Lancet editor takes seven years to act on Wakefield's declaration of Legal Aid Board involvement

From "ARCH" <arch@btclick.com>

Herewith Andrew Wakefield's "forgotten" letter published in the 2nd May
1998 issue of The Lancet declaring his agreement  "to help evaluate a small
number of these children on behalf of the Legal Aid Board. These children
have all been seen expressly on the basis that they were referred through
the normal channels (eg, from general practitioner, child psychiatrist, or
community paediatrician) on the merits of their symptoms."
 
He would have shown it to his fellow researchers and paediatric colleagues
prior to submitting it to The lancet.
 
In addition, the letter would have gone through acceptance and proof
stages, following pre publication procedures, which involved sending him
and the other authors proof correspondence from the correspondents'
enquiries, so that he and his fellow researchers could reply to them in the
same issue.
 
This having been done, the letters would have gone for publication, another
delay of several weeks at least, following a further proof reading of the
entire issue.
 
The issue in which "Ileal-lymphoid-nodular hyperplasia, non-specific
colitis and pervasive-developmental disorder in children.  Lancet  1998;
351: 637-42." was published is dated 28th February 1998.
 
Therefore, The Lancet and Richard Horton and his study colleagues, such as
Simon Murch,were fully aware of his declaration,"to help evaluate a small
number of these children on behalf of the Legal Aid Board" six weeks or so
in advance , before his letter of reply and that of Dr. Walker-Smith in the
same issue,were eventually published.
 
The lancet have had seven years to respond to his declaration. Why did they
only do so last week as if it was a total surprise ?
 
Richard
 
 
Reference
http://www.thelancet.com/journal/vol351/iss9112/full/llan.351.9112.correspon
dence.7074.1
 
Department of Public Health Medicine, Wiltshire Health Authority, UK 




1 Wakefield AJ, Murch SH, Anthony A, et al. Ileal-lymphoid-nodular
hyperplasia, non-specific colitis and pervasive-developmental disorder in
children.  Lancet  1998; 351: 637-42. [Text]

Author's reply 


Sir--D R Walker states that "biased selection of patients will influence
what you hear". Bias occurs in science when data are either wittingly or
unwittingly concealed. Does he condone the exclusion of a potentially
significant element of the history? He asks for virological evidence: we
refer him to our abstract (Gut 1998; 42: A86). Sadly, Walker casts the
value of the medical history, the process of peer review, and this
paediatric diaspora to the scrapheap of bad science and anecdote.


Leonard Sinclair and Peter Richmond and David Goldblatt correctly point out
the inappropriate use of adult reference ranges. We stated that IgA levels
were low in four out of 12 affected children. The normal range for IgA in
this age group is 05-24 g/dL, and, only one child was outside the normal
range. Similarly, the appropriate age-related range for alkaline
phosphatase is 250-800 U/L. These errors do not affect the conclusions of
the paper, particularly the identification of ileal lymphoid nodular
hyperplasia and colonic inflammation in a group of children with
developmental disorder.


A Rouse suggests that litigation bias might exist by virtue of information
that he has downloaded from the Internet, from the Society for the
Autistically Handicapped. Only one author (AJW) has agreed to help evaluate
a small number of these children on behalf of the Legal Aid Board. These
children have all been seen expressly on the basis that they were referred
through the normal channels (eg, from general practitioner, child
psychiatrist, or community paediatrician) on the merits of their symptoms.
AJW had never heard of the Society for the Autistically Handicapped and no
fact sheet has been provided for them to distribute to interested
parties.The only fact sheet that we have produced is for general
practitioners, which describes the background and protocol for
investigation of children with autism and gastrointestinal symptoms.
Finally all those children referred to us (including the 53 who have been
investigated already and those on a waiting list that extends into 1999)
have come through the formal channels described above. No conflict of
interest exists.


The authors stand by their findings. We recommend that paediatric
gastroenterologists investigate this problem further, since it is our
belief that there is both a large unmet need in the community and a
possible window-of-opportunity for some children with autism.

A J Wakefield