2011年11月16日水曜日

脳卒中後のBMIと予後:obesity paradox

脳卒中後のBMIと予後:obesity paradoxに関する研究を紹介します。

Wolfram Doehner, et al: The association of body mass index and presence of cachexia with survival and disability after stroke: data from 1,521 hospitalised patients with 30 months follow-up

急性期脳卒中とTIAの患者1521人を対象に、BMIで5群(悪液質18.5未満、標準18.5-25、過体重25-30、軽度肥満30-35、中等度以上肥満35以上)に分類しました。アウトカムは30か月後の死亡、脳卒中再発、施設生活、ADL介助(Barthel index 60点未満など)です。

結果ですが、BMIが低ければ低いほど、死亡率、死亡率+脳卒中再発率、施設生活、ADL介助が高かったです。BMIは多変量解析でも独立した予後因子でした。つまり、急性期脳卒中とTIAの患者においてもobesity paradoxが成立するという結論です。

この研究ではBMI18.5未満を悪液質と呼んでいますが、BMI18.5未満はあくまでるいそうであって、悪液質ではありません。Evansなどの悪液質の診断基準も使用していませんので、この点には注意が必要です。

るいそう患者で脳卒中の予後が悪いことは理解できますが、BMI35以上の群でもっとも予後がよい点に関しては日本では当てはまらないのではないかと感じてしまいます。BMIが25以上で予後が悪いという報告もありますので。ただ、この著者らはStrokeにも脳卒中のObesity Paradoxに関して投稿していますので無視はできません。

Background: Overweight and obesity are established risk factors for cardiovascular disease including stroke. In patients with established cardiovascular disease, increasing evidence suggests an inverse relationship between body mass index (BMI) on outcome, which has been termed obesity paradox. The impact of body weight in general and presence of cachexia specifically on outcome after stroke is not well established. We aimed to investigate the relationship between BMI and mortality as well as functional outcome in patients after stroke.

Patients and methods: We analysed data from of the Telemedical Project for Integrative Stroke Care project. In 1,521 patients suffering from an acute stroke or TIA data on BMI at time of hospital admission and on subsequent outcomes were available. Patients were grouped by BMI as cachectic (BMI ≤18.5), reference group (BMI >18.5 to 25) overweight (BMI >25 to 30), mild obesity (BMI >30 to 35) and advanced obesity (BMI >35, all kg/m2). Outcome measures after 30 months included all-cause mortality, recurrent stroke, need for institutional care, and dependency (institutionalisation, Barthel index <60 or modified Rankin score >3).

Results: During 30 months of follow-up, 401 patients (27%) died. Mortality rates at 30 months were 61%, 33%, 24%, 18%, and 13% in the BMI subgroups ≤18.5,>18.5–25, >25–30, >30–35, and >35 kg/m2, respectively (P < 0.001). Rates for the combined endpoint of death or recurrent stroke were 64%, 40%, 31%, 22%, 18%, respectively (p < 0.001). Also, institutional care and dependency followed the same stepwise pattern with lowest rates in obese subjects (all p < 0.001). BMI was a significant inverse predictor for poor outcome after multivariable adjustment for age, sex, co-morbidity, living in partnership, and stroke severity: Compared to BMI 18-5-25 (HR 1.0, i.e., reference group) risk for death or recurrent stroke was higher in patients with BMI < 18.5 (HR 2.74, 95%CI 1.23–6.03), but lower in patients with overweight (HR 0.79; 95%CI 0.60–1.03, p = 0.08), mild obesity (HR 0.56, 95%CI 0.37–0.86; p < 0.01) and advanced obesity (HR 0.51, 95%CI 0.27–0.97; p < 0.05). When patients’ obesity (BMI > 30) are considered as reference group, risk for death or recurrent stroke more than five times increased in patients with BMI < 18.5, and two times increased in patients with BMI 18.5–25. Similarly, the risk for death or institutional care or and dependency was highest in patients with cachexia (BMI < 18.5), and decreased stepwise with increasing BMI being lowest in obese and very obese patients.

Conclusion: Patients hospitalised for stroke or TIA with low BMI (BMI < 25) and particularly with cachexia show increased subsequent morbidity and mortality. In contrast, obese patients have better outcome for mortality or recurrent stroke, need for institutional care, and dependency than patients with normal BMI. A better outcome after stroke in obese patients is in contrast to data from primary prevention studies, but concurs with observations of an obesity paradox in other cardiovascular diseases including heart failure and diabetes mellitus. Treatment strategies to increase or maintain body weight in patients with stroke or TIA should be tested.

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