Heikki Peltolaa ∙ Annamari Patjab ∙ Pauli Leinikkib ∙ Martti Valleb ∙ Irja Davidkinb ∙ Mikko Pauniob
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| AAP: This 14-year prospective study of 3 million adverse events tracked subjects who developed gastrointestinal symptoms or signs lasting 24 hours or more starting one hour after MMR vaccination. Researchers also checked hospital and health center records or interviewed local public health nurses. No evidence was found for MMR vaccine-associated inflammatory bowel disease or autism. |
“Concern1 of potential loss of confidence in measles, mumps, and rubella (MMR) vaccine has been raised by a recent paper2 that suggested a causal association between this vaccine (or another environmental trigger) and a new syndrome of chronic inflammatory bowel disease and autism. Characteristically, all children described developed intestinal symptoms within days or soon after vaccination.”
Conflicts of interest: This study was based on inherently unreliable data and funded by Merck, which makes the current formulation (MMR-II) of the measles, mumps, and rubella vaccine, and stands to profit from results that disprove any dangers.
F. Edward Yazbak, MD: Makela et al. were so intent on shooting down Wakefield’s work that even in a paper titled “Neurologic disorders after MMR,” they found a way to mention that no hospitalized children with autism had IBD. But regardless of what Makela says, the fact is that the number of individuals who received assistance for IBD from the Social Security Institution in Finland doubled in nine years (from 9,737 in 1992 to 20,807 in 2001).
The whole study is based on ONE comparison. If the children in the first group developed symptoms of encephalitis and meningitis within two weeks of vaccination, then causation is implied (medically and medico-legally). In this case, a comparison with the control group is meaningless and the author’s conclusion is unwarranted.[8]
WHAT THE COCHRANE REVIEW SAID:
■ This study suffered from a “moderate” risk of bias.
■ It was “weakened” by the loss of 14% of the original birth cohort and the effects of the rather long time frame of follow up. What the impact of either of these factors was in terms of confounders is open to debate.
■ The long follow up for autism was due to the lack of a properly constructed causal hypothesis.
■ The study failed to report complete vaccine identification information, including lot numbers, adjuvants, preservatives, strains, product and manufacturer.
■ There was a lack of adequate description of exposure (vaccine content and schedules).
■ The authors provided “inadequate” explanations for missing information, even though there were clearly missing unintended-event data on as many as 20% of the participants.
■ The study had discrepancies in reporting of denominators and was classified to be at moderate risk of bias.
What the IOM said: The study suffered from one primary limitation: its exclusive reliance on hospitalization records. This made it impossible to identify children with ASD who were not hospitalized, but rather seen in an outpatient setting. The IOM went on to say that “While the authors stated that it is common in Finland for children with autism to be admitted to the hospital for observation and testing, a diagnosis of autism does not always involve hospitalization.”[9]
What Science-Based Medicine.com said: “Using ‘hospitalizations’ as criteria for finding children with autism (is) not a good way to find autism cases, I agree.”[10]
SUMMARY:
The “Finnish MMR study” fails to make explicit the exact definition of ‘caseness’, particularly with respect to autism. The criticisms leveled at the study are crucially important in this respect. First, there is a failure to differentiate between autism per se, and the sub-group who are proposed to be at increased risk (i.e. those with regressive onset). There is also a degree of circularity in the statement that those whose encephalitis was ‘unrelated to vaccination’ were excluded. To deselect particular cases before analysis, on the basis of a proposed non-relationship between exposure and outcome is poor epidemiological practice. Further, it implies that decisions about causality were made after the event, on the basis of criteria which were not made explicit to the reader. At face value, the exclusion of these cases would appear to work in favor of those proposing a possible association between exposure and hospitalization; but this would only be the case if the lack of association was real. No evidence is presented which allows formulation of an opinion on this. The most problematic factor, however, is in the assumption that children hospitalized ‘for autism’ somehow represent the very well defined group of children that are proposed to be at risk of an adverse event following vaccination. This assumption simply has no validity, and neither, therefore, do any conclusions based on data related to this group.