Association of sudden infant death syndrome with VEGF and IL-6 gene polymorphisms.

In the UK, Sudden Infant Death Syndrome (SIDS) is a major cause of postperinatal mortality up to the end of the first year of life. Several studies have found an association between cytokine IL-10 genotypes and SIDS. The aim of the present work was to test the hypothesis that SIDS is associated with high producer gene polymorphisms for certain proinflammatory cytokines and with low producer gene polymorphisms of certain antiinflammatory cytokines.

Interleukin 10 genotype as a risk factor for sudden infant death syndrome: determination of IL-10 genotype from wax-embedded postmortem samples.

In a previous study an association was shown between SIDS and an interleukin-10 (IL-10) genotype. That study was carried out on frozen, unfixed tissue samples, but these are difficult to obtain. Fixed samples used for pathological examination are available.

Association of IL-10 genotype with sudden infant death syndrome.

Sudden infant death syndrome (SIDS) is a major cause of infant death of unknown etiology. We propose that SIDS results from a genetically determined imbalance in the production of inflammatory and anti-inflammatory cytokines in response to the infant's microbial flora. We were especially interested to know the relationship between SIDS and genetically determined higher or lower production of IL-10, an anti-inflammatory cytokine.

An association between sudden infant death syndrome (SIDS) and Helicobacter pylori infection.

Background: Helicobacter pylori has recently been detected in the stomach and trachea of cases of sudden infant death syndrome (SIDS) and proposed as a cause of SIDS.

Aims: To establish the incidence of H pylori in the stomach, trachea, and lung of cases of SIDS and controls.

Methods: Stomach, trachea, and lung tissues from 32 cases of SIDS and eight control cases were examined retrospectively.