New Possible Link to SIDS Found

High levels of protein in infants' brains provide clue to cause of fatal syndrome

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MONDAY, Nov. 10, 2003 (HealthDayNews) -- High levels of a particular cytokine in the brains of infants may be linked to Sudden Infant Death Syndrome (SIDS).

The discovery comes from a Belgian study in the Nov. 11 issue of Neurology.

Researchers studied the brains of 19 infants who died from SIDS and eight who died from other conditions and compared the level of various cytokines -- a class of proteins involved in regulating the immune system -- in both groups of infants.

The study found the brains of all 19 infants who died from SIDS showed strong or moderate levels of the cytokine interleukin-1 in the same regions of the brain stem.

In comparison, the brains of six of the infants who didn't die of SIDS showed weak, negligible or no level of interleukin-1 in the same regions while the other two had a moderate level.

"We detected a pattern of cytokine in the SIDS brain that could overturn a delicate balance in molecular interactions in vital brain centers," study author Dr. Hazim Kadhim says in a prepared statement.

"It seems that high levels of interleukin-1 could be a common denominator in SIDS," he says.

But the ages of the infants in this study were not exactly matched. The infants in the SIDS group ranged in age from 6 weeks to 10 months at the time of their death. The non-SIDS infants were one day to 18 months old when they died.

That means the results are open to criticism, says an editorial in the same issue of Neurology.

"Since the SIDS and control infants were not age-matched, it's difficult to say how normal developmental changes in cytokine levels impacted the results," writes editorial author Dr. Bradley T. Thach of Washington University School of Medicine in St. Louis.

"Another crucial question is what is the cause of the elevated cytokines in SIDS?" Thach writes.

More information

Here's where you can learn more about SIDS.

SOURCE: American Academy of Neurology, news release, Nov. 10, 2003


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