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Biomedical subjects

M M Erickson

Publications and source records attributed to M M Erickson.

7 recordsLinked to original sources
PubMed1983

Elevation of postmortem triiodothyronine in sudden infant death syndrome and in infants who died of other causes: a marker of previous health.

We measured serum concentrations of thyroxine (T4), triiodothyronine (T3), reverse T3, free T4, thyroid-stimulating hormone, and cortisol in 62 victims of sudden infant death syndrome (SIDS) in 30 infants who died of known causes and in 15 living controls. The mean T3 value was elevated in 69% of those with SIDS. 37% of the others who died, and in no control infants. After excluding those who died of known cause who had abnormal thyroid function (abnormal postmortem concentrations of T4, free T4, or reverse T3), the T3 values were elevated in 63% of those remaining. When the data were analyzed on the basis of case histories and autopsy findings, those infants who were in good health and died suddenly of accidental causes had an elevation in mean T3 similar to that seen in SIDS victims; those who died under conditions known to alter thyroid metabolism did not. The T4, free T4, reverse T3, thyroid-stimulating hormone, and cortisol values were not useful in differentiating those with SIDS from the living controls, or those who were healthy at the time of death. We were unable to find any difference in T3 serum concentrations between the total group who had SIDS and those who had SIDS with minor infections, with petechiae on intrathoracic organs, with premature birth, or those who were resuscitated. Our data point out the importance of using appropriate controls when evaluating SIDS. The normal reverse T3 values in SIDS, as well as confirmation of the normal T4 and free T4 values, constitute evidence against chronic persistent alveolar hypoventilation or prolonged episodes of hypoxia immediately preceding death from SIDS.

Female↗
PubMed1983

Tissue mineral levels in victims of sudden infant death syndrome I. Toxic metals--lead and cadmium.

Lung, liver, kidney, and rib specimens were obtained at autopsy from 66 sudden infant death syndrome (SIDS) infants and 23 infants who died suddenly from other causes between the ages of 4-26 wk. Tissue levels of lead and cadmium were measured by atomic absorption spectroscopy and are expressed as microgram/g dry weight. Because these metals are cumulative with age in storage tissues, the levels were corrected for age (adjusted to age 13 wk). The SIDS liver and rib specimens contained significantly more lead than non-SIDS tissues (liver, 1.095 microgram/g versus 0.761 microgram/g, P less than 0.05; rib, 1.754 microgram/g versus 1.041 microgram/g, P less than 0.01, respectively). There were no significant differences in cadmium concentration between the SIDS and non-SIDS tissues. All four tissues showed significant increases with age in both lead and cadmium concentrations in SIDS. The increase in lung lead concentration with age was significantly greater in SIDS than in non-SIDS cases, P less than 0.05. In non-SIDS only kidney cadmium showed an increase with age (P less than 0.0001). These data collectively suggest an increased exposure of the SIDS infant to lead either prenatally and/or postnatally. Any physiologic effects of the increased tissue lead levels are unknown. They may be only a marker of the known epidemiology of SIDS.

Age Factors↗
PubMed1983

Tissue mineral levels in victims of sudden infant death syndrome II. Essential minerals: copper, zinc, calcium, and magnesium.

Deficiencies of various vitamin and minerals per se have been suggested as possible causes of sudden infant death syndrome (SIDS). Further, a deficiency of essential minerals may lead to enhanced toxicity of toxic elements, in particular, lead and cadmium to explore the possibility of mineral deficiencies or interactions with the toxic metals, lead and cadmium, lung, liver, kidney, and rib specimens were obtained at autopsy from 66 SIDS infants and 23 infants who died suddenly from other cases. Tissue copper, zinc, calcium, and magnesium were measured by atomic absorption spectroscopy. No differences were found between SIDS and non-SIDS for any element in any tissue except for more magnesium in the liver (P less than 0.0001) and less copper in the lungs (P less than 0.02) in the SIDS group. Only sporadic interactions between toxic and essential elements could be found. We found no evidence of any essential mineral deficiencies per se or significant interactions of essential and toxic minerals that might potentiate the effects of toxic metals. The physiologic significance, if any, of the higher liver magnesium and lower lung copper found in SIDS is unclear.

Cadmium↗