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zoom RSS セロトニンの欠乏が乳児突然死症候群(SIDS)の原因か

<<   作成日時 : 2010/02/06 19:05   >>

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 新たな研究によると、呼吸や心拍の制御に重要な役割をしている脳内化学物質セロトニンの欠乏が乳児突然死症候群(SIDS)の原因の可能性が出てきた。SIDSで死亡した乳児はセロトニンが低いという。
 SIDSは1才未満乳児の原因不明の突然死であり、仰向けで寝かせるようにというキャンペーンにより米国では減少傾向にあるが、今も2,000人に1人の乳児が死亡している。
 脳内の重要な神経伝達物質であるセロトニンがSIDSの原因として長い間疑われてきた。セロトニンの不足が、乳児が入眠中に酸素低下と二酸化炭素増加に対して反応する方法に影響すると想定されてきた。正常の場合は酸素が不足すると覚醒して酸素を取り込もうとする動きを起こす。しかし、SIDSの乳児は重要な保護システムが上手く働かず覚醒しない。
 セロトニンとそれを作る酵素トリプトファン水酸化酵素(TPH2)を測定したところ、セロトニンレベルが26%低く、TPH2レベルが22%低かった。
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細菌感染による乳幼児突然死症候群(SIDS)
http://kurie.at.webry.info/200809/article_16.html
『おしゃぶり』は乳児突然死を予防する
http://kurie.at.webry.info/200706/article_68.html
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Serotonin May Be Key to Sudden Infant Deaths
Deficiency hampers babies' ability to respond to low oxygen, study suggests
By Serena GordonHealthDay Reporter
http://health.msn.com/kids-health/articlepage.aspx?cp-documentid=100253829

TUESDAY, Feb. 2 (HealthDay News) -- Lack of the brain chemical serotonin may be crucial to sudden infant death syndrome (SIDS), new research finds.

Babies who died of SIDS had significantly lower levels of serotonin -- an important regulator of involuntary functions such as breathing and heart rate -- compared to babies who died of other causes, the study found. This finding may eventually lead to a test that could screen newborns to spot those most vulnerable to SIDS.

"This study is confirming that SIDS is a serotonin problem, and we're getting closer to the fundamental mechanism behind SIDS," said the study's senior author, Dr. Hannah C. Kinney, a neuropathologist at Children's Hospital Boston and a professor of pathology at Harvard Medical School.

"The goal is to develop a test to identify which babies are at risk, and then to find a drug that might be able to help them through the critical period. But these are long-term goals," she said.

Results of the study are published in the Feb. 3 issue of the Journal of the American Medical Association.

SIDS involves the sudden, unexplained death of an infant under one year of age, according to background information in the study. Although the rate of SIDS has decreased in the United States -- largely as a result of a national Back-to-Sleep campaign that encouraged parents to put babies to sleep on their backs one out of every 2,000 American babies is still dying of SIDS, the authors note.

Researchers have long suspected that a lack of serotonin, an important neurotransmitter in the brain, may be a factor in SIDS deaths. Neurotransmitters are chemicals that transmit messages from one brain cell to another. Experts have theorized that a lack of serotonin affects the way a baby responds to a loss of oxygen and a buildup of carbon dioxide while sleeping. In babies with a normally functioning system, the lack of oxygen would cause them to awaken and turn their head to get fresh oxygen.

In babies who die of SIDS, this important protective mechanism is either underdeveloped or lacking, and they don't awaken. That may be one reason why the Back-to-Sleep campaign was so successful in reducing SIDS. By putting babies to sleep on their backs and taking soft, fluffy bedding out of the crib, parents are taking away environmental stressors that may contribute to SIDS, the researchers said.

In the current study, Kinney and her colleagues measured levels of serotonin and trytophan hydroxylase (TPH2) in 35 babies who died from SIDS and in 12 babies who died of other, known causes. TPH2 is an enzyme that helps make serotonin. In the group of babies who had died of other causes, the researchers included infants who had experienced oxygen deprivation near death to rule that factor out as a cause of lower serotonin levels.

They found that serotonin levels were 26 percent lower and TPH2 levels were 22 percent lower in babies who died of SIDS compared to babies who died of other causes.

"This study is getting close to the underlying mechanism," said Dr. Raymond Pitetti, associate director of emergency medicine at Children's Hospital of Pittsburgh.

"The goal would be to develop a screening tests so we can identify someone who might need a monitor or to be more closely watched," he said.

In the meantime, he and Kinney advised parents to continue to put their babies to sleep on their back, to avoid soft bedding, to ensure adequate ventilation in the room where the baby sleeps and maybe even add a ceiling fan to the room. Some research has suggested that putting babies to bed with a pacifier in the mouth may help prevent SIDS, too.

"The most important thing for parents to know is that SIDS is a biological problem. It's a disease process, and right now, there's no way to identify it in advance," said Kinney. That why it's so important to take away any environmental challenges, like soft bedding and sleeping on the stomach, she added.

More information

The American Lung Association has advice on preventing SIDS.
SOURCE: Hannah C. Kinney, M.D., neuropathologist, Children's Hospital Boston, and professor, pathology, Harvard Medical School, Boston, Mass.; Raymond Pitetti, M.D., associate director, emergency medicine, Children's Hospital of Pittsburgh, Penn.; Feb. 3, 2010 Journal of the American Medical Association

Copyright @2010 HealthDay. All Rights Reserved.

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Brainstem Serotonergic Deficiency in Sudden Infant Death Syndrome

Jhodie R. Duncan, PhD; David S. Paterson, PhD; Jill M. Hoffman, BS; David J. Mokler, PhD; Natalia S. Borenstein, MS; Richard A. Belliveau, BA; Henry F. Krous, MD; Elisabeth A. Haas, BA; Christina Stanley, MD; Eugene E. Nattie, MD; Felicia L. Trachtenberg, PhD; Hannah C. Kinney, MD

JAMA. 2010;303(5):430-437.

Context Sudden infant death syndrome (SIDS) is postulated to result from abnormalities in brainstem control of autonomic function and breathing during a critical developmental period. Abnormalities of serotonin (5-hydroxytryptamine [5-HT]) receptor binding in regions of the medulla oblongata involved in this control have been reported in infants dying from SIDS.

Objective To test the hypothesis that 5-HT receptor abnormalities in infants dying from SIDS are associated with decreased tissue levels of 5-HT, its key biosynthetic enzyme (tryptophan hydroxylase [TPH2]), or both.

Design, Setting, and Participants Autopsy study conducted to analyze levels of 5-HT and its metabolite, 5-hydroxyindoleacetic acid (5-HIAA); levels of TPH2; and 5-HT1A receptor binding. The data set was accrued between 2004 and 2008 and consisted of 41 infants dying from SIDS (cases), 7 infants with acute death from known causes (controls), and 5 hospitalized infants with chronic hypoxia-ischemia.

Main Outcome Measures Serotonin and metabolite tissue levels in the raphe' obscurus and paragigantocellularis lateralis (PGCL); TPH2 levels in the raphe' obscurus; and 5-HT1A binding density in 5 medullary nuclei that contain 5-HT neurons and 5 medullary nuclei that receive 5-HT projections.

Results Serotonin levels were 26% lower in SIDS cases (n = 35) compared with age-adjusted controls (n = 5) in the raphe' obscurus (55.4 [95% confidence interval {CI}, 47.2-63.6] vs 75.5 [95% CI, 54.2-96.8] pmol/mg protein, P = .05) and the PGCL (31.4 [95% CI, 23.7-39.0] vs 40.0 [95% CI, 20.1-60.0] pmol/mg protein, P = .04). There was no evidence of excessive 5-HT degradation assessed by 5-HIAA levels, 5-HIAA:5-HT ratio, or both. In the raphe' obscurus, TPH2 levels were 22% lower in the SIDS cases (n = 34) compared with controls (n = 5) (151.2% of standard [95% CI, 137.5%-165.0%] vs 193.9% [95% CI, 158.6%-229.2%], P = .03). 5-HT1A receptor binding was 29% to 55% lower in 3 medullary nuclei that receive 5-HT projections. In 4 nuclei, 3 of which contain 5-HT neurons, there was a decrease with age in 5-HT1A receptor binding in the SIDS cases but no change in the controls (age x diagnosis interaction). The profile of 5-HT and TPH2 abnormalities differed significantly between the SIDS and hospitalized groups (5-HT in the raphe' obscurus: 55.4 [95% CI, 47.2-63.6] vs 85.6 [95% CI, 61.8-109.4] pmol/mg protein, P = .02; 5-HT in the PGCL: 31.4 [95% CI, 23.7-39.0] vs 71.1 [95% CI, 49.0-93.2] pmol/mg protein, P = .002; TPH2 in the raphe' obscurus: 151.2% [95% CI, 137.5%-165.0%] vs 102.6% [95% CI, 58.7%-146.4%], P = .04).

Conclusion Compared with controls, SIDS was associated with lower 5-HT and TPH2 levels, consistent with a disorder of medullary 5-HT deficiency.

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セロトニンの欠乏が乳児突然死症候群(SIDS)の原因か 医師の一分/BIGLOBEウェブリブログ
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