisis, states that in her opinion, the distinction between acute and community paediatrics needs to disappear. She is not alone in this view. I suspect very many paediatricians will agree with her.
We all need a good basic training in paediatric medicine as a foundation for our work and for any special interest. There is already much o...
Dear Editor,
I thank Dr Fenton for his interest and insightful comment. It seems that there has been a printing mistake. The criteria for diagnosis of urinary tract infection was >100,000 bacteria per ml in mid stream urine specimen, and not, >100 bacteria per ml, as was mistakenly published.
The criteria for diagnosis of UTI was any bacteria in suprapubic aspirate (as per AAP guidelines[1]), an...
Dear Editor
Dr Mather’s and Dr Bannon’s articles are timely reminders of the crisis facing community paediatrics today. When I am asked what I do as a community paediatrician I say that “I generally endeavour to manage children with physical, behavioural and emotional difficulties in their locality rather than them having to come to see me in a hospital.” If then Dr Bannon’s layperson wants a sentence or two m...
Dear Editor,
I was touched to read the article “From containers to classrooms: converting capitalism’s swords into ploughshares” and the accompanying reference: http://www.starfish-initiative.org
There are many noble endeavours in the developing and developed world like the Starfish Initiative. Another such is the online availability of BMJ and ADC to paediatricians and doctors in the developing world,...
Dear Editor,
The paper by Ladhani et al on vitamin D deficiency reminds us of our wider duty of care to children in considering background nutrition [1].
Prolonged breast feeding has been recognised as a risk factor for vitamin D deficiency [2]; it will be interesting to observe whether its incidence will increase with the international drive to promote exclusive breast feeding for the first six m...
Dear Editor,
We thank Allgrove for drawing attention to the growing problem of vitamin D deficiency in children [1]. However, we wish to comment on several of the points raised in the commentary.
As observed by Allgrove, a daily dose of vitamin D less than 10 mcg (400 IU) does not prevent vitamin D deficiency (serum 25(OH)D <25 nmol/L) in all newborn full-term infants [2]. This evidence conflicts...
Dear Editor,
We read with great interest the a.m. review which comes to the conclusion that immunosuppressive therapy does not significantly improve the outcome of children with acute myocarditis. This is in accordance with an important review concerning the adult age [1]. However, both reviews show one decisive drawback. They do not take the essential changes in pathogenetic considerations and diagnostic methods...
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