The authors state that “mercury is toxic to the environment”. But is
it?
Because mercury (Hg) is what humans call an “element”, it cannot be
broken down into something simpler, and leaving aside Hg exportation
effects via human space travel and other unknowns, all of the element
mercury (Hg) that was originally here on this planet is still here, though
in a variety of forms – elemental, ionic, organic.
The authors state that “mercury is toxic to the environment”. But is
it?
Because mercury (Hg) is what humans call an “element”, it cannot be
broken down into something simpler, and leaving aside Hg exportation
effects via human space travel and other unknowns, all of the element
mercury (Hg) that was originally here on this planet is still here, though
in a variety of forms – elemental, ionic, organic.
Presumably, the planet, it’s mercury, and non-human life itself,
proceeded collectively in that which humans call “the environment”, for
millions/billions of years. There always were areas of the planet that
were unsuitable for occupation by many forms of life due to high levels of
naturally occurring mercury. In areas which humans call “mercury mines”,
Hg occurs in combination with sulphur as cinnabar, as well as in the form
which humans call “quicksilver”.
It seems likely that humans will continue to populate, and
industrialize, the entire planet. It will be increasingly difficult to
conceive of any environment other than “man’s environment”, since humans
and human influence will be everywhere. Mercury is toxic, but only to
“man’s environment”.
Retaining the mercury sphygmomanometer seems to be happening de
facto, via the endless debate about electronic device suitability, and
suggests a common sense obligation to a safer, and more consumer friendly
mercury device that has undergone some evolution from it’s unsafe,
unsealed, unlabelled, nineteenth century origins.
Wherever mercury is used in a therapeutic device, the presentation of
the device should reflect the respect for health and safety implied in
the term “health professional”. Accuracy is not the only consideration.
We noted with interest the article published by Ladhani and
colleagues [1] highlighting the problem of vitamin D deficiency. We agree
that this remains a problem, especially in “at risk” ethnic minority
groups.
In Oldham, which has a population of 49992 children, 20.8% are
Asians (Census 2001). Between December 2002 and March 2004, we identified
9 cases of hypocalcaemia /rickets secondary to Vi...
We noted with interest the article published by Ladhani and
colleagues [1] highlighting the problem of vitamin D deficiency. We agree
that this remains a problem, especially in “at risk” ethnic minority
groups.
In Oldham, which has a population of 49992 children, 20.8% are
Asians (Census 2001). Between December 2002 and March 2004, we identified
9 cases of hypocalcaemia /rickets secondary to Vitamin D deficiency. We
excluded those with vitamin D deficiency secondary to other conditions of
non-nutritional aetiologies. All of the 9 children had biochemical
changes of raised alkaline phosphatase, levels of 25-OHD below 10 ng/ml and
3 had radiological evidence of rickets. 8/9 of these were of Asian extraction and 5/9 were male.
Presentation of
these children were divided into those with hypocalaemic symptoms and
those with clinical rickets. 6/9 of them presented with hypocalcaemic
symptoms and their ages ranged from 6 days to 13 years of age. These
included 2 neonates who presented with focal seizures, 2 toddlers under
two years, presented with generalized seizures and 2 thirteen year
old, presented with cramps/carpopedal spasms. 3/9 presented with signs of
rickets and were aged between 15 to 19 months old.
The 2 neonates involved were born at term with their birth weights on the
25th centiles. Calcium levels were 1.39 and 1.54 mmol/l respectively.
Both were on formula feeds, and tests on maternal blood, revealed levels of
parathyroid and calcium suggestive of vitamin D deficiency. Four toddlers
were still breast-fed, all of whom were confirmed from dietary history to
have limited solid intake. Of the two teenagers, one had a diet low in
calcium and the other had background problems of abdominal pain.
All the children were treated with Vitamin D and 3 children also received
oral calcium supplements. All responded to treatment with normalisation
of biochemical bone profiles and vitamin D/PTH levels.
There is no information on the prevalence of rickets in the
UK, however, there are reports to say that this is growing.[2] Our experience
and reports across the UK, shows that the ethnic minority population still
remains at risk of vitamin D deficiency. Efforts to promote vitamin D
supplementation as recommended by the Department of Health need to be
implemented and targeted at the risk group.
References
1.Ladhani S, Srinivasan L, Buchanan C, Allgrove J. Presentation of
vitamin D deficiency. Arch Dis Child 2004; 89: 781-784.
2. Mughal MZ. Resurgence of vitamin D deficiency rickets in the UK.
Osteoporosis Review 2005; 13 (1): 10-13.
3. Department of Health, Nutrition and Bone Health: with particular
reference to calcium and vitamin D. Report of the Subgroup on Bone Health,
Working Group of the nutritional Status of the Population of the Committee
on Medical Aspects of the Food Nutrition Policy. Rep Health Soc
Subj (Lond) 1998;49: iii-ivii,1-24.
Singh-Grewal et al.1 confirm earlier findings that the complications and disadvantages of male neonatal circumcision outweigh any possible health benefit and, therefore, non-circumcision produces the highest medical utility.2,3
Singh-Grewal et al.1 confirm earlier findings that the complications and disadvantages of male neonatal circumcision outweigh any possible health benefit and, therefore, non-circumcision produces the highest medical utility.2,3
Unfortunately, their report on urinary tract infection (UTI) is incomplete because they have failed to mention the value of breastfeeding in reducing UTI in infants.1 Pisacane et al. report that breastfed infants have a relative risk of 0.38 compared to those infants who are fed with breastmilk substitute, a 62 percent reduction.4 This is caused by oligosaccharides that prevent adhesion of pathogens to uroepithelial tissue.5 Marild et al. report that the protective effect of breastfeeding continues after weaning.6
Breastfeeding is free of the complications associated with circumcision. The American Academy of Pediatrics recommends breastfeeding, not circumcision, to reduce the incidence of UTI and other infections.7
George C. Denniston, MD, MPH President
George Hill, Bioethicist Executive Secretary
Doctors Opposing Circumcision
Suite 42
2442 NW Market Street
Seattle, Washington 98107-4137
USA.
We read with interest the article written by Weston and colleagues [1] on the effects of probiotics (Lactobacillus fermentum PCCTM) on atopic
dermatitis (AD). They showed that the reduction in SCORAD index over time
was significant in the probiotic group but not the placebo group and that
significantly more children receiving probiotics had a SCORAD index that
was better than baseline at week 16 compar...
We read with interest the article written by Weston and colleagues [1] on the effects of probiotics (Lactobacillus fermentum PCCTM) on atopic
dermatitis (AD). They showed that the reduction in SCORAD index over time
was significant in the probiotic group but not the placebo group and that
significantly more children receiving probiotics had a SCORAD index that
was better than baseline at week 16 compared with the placebo group. On a
statistical point of view, the difference between L. fermentum and placebo
groups was rather moderate, reaching a low level of significance.
One
could conclude that the benefit of probiotics treatment in clinical
practice is rather faint. On the contrary, the effect is quite impressive
since this study shows a decrease in SCORAD index of 18.2 points at the
end of the study. This is a remarkable effect since decrease in SCORAD
index in therapeutic studies rarely reaches such levels. For example, in
studies on topical steroids, the decrease in SCORAD index is 16 in the
initial phase of treatment (once daily for 2 weeks) and 8 in the
maintenance phase (twice weekly for 16 weeks).[2]
As impressive is the
decrease in SCORAD index observed in the placebo group since it reached
10.2 points. It is common to observe a decrease in SCORAD index in double
blind randomized studies. However, to the best of our knowledge a placebo
intervention in AD treatment studies never allows to induce more than 5
points improvement in total SCORAD score. Such a high value in the study
from Weston and colleagues is quite unusual and questions on the potential
therapeutic effect of the agent orally absorbed by the “placebo” group.
Actually, the same question could be addressed for another study on
therapeutic effect of probiotics in AD. Viljanen and colleagues compared
L. rhamnosus GG, a mixture of 4 probiotics and placebo in a randomized
study conducted in 230 infants with atopic eczema/dermatitis syndrome.[3] They observed a reduction of 25.4 points in SCORAD in L. rhamnosus GG
treated group, a 22.8 points reduction in the mixture of 4 probiotics
treated group and an impressive 20.9 points reduction in the placebo group
as well. When looking at the placebos used in these 2 studies, one could
find an explanation to this very unusual effect of placebo in AD.
Cellulose and maltose dextran were respectively used in the studies of
Weston and colleagues and Viljanen and colleagues. Substances chosen as
placebo both could be considered as prebiotics. Prebiotics are defined as
non digestible substances which are beneficial for the host by
specifically stimulating the growth and/or the activity of a limited
number of bacterial strains still established in floral gut. Although
further investigations are necessary, preliminary data suggest that the
consumption of prebiotics can modulate immune parameters including Th1/Th2
balance.[3,4] Thus, specific prebiotics could act on the gut flora to
induce an immunomodulation that could be beneficial to the decrease of AD
manifestations.
We recently carried out a study (submitted) comparing the
efficiency of synbiotics (probiotic Lactobacillus rhamnosus Lcr35 plus
prebiotics) with prebiotics alone as a control, in the treatment of
moderate and severe AD in children above 2 years showing that both groups
had a reduction in SCORAD of more than 15 points after 3 months of
treatment.
There is undoubtedly a place for probiotics in the treatment of AD, but
many variables could influence their therapeutic effects and remain to be
studied: dose, duration of treatment, strain and genius of probiotics, all
parameters that might lead to different results. We would like to stress 2
important issues in conducting therapeutic studies of AD with pre-, pro-
or synbiotics. First, the choice of a true placebo (and not a compound
with prebiotic characteristics) seems to be a critical point. Second,
probiotics, but also prebiotics and symbiotics are therapeutic agents of
AD of potential value to be explored.
References
1 Weston S, Halbert A R, Richmond P, Prescott S L. Effects of
probiotics on atopic dermatitis: a randomised controlled trial. Arch Dis
Child. Published Online First: 29 April 2005.
2 Van Der Meer JB, Glazenburg EJ, Mulder PG, Eggink HF, Coenraads
PJ. The management of moderate to severe atopic dermatitis in adults with
topical fluticasone propionate. The Netherlands Adult Atopic
DermatitisStudy Group. Br J Dermatol. 1999;140:1114-21.
3 Viljanen M, Savilahti E, Haahtela T, et al. Probiotics in the
treatment of atopic eczema/dermatitis syndrome in infants: a double-blind
placebo-controlled trial? Allergy 2005;60:494-500
4 Schley PD, Field CJ. The immune-enhancing effects of dietary
fibres and prebiotics. Br J Nutr 2002; 87 Suppl 2:S221-30.
We read with great interest the article by SE Jones et al.
highlighting the worrying trend of increasing obesity detected by use of
routinely collected data. In 2002-2003 we carried out a prospective
observational study aimed at estimating the problem of obesity in children
presenting to the outpatient department of Royal Glamorgan Hospital. The
hospital caters to the population of Rhondda, Cynon and...
We read with great interest the article by SE Jones et al.
highlighting the worrying trend of increasing obesity detected by use of
routinely collected data. In 2002-2003 we carried out a prospective
observational study aimed at estimating the problem of obesity in children
presenting to the outpatient department of Royal Glamorgan Hospital. The
hospital caters to the population of Rhondda, Cynon and Taff Ely which are
amongst the most deprived areas in Europe.
We used Weight and height
measurements (which are routinely done for all children visiting the
outpatients), to calculate the Body Mass Index (BMI). These were then
plotted on standard BMI centile charts. Using the guidelines published by
the Child Growth Foundation those above the 98th centile were considered
obese while those between the 91st and 98th centile were classed as
overweight.
Of the 1184 children attending the outpatients, 992 satisfied the
study criteria: those excluded were infants less than 6 months and others
where it was difficult to accurately make these measurements. 133 (13.4%)
were obese and 132 (13.3%) were overweight. Although there was no
difference in the proportion of overweight girls (13.7%)and overweight
boys (13.2%), a higher percentage of girls (15.2%) was significantly obese
compared to boys (11.6%). The percentage of overweight or obese children
from the three valleys was comparable - Rhondda (27%), Taff Ely (27.5%)
and Cynon (29.4%). Only 18.4% of the children coming from outside these
areas were either obese or overweight. Analysis of the various age groups
showed only 13.6% of the infants>6 months and 15.5% of the 1 to 3 year
olds to be obese or overweight. The proportion of overweight or obese
children increased with age to reach 39.5% in 11 to 15 year olds.
The problem of obesity is on the increase and perhaps
disproportionately so in the more deprived areas. Inclusion of a BMI
calculation for all children presenting at any point of healthcare can
help highlighting the problem. This may be specially important in deprived
areas where a chubby child is presumed to be the healthy one.
We appreciate Drs. Flaherman and Newman’s comments on our manuscript and welcome the opportunity to respond. First we would like to point out that the clinical risk factor score for a bottle-fed infant with birth weight 4.1 kg would only be higher than for a breast-fed infant of less than 38 weeks gestation if the latter infant’s birthweight were in the lowest birthweight category (2000g–2500g).
We appreciate Drs. Flaherman and Newman’s comments on our manuscript and welcome the opportunity to respond. First we would like to point out that the clinical risk factor score for a bottle-fed infant with birth weight 4.1 kg would only be higher than for a breast-fed infant of less than 38 weeks gestation if the latter infant’s birthweight were in the lowest birthweight category (2000g–2500g).
Although birthweight appears to make a large contribution to our clinical risk score, it is important to remember that all the infants, except those in the lowest birthweight category, receive points for their birthweight. We could have centred our birthweight score on the middle birthweight category but that would have involved subtracting points for birthweights in lower categories and adding points for birthweights in higher categories. The net effect would have been a fixed decrease in all the infants’ clinical risk factor scores, but no difference in the measures of predictive accuracy.
In our
published analysis, we treated birthweight as a continuous variable and in
univariate logistic regression observed an OR of 1.8 (95% CI 1.2-2.8) for
developing hyperbilirubinemia with each kilogram increase in birthweight.
When we considered birthweight as a six level ordinal variable (using 500
g intervals), we again observed a stepwise increase in risk of
hyperbilirubinemia with increasing birthweight interval (OR=1.3; 95% CI
[1.1-1.6]). The OR remained virtually unchanged when controlling for
covariates such as gestational age, gender, and gestational diabetes. The
figure below illustrates this linear relationship between birthweight and
development of hyperbilirubinemia and argues against a threshold effect.
We should point out, however, that when the six birthweight categories
were considered as indicator variables, we did not have sufficient sample
size to detect the stepwise increased risk of hyperbilirubinemia with each
increasing birthweight interval (see figure 1).
Figure 1.
Interestingly, unlike the infants in Newman’s studies, [1,2] the risk
of hyperbilirubinemia in our study infants did not decrease with each
additional week of gestational age over the range of 35-42 weeks. Near
term infants (<38 week GA) had the highest risk (15%), term infants
(38-39 weeks GA) had the lowest risk (9%), and post-term infants (>40
weeks GA) had an intermediate risk of hyperbilirubinemia (12%), though the
association of post-term gestational age with hyperbilirubinemia was not
statistically significant in univariate analysis.
We agree with Flaherman and Newman that clinical risk factors
obtained from the history and physical examination may increase the
predictive accuracy of the predischarge bilirubin measurement.[1] We plan
to explore this hypothesis in future studies, but we remain cautious about
the use of potentially ambiguous and subjective risk factors such as
maternal race and infant bruising and cephalohematoma. Misclassification
of these variables could decrease their generalizability in predicting
risk of hyperbilirubinemia. Finally, in addition to considering the
incremental benefit of incorporating risk factors, we must also consider
the incremental cost and complexity of including these factors in any
systematic universal screening protocol.
References
1. Newman TB, Liljestrand P, Escobar GJ. Combining clinical risk
factors with serum bilirubin levels to predict hyperbilirubinemia in
newborns. Arch Pediatr Adolesc Med 2005;159(2):113-9.
2. Newman TB, Xiong B, Gonzales VM, Escobar GJ. Prediction and prevention
of extreme neonatal hyperbilirubinemia in a mature health maintenance
organization. Arch Pediatr Adolesc Med 2000;154(11):1140-7.
Dr. Kanjilal makes some important observations but is mistaken in
several of her assertions. First, she suggests that because we limited
our study sample to infants for whom pre and post discharge TSBs were
performed our results are affected by some form of selection bias. The
bias she is referring to is verification bias, in which only patients with
“positive” or more concerning test results have a...
Dr. Kanjilal makes some important observations but is mistaken in
several of her assertions. First, she suggests that because we limited
our study sample to infants for whom pre and post discharge TSBs were
performed our results are affected by some form of selection bias. The
bias she is referring to is verification bias, in which only patients with
“positive” or more concerning test results have a follow-up test to verify
the original results. By decreasing the number of patients with
“negative” test results, this bias has the effect of overestimating test
sensitivity and underestimating specificity. However, as we point out in
our manuscript, we studied infants enrolled in an early discharge follow-
up program and minimized the potential for verification bias by
restricting our sampling frame to months during which >75% of enrolled
infants had postdischarge TSB measurements performed. In fact, for the
majority of these months, >90% of enrolled infants had postdischarge
TSBs measured.
The second point on which Dr. Kanjilal is mistaken concerns the
inclusion of “interrelated” factors “like vacuum and cephalohematoma” in
our clinical risk factor scoring system. As summarized in Table 2, vacuum
extraction is included in the scoring system but cephalohematoma is not.
In fact, contrary to our expectation, cephalohematoma was not associated
with development of postdischarge TSB>95%ile. This simply may be a
result of poor documentation of cephalohematoma in the admission and
discharge physical examinations (misclassification bias), but it raises
concerns about the use of subjective factors in clinical risk factor
scoring systems. Our results suggest that using more objective findings,
such as use of vacuum extraction during delivery--a common cause of
cephalohematoma-- may provide more accurate information about subsequent
risk of hyperbilirubinemia.
Finally, our finding that breastfeeding increases the risk of
hyperbilirubinemia is not new and should not be interpreted as a
recommendation against breastfeeding. As pediatricians who routinely care
for newborn infants, we recognize the benefits of breastfeeding and
strongly support its use. However, at the same time we are cognizant of
the potential risks of dehydration and hyperbilirubinemia posed by
inadequate intake in breastfed infants. The results of our study should
be interpreted as yet another invocation for healthcare systems and
providers to guarantee adequate lactation support for breastfeeding
mothers and early identification and treatment of breastfeeding problems
that may result in inadequate intake for infants.
As Dr. Kanjilal suggests, a prospective validation of alternative
risk assessment strategies is needed to confirm the results of our study
as well as other studies of alternative screening strategies. Further
studies are needed to evaluate the incremental benefit of using clinical
risk factors in addition to the predischarge TSB to predict which infants
are at risk of developing severe hyperbilirubinemia. And finally, more
studies are needed to evaluate the cost-effectiveness of alternative
strategies for screening and tracking infants for their risk of developing
severe hyperbilirubinemia in order to prevent the occurrence of
kernicterus, an uncommon but devastating, costly, and entirely preventable
condition.
We read with interest the article written by Shaw and Bishop [1] on
the use of bisphosphonates and would like to report the following adverse
reaction. A breast-fed full term neonate with clinically diagnosed
osteogenesis imperfecta type III was treated on day nine of life with IV
pamidronate (0.5mg/kg od for three days) on the advice of a tertiary centre.
Serum calcium had been measured at 24 hours o...
We read with interest the article written by Shaw and Bishop [1] on
the use of bisphosphonates and would like to report the following adverse
reaction. A breast-fed full term neonate with clinically diagnosed
osteogenesis imperfecta type III was treated on day nine of life with IV
pamidronate (0.5mg/kg od for three days) on the advice of a tertiary centre.
Serum calcium had been measured at 24 hours of age and was 2.72 mmol/L
(corrected) with a normal PTH of 1.4 pmol/l. Two days after the third
dose, the baby had four short-lived generalised seizures. Ionised calcium
measured at the time of the fits was 0.96 mmol/L and total serum calcium
was 1.73 mmol/L. The remainder of the biochemistry was unremarkable. The
serum calcium level was treated with an infusion of IV calcium gluconate
and a short course of oral calcium supplements and rose rapidly. No
further seizures were observed. We postulate that these seizures were
caused by hypocalcaemia secondary to pamidronate therapy.
The introduction of cyclical pamidronate therapy in recent years has
been shown to be both effective and safe for the treatment of osteogenesis
imperfecta in infants and young children.[2] Previous studies in children
have demonstrated a mild drop in serum calcium levels following
administration but none have described these as being severely symptomatic
and levels rapidly return to normal driven by an elevation in parathormone
production.[3,4] Hypocalcaemic seizures following bisphosphonate
administration have only previously been reported in a 92 year old woman
with vitamin D deficiency.[5] This is therefore the first report of
hypocalcaemic seizures secondary to bisphosphonate administration in the
neonatal age group. With the recommendation that bisphosphonates are used
as early as possible in children with osteogenesis imperfecta to gain
maximum benefit [6], monitoring of serum calcium levels is advisable when
pamidronate is used in neonates.
References
1 Shaw NJ, Bishop NJ. Bisphosphonate treatment of bone disease. Arch
Dis Child 2005; 90:494-499.
2 Glorieux FH, Bishop NJ, Plotkin H, Chabot G, Lanoue G, Travers R
Cyclical administration of pamidronate in children with severe
osteogenesis imperfecta. N Eng J Med 1998; 339:947-952.
3 Rauch F, Plotkin H, Travers R, Zeitlin L, Glorieux FH. Osteogenesis
Imperfecta Types I, III and IV: Effect of Pamidronate Therapy on Bone and
Mineral Metabolism. J Clin Endocrinol Metab 2003; 88:986-992.
4 Astrom E, Soderhall S. Beneficial effect of long term intravenous
bisphosphonate treatment of osteogenesis imperfecta. Arch Dis Child 2002;
86:356-364.
5 Maclsaac RJ, Seeman E, Jerums G. Seizures after alendronate. J R
Soc Med 2002; 95:615-616.
6 Plotkin H, Rauch F, Bishop NJ, Montpetit K, Ruck-Gibis J, Travers
R, Glorieux FH. Pamidronate treatment of severe osteogenesis imperfecta in
children under 3 years of age. J Clin Endocrinol Metab 2000; 85:1846-50.
Notwithstanding the characterisation of laparoscopic cholecystectomy
as the so-called "gold standard" [1], what needs to be acknowledged is
that, in comparison with open cholecystectomy, the former is associated,
not only with an increased risk of common bile duct injury [1-2], but also
with what has belatedly become increasingly recognised as the increased
risk of gallstone spillage (i.e. spillage...
Notwithstanding the characterisation of laparoscopic cholecystectomy
as the so-called "gold standard" [1], what needs to be acknowledged is
that, in comparison with open cholecystectomy, the former is associated,
not only with an increased risk of common bile duct injury [1-2], but also
with what has belatedly become increasingly recognised as the increased
risk of gallstone spillage (i.e. spillage into the peritoneal cavity), some of the adverse sequelae of which can
manifest themselves as long as twenty years postoperatively.[3]
In their protean manifestations, the adverse sequelae of gallstone spillage range from
intraperitoneal, retroperitoneal, and pelvic abscesses, to intrathoracic manifestations such as empyaemas and even cholelithoptysis.[3,4] include intestinal obstruction and lodgement in distal hernial sacs.[3] Gallstone spillage is estimated to
occur in up to 30% of laparoscopic cholecystectomies [4], but even this might be an underestimate, the latter best remedied, according to one view, by prospective studies documenting, in the same cohort, not only bile duct injury, but also gallstone spillage and its long-term sequelae.[5] The time is also long overdue to ask whether, in view of the above, it is fair to ask surgeons who are already accomplished and skilled in the three-dimensional modality of open cholecystectomy to address the steep learning curve of the two-dimensional perspective of laparoscopic cholecystectomy irrespective of whether or not they are comfortable with the switch.
Yours sincerely,
OMP Jolobe
References
(1) Jaffray B. Minimally invasive surgery
Archives of Disease in Childhood 2005:90:537-42.
(2) Johnson A. Laparoscopic surgery
Lancet 1997:349:631-5.
(3) Sathesh-Kumar T., Saklani AP., Vinayagam R., et al. Spilled gallstones during laparoscopic cholecystectomy: a review of the
literature
Postgraduate Medical Journal.
(4) Patterson EJ and Nagy AG
Don't cry over spilled stones? Complications of gallstones spilled during
laparoscopic cholecystectomy: case report and literature revies. Canadian Journal of Surgery 1997:40:300-4.
(5) Jolobe OMP
Multidisciplinary approach to biliary complications of laparoscopic
cholecystectomy (letter). British Journal of Surgery 1998:85:1450.
Levine and Olver have raised issues of great concern for the society
(Arch Dis Child May 2005). Children are the future of this nation, as of
any other. Levine and Olver have shown that 8 of 24 paediatric departments
in the major cities of the UK have lost their paediatric identity over the
past decade.
To my knowledge, there is no other country where this has happened.
Canada, Australia, New...
Levine and Olver have raised issues of great concern for the society
(Arch Dis Child May 2005). Children are the future of this nation, as of
any other. Levine and Olver have shown that 8 of 24 paediatric departments
in the major cities of the UK have lost their paediatric identity over the
past decade.
To my knowledge, there is no other country where this has happened.
Canada, Australia, New Zealand and the US all have robust academic
paediatric departments that represent the cutting edge of children's
research and academic clinical activity in every single major conurbation
in the developed world.
We are either being astoundingly clever with our resource planning, or
astoundingly unimaginative.
In a significantly resource-limited city like Calcutta in India, there are
four medical colleges with heads of departments in paediatrics for each of
the colleges. If there is a new health problem in children within the
conurbation requiring academic reflection, society (i.e. the media,
charities, non-governmental organisations, government strategists) involve
the academic head of paediatrics in the planning process. Not so perhaps
in many of the major cities of the UK, where you will be hard-pressed to
discover the possible leaders in academic Child Health among the
histopathology, immunology - perhaps even astrophysics - divisions of the
university.
The authors state that “mercury is toxic to the environment”. But is it?
Because mercury (Hg) is what humans call an “element”, it cannot be broken down into something simpler, and leaving aside Hg exportation effects via human space travel and other unknowns, all of the element mercury (Hg) that was originally here on this planet is still here, though in a variety of forms – elemental, ionic, organic.
...
Dear Editor,
We noted with interest the article published by Ladhani and colleagues [1] highlighting the problem of vitamin D deficiency. We agree that this remains a problem, especially in “at risk” ethnic minority groups.
In Oldham, which has a population of 49992 children, 20.8% are Asians (Census 2001). Between December 2002 and March 2004, we identified 9 cases of hypocalcaemia /rickets secondary to Vi...
Dear Editor,
We read with interest the article written by Weston and colleagues [1] on the effects of probiotics (Lactobacillus fermentum PCCTM) on atopic dermatitis (AD). They showed that the reduction in SCORAD index over time was significant in the probiotic group but not the placebo group and that significantly more children receiving probiotics had a SCORAD index that was better than baseline at week 16 compar...
Dear Editor,
We read with great interest the article by SE Jones et al. highlighting the worrying trend of increasing obesity detected by use of routinely collected data. In 2002-2003 we carried out a prospective observational study aimed at estimating the problem of obesity in children presenting to the outpatient department of Royal Glamorgan Hospital. The hospital caters to the population of Rhondda, Cynon and...
Dear Editor,
We appreciate Drs. Flaherman and Newman’s comments on our manuscript and welcome the opportunity to respond. First we would like to point out that the clinical risk factor score for a bottle-fed infant with birth weight 4.1 kg would only be higher than for a breast-fed infant of less than 38 weeks gestation if the latter infant’s birthweight were in the lowest birthweight category (2000g–2500g).
...Dear Editor,
Dr. Kanjilal makes some important observations but is mistaken in several of her assertions. First, she suggests that because we limited our study sample to infants for whom pre and post discharge TSBs were performed our results are affected by some form of selection bias. The bias she is referring to is verification bias, in which only patients with “positive” or more concerning test results have a...
Dear Editor,
We read with interest the article written by Shaw and Bishop [1] on the use of bisphosphonates and would like to report the following adverse reaction. A breast-fed full term neonate with clinically diagnosed osteogenesis imperfecta type III was treated on day nine of life with IV pamidronate (0.5mg/kg od for three days) on the advice of a tertiary centre. Serum calcium had been measured at 24 hours o...
Dear Editor,
Notwithstanding the characterisation of laparoscopic cholecystectomy as the so-called "gold standard" [1], what needs to be acknowledged is that, in comparison with open cholecystectomy, the former is associated, not only with an increased risk of common bile duct injury [1-2], but also with what has belatedly become increasingly recognised as the increased risk of gallstone spillage (i.e. spillage...
Dear Editor,
Levine and Olver have raised issues of great concern for the society (Arch Dis Child May 2005). Children are the future of this nation, as of any other. Levine and Olver have shown that 8 of 24 paediatric departments in the major cities of the UK have lost their paediatric identity over the past decade.
To my knowledge, there is no other country where this has happened. Canada, Australia, New...
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