Ramsay et al. are right to draw attention to the fact that many
'herbal creams' for atopic eczema contain potent or very potent topical
steroids. Their research echoes that done by Keane et al. [1] which showed
that of 11 Chinese herbal treatments obtained from patients attending
dermatology outpatient clinics at King's College Hospital, eight contained
dexamethasone at a mean concentrati...
Ramsay et al. are right to draw attention to the fact that many
'herbal creams' for atopic eczema contain potent or very potent topical
steroids. Their research echoes that done by Keane et al. [1] which showed
that of 11 Chinese herbal treatments obtained from patients attending
dermatology outpatient clinics at King's College Hospital, eight contained
dexamethasone at a mean concentration of 456 µg/g.
What is ironic about this is that patients or their parents or carers
often turn to 'herbal creams' because of steroid phobia - the misplaced
belief that corticosteroids are unsafe, even when used properly and under
the guidance of a clinician.[2] In the absence of almost any guidance
about their use, people may apply 'herbal creams' to areas of sensitive
skin such as the face and flexures, and they may use them for protracted
periods, possibly causing precisely the damage they were seeking to avoid.
The problem is the more frustrating because atopic eczema can usually
be more effectively treated than most people imagine. Even in severe
cases, the proper use of emollients and corticosteroids can produce
dramatic improvement in most cases of eczema. This was demonstrated
clearly by Cork et al. in their recent audit of adverse drug reactions to
aqueous cream in children with atopic eczema.[3] The availability of new
topical immunomodulators for those whose eczema does not respond to
topical corticosteroids - for whatever reason, including non-compliance
through steroid phobia - may be expected to reduce the burden of atopic
eczema still further.
All this being so, doctors should advise their patients to be
extremely cautious in experimenting with so-called 'herbal treatments' for
skin diseases. As an eminent professor of dermatology said recently, "if
an 'alternative' treatment for a skin disease appears to work like magic,
one should be extremely wary of it."
References
(1) Keane F.M., Munn S.E., du Vivier A.W.P., Taylor N.F. and Higgins
E.M., Analysis of Chinese herbal creams prescribed for dermatological
conditions; BMJ 27 February 1999;318:563-564
(2) Charman C.R., Morris A.D., Williams H.C., Topical corticosteroid
phobia in patients with atopic eczema; British Journal of Dermatology
2000; 142: 931-936.
(3) Cork M J et al. An audit of adverse drug reactions to aqueous
cream in children with atopic eczema Pharmaceutical Journal, 2003; 747-748
(29 November.)
We read with interest the study on the use of high dose ibuprofen in
cystic fibrosis (CF) by Arranz et al.[1] Whilst we appreciate the possible
beneficial effects of high dose ibuprofen on lung function, we are
concerned that its non-critical use could be associated with some risks,
despite monitoring of drug levels.
The authors quote an earlier report showing that ibuprofen can be
u...
We read with interest the study on the use of high dose ibuprofen in
cystic fibrosis (CF) by Arranz et al.[1] Whilst we appreciate the possible
beneficial effects of high dose ibuprofen on lung function, we are
concerned that its non-critical use could be associated with some risks,
despite monitoring of drug levels.
The authors quote an earlier report showing that ibuprofen can be
used in patients with CF to slow the deterioration in pulmonary function
‘without unacceptable side effects’.[2] It is, however, important to note
that in the cited article the CF patients with liver disease, renal
disease, hypersensitivity to non-steroidal anti-inflammatory drugs
(NSAID), allergic broncho-pulmonary aspergillosis, colonized with
Burkholderia cepacia, and cardiovascular, neurologic, haematologic, or
peptic ulcer disease had been excluded and only those with mild
respiratory involvement were studied.[2] It is unclear whether similar
exclusion criteria were applied by Arranz et al.[1]
Liver disease develops in approximately 25% of CF patients and
represents their third most common cause of death.[3,4] The main
hepatological complication of CF is biliary cirrhosis with development of
portal hypertension and oesophageal varices.[3,4] Detection of liver
disease in CF can be difficult given its often insidious onset of clinical
and biochemical features.[3,4] NSAIDs such as ibuprofen can trigger a
potentially life-threatening gastrointestinal bleeding in portal
hypertension, including patients with CF-related liver disease.[5]
We would suggest a careful exclusion of liver involvement using
clinical examination, abdominal ultrasound and laboratory tests before
advocating the use of high dose NSAIDs in CF patients.
References
(1) Arranz I. et al. Population pharmacokinetics of high dose
ibuprofen in cystic fibrosis. Arch. Dis. Child. 88, 1128-1130 (2003).
(2) Konstan MW, Byard PJ, Hoppel, CL and Davis PB. Effect of
High-Dose Ibuprofen in Patients with Cystic Fibrosis. N Engl J Med 332,
848-854 (1995).
(3) Colombo,C. et al. Liver disease in cystic fibrosis: A prospective
study on incidence, risk factors, and outcome. Hepatology 36, 1374-1382
(2002).
(4) Tanner, M.S. & Taylor, CJ. Liver disease in cystic fibrosis.
Arch. Dis. Child 72, 281-284 (1995).
(5) De Ledinghen,V. et al. Anti-inflammatory drugs and variceal
bleeding: a case-control study. Gut 44, 270-273 (1999).
Sudden unexpected death due to epilepsy (SUDEP)is a concept that
suggests the cause of death relates to an epileptic disorder. This paper
makes no mention of the fact that some cases of "SUDEP" may result when a
long QT syndrome (LQTS) has been misdiagnosed as epilepsy. How many the
studies of epilepsy mortality looked specifically at cardiac causes of
"epilepsy deaths", beyond considering those who a...
Sudden unexpected death due to epilepsy (SUDEP)is a concept that
suggests the cause of death relates to an epileptic disorder. This paper
makes no mention of the fact that some cases of "SUDEP" may result when a
long QT syndrome (LQTS) has been misdiagnosed as epilepsy. How many the
studies of epilepsy mortality looked specifically at cardiac causes of
"epilepsy deaths", beyond considering those who appeared to have drowned?
The accurate diagnosis of LQTS is important as the prognosis,
treatment and genetic implications are quite different from those
recommended for most forms of epilepsy.
LQTS can be easily confused with epilepsy. In one study of 78 members
from five families screened for LQTS, 36 were found to be affected. Of
the 10 deceased individuals six had been symptomatic during childhood,
three had been diagnosed with epilepsy, two had drowned and two had died
suddenly of unknown cause.[1]
I believe that the attribution of a sudden death to SUDEP is not very
helpful unless the diagnosis of LQTS has been reasonably excluded.
Reference
(1) Bradley T, Dixon J, Easthope R. Unexplainedfainting, near
drowning and unusual seizures in childhood: screening for long QT syndrome
in New Zealand NZMedJ 1999; 112;299-302.
In the guideline review the author underlines the importance of an accurate analysis of sweat electrolytes in newborns who had undergone CF neonatal screening.(1)
As there is limited experience with sweat tests in the first weeks of life we wish to report our experience in Tuscany regarding quantitative measurement of sweat electrolytes in newborns posi...
In the guideline review the author underlines the importance of an accurate analysis of sweat electrolytes in newborns who had undergone CF neonatal screening.(1)
As there is limited experience with sweat tests in the first weeks of life we wish to report our experience in Tuscany regarding quantitative measurement of sweat electrolytes in newborns positive to CF neonatal screening.(2-5)
From July 1st 1991 to November 31st 2003, 1012 out of 334,854 newborns (558 females 55.1% and 454 males 44.9%) resulted positive to our neonatal screening programme that, due to the high allelic heterogeneity in our region, consists in an IRT/IRT protocol with meconium lactase complementary test.(2)
A minimum sweat weight of 60 mg was collected in 97.6% of newborns tested (mean ± SD 149.4 ± 51 mg).
Sixty-eight (6.7%) of the 1012 newborns, 30 females and 38 males, had chloride values above the traditional 60 mmol/l cut-off and showed clinical manifestations of the disease.
Fifteen (1.4%) had "borderline" (40 to 60 mmol/l) sweat chloride levels but 2 (13.3%) subsequently developed symptoms of CF.
In the 944 newborns who tested positive with a chloride value below 60 mmol/l, the mean chloride value ± SD observed was 16.08 ±7.2 mmol/l (95% confidence interval, 15.6-16.5). As the upper limit of normal sweat chloride in newborns is not well-defined, we calculated the sweat chloride percentiles (table 1).
The sweat test is usually performed successfully on newborns as an adequate amount of sweat is easily collected. Other experiences show that sweat chloride values greater than 30 mmol/l are highly unusual in newborns undergoing evaluations after positive CF screening.(3-5) A key point in the guidelines states that a sweat chloride value of less than 40 mmol/l is normal, however, we would like to emphasisethat this is not true of the newborns we screened for CF.
Table 1 Percentiles of chloride values (mmol/l) in newborns positive to neonatal screening
Percentile
3rd
5th
10th
25th
50th
75th
90th
95th
97th
99th
Chloride (mmol/l)
7.4
8.3
9.1
11.2
15
19.8
25.5
30.5
35.1
40.8
References
1. Baumer JH. Evidence based guidelines for the performance of the sweat test for the investigation of cystic fibrosis in the UK. Arch Dis Child 2003;88:1126-1127
2. Taccetti G, Festini F, Mergni G et al. Neonatal screening for cystic fibrosis: the tuscan experience. Pediatr Pulmonol 2003;Suppl 25: 221-222
3. Farrell PM, Koscik RE. Sweat chloride concentration in infants homozygous or heterozygous for F508 cystic fibrosis. Pediatrics 1996;97:524-528
4. Massie J, Gaskin K, Van Asperen P, Wilcken B. Sweat testing following newborn screening for cystic fibrosis. Pediatr Pulmonol 2000;29:452-456
5. Padoan R, Bassotti A, Seia M, Corbetta C. Negative sweat test in hypertripsinemic infants with cystic fibrosis carrying rare CFTR mutations. Eur J Pediatr 2002;161:212-215
Regarding the article by Wing et al.[1]
It is my hypothesis that the percentage of individuals of higher testosterone is increasing worldwide, more in some places than others. I suggest this is the cause of the "secular trend." Among a number of characteristics that may result from this increase in numbers of individuals of higher testosterone, I suggest increasing obesity is one. An obesity epidemi...
Regarding the article by Wing et al.[1]
It is my hypothesis that the percentage of individuals of higher testosterone is increasing worldwide, more in some places than others. I suggest this is the cause of the "secular trend." Among a number of characteristics that may result from this increase in numbers of individuals of higher testosterone, I suggest increasing obesity is one. An obesity epidemic is occurring within children. (See "Obesity Epidemic in Children..." at http://www.anthropogeny.com/research.html)
Wing,et al, report that "sleep disordered breathing," "predominantly obstructive," occurs with greater frequency within obese children. I suggest this may also be due testosterone. Cistulli, et al, reported that in a 13-year-old boy that "Our data strongly suggest that the mechanism by which testosterone administration may induce or exacerbate OSA is through an influence on neuromuscular control of upper airway patency during sleep."[2]
I suggest the findings of Wing, et al, may represent the combined effects of testosterone on "sleep disordered breathing" and obesity in the children of their study.
References
1. YK Wing, SH Hui, WM Pak, CK Ho, A Cheung, AM Li, and TF Fok. A controlled study of sleep related disordered breathing in obese children. Arch Dis Child 2003; 88: 1043-1047
2. Reeves-Hoche MK, Meck R, Zwillich CW. Nasal CPAP: an objective evaluation of patient compliance. Am J Respir Crit Care Med. 1994 Feb;149(2 Pt 1):530-2).
We were interested in the paper by Goldwater calling for a critical review
of approaches to research in sudden infant death syndrome (SIDS).[1]
We
would agree that SIDS research needs to be continually re-assessed due
both to difficulties in establishing this ‘diagnosis’, and to problems
associated with understanding aetiological mechanisms. However, the
suggestion that the fall in SIDS rates has...
We were interested in the paper by Goldwater calling for a critical review
of approaches to research in sudden infant death syndrome (SIDS).[1]
We
would agree that SIDS research needs to be continually re-assessed due
both to difficulties in establishing this ‘diagnosis’, and to problems
associated with understanding aetiological mechanisms. However, the
suggestion that the fall in SIDS rates has not been due to ‘reducing the
risks’ (RTR) campaigns but instead is merely ‘a reflection of natural
variation’ is of great concern. Although data from Sweden and Australia
are used to support this contentious proposition, examination of the data
is not confirmatory.
While SIDS rates in Sweden have been less pronounced than in certain
other Scandinavian countries, (at 0.3/1000 live births in 1970), by the
time the Swedish back to sleep campaign was launched in 1991 the rate had
risen to 1.2; it subsequently dropped to 0.4 in 1994 and has remained low
ever since.[2,3] SIDS rates in Finland were lower than in Sweden, but even
there the trends are similar.[2] Examination of Australian Bureau of
Statistics data also does not support Goldwater’s contention. These data
clearly show continued and consistent falls in SIDS rates in all parts of
Australia since information become available on risk factors (in the late
1980s). Any increases in rates have been temporary, minimal, not
sustained and not statistically significant. Similar falls have been
shown in many other countries.[3] Thus, there can be no doubt that the
marked decline in SIDS rates has been due to the RTR campaigns, sponsored
by extremely hard working and well-motivated SIDS organisations, and not
to random variation. To question the effectiveness of the RTR campaign
has the potential to encourage parents to ignore well-established safety
messages about infant sleeping, and thus to put their infants lives
needlessly at risk.
References
1. Goldwater PN. Sudden infant death syndrome: a critical review of
approaches to research. Arch Dis Child 2003;88:1095-1100.
2. Sudden infant death in the Nordic countries. Results of the Nordic
Study of Sudden Infant Death Syndrome, 1990-1996. TemaNord, Nordic Council
of Ministers, Copenhagen, Denmark. 1997:600.
The report of 2 cases of Kawasaki disease (KD) presenting with lobar
pneumonia[1] is interesting.
We have recently seen a six year old boy
presenting similarly. The main feature in our case was that the child’s
degree of illness was in excess of that one would expect with bilateral
patchy changes on the chest Xray. Other concerns were an ESR of 80mm in
the first hour, a platelet count of 495...
The report of 2 cases of Kawasaki disease (KD) presenting with lobar
pneumonia[1] is interesting.
We have recently seen a six year old boy
presenting similarly. The main feature in our case was that the child’s
degree of illness was in excess of that one would expect with bilateral
patchy changes on the chest Xray. Other concerns were an ESR of 80mm in
the first hour, a platelet count of 495 x 109/L and CRP of 34mg/L. He
developed red, dry eyes 5 days after admission with skin peeling on the
7th day. He was treated with IV Immunoglobulin and Aspirin. Within 48
hours there was dramatic resolution of his symptoms and pulmonary
manifestations. An ECHO cardiogram showed normal coronary arteries.
The report by Uziel et al. underlines the need to be aware of
atypical presentations of KD. However it is remarkable that despite the
clinical variability of KD, the diagnosis rate in similar in different
series. For example the recent study in the US gave a KS incidence of
17.1/100,000 in the <_5 years="years" age="age" group="group" in="in" us2="us2" whereas="whereas" the="the" irish="irish" incidence="incidence" was="was" reported="reported" as="as" _15.2="_15.2" _100000.3="_100000.3" agreement="agreement" relation="relation" to="to" diagnosis="diagnosis" of="of" condition="condition" is="is" converging="converging" main="main" issue="issue" now="now" being="being" atypical="atypical" cases="cases" like="like" this="this" one.="one." p="p"/>References
(1) Uziel Y, Hashkes PJ, Kassem E, Gottesman G, Walach B. “Unresolving
pneumonia” as the main manifestation of atypical Kawasaki disease. Arch
Dis Child 2003;88:940-42.
(2) Holman RC, Curns AT, Belay ED, Steiner CA, Schonberger LB.
Kawasaki Syndrome Hospitalizations in the United States, 1997 and 2000.
Pediatrics 2003; 112:495-501.
(3) Lynch M, Holman RC, Mulligan A, Belay ED, Schonberger LB. Kawasaki
syndrome hospitalizations in Ireland, 1996 through 2000. The Pediatr
Infec Dis Journal 2003;22(11):959-63 .
Dear Editor
Ramsay et al. are right to draw attention to the fact that many 'herbal creams' for atopic eczema contain potent or very potent topical steroids. Their research echoes that done by Keane et al. [1] which showed that of 11 Chinese herbal treatments obtained from patients attending dermatology outpatient clinics at King's College Hospital, eight contained dexamethasone at a mean concentrati...
Dear Editor
We read with interest the study on the use of high dose ibuprofen in cystic fibrosis (CF) by Arranz et al.[1] Whilst we appreciate the possible beneficial effects of high dose ibuprofen on lung function, we are concerned that its non-critical use could be associated with some risks, despite monitoring of drug levels.
The authors quote an earlier report showing that ibuprofen can be u...
Dear Editor
Sudden unexpected death due to epilepsy (SUDEP)is a concept that suggests the cause of death relates to an epileptic disorder. This paper makes no mention of the fact that some cases of "SUDEP" may result when a long QT syndrome (LQTS) has been misdiagnosed as epilepsy. How many the studies of epilepsy mortality looked specifically at cardiac causes of "epilepsy deaths", beyond considering those who a...
In the guideline review the author underlines the importance of an accurate analysis of sweat electrolytes in newborns who had undergone CF neonatal screening.(1)
As there is limited experience with sweat tests in the first weeks of life we wish to report our experience in Tuscany regarding quantitative measurement of sweat electrolytes in newborns posi...
Dear Editor
Regarding the article by Wing et al.[1] It is my hypothesis that the percentage of individuals of higher testosterone is increasing worldwide, more in some places than others. I suggest this is the cause of the "secular trend." Among a number of characteristics that may result from this increase in numbers of individuals of higher testosterone, I suggest increasing obesity is one. An obesity epidemi...
Dear Editor
We were interested in the paper by Goldwater calling for a critical review of approaches to research in sudden infant death syndrome (SIDS).[1]
We would agree that SIDS research needs to be continually re-assessed due both to difficulties in establishing this ‘diagnosis’, and to problems associated with understanding aetiological mechanisms. However, the suggestion that the fall in SIDS rates has...
Dear Editor
The report of 2 cases of Kawasaki disease (KD) presenting with lobar pneumonia[1] is interesting.
We have recently seen a six year old boy presenting similarly. The main feature in our case was that the child’s degree of illness was in excess of that one would expect with bilateral patchy changes on the chest Xray. Other concerns were an ESR of 80mm in the first hour, a platelet count of 495...
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