Oxygen deficit again hinted as SIDS cause.

Oxygen deficit again hinted as SIDS cause

A new study supports a growing but controversial body of evidence that sudden infant death syndrome, or SIDS, is the deadly culmination of an underlying disease characterized by a chronic oxygen deficit. The finding strengthens the possibility that a biochemical "marker" might be found to identify infants at highest risk.

SIDS--the sudden, unexplained death of an apparently healthy child--is most common among infants 2 to 4 months old and only rarely occurs after 9 months. Although no specific biological mechanism has been linked to the syndrome, some research suggests an association with cardiopulmonary deficiencies, defective central respiratory control or both.

Researchers at the National Hospital in Oslo, Norway, measured levels of hypoxanthine in the eye fluids of 32 infants who had died of SIDS. Hypoxanthine is a breakdown product of the common cellular chemical adenosine monophosphate, or AMP. Increased levels of hypoxanthine indicate low oxygen levels, or hypoxia, in body tissues -- especially when measured in eye fluids, which lack hypoxanthine-destroying enzymes. Compared with children who died from trauma and with infants who died suddenly of known causes, the SIDS victims had much higher hypoxanthine levels, the researchers report in the October PEDIATRICS.

While physicians cannot safety measure hypoxanthine levels in the eyes of living infants, other indicators of chronic hypoxia may prove useful. In research reported in the April 30, 1987, NEW ENGLAND JOURNAL OF MEDICINE, Enid Gilbert and her co-workers at the University of Wisconsin School of Medicine in Madison found elevated levels of a particular type of hemoglobin--hemoglobin F--in the blood of SIDS victims. High levels of hemoglobin F had previously been found in infants born to mothers with chronic low oxygen resulting from severe asthma, anemia or heart failure. The Wisconsin team is seeking to confirm that hemoglobin F levels may have value as a marker for some infants at risk for SIDS.

The new study, "is exciting to us and it's very important," Gilbert told SCIENCE NEWS. "The report is supportive of our findings."

The Norwegians, led by Torleiv O. Rognum, note that with a hypoxia-induced accelerated conversion of AMP to hypoxanthine, there is a buildup of adenosine. Adenosine is known to inhibit respiration. This added inhibition, on top of an initial hypoxia, may result in a "vicious circle" of oxygen deprivation, they say.