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Editor,—Kerr et al claimH pylori as a potential etiologic factor in SIDS. Fatal systemic ammonia intoxication through hydrolysis of urea by H pylori produced urease in the lungs and trachea, following aspiration of gastric juice, was proposed as a possible pathogenic pathway. In general we cannot agree with this hypothesis. The molecular procedure (nested PCR and ELISA based detection) used in this study could explain some inconsistent data—for example, H pylori DNA detection in lungs or trachea but not in the stomach. Furthermore, it is debatable whether haematoxylin and eosin (H&E) routine staining is an efficient method to visualise Helicobacter like organisms. A Warthin-Starry-silver stain, modified Giemsa or immunochemistry would have been more advisable.
We also regret that no histopathological data were given which could have provided essential information about a possible infectious etiology. From our experience, we observed that an acuteH pylori infection always causes marked inflammatory changes of the gastric mucosa.
We also find that the negative control group was not a good reference, as this group did not comprise enough cases and was too heterogeneous (including two premature cases with apparently no normal environmental contact, one case with pneumonia (aspiration pneumonia?)).
The discussion is totally speculative—for example, the role of interleukin 1 in H pylori infection: the main cytokines involved are (decreased production of) transforming growth factor, (local production of) tumour necrosis factor (TNF), interleukin 2 and interleukin 8. From the data presented, only the presence of H pylori DNA in the respiratory system (some cases without infection of the gastric mucosa) can be claimed. All other conclusions are not substantiated and should be considered as speculative until further evidence is provided—for example, culturing of H pylori from tracheal or lung fluid.
Even if the presence of viable H pyloricells in the respiratory system can be established, some kind of experimental model should be used to establish H pylori as a causative agent in SIDS.
Recent findings established by the Children's Hospital of Bamberg, Germany, suggest a hypoplasia of the basilar artery as a more plausible explanation for SIDS. It has been shown that this anatomical defect can cause blockage of the cerebral blood circulation especially in the prone sleeping position when the head is turned aside. This hypoplasia can be detected by ultrasound. Data of this study1performed by the same hospital, seem to confirm this hypothesis. Among 3506 births over the last two years, 31 newborns (0.88%) could be identified with marked hypoplasia of the basilar artery, six of these newborns were considered as high risk cases (1.7‰). The babies were given a monitor and the parents were instructed in resuscitation. None of the children born and screened in the Children's Hospital of Bamberg died from SIDS in the last years, whereas two babies not participating in the screening programme died out of 1130 house born babies in the region of Bamberg (1.8‰). For statistical significance 5000 births are necessary; a number that will be reached end of the year 2001. Further reports are pending.
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