Time To Revisit Deer Part 3 (Wakefield situation)

August 4, 2011

http://www.ageofautism.com/2011/07/time-to-revisit-deer-3.html

By Hewitt

This is the third part of an analysis of Deer’s (in photo) claims

that Dr Wakefield fixed the findings in the 1998 Lancet paper

'Ileal-lymphoid-nodular hyperplasia' (Lancet, 1998; vol. 351,

p.637), a small clinical case series of 12 patients with autism and bowel

disease treated at the Royal Free Hospital in 1996/97. The British

Medical Journal editors not only published Deer’s claims on 5

January 2011

[HERE], but

backed them with the charge of academic fraud against Wakefield. Using

the UK General Medical Council (GMC) transcripts and research papers,

Parts 1 and 2 questioned the way Deer selected his evidence to support

serious allegations of fraud.

Scientific fraud

To substantiate scientific fraud the accuser must show that the

original findings were changed – ‘fixed’, ‘falsified’, ‘fabricated’ in

the BMJ’s words – to advance a particular interest or theory that the

original findings do not support. These analyses of Deer’s claims test if

this is so. Part one examined Deer’s claim that three of the nine

children reported with regressive autism did not have an autism diagnosis

[

HERE]. Part two examined the claim that, “despite the paper

claiming that all 12 children were ‘previously normal,’ five had

documented pre-existing developmental concerns” and could not have

regressive autism

[

HERE]. Deer used GP records and local consultants’ letters from the

early 1990s that were not available to Wakefield and his team when

investigating the Lancet paper children in the mid-1990s, and which only

became available 16 or so years later to the GMC fitness to practice

hearing against Dr Wakefield and Professors and Simon

Murch sitting between 2007 and 2010. Of the volumes of documents used as

evidence in the GMC hearing, the Royal Free team in the mid-1990s would

have only the following: the General Practitioner’s (GP) referral letters

summarising each child’s case; four consultants’ letters which two GPs

appended to their referral letters; and the results of their own clinical

investigations at the Royal Free. The two analyses of Deer’s evidence

showed that he selected extracts from the GMC transcripts that appeared

to support his claims but failed to examine statements from the GMC

hearing that countered his claims. That medical clinicians disagree over

the interpretation of symptoms – as the GMC hearing showed in abundance –

does not constitute fraud. In other words the first two analyses of

Deer’s evidence found no evidence of Wakefield’s alleged fraud.

Deer’s claim

The third and present part examines Deer’s claim that “In nine cases,

unremarkable colonic histopathology resultsnoting no or minimal

fluctuations in inflammatory cell populationswere changed after a

medical school ‘research review’ to ‘non-specific colitis’”. Seen

in the context of an article claiming Wakefield fixed his results, this

claim suggests further fixing took place by colleagues, not just

Wakefield, attending the review. However, as discussed below, the review

was a means whereby clinicians reached agreement on the different

interpretations of the children’s bowel condition. This claim is examined

in the light of the published GMC transcripts of the hearing against the

three doctors. Child 11’s case is the exception – a private patient from

the US, his case was discussed only in passing and so cannot be

independently verified from the GMC transcripts. So nine cases becomes

eight. We can judge the accuracy, selectivity and interpretive license

Deer applies to his evidence against Wakefield. His claims that Wakefield

fixed his results are summarised in a list of bullet-points at the end of

his BMJ article.

Deer’s article provides little in evidence to back up his third claim. Of

the nine children, only child 3 is singled out as “a prime example” of a

bowel disease case. No evidence is provided in the body of the article on

the other children’s bowel condition. We examine what Deer says about

this child before commenting on the other seven children. The procedure

is simple: Deer’s quotes and his endnotes referencing GMC and other

evidence are given in italics followed by other statements of evidence

from the GMC ignored by Deer. We end up with two lists of statements from

the GMC: one from Deer supporting his allegations and the other from GMC

witness statements countering his claims – both lists containing matching

statements that contradict each other. Of course disputation is the stuff

of scientific debate and the driver of scientific progress. But at no

point can disputed statements count as evidence of fraud. They cannot

stand as the last word on whether Wakefield fixed his results when other

statements by medical clinicians and experts to the GMC hearing undermine

the thrust of his allegations of fraud – a charge the GMC did not level

against Wakefield or the other two doctors.

The children

This is what Deer says of child 3.

Quote 1 “What was unquestionably true was that child 3 had serious

bowel trouble: intractable, lifelong, constipation. This was the most

consistent feature among the 12 children’s symptoms and signs but, being

the opposite of an expected finding in inflammatory bowel disease,

it was nowhere mentioned in the paper.

108 a) Ajjegowda Shantha. GP records and evidence to the panel. Day 5.

( -. Evidence to the panel. Day 91.

109 Murch S, Thomson M, - J. Author’s reply [letter]. Lancet

1998; 351:908

110 Squires RH and Colletti RB, Indications for pediatric

gastrointestinal endoscopy: A medical position statement of the North

American Society for Pediatric Gastroenterology and Nutrition. Journal of

Pediatric Gastroenterology and Nutrition 1996; 23: 107-110.

111 Ian Booth. Evidence to the panel. Day 41. “Looking for inflammatory

bowel disease would be a most unusual way of approaching a patient with

severe, long-standing constipation.”

Deer’s central contention is that, although the children, including child

3, may have displayed bowel symptoms, none had inflammatory bowel disease

(IBD) as claimed in the Lancet paper, and that at worst they had

constipation which Deer claims was not consistent with IBD. However the

lack of mention of constipation in the Lancet paper is evidence of its

initial and provisional status as a small case series – which the Lancet

called an ‘Early Report’ – which presents initial findings that

subsequent more rigorous research sustains or refutes. As the research

developed after 1998, further papers by Royal Free team members referred

to constipation in the context of IBD, supporting contradictory findings

that challenge what Deer says about the children’s bowel ‘trouble’:

Furlano RI et al. 'Colonic CD8 and T-cell infiltration with

epithelial damage in children with autism', Jn Pediatrics 2001,

138, 3. Torrenti, F et al. 'Focal-enhanced gastritis in regressive autism',

Am Jn Gastroenterology 2004, 99, 598-605. Afzal N, et al. 'Constipation with acquired megarectum in children

with autism', Pediatrics 2003, 112:939-42.

Regarding endnote 110, the protocol was issued in 1996, prior to the

above research, and considers the use of endoscopy in general

paediatric gastroenterology. It does not address the use of endoscopy in

diagnosing gastroenterological problems in autistic children.

Regarding 111, the above research into the presence of constipation in

the context of IBD suggests a different view to Professor Booth's.

Further, the following exchange took place at the GMC hearing between

-’s counsel and Dr V , defence expert witness in

gastroenterology: " Q Staying with constipation, do you come

across constipation as a feature of inflammatory bowel disease? A

Absolutely, yes” (Day 101-38).

So the 1998 paper was the first of several papers on autism and bowel

disease from members of the Royal Free team which subsequently went on to

develop more rigorous findings, including the co-presence of constipation

and IBD and the significance of the children’s histopathology.

Deer goes on to argue that, following the initial histology reports, the

bowel findings were changed by a medical school “review” – a statement

suggesting that, if the changes amounted to ‘fixing the data’, the

responsibility lay with participating colleagues seeking agreement on

conflicting histopathology readings. Responsibility for these changes

cannot rest on Wakefield alone, contrary to what the BMJ editors’ contend

in their accompanying editorial to Deer's piece.

Quote 2: as I revealed in the BMJ last April, the hospital’s pathology

service found the children’s colons to be largely normal, but a medical

school “review” changed the results.

115 Deer B. Wakefield’s “autistic enterocolitis” under the

microscope. BMJ 2010; 340:838-41.

What Deer’s article does not reveal are the purpose, rigour and

exemplary professionalism of these reviews that “changed results”.

Without more exact procedures to determine medical findings associated

with autism and bowel disease, early findings must inevitably rely on

individual interpretations, with their greater risk of error and

inexactness. Yet these same moves towards accuracy, when subject to

critical peer review among scientists and clinicians, play an important

role in reaching greater accuracy in interpretation. In the case of

histological readings of bowel samples, different histopathologists can

arrive at different readings. Given the critical importance of these

findings for the outcome of the patient’s clinical care, a process of

checking and debating different views is imperative. With this in mind

Professor instituted two new practices to review the

biopsies of children treated by his team, including, but not limited to,

the Lancet 12: first, weekly clinical reviews of the histological

findings attended by general histopathologists who had produced the

initial reports, an expert in bowel histopathology, the appropriate

clinicians and medical scientists; secondly, a blinded review of the

initial histology findings conducted by the expert bowel histopathologist

(the GMC panel did not examine the blinded reviews). The transcripts

record the added rigour the weekly reviews imposed, in subjecting initial

reports, constrained by time and resources as witnesses indicated (see eg

Day 33-3), to close scrutiny and a deliberative process of reaching

consensus on their significance. Work pressures on the hospital pathology

department meant that the Lancet children were one small group among 700

or so cases per week received from different departments (Day 3 –

36).

Apart from child 3, Deer provides no evidence in the body of his article

to support the claim that “unremarkable colonic histopathology results”

were changed for the other eight children. The nine children can only be

identified from the table attached to the article, where under a column

headed ‘non-specific colitis’ he compares what was said in the Lancet

paper for each of the 12 children with what he claims the records show,

placing a ‘Yes’ or ‘No’ against each child to substantiate or

refute the Lancet data. 'No’s' are placed against child 3, 4, 5, 7, 8, 9,

10, 11 and 12. Whereas the Lancet said that these children exhibited

findings of non-specific IBD, Deer claims these children showed

“unremarkable” histopathology results that were subsequently

changed.

Given the significance of this claim for his general claim that Wakefield

fixed the Lancet paper results, it is surprising that this evidence is

not included in the article itself (apart from child 3’s). Deer confines

the evidence to a different paper which readers of his BMJ article may

have missed. A link ‘web extra’, to a ‘background document’ with Deer’s

data, is found on the left column of the article’s webpage. This goes to

a pdf document – each page headed with Deer’s own web address – on a

separate part of the BMJ’s website. The ‘web extra’ provides two tables

separating out the content from the single table in the article into

Table 1, what the Lancet paper says, and Table 2, what Deer says. In

Table 2, the column refuting the existence of non-specific colitis has

‘no’s’ and a footnote against each of the nine children. The footnotes

cite the first histology reports on the children’s biopsies (small and

large bowel biopsies numbered I, II, III, etc) produced by the Royal

Free’s general histopathologists, other reports and Deer’s comments. No

reference is given to the findings of the later blinded readings by the

expert bowel histopathologist and scant reference to the more rigorous

analyses of -’s weekly reviews. Important parts of the Royal

Free team’s research procedures and findings are missing.

If the initial histology reports written by the Royal Free’s team of

general histopathologists, which Deer quotes in his footnotes to Table 2,

are compared with the subsequent data from the expert histopathologist in

gastroenterology available to the GMC, we see markedly different readings

regarding the presence and extent of inflammation in the children’s

bowel. We will look in detail at the matching reports for child 3 first

and then, to save time, compare short extracts from the matching reports

for the other seven children (excluding 11). Bold text is used throughout

to emphasise conflicting statements in the matching reports.

CHILD 3

Quote 3: [Footnote] 56. Histology report. ‘I. Shows small

bowel mucosa with an increase in intra-epithelial small lymphocytes, but

no architectural abnormality. II. Shows small bowel mucosa with

prominent lymphoid follicles. III-VII. Each show large bowel-type mucosa

within normal histological limits.’ The pathology service

comments: ‘Mild inflammatory and reactive changes in the small bowel

samples, of uncertain significance on morphological grounds alone. No

microbes or granulomas identified in any of these samples.’”

The initial histology report for child 3 – in common with initial

reports for the other 8 children – identifies signs of inflammation which

are considered unproblematic. By contrast child 3’s discharge summary

written by Dr Casson (a member of the Royal Free team and co-author

of the Lancet paper) on 16 September 1996 draws on the further

histopathology review of the results and stresses the pathology of

inflammation in the child’s bowel:

“Overall appearances were normal until the ascending colon.

Here one definite apthoid ulcer was seen and towards the

caecum there were multiple prominent colonic lymphoid follicles.

The terminal ileum also appeared abnormal showing marked lymphonodular

hyperplasia though there was no ulceration. Histology possibly

demonstrates mild chronic inflammation within the lamina propria of

the terminal ileum. It should be noted that it is difficult to

estimate whether or not this is within normal limits. … Throughout the

large bowel there was a patchy increase in chronic inflammatory cells

with an occasional prominent lymphoid follicle with a germinal

centre. There was also an occasional focus of acute cryptitis

within the ascending colon. There was also mild crypt

distortion. …. The patchy distribution of this inflammation and

the involvement of the terminal ileum are in keeping with a diagnosis of

Crohn’s disease.”

Subsequently the diagnosis of Crohn’s was replaced by ‘non-specific’ or

‘indeterminate colitis’, reflecting the limited knowledge in the

paediatric gastroenterology community in the mid-1990s of how to read

bowel symptoms in autistic children. Professor - explains his

logic at the time: “I believed these children had significant

inflammatory bowel disease but it was not Crohn’s disease and was not

ulcerative colitis. That is why the actual words, ‘indeterminate colitis’

were used here” (Day 74-42-3).

CHILD 4

Quote 4: 60. Histology report. “I. Small bowel type mucosa with a

lymphoid follicle. II-VII. Large bowel mucosa, some with attached

muscularis mucosae, with no evidence of architectural distortion or

increase in inflammatory cells in the lamina propria. Lymphoid follicles

with germinal centres are present in many of the biopsies. No cryptitis

or crypt abscesses are seen. The surface epithelium appears intact. No

granulomas, ova or parasites are seen.” The pathology service comments:

“Large bowel series with terminal ileum, with no histopathological

abnormality.”

Comparing this initial report with the following exchange between

and his QC, we see why he took the subsequent results more

seriously and why he placed more credence on the reports of the expert

bowel histopathologist, Dr Dhillon:

Q Just take as an example – we could do the exercise and I am going to do

it in due course when we go through the individual cases, but in some

cases Dr Dhillon appears to have found a description of the pathology

there that is not present in the original report.

A There are differences. There are some children where there are

differences, yes.

Q Taking as an example ... Child 4...You have written there....

A It says, “Lymphoid nodular hyperplasia. Dhillon differs – 2/5 Paneth

cell metaplasia. Increased eosinophils 5/5 mild increase in inflammatory

cells”, And then I have written after that, “routine – normal”, rather as

an aide memoir to myself saying that the routine report had been reported

as normal....

Q ....I asked you whether the Dhillon findings were the same as the

routine, were they in all cases the same as the routine?

A ....They were not the same in all cases, no.

Q Taking that as an example, you have got “Dhillon differs” – you have

written that to yourself.

A I have.

Q What did you mean by that?

A He considered that there was more significant

histopathological abnormality than the routine report. Obviously the

routine report says it is normal and he, for example, says, “Mild

increase in inflammatory cells”. I agreed with that, otherwise I would

not have written it.

Q And 2/5, what does that mean?

A That is the two out of five paneth cells there was metaplasia

CHILD 5

Quote 5: 64 Histology report. “Specimen I consists of fragments of

small intestinal mucosa which includes lymphoid follicles but

which is without pathological abnormality. Specimens II, III and

IV are large bowel mucosa fragments with normal crypt

architecture. There is at best a minimal increase in chronic

inflammatory cells within the superficial lamina propria. No active

inflammation is seen. Specimens III and IV show minor crypt

architecture distortion, including occasional bifid forms. Paneth cell

metaplasia is not seen. No excess chronic inflammatory cells are seen. A

very occasional polymorph is seen within surface crypt epithelium. No

ova, granulomas or parasites are seen in any of these biopsies.” The

pathology service comments: “Large bowel series; minor changes the

significance of which are uncertain but do not amount to the diagnosis of

inflammatory bowel disease.” Also of interest: child 5 was reported

by endoscopist and Lancet co-author Simon Murch as not having ileal

lymphoid hyperplasia, but the published Lancet paper said that he did

have this.

Child 5’s discharge summary which the Royal Free sent to the GP is

referred to on Day 11 (p.52): “he has apparently been having bouts of

diarrhoea on and off since he was 4 years of age. There is no blood

or mucous in the stool. He has occasional abdominal pain during which

he suddenly clutches his abdomen and flexes his knees. This has a

duration of about 10 minutes and then resolves.

The histology report in footnote 64 is discussed in Mr 's

examination of Professor - (Day 78-45/6), which again provides

insight into how he read the histology report in a way

significantly different from Deer.

Q I would like your comments on the findings first.

A Specimen I is in accord with the endoscopic appearances. The II, III

and IV, “there is minimal increase in chronic inflammatory cells within

the superficial lamina propria”, that is a definite abnormality that

suggests chronic inflammation, but the adjective “minimal” is used

and there is “no active”, that means acute, inflammation. III and IV says

“minor crypt architecture distortion including occasional bifid forms”.

That clearly indicates that there has been previous damage from

inflammation, damage in crypt architecture, and the crypts have

responded to that abnormality by, instead of having a single form,

they have developed a double or bifid form.

In III and IV the opinion was that there was no excess chronic

inflammatory cells and a very occasional polymorph was seen within the

surface crypt epithelium. That is certainly abnormal, which is an

indicator of some acute inflammation.

CHILD 7

Quote 6: 72 Histology report. “I-II. Two pieces of small

intestinal type mucosa with essentially normal villous architecture.

There is no increase in inflammatory cells in the lamina propria or in

intraepithelial lymphocytes. Part of a lymphoid follicle is included. No

parasites or granulomas are identified. III-IV. Sections from all sites

show large bowel mucosa with no abnormality of crypt architecture or

significant increase in inflammatory cells in the lamina propria. Some of

the biopsies contain lymphoid follicles. No granulomas or parasites are

seen.” The pathology service comments: “Small bowel biopsy and large

bowel series without significant histological abnormality.”

The colonoscopy report showed “Slight evidence of vascular

abnormality in rectum and sigmoid but otherwise essentially normal.

The terminal ileum however demonstrated a marked degree of

lymphonodular hyperplasia” (Day 1 – 57). Commenting on his

post-admission letter to Child 7’s GP, when examined by GMC QC Ms ,

- points out: “It was an interesting letter from my

perspective because clearly something had been found that was considered

significant”, namely the finding of evidence of bowel inflammation and

indeterminate colitis” (Day 6 – 31). Again -, drawing on

his long-standing experience and expertise in gastroenterology, placed

greater significance on the presence of lymphonodular

hyperplasia.

CHILD 8

Quote 7: 76 Histology report. “I. These are both fragments of

poorly orientated, but normal small bowel mucosa. A lymphoid reactive

centre is seen in each sample. II-IV. These are all pieces of normal

colonic type mucosa containing occasional lymphoid aggregates. Minimal

inflammatory changes may be the result of operative

artefact.”

Following GP treatment for constipation, child 8 was admitted to her

local hospital after she became unsettled during the night, was screaming

for a week, had diarrhoea (“6 bowel motions/day) and complained of

abdominal pain. On arriving at the Royal Free, the question for Professor

- was whether the histology report indicated the presence of

inflammation in the bowel. In his examination by Ms , he rejects the

general histopathologist’s suggestion that signs of inflammation were

artificial due to problems in extracting the biopsy (an ‘operative

artefact’), rather than evidence of real inflammation, because there was

insuficient time for the small bowel specimens to become inflamed after

removal (Day 80 – 37). - concludes that it is “Not Crohn’s or

ulcerative colitis, no, but the fact reported there is “minimal

inflammatory changes”.

When Mr QC questions Dr , the defence expert witness in

gastroenterology (Day 103-6), about the presence of inflammation in child

8’s bowel, he replies, “No, it is not entirely normal. It is not,

frankly, grossly abnormal, but a lymphoid reaction is implying, as we

have discussed in previous patients, that there is some overactivity

of the lymphoid tissue, thereby implying some degree of

inflammation.”

CHILD 9

Quote 8: 80 Histology report. “I. Small bowel mucosa showing no

histological abnormality. II-VII. Large bowel mucosa showing prominent

lymphoid follicles but no histological abnormality.”

Again at variance with the general histopathologist’s original report

above, the colonoscopist’s report found “a marked increase in the size

and number of prominent lymphoid nodules”, which - relayed

to the GP, adding that, “The colon was endoscopically normal except for

an area at the hepatic flexure which was slightly erythematous.

Histologically there was an increase in chronic inflammatory cells

throughout the colon with a moderate increase in intra-epithelial

lymphocytes.... Our diagnosis is indeterminate colitis with

lymphoid nodular hyperplasia” (Day 4-13).

Later Dr , when examined by Mr QC, explained that large

bowel mucosa showing prominent lymphoid follicles was “...an unusual

feature because lymphoid hyperplasia...is normally in the terminal ileum”

(Day 103 - 16).

CHILD 10

Quote 9 : 84 Histology report. “I. The specimen consists of small

bowel and have sampled a Peyer’s patch. Where present, the overlying

villae appear unremarkable. The lymphoid tissue shows reactive changes.

Parasites and granulomas are not seen. II-VI. All these biopsies show

large bowel mucosa with occasional isolated bifid glands. The

inflammatory population is within normal limits. Parasites and granulomas

are not seen.” The pathology service comments: “No significant

histological abnormality.” A supplementary report was requested,

following a weekly histology meeting with clinicians, and possibly with

Wakefield. This said: “These biopsies have been reviewed following a

clinicopathological meeting. The ileal biopsy shows confluent lymphoid

aggregates within otherwise unremarkable small intestine. The large bowel

biopsies show a very subtle scattering of chronic inflammatory cells

within the lamina propria. The superficial lamina propria contains focal

nuclear debris and the surface epithelium appears slightly degenerate.

No active inflammation is seen. More levels have been cut and no

granulomas have been identified.” The pathology service comments:

“Minor abnormalities. ? Significance.” Child 10’s biopsies were

also examined at another centre. Following the supply of samples to the

University Hospital of Wales, Cardiff, Huw , consultant paediatric

gastroenterologist, wrote: “I’ve now had a chance to review 10’s

intestinal biopsies kindly sent down from the Royal Free hospital, and

although there are lymphoid follicles present in the small intestine

these are often regarded as a normal finding, and certainly our

pathologists here would suggest that the colonic biopsies were within

normal limits. Certainly they do not feel he has good evidence

of gut inflammation in the biopsies.”

The long footnote records a process of uncovering problematic

signs in child 10’s bowel which are not initially understood. First, the

general histopathologist’s report identifies reactive changes in the

lymphoid tissue, but no significant histological abnormality. Secondly,

the biopsies were reviewed, which confirmed the initial findings, but

uncertainty remains over their significance. Thirdly, but absent from the

footnote, Dr Murch’s colonoscopy report (Day 25 - 59) states

unambiguously, “This colonoscopy was definitely abnormal, in

probably a more striking example of the pattern seen in the cohort of the

autistic children. The rectum showed definite mild abnormality, with a

slightly granular mucosa and abnormal vascular pattern. Prominent

lymphoid follicles could be seen throughout the colon, with no other

mucosal abnormality. The caecum showed an eryhthematous, granular mucosa

around a swollen ileo-caecal valve, while the terminal ileum showed minor

inflammatory change and striking lymphoid hyperplasia distally.

I suspect that the biopsies will show unequivocal

abnormality!”

When these concerns were placed side by side with the University Hospital

of Wales report, which viewed the biopsies as unproblematic, the Royal

Free clinicians had to decide whether child 10’s inflammation was

pathological and required treatment. Presumably because of their

experience and duty of care, the team decided that treatment was

warranted.

CHILD 12

Quote 10: 92 Histology report. “I-IV. Pieces of large bowel

mucosa including lymphoid follicles with germinal centres. There

is no architectural abnormality and no increase in inflammatory cells in

the lamina propria. No organisms or granulomas are seen.”

Again in the hands of an expert gastroenterologist, the unremarkable

is viewed with more concern. Dr Murch finds “Appearances almost

normal to caecum. Again there were minor changes in the rectum and caecum

(slight changes in vascularity and prominent lymphoid follicles). The

ileo-caecal valve could not be identified”. Pieces of large bowel

mucosa including lymphoid follicles with germinal centres...” (Day 25

- 63). Examined by Mr QC, Professor - summed up his

conclusion that “the finding of lymphoid follicles, especially with

germinal centres, in the large bowel mucosa is an abnormal finding”

(Day 82 - 21).

Conclusion

This study of the GMC transcripts shows that Deer has constructed his

allegations of fraud against Wakefield in two ways. First he redefines

what constitutes fraud. Academic fraud is no longer confined to

researchers who deliberately change their original data in publications

promoting scientific preconceptions the original data do not support.

According to this conventional view, the accuser would have to compare

only the researchers’ own original data with the published data. For Deer

fraud is committed and substantiated if there is, besides the original

research data, additional data the researchers did not have access to

that is different from the published data. We have seen that Deer either

did not have access to or did not use all the original data generated by

the Royal Free team, such as the results of the blinded histopathology

reviews and the weekly reviews. But we have also seen that Deer makes

considerable use of additional information, such as GP and local

consultant records which the Royal Free team would not be aware of at the

time the case series was conducted. For example, the first and second

analyses of Deer’s article showed that he drew on GP and local consultant

records, most not available to the team, that appeared to show that three

of the children were not autistic and that five (including child 11) had

pre-existing developmental concerns before and not after the MMR. The

analyses used other statements, some from the same witnesses, to show

that the children were indeed autistic and that the pre-existing

conditions were not relevant to the conditions that did emerge after MMR

(except for one child who had the measles jab before his MMR). Of course

these different views may be matters for further debate – though relating

to records taken in some cases 20 plus years ago. But the fact that

debate is possible means these are not matters of indisputable truth,

against which differing findings can be viewed as fraudulent.

The second way in which Deer constructs his case for fraud is by

selecting statements from the GMC hearing in such a way that differences

of interpretation and matters of legitimate scientific debate are

foreclosed to produce the impression that the selected statements stand

as the only account available. For example, when we compare Deer’s

evidence with other statements from the GMC transcripts, we see that

there were differences in the conclusions clinicians reached on the

significance of the children’s bowel symptoms, specifically regarding the

evidence of inflammation. But rather than acknowledge the normal scope of

interpretative variation in histopathology findings, Deer provides the

reader only with the ‘unremarkable’ accounts of the initial

histopathology reports in seeking to undermine the histological evidence

of ‘non-specific colitis’ in nine of the 12 children summarised in the

Lancet paper.

Deer’s reconstructions of scientific fraud – of the definition and data

determining fraud – are endorsed by the BMJ editors in an editorial

introducing his article. The editors allege that “Wakefield altered

numerous facts about the patients’ medical histories in order to support

his claim to have identified a new syndrome”. Yet not one example of an

original fact altered to fit a preconceived syndrome – so constituting

fraud – is given by Deer or the BMJ. Discrepancies between the Lancet

published data and other data refer in the main to data the Lancet team

did not see because they were not part of the original findings. Where

data were changed, this was part of the routine processes of reviewing

data to seek greater factual accuracy and of reaching a consensus on

different interpretations. Not only Deer but more surprisingly the BMJ

editors represent the routine but complex processes of making clinical

judgments as fixing the data - a travesty of the clinical

process.

Deer’s binary view of the truth – where this is no room for

interpretation, debate over gradations of meaning, and for reaching

consensus – obscures the true nature of clinical investigation and the

process of medical advance.

Posted by Age of Autism at July 30, 2011 at 5:45 AM in

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August 4, 2011