437 SERUM 25-HYDROXY-VITAMIN D (25-OHD) CONCENTRATIONS AND BONE HISTOLOGY IN SUDDEN INFANT DEATH SYNDROME (SIDS)

Abstract

Based on an increased winter incidence, less time outside, increased “microscopic rickets,” and a speculation that hypocalcemia and laryngospasm are a terminal event, the possibility of vitamin D deficiency in SIDS has been raised. Further, evidence of growth arrest in costochondral junctions has been reported in 90% of unexplained infant deaths. Post mortem serum samples and sixth ribs were collected from 23 SIDS and 7 control infants. Ribs were immediately placed in Millonig's fixative and processed without decalcification. The mean ± S.D. of serum 25-OHD in the SIDS cases was 21.0 ± 7.9 ng/ml, control post mortem samples were 13.2 ± 9.3 ng/ml. The mean of the SIDS is well above hypocalcemic or rachitic ranges (<6 ng/ml) and did not differ from normal adults (24 ± 9.7 ng/ml) or 39 living premature and SGA infants at 3 months of age (26 ± 9.9 ng/ml). Serum calcium values were within physiological ranges (mean ± S.D. SIDS 9.34 ± 1.8 mg%, control 9.22 ± 1.85 mg%). Of currently analyzed rib specimens, normal histology with normal costochondral junctions and normal mineralization has been found. Thus, vitamin D deficiency per se, as reflected by serum 25-OHD, can be ruled out as a cause of a SIDS. We have not been able thus far to confirm the finding of postnatal growth abnormalities in rib cartilage and bone in SIDS.

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