抽菸增加抽搐和ALS風險
作者:Allison Gandey
出處:WebMD醫學新聞
November 25, 2009 — 醫師有新理由鼓勵病患戒菸了!一篇新研究發現,抽菸者發生抽搐的機會是未抽菸者的2倍。另一篇報告指出,抽菸確定是偶發肌萎縮性脊髓側索硬化症(amyotrophic lateral sclerosis,ALS)的風險因素。
布萊根婦女醫院與哈佛醫學院的Barbara Dworetzky醫師等研究者表示,我們觀察發現,相較於未曾抽菸者,目前有抽菸者發生抽搐的風險達2倍,癲癇風險適度增加但不顯著,且與中風無關。
這項研究線上發表於11月18日的Epilepsia雜誌。研究者使用「Nurses' Health Study」的資料評估246名病患,這些研究對象是25-42歲女性,郵寄有關生活型態和醫療史(包括癲癇和抽搐)的問卷給她們。
校正中風、腦腫瘤、高血壓、其他可能的干擾因素之後,研究者發現抽菸和抽搐風險之間的顯著關聯。
【抽菸狀態和抽搐風險】 抽菸狀態
相對風險
95% 信心區間
未曾抽菸
1.00
參考用
以前抽菸
0.98
0.58 – 1.66
現在抽菸
2.60
1.53 – 4.42
以前曾經抽菸和目前有抽菸者,癲癇或復發非引發性抽搐的風險皆略為增加。相對風險為1.46和1.27,但是未達統計上的顯著差異。
另一篇報告中,波士頓Tufts大學、Baystate醫學中心的Carmel Armon醫師指出抽菸和ALS之間的關聯。
Armon醫師在新聞稿中表示,運用實證醫學方法,分辨設計較佳的研究和有限制而無法信賴的研究。設計較佳的研究一致顯示抽菸增加了發生ALS的風險。有些發現認為,抽菸可能與直接誘發此病有關。
【建立ALS的風險因素】
Armon醫師檢視了28篇研究,其中,七篇符合納入規範。在發表於11月17日Neurology期刊的報告中,他指出,只有一篇研究提供等級2的證據,其他的是等級3的證據。這些研究都顯示,抽菸與ALS風險增加有關。等級2的研究顯示,這是一種劑量反應關係,戒菸之後,風險逐年下降。其他提供等級4-5證據的文章,不足以用來提出結論。
Armon醫師表示,確認抽菸是ALS的風險因素有三方面的影響,首要的就是,發現環境與發生ALS的關聯,這在之前未曾被確認過。
Armon醫師表示,抽菸毫無可取之處,戒菸可以減少未來發生ALS的機會,而抽菸引起其他人類疾病的機轉已經被充分瞭解,確認它在發生ALS的角色將有助於確認發生此病的生物過程。
尼古丁是一種興奮性的神經傳導物質,會促進釋放穀氨酸鹽,穀氨酸鹽在癲癇和ALS都有關聯。尼古丁這種刺激物質會發生高血壓和造成失眠,抽菸也會因長期曝露於一氧化碳而引起組織缺氧。
Armon醫師認為,除非有高於等級2的新證據才可能推翻這些結論。
國家健康研究中心與癲癇基金會的研究資金支持抽菸和抽搐之關聯的研究。Armon醫師也接受國家健康研究中心的研究支持。他擔任Neurology的編輯委員,為麻州公衛部門提供諮商服務,提供有關ALS風險因素和因果關係的專家證詞。Armon還接受eMedicine.com更新電子化章節的版稅 。eMedicine出現在Medscape,兩者都屬於WebMD。
Epilepsia.線上發表於2009年11月18日。
Smoking Increases Seizures and Risk for ALS
By Allison Gandey
Medscape Medical News
November 25, 2009 — Physicians have new reasons to encourage patients to quit smoking. A new study has found that smokers are 2 times more likely to have seizures compared with nonsmokers. Another report says the habit may now be considered an established risk factor for sporadic amyotrophic lateral sclerosis (ALS).
"We observed a doubling in the risk of seizures and a modest nonsignificant increase in epilepsy in current compared with never smokers that appeared to be independent of stroke," report the investigators, led by Barbara Dworetzky, MD, from Brigham and Women's Hospital and Harvard Medical School in Boston, Massachusetts.
Their work was published online November 18 in Epilepsia. Investigators used data from the Nurses' Health Study to evaluate 246 patients. The participants were women aged 25 to 42 years who had mailed in questionnaires about their lifestyle and medical history, including epilepsy and seizure activity.
After adjusting for stroke, brain tumor, hypertension, and other potential confounding factors, researchers observed a significant association between smoking and risk for seizure.
Smoking Status and Risk for Seizure
Smoking Status Relative Risk 95% Confidence Interval
Never 1.00 Reference
Past 0.98 0.58 – 1.66
Current 2.60 1.53 – 4.42
The risk for epilepsy or recurrent unprovoked seizures was modestly elevated with both past and current smoking. The relative risk was 1.46 and 1.27, but this was not statistically significant.
In another report, Carmel Armon, MD, from Tufts University, in Boston, and the Baystate Medical Center in Springfield, Massachusetts, outlined the link between smoking and ALS.
"Application of evidence-based methods separates better-designed studies from studies with limitations that may not be relied on," Dr. Armon said in a news release. "The better-designed studies show consistently that smoking increases the risk of developing ALS. Some findings suggest that smoking may be implicated directly in causing the disease," he said.
Established Risk Factor for ALS
Dr. Armon identified 28 studies. Of these, 7 articles met the inclusion criteria. Reporting in the November 17 issue of Neurology, he points out that only 1 study provided class 2 evidence, and another provided class 3 evidence. Both of these studies demonstrated an increased risk for ALS with smoking. The class 2 study showed a dose-response effect and risk decreasing with number of years since quitting smoking. The remaining articles provided class 4 or 5 evidence, which may not be relied on to draw conclusions.
Identifying smoking as an established risk factor for ALS has 3 implications, Dr. Armon said. "First and foremost, the findings provide a link between the environment and the occurrence of ALS, where none had been previously identified with this level of certainty," he noted.
"Since smoking has no redeeming features, avoidance may reduce the occurrence of ALS in the future, and since some of the mechanisms by which smoking causes other diseases in humans are understood fairly well, recognizing its role in the occurrence of ALS may help pinpoint the biological processes that initiate the disease," Dr. Armon said.
Nicotine is an excitatory neurotransmitter that enhances glutamate release. Glutamate plays a role in both epilepsy and ALS. Nicotine is a stimulant that may increase blood pressure and impair sleep. Smoking also causes tissue hypoxia from chronic carbon monoxide exposure.
Dr. Armon suggests that to change these conclusions, new evidence would need to be class 2 or higher.
The study linking smoking and seizures was supported by the National Institutes of Health and a research grant from the Epilepsy Foundation. Dr. Armon also received research support from the National Institutes of Health. He serves on the editorial board of Neurology, serves as a consultant to the Massachusetts Department for Public Health, and has given expert testimony related to risk factors and causation in ALS. Dr. Armon also receives royalties from eMedicine.com for updating electronic chapters. eMedicine appears on Medscape, and both are owned by WebMD.
Epilepsia. Published online November 18, 2009.
Neurology. 2009;73:1693–1698.