Helicobacter pylori Antigen in Stool Is Associated With SIDS and Sudden Infant Deaths due to Infectious Disease

Stray-Pedersen, Arne; Vege, Åshild; Rognum, Torleiv O.

doi:10.1203/pdr.0b013e31818095f7

Cited by 18 publications

(10 citation statements)

References 37 publications

(45 reference statements)

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“…Of special interest with regard to the findings in the present study is that Helicobacter pylori antigene in stool is reported to be associated with SIDS [29]. The study suggests that H. pylori infection represents a biomarker of increased vulnerability to infections and an increased risk of sudden death before 5 months of age.…”

Section: Discussionsupporting

confidence: 49%

IL-1 gene cluster polymorphisms and sudden infant death syndrome

et al. 2010

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Section: Discussionsupporting

confidence: 49%

IL-1 gene cluster polymorphisms and sudden infant death syndrome

et al. 2010

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“…In spite of absence of fatal inflammatory reaction, a significant proportion of SIDS victims have levels of IL-6 in the cerebrospinal fluid in the same range as infants with fatal infection (5,8). Furthermore, SIDS cases have significantly more frequent Helicobacter pylori in their stools than controls (9), and the prevalence of S. aureus in nasopharyngeal flora is significantly higher in SIDS cases compared to age-matched controls (4). These observations are interesting as Von Bernuth et al (10), have reported nine infants and children with autosomal recessive MyD88 deficiency that suffered life-threatening often recurrent bacterial infection.…”

Section: Discussionmentioning

confidence: 99%

Altered gene expression and possible immunodeficiency in cases of sudden infant death syndrome

et al. 2016

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Background: A large number of studies have tried to uncover a genetic predisposition for sudden infant death syndrome (SIDS), but there is still uncertainty concerning the pathogenesis of these deaths. The purpose of this study was to investigate mRNA gene expression in SIDS cases and controls, in order to uncover genes that are differentially expressed in the two groups. Methods: Tissue from brain, heart, and liver from 15 SIDS cases and 15 controls were included in the study, and mRNA expression was determined using the Illumina whole genome gene expression DASL HT assay. results: Seventeen genes showed significantly altered expression compared to controls, after correction for multiple testing. Three genes involved in the immune system were of particular interest, including the downregulation of MyD88 in tissue from SIDS brains, as well as the downregulation of the genes encoding CCL3 and UNC13 in the liver. conclusion: These findings indicate that there is an altered expression of genes involved in the inflammatory process in a proportion of SIDS cases, which further strengthen the hypothesis that impaired immune response play a role in this syndrome.

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“…Stray‐Pedersen et al. (21) found evidence that Helicobacter pylori infection in infancy may be involved as a triggering pathogen for sudden death during the first 5 months after birth.…”

Section: Discussionmentioning

confidence: 99%

“…By in situ hybridization, An et al (20) found evidence to suggest that a virus infection may be involved in the genesis of sudden infant death syndrome, at least when the death occurs between the ages 3 weeks and 4 months. Stray-Pedersen et al (21) found evidence that Helicobacter pylori infection in infancy may be involved as a triggering pathogen for sudden death during the first 5 months after birth.…”

Section: Differences Between the Counts Of Cd15mentioning

confidence: 99%

Obstruction of the lung capillaries by blood platelet aggregates and leucocytes in sudden infant death syndrome

Hanssen

Jørgensen

2010

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Altogether 34 cases of sudden infant death were studied postmortem with particular emphasis on the pathological changes in the lungs. Light microscopy, including application of immunohistochemical methods, and transmission electron microscopy were used for the identification of blood platelets and white blood cell types in alveolar capillaries. The main findings were platelet aggregates and a varying number of neutrophil polymorphonuclear granulocytes in the lung capillaries, mixed with a smaller number of lymphocytes. The findings may be interpreted as an early sign of inflammation with capillary thrombosis, resulting in ischaemia, i.e. arrest of flow. In 21% of the cases, inflammatory cells had also expanded focally into alveolar spaces, creating the picture of localized areas of bronchopneumonia. An infant dying suddenly of a traumatic head injury served as a control. Neither platelets nor leucocytes were observed in the alveolar capillaries of this infant. In conclusion, in lungs from cases of sudden infant death syndrome, the alveolar capillaries are obstructed by platelet aggregates and leucocytes, interpreted as signs of an initial stage of lung inflammation with ischaemia.

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Helicobacter pylori Antigen in Stool Is Associated With SIDS and Sudden Infant Deaths due to Infectious Disease

Cited by 18 publications

References 37 publications

IL-1 gene cluster polymorphisms and sudden infant death syndrome

IL-1 gene cluster polymorphisms and sudden infant death syndrome

Altered gene expression and possible immunodeficiency in cases of sudden infant death syndrome

Obstruction of the lung capillaries by blood platelet aggregates and leucocytes in sudden infant death syndrome

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