ライフサイエンスコーパス: acamprosate

コーパス検索結果 (１語後でソート)

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1 s) would have a better treatment response to acamprosate.

2 onclude that calcium is the active moiety of acamprosate.

3 in agreement with the established profile of acamprosate.

4 Most assessed acamprosate (27 studies, n = 7519), naltrexone (53 studi

5 nt with 16 weeks of naltrexone (100 mg/d) or acamprosate (3 g/d), both, and/or both placebos, with or

6 ment for 16 weeks with naltrexone, 100 mg/d, acamprosate, 3 g/d, or both, and/or placebo; 4 groups re

7 their drinking behavior was not affected by acamprosate, an FDA-approved drug for the treatment of a

8 o significant differences were found between acamprosate and naltrexone for controlling alcohol consu

9 The PREDICT study tested acamprosate and naltrexone vs placebo in 426 randomly as

10 comparing combinations of medications (i.e., acamprosate and naltrexone) and behavioral interventions

11 Both acamprosate and oral naltrexone were associated with red

12 cent reports documenting that naltrexone and acamprosate are more effective than placebo in the treat

13 Along with a few other medications, acamprosate (Campral-calcium-bis (N-acetylhomotaurinate)

14 ly inactive molecule and that the effects of acamprosate described in more than 450 published origina

15 In particular, acamprosate does not interact with NMDA receptors or met

16 Here we show that acamprosate does not interact with proposed glutamate re

17 Acamprosate (grade A, from large-scale studies in Europe

18 Intervention Four weeks of acamprosate (initial oral loading followed by 1998 mg da

19 here is accumulated evidence suggesting that acamprosate interferes with the glutamate system, the mo

20 Acamprosate is approved for the treatment of alcoholism,

21 Surprisingly, calcium salts produce acamprosate-like effects in all three animal models.

22 s to the pathogenesis of alcoholism and that acamprosate may exert its actions by intervening in this

23 ly; risk was not significantly increased for acamprosate or topiramate.

24 h fared better on drinking outcomes, whereas acamprosate showed no evidence of efficacy, with or with

25 Acamprosate showed no significant effect on drinking vs

26 atient), and MM plus combined naltrexone and acamprosate therapy ($1003 per patient).

27 ntral glutamate are reduced across time when acamprosate therapy is initiated at the onset of alcohol

28 ocusing only on effectiveness, MM-naltrexone-acamprosate therapy is not significantly better than MM-

29 g cost and cost-effectiveness, MM-naltrexone-acamprosate therapy may be a better choice, depending on

30 e glutamate to creatine ratio across time by acamprosate (time x treatment interaction: F(,) = 13.5,

31 Meta-analyses of trials comparing acamprosate to naltrexone found no statistically signifi

32 tinal symptoms were significantly greater in acamprosate-treated individuals, in agreement with the e

33 The models predicted acamprosate treatment response with a mean sensitivity a

34 ation and serum metabolite levels to predict acamprosate treatment response.

35 ients with high plasma calcium levels due to acamprosate treatment showed better primary efficacy par

36 e (no alcohol consumption during 3 months of acamprosate treatment) while nonresponse was defined as

37 he NNT to prevent return to any drinking for acamprosate was 12 (95% CI, 8 to 26; risk difference [RD

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