scholarly journals Sudden infant death syndrome: Melatonin, serotonin, and CD34 factor as possible diagnostic markers and prophylactic targets

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0256197
Author(s):  
Dmitry Ivanov ◽  
Ekaterina Mironova ◽  
Victoria Polyakova ◽  
Inna Evsyukova ◽  
Michail Osetrov ◽  
...  
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Melatonin Receptors ◽  
Infant Mortality Rate ◽  
Immunohistochemical Method ◽  
Control Group ◽  
Sudden Infant ◽  
Predictive Diagnosis ◽  
Cardiovascular Damage

Sudden infant death syndrome (SIDS) is one of the primary causes of death of infants in the first year of life. According to the WHO’s data, the global infant mortality rate is 0.64–2 per 1,000 live-born children. Molecular and cellular aspects of SIDS development have not been identified so far. The purpose of this paper is to verify and analyze the expression of melatonin 1 and 2 receptors, serotonin (as a melatonin precursor), and CD34 molecules (as hematopoietic and endothelial markers of cardiovascular damage) in the medulla, heart, and aorta in infants who died from SIDS. An immunohistochemical method was used to investigate samples of medulla, heart, and aorta tissues of infants 3 to 9 months of age who died from SIDS. The control group included children who died from accidents. It has been shown that the expression of melatonin receptors as well as serotonin and CD34 angiogenesis markers in tissues of the medulla, heart, and aorta of infants who died from SIDS is statistically lower as compared with their expression in the same tissues in children who died from accidents. The obtained data help to clarify in detail the role of melatonin and such signaling molecules as serotonin and CD34 in SIDS pathogenesis, which can open new prospects for devising novel methods for predictive diagnosis of development and targeted prophylaxis of SIDS.

Apnea, Hypoxemia, and Aborted Sudden Infant Death Syndrome

PEDIATRICS ◽  
1978 ◽  
Vol 62 (5) ◽  
pp. 686-691
Author(s):  
June P. Brady ◽  
Ronald L. Ariagno ◽  
John L. Watts ◽  
Steven L. Goldman ◽  
Fe M. Dumpit
Keyword(s):  
Heart Rate ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Total Duration ◽  
Periodic Breathing ◽  
Sudden Infant Death ◽  
Control Group ◽  
Sudden Infant ◽  
Nasal Catheter ◽  
End Tidal

To find out whether there is any relationship between the ventilatory response to hypoxia and the sudden infant death syndrome (SIDS), we studied the effects of mild induced hypoxia (PIO2, 120 mm Hg = 17% oxygen) in 16 infants aged 2 weeks to 6 months. Eight had recurrent apneic spells (apnea group) (five had aborted SIDS and three had recurrent apnea in the intensive care nursery) and eight were "well" preterm infants about to fly in a pressurized airplane (PIO2, 120 mm Hg) (control group). Mean birth weights were 2,245 and 1,400 gm and mean gestational ages were 35 and 30 weeks. Postconceptual ages (41.8 and 41.3 weeks) were almost identical. Heart rate was obtained from an ECG, and respiratory rate and pattern were obtained from a pneumogram. In addition, end-tidal PCO2 and PN2 or PO2 were obtained with a nasal catheter and gas analyzers. In the apnea group with inhalation of 17% oxygen, we observed an increase in periodic breathing and an increase in both rate and total duration of respiratory pauses. In the control group there were no significant changes. Heart rate and PCO2 did not change in either group. Our findings suggest that infants prone to apnea may have unique respiratory responses to mild induced hypoxia.

Sudden Infant Death Syndrome in a Twin: A Comparison of Sibling Histories

PEDIATRICS ◽  
1986 ◽  
Vol 78 (1) ◽  
pp. 146-150
Author(s):  
A. Kahn ◽  
D. Blum ◽  
M. F. Muller ◽  
L. Montauk ◽  
A. Bochner ◽  
...  
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Clinical Risk Factor ◽  
Control Group ◽  
Sudden Infant ◽  
First Year ◽  
Control Infant ◽  
The Mean ◽  
First Year Of Life

To determine possible characteristics of infant victims of sudden death, we examined 114 items related to the pre- and postnatal histories of 42 pairs of twins one of whom died of sudden infant death syndrome (SIDS) leaving a surviving sibling. Interviews with the parents were conducted after the occurrence of SIDS, and the data were checked with records held by gynecologists and pediatricians. To evaluate the specificity of any factors, we studied a control group of 42 age- and sex-matched pairs of twins, both of whom survived the first year of life. Only 11 of 114 characteristics were significantly related to SIDS: future victims had a smaller weight and height at birth, stayed longer in the nursery, and followed a moving object with their eyes, had head control, and smiled at a later age than their surviving siblings. They also fatigued more often during feeding (11/42) and had reduced arm and neck tonus (9/42). They were described as longer sleepers than their surviving siblings. During sleep, some SIDS twins, but no surviving twin, were found to be cyanotic at least once or pale (4/42) and were repeatedly covered with abundant sweat (8/42). In the control group of normal twins, the occurrence of most of these characteristics was found with a frequency comparable to that seen in the SIDS infants; the specificity of these characteristics is thus considered doubtful. The mean birth weight and height were significantly greater in the control group, and no control infant had an episode of cyanosis or pallor or repeated episodes of profuse sweating observed during their sleep. It is concluded that, if further research validates the occurrence of night hyperhydrosis in some future SIDS victims, this symptom could be a clinical risk factor.

scholarly journals Preliminary Study on the Cytoarchitecture of the Human Parabrachial/Kölliker-Fuse Complex, with Reference to Sudden Infant Death Syndrome and Sudden Intrauterine Unexplained Death

2004 ◽  
Vol 7 (2) ◽  
pp. 171-179 ◽  
Author(s):  
Anna Maria Lavezzi ◽  
Giulia Ottaviani ◽  
Gianmario Ballabio ◽  
Lino Rossi ◽  
Luigi Matturri
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Animal Species ◽  
Experimental Studies ◽  
Sudden Infant Death ◽  
Parabrachial Nucleus ◽  
Control Group ◽  
Sudden Infant ◽  
Human Beings ◽  
Unexplained Death

The parabrachial/Kölliker-Fuse complex has been defined, in different animal species, to lie in the dorsolateral part of the pontine tegmentum and to be subdivided into three well-defined regions: the medial parabrachial nucleus, the lateral parabrachial nucleus, and the Kölliker-Fuse nucleus. Experimental studies have shown that the parabrachial/Kölliker-Fuse complex is involved in a variety of functional activities and above all plays an important role in respiratory modulation. In human brainstem, the cytoarchitecture and physiology of this complex have not yet been fully characterized. The aim of the present study was to examine fetal and infant human brainstems in order to define the precise morphology of the three nuclei of the parabrachial/Kölliker-Fuse complex, and to determine whether this nervous center shows morphologic alterations in sudden infant death syndrome (SIDS) and in sudden intrauterine unexplained death (SIUD). In serial sections of 31 brain-stems of subjects aged from 32 gestational wk to 10 months of life, we studied, by morphologic and morphometric analyses, the cytoarchitecture and the extension of the three nuclei of the parabrachial/Kölliker-Fuse complex. All the morphometric parameters were very similar in SIUD and SIDS cases to those of the respective control group, as shown by the absence of significant statistical differences between the two fetus and infant groups. We observed that the features of both the lateral and the medial parabrachial nuclei are largely consistent with those reported in experimental studies. In contrast, the Kölliker-Fuse nucleus appears to be more developed in human beings than in other animal species, showing a greater extension and a more complex structure, as well as subdivision into two subnuclei (compactus and dissipatus).

Diaphragm Strength in Near-Miss Sudden Infant Death Syndrome

PEDIATRICS ◽  
1982 ◽  
Vol 69 (6) ◽  
pp. 782-784
Author(s):  
Charles B. Scott ◽  
Bruce G. Nickerson ◽  
Charles W. Sargent ◽  
Paula C. Dennies ◽  
Arnold C. G. Platzker ◽  
...  
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Near Miss ◽  
Diaphragm Muscle ◽  
Control Group ◽  
Sudden Infant ◽  
Transdiaphragmatic Pressure ◽  
Airway Occlusion ◽  
The Mean

Diaphragm muscle strength was measured as maximal transdiaphragmatic pressure during airway occlusion in ten near-miss sudden infant death syndrome infants aged 4.1 ± 0.6 (SE) months post-term, range 2 to 7 months, and ten control infants aged 4.5 ± 0.8 months post-term, range 0.8 to 8 months. In the near-miss sudden infant death syndrome group, the mean maximal transdiaphragmatic pressure was 106 ± 6 cm H2O, range 78 to 132 cm H2O, compared with a mean maximal transdiaphragmatic pressure of 86 ± 4 cm H2O, range 69 to 106 cm H2O, in the control group. Diaphragm strength is normal or increased in near-miss sudden infant death syndrome infants.

On Listening to Parents: The Sudden Infant Death Syndrome Over 25 Years

PEDIATRICS ◽  
1996 ◽  
Vol 97 (6) ◽  
pp. 896-897
Author(s):  
Shirley Tonkin
Keyword(s):  
New Zealand ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Full Employment ◽  
Medical Officer ◽  
Sudden Infant Death ◽  
The United States ◽  
Infant Mortality Rate ◽  
Congenital Defects ◽  
Sudden Infant

I have been watching the sudden infant death syndrome (SIDS) epidemic in New Zealand over 25 years. I've seen it both coming and going. As a medical officer with the government Department of Health, I had access to official statistics from 1960. New Zealand has a small, circumscribed, stable population, a good universal public health system, a good standard of infant health, and almost full employment. However, in 1970, because New Zealand had a high postneonatal infant mortality rate in comparison with other countries such as the United States, I decided to home visit each family in Auckland (population 500 000) where an infant's death had occurred. I expected to learn of such deaths from hospital records, and although I had learned that there were approximately 80 such deaths in Auckland annually, the hospital could supply me with the names of only 10. This lack of deaths occurring in hospital explains why pediatricians were unaware of the situation. "The coroner may know of some deaths that have happened in people's homes," I was told. The coroner gave me a long list. In that year over 70 babies had died unexpectedly in their own homes, unattended by any medical practitioner. I checked the death certificates. Twenty of these home deaths were inevitable from severe congenital defects, 25 had died of unrecognized infections, but the other 25 had not been sick. They had been well cared for. They had simply been found dead after having been put down for sleep in the usual manner.

Oculocardiac Reflex in Near Miss for Sudden Infant Death Syndrome Infants

PEDIATRICS ◽  
1983 ◽  
Vol 71 (1) ◽  
pp. 49-52 ◽  
Author(s):  
André Kahn ◽  
Jalil Riazi ◽  
Denise Blum
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Near Miss ◽  
Cardiac Response ◽  
Control Group ◽  
Sudden Infant ◽  
First Year ◽  
First Year Of Life

To gain insight into the role of the vagus nerve in sudden infant death syndrome (SIDS), 180 infants ranging in age from 1 to 66 weeks were examined with respect to cardiac response to ocular compression. There were 35 near-miss infants, 76 normal siblings of SIDS victims, and 69 normal control infants. Asystoles within the control group ranged from 0.3 to 1.8 seconds. Ten of 35 (28%) near-miss infants and 10/76 (13%) siblings had asystoles >2.0 seconds when first tested. When statistically compared, the near-miss infants were significantly different from both the control infants and the siblings (Kruskal-Wallis procedure: P < .01, and P < .05, respectively). It is concluded that in the first year of life a significant number of near-miss infants have an exaggerated cardiac response to ocular compression. Furthermore, the presence of prolonged asystoles in certain siblings indicates that vagal hypersensitivity, as manifested by ocular compression, may be, in part, hereditary.

scholarly journals Substantia Nigra Abnormalities Provide New Insight on the Neural Mechanisms Underlying the Sleep-Arousal Phase Dysfunctions in Sudden Infant Death Syndrome

ASN NEURO ◽  
2020 ◽  
Vol 12 ◽  
pp. 175909142096269 ◽  
Author(s):  
Anna M. Lavezzi ◽  
Riffat Mehboob ◽  
Graziella Alfonsi ◽  
Stefano Ferrero
Keyword(s):  
Substantia Nigra ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Maternal Smoking ◽  
Great Part ◽  
Pathological Finding ◽  
Sudden Infant Death ◽  
Control Group ◽  
Sudden Infant ◽  
Sleep Arousal

The purpose of this study was to research possible developmental alterations of the substantia nigra (SN) in sudden infant death syndrome (SIDS), a syndrome frequently attributed to arousal failure from sleep. Brain stems of 46 victims of sudden infant death, aged from 1 to about 7 months (4 to 30 postnatal weeks), were investigated. Twenty-six of these cases were diagnosed as SIDS, due to the lack of any pathological finding, while the remaining 20 cases in which the cause of death was determined at autopsy served as controls. Maternal smoking was reported in 77% of SIDS and 10% of controls. Histopathological examination of the SN was done on 5-µm-thick sections of caudal midbrain stained with both hematoxylin-eosin and Klüver-Barrera. Densitometry, immunohistochemistry and histochemistry were applied to highlight the neuronal concentration, the tyrosine hydroxylase (TH) expression, and the presence of neuromelanin (NM) in this structure. Hypoplasia of the pars compacta portion of the SN was observed in 69% of SIDS but never in controls; TH expression was significantly higher in controls than in SIDS; and NM was observed only in 4 infants of the control group but not in SIDS. A significant correlation was found between SIDS, hypoplasia/low neuronal density, low TH expression in the pars compacta, and maternal smoking. Because the SN pars compacta, being the major dopamine brain center, controls many functions, including the sleep-arousal phase, its alterations, especially concurrently with smoking exposure, may contribute to explain the pathogenesis of SIDS that occur in the great part of cases at awakening from sleep.

Polysomnographic Studies of Infants Who Subsequently Died of Sudden Infant Death Syndrome

PEDIATRICS ◽  
1988 ◽  
Vol 82 (5) ◽  
pp. 721-727
Author(s):  
A. Kahn ◽  
D. Blum ◽  
E. Rebuftat ◽  
M. Sottiaux ◽  
J. Levitt ◽  
...  
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Indirect Evidence ◽  
Sudden Infant Death ◽  
Control Group ◽  
Sudden Infant ◽  
Peripheral Chemoreceptor ◽  
Code Number ◽  
The Future ◽  
Central Apneas

The polygraphic findings from 11 future victims of sudden infant death syndrome (SIDS) are reported and compared with those of matched pairs of control infants. The recordings had been done to alleviate parental anxiety about sleep apnea. Four infants had siblings who were victims of SIDS. Two infants were studied 3.5 to 9.5 weeks before their deaths because of an unexplained apparent life-threatening event that had occurred during sleep. For each victim of SIDS, two control infants were selected from the 2,000 infants who had been tested in the same hospitals. They were matched for sex, gestational age, postnatal age, and weight at birth with the SIDS victims. Their polygraphic recordings had been performed within similar conditions. Each record was allocated a random code number and was analyzed without knowledge of the patient's identity by two independent scorers. Most sleep and cardiorespiratory variables studied did not differentiate SIDS victims from control infants. Only four variables significantly characterized the future SIDS victims: the maximal duration of central apneas, the number of sighs followed by a central apnea, the presence of obstructive apneas, and the presence of mixed apneas. Central apneas were longer during all sleep states in the SIDS victims compared with their matched controls, but none exceeded 14 seconds. Sighs immediately followed by an apnea were significantly less frequent in the future SIDS group. Obstructive and mixed sleep apneas were seen in eight of 11 SIDS victims and in only three of 22 control infants. They were significantly more frequent (total number of episodes: 89 in the SIDS group and three in the control group) and lasted longer in the SIDS victims than in the control group. The present data thus confirm some previous reports of an increase in obstructed breathing in infants who eventually die of SIDS. The observation of a reduced number of sighs followed by an apnea in this group raises the possibility of a lower peripheral chemoreceptor response in some of these infants. Although these observations do not establish risk predictors for infants who eventually become victims of SIDS, they add further indirect evidence for a possible sleep-related impairment of respiratory controls in some of these infants.

scholarly journals Sudden infant death syndrome: deletions of glutathione-S-transferase genes M1 and T1 and tobacco smoke exposure

2021 ◽  
Author(s):  
Anthea Mawick ◽  
Heidi Pfeiffer ◽  
Marielle Vennemann
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Tobacco Smoke ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Control Group ◽  
Sudden Infant ◽  
Gene Deletions ◽  
Group A

AbstractIn developed countries, sudden infant death syndrome (SIDS) is the leading cause of death in infants in their first year of life. The risk of SIDS is increased if parents smoked during pregnancy and in presence of the child. Glutathione S-transferases (GSTs) catalyse the conjugation of glutathione with electrophilic compounds and toxins, making them less reactive and easier to excrete. As a gene dose effect was observed for GSTM1 and GSTT1, the aim of this study was to investigate whether there is a connection between homozygous or heterozygous gene deletions of GSTM1 or GSTT1 and the occurrence of SIDS. We found that heterozygous deletion of GSTM1 occurred significantly more frequently in the SIDS case group compared to the control group. A homozygous deletion of GSMT1 was slightly more frequently in the control group. A homozygous gene deletion of GSTT1 showed no significant difference between the SIDS group and the control group. We also found that in the SIDS group, the number of victims that were exposed to cigarette smoke was significantly higher than the number of victims without cigarette smoke exposure and that the mean lifetime of children whose mothers smoked was shorter in comparison with non-smoking mothers. In SIDS cases with homozygous gene deletions of GSTM1, the median life span of children with tobacco smoke exposure was 60 days shorter than without smoke exposure. In conclusion, the absence of these two genes is not the only trigger for SIDS but could be a critical aspect of SIDS aetiology, particularly in SIDS cases with smoking parents.

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