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Editor,—We read with great interest the paper byKerr et al on the association betweenH pylori infection and SIDS. However, we cannot agree with the speculation the authors made.
Recently, we performed a similar retrospective analysis of nine cases of SIDS and eight controls collected in our hospital over the past two years. Controls were selected from infants with known cause of death, including congenital malformation, infection, metabolic disease, and drug intoxication (see table).
The formalin-fixed and paraffin-embedded stomach, trachea, and lung specimens obtained during postmortem examination were retrieved. Initial histological examination was performed by an experienced pathologist to look for any evidence of H pylori colonisation in these specimens. In addition, we used three different PCR assays that amplify two regions of the ureB gene1 2 and the cagA gene3 to detect the presence of H pylori DNA in these samples.
Histological examination failed to show anyHelicobacter like organism in these samples. Moreover, despite using three different sensitive PCR assays, we failed to show the presence of H pylori DNA in the stomach, lung, or trachea of the SIDS and control patients.
Viable H pylori has recently been recovered from the vomitus of infected children and adults.2Conceivably, it could lead to silent aspiration of gastric contents into the lung and result in bronchopneumonia. However, the failure to detect the organism in the stomach, trachea, and lung specimens, together with the absence of features to suggest aspiration pneumonia as the cause of death in these infants, argue against the validity of this speculation. With the high prevalence of H pylori infection in Chinese, one would expect a parallel high incidence of SIDS in our ethnic group, which does not fit into any epidemiological observations. Taken together, the significance ofH pylori as a cause of SIDS is highly questionable.