Problems on the diagnosis of sudden infant death syndrome

We evaluated height as a potential risk factor for breast cancer in a case-control study of 747 young women diagnosed with invasive breast cancer before age 46 years and 961 control subjects recruited by random digit dialing. We found that total height attained did not affect a woman's risk of the disease. The age when a women reached her maximum height, however, was a risk factor for breast cancer. There was a trend of decreasing risk of breast cancer in relation to increasing age of height attainment, culminating in a 30% reduction in the risk of breast cancer for women who reached their maximum height when they were 18 years or older compared with women who reached their maximum height when they were 13 years old or less (odds ratio = 0.7; 95% confidence interval = 0.5-1.0). Although the age at menarche was correlated with the age at maximum height, the effect of age at maximum height persisted after adjustment for age at menarche. Previous studies have reported that age at menarche is an important determinant of risk, but this study indicates that age when maximum height is reached may be another, and possibly more important, landmark of puberty that is related to breast cancer risk. The physiologic basis for this claim may lie in the influence on breast development of exposure to growth hormone and insulin-like growth factor during puberty, and on a decreased time between the end of puberty and a woman's first livebirth, both of which are believed to affect a woman's risk of breast cancer.     

Relationship of passive cigarette-smoking to sudden infant death syndrome

The smoking habits of 56 families who lost babies to the sudden infant death syndrome (SIDS) were compared to those of 86 control families. A higher proportion of SIDS mothers smoked both during pregnancy (61% vs. 42%) and after their babies were born (59% vs. 37%). SIDS mother also smoked a significantly greater number of cigarettes than controls. Exposure to cigarette smoke ("passive smoking") appears to enhance the risk of SIDS for reasons not known.     

Fetal hemoglobin levels in sudden infant death syndrome

OBJECTIVE: The aim of this study was to determine and compare fetal hemoglobin levels from infants dying of the sudden infant death syndrome (SIDS) with aged-matched control infants dying of other causes. Similar previous studies have reported both elevated and normal levels of fetal hemoglobin in whole blood samples from infants dying of SIDS. DESIGN: Triton-acid-urea gel electrophoresis and densitometry were used to determine fetal hemoglobin levels in postmortem whole blood samples from infants dying of SIDS and from appropriately age-matched control infants. Whole blood samples were analyzed blindly and matched for postgestational age. Infant ages at death ranged from birth to less than 1 year. MAIN OUTCOME MEASURES: Fetal hemoglobin in whole blood from infants dying of SIDS and control infants. RESULTS: During the period of postnatal development most associated with SIDS cases (2 to 6 months after birth), fetal hemoglobin levels were found to be significantly elevated in postmortem whole blood samples from SIDS infants compared with gestational age-matched control infants dying of causes other than SIDS. CONCLUSION: We conclude that levels of fetal hemoglobin are elevated in postmortem whole blood of SIDS infants compared with controls. Furthermore, the apparent conflict in the literature regarding fetal hemoglobin levels in SIDS infants and controls is most likely due to variability in the control data of some studies.     

Brown fat retention in sudden infant death syndrome

This study was undertaken to confirm the findings of Naeye with regard to the pathological retention of the so-called brown fat cells in the periadrenal adipose tissue of infants who die of the sudden infant death syndrome. The percent of multilocular fat cells was determined in histological sections of periadrenal adipose tissue obtained from a series of 289 autopsies. In general, our morphological observations confirm his. However, our results indicate that the percent of periadrenal multilocular cells cannot be used as a diagnostic criterion in any single case. Futhermore, we consider that the mechanism for this delay in transformation remains unclear.     

Tritiated-naloxone binding to brainstem opioid receptors in the sudden infant death syndrome

The sudden infant death syndrome (SIDS) is defined as the sudden death of an infant under 1 year of age that remains unexplained after a thorough case investigation, including a complete autopsy. We hypothesized that SIDS is associated with altered 3H - naloxone binding to opioid receptors in brainstem nuclei related to respiratory and autonomic control. We analyzed 3H - naloxone binding in 21 regions in SIDS and control brainstems using quantitative tissue receptor autoradiography. Three groups were analyzed: SIDS (n = 45); acute controls (n = 14); and a chronic group with oxygenation disorders (n = 15). Opioid binding was heavily concentrated in the caudal nucleus of the solitary tract, nucleus parabrachialis medialis, spinal trigeminal nucleus, inferior olive, and interpeduncular nucleus in all cases analyzed (n = 74). The arcuate nucleus on the ventral medullary surface contained negligible binding in all cases (n = 74), and therefore binding was not measurable at this site. We found no significant differences among the three groups in the age-adjusted mean 3H - naloxone binding in 21 brainstem sites analyzed. The only differences we have found to date between SIDS and acute controls are decreases in 3H - quinuclidinyl benzilate binding to muscarinic cholinergic receptors and in 3H - kainate binding to kainate receptors in the arcuate nucleus in alternate sections of this same data set. The present study suggests that there is not a defect in opioid receptor binding in cardiorespiratory nuclei in SIDS brainstems.     

Cerebral white matter lesions in sudden infant death syndrome

In 21.6% of infants who died of sudden infant death syndrome, the cerebral white matter showed areas of leukomalacia. Of those infants with congenital heart disease, 24.8% had lesions, whereas 4.4% of infants who died from known acute causes had lesions. The sites of the cerebral white matter lesions, subcortical or periventricular, seem to be related to the age of the infant.     

Enigma in swaddling clothes: sudden infant death syndrome

SIDS strikes suddenly, and its cause is unknown. It elicits trauma such as profound guilt and calls into question a lost parental role and status, the ability of parents to fulfill the societal expectation of child rearing, and the legitimacy of the grief process for which the parents are unprepared. Grief includes reactions to loss and separation anxiety and results from lost attachments experienced by parents. Counselors can help rebuild the emotional constellations of bereaved parents, ease the communication between the parents, and interpret the needs of one parent to the other. When counseling bereaved parents they should enlist the help of resilient and emotionally mature family members. Because many bereaved parents abruptly leave their homes to forget and recover, helping professionals should move swiftly yet cautiously to aid immediate and extended families. Their efforts may be the first and last change to intervene.     

Potential role of microbiological agents in sudden infant death syndrome

The potential role of microbiological agents was investigated in 10 cases of Sudden Infant Death Syndrome in Budapest between September 1996 and December 1997. Autopsy, histological examination and microbiological tests were performed on samples of blood, cerebrospinal fluid, pharyngeal and bronchial samples from infants under six months died suddenly, without previous diseases. The multifactorial pathomechanism of SIDS was suggested by detection of Parainfluenza Type virus antigen, isolation of toxin producing Staphylococcus aureus, Enterobacteriaceae and Candida albicans strains in large number of more samples of the same infant.     

Brainstem 3H-nicotine receptor binding in the sudden infant death syndrome

Maternal cigarette smoking during pregnancy has been shown to be a major risk factor for the sudden infant death syndrome (SIDS). We hypothesized that SIDS is associated with altered 3H-nicotine binding to nicotinic receptors in brainstem nuclei related to cardiorespiratory control and/or arousal. We analyzed 3H-nicotine binding in 14 regions in SIDS and control brainstems using quantitative tissue receptor autoradiography. Three groups were analyzed: SIDS (n = 42), acute controls (n = 15), and a chronic group with oxygenation disorders (n = 18). The arcuate nucleus, postulated to be important in cardiorespiratory control and abnormal in at least some SIDS victims, contained binding below the assay detection limits in all (SIDS and control) cases. We found no significant differences among the 3 groups in mean 3H-nicotine binding in the 14 brainstem sites analyzed. When a subset of the cases were stratified by the history of the presence or absence of maternal cigarette smoking during pregnancy, however, we found that there was no expected increase (upregulation) of nicotinic receptor binding in SIDS cases exposed to cigarette smoke in utero in 3 nuclei related to arousal or cardiorespiratory control. This finding raises the possibility that altered development of nicotinic receptors in brainstem cardiorespiratory and/or arousal circuits put at least some infants, i.e. those exposed to cigarette smoke in utero, at risk for SIDS, and underscores the need for further research into brainstem nicotinic receptors in SIDS in which detailed correlations with smoking history can be made.     

Evidence for retarded kidney growth in sudden infant death syndrome

The aim of the study was to compare the growth rate of the kidneys of infants who died of sudden infant death syndrome (SIDS) and control babies under 1 year; 227 infants who died in St. Petersburg from 1983 to 1990 and who met the criteria for SIDS were included in the study; 138 infants who died suddenly of respiratory infections within the same period constituted a control group. The infants did not have signs of dehydration, malformations, tumours or intrauterine infections. Morphologically the kidneys were intact. Factors which might influence the weight of the kidneys at the time of death were: the cause of death (whether SIDS or not), gender, gestational age, weight, length and ponderal index at birth, age, weight and length at death. Stepwise (forward) linear regression analysis identified three variables which in combination most accurately and independently influenced the predicted weight of the kidneys. These were the cause of death, gender and weight at the time of death. The weight of the kidneys increased by 6.0 g for each increase in total body weight of 1,000 g [95% confidence interval (CI) 5.0-7.0 g], in boys the kidney weight was 3.3 g (95% CI 1.6-5.0 g) higher than in girls and in the SIDS babies kidney weight was 2.5 g (95% CI 0.8-4.2 g) less than controls. Delayed kidney growth may be an indicator of increased risk of SIDS in infants under 1 year and may contribute in some cases.     

Comparison of [125I]iodomelatonin binding sites in infant cerebellum of sudden infant death syndrome and non-sudden infant death syndrome

A tributyltin chloride (TBTCl)-resistant bacterium, Alteromonas sp. M-1, was isolated from coastal seawater. This bacterium grew in medium containing 125 microM TBTCl. TBTCl added to the medium was taken up by this bacterium, however, the amount of TBTCl in the cellular fraction was low after the logarithmic phase, suggesting the existence of a TBTCl-efflux system. A genetic library was constructed using plasmid vector pUC 19. Three positive clones were obtained, by which E. coli was transformed to TBTCl resistance. Of the three clones, the shortest fragment from HindIII-library was analyzed. This fragment was 1.8 kb long and contained one complete open reading frame. The predicted amino acid sequence of this open reading frame had a homologous domain to transglycosylases of bacteriophage and E. coli. TBTCl-tolerant marine bacteria other than Alteromonas sp. M-1 were obtained from natural seawater to which TBTCl was added. DNA-DNA hybridization was performed between the three cloned fragments from Alteromonas sp. M-1 and chromosomal DNA of the TBTCl-tolerant bacteria. Some strains hybridized with the fragments and some did not, suggesting that several genes are responsible for TBTCl tolerance.     

DTP vaccine and infant sudden death syndrome. Meta-analysis

BACKGROUND: At the beginning of 1994, five cases of sudden infant death syndrome after DTP immunization appeared in Spain. In order to study a causal relationship a meta-analysis of the different studies that assess this possibility has been conducted. METHODS: The selection criteria was epidemiological study, case-control or cohort, assessing risk of sudden infant death syndrome in immunized versus non-immunized infants or risk of sudden infant death syndrome in recently immunized infants versus immunized infants beyond 30 days. Pooled risk ratios were calculated from adjusted risk ratios, when available, of the different studies, by a meta-analysis according the method described by Greenland. RESULTS: One cohort and four case-control studies were selected. Pooled risk ratio for immunized versus non-immunized infants was 0.67 (95% CI = 0.60-0.75). When comparing risk of sudden death syndrome in up to 30 days immunized infants versus more than 30 days immunized infants, the pooled risk ratio was 1.00 (95% CI = 0.84-1.20). CONCLUSIONS: DTP-immunization does not seem to increase the risk of sudden infant death syndrome. The risk of sudden infant death syndrome is not greater in the first thirty days following immunization. These data indicate a lack of association between DTP immunization and sudden infant death syndrome.