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1 the voluntary withdrawal of fenfluramine and dexfenfluramine.
2 as pulmonary vascular effects reminiscent of dexfenfluramine.
3 rexic agents: fenfluramine and its d-isomer, dexfenfluramine.
4 ollowing anorexigen treatment were uncommon (dexfenfluramine, 2.3%; phentermine/fenfluramine, 2.4%, a
5 ntrol analysis of 6532 subjects who received dexfenfluramine, 2371 who received fenfluramine, and 862
6 patients), investigational sustained-release dexfenfluramine (352 patients), or placebo (354 patients
7 women) had been randomly assigned to receive dexfenfluramine (366 patients), investigational sustaine
8 different in treated and untreated subjects (dexfenfluramine, 9.0%; phentermine/fenfluramine, 4.0%; a
9      Fluoxetine, sibutramine, sertraline and dexfenfluramine all produced a significant reduction in
10 dence interval, 2.9 to 56.4) with the use of dexfenfluramine alone, 24.5 (5.9 to 102.2) with the use
11           We examined patients who had taken dexfenfluramine alone, dexfenfluramine and phentermine,
12 ients who took fenfluramine and phentermine, dexfenfluramine alone, or dexfenfluramine and phentermin
13  disorders in persons taking fenfluramine or dexfenfluramine alone, particularly for more than three
14 athic valvular disorders, 5 after the use of dexfenfluramine and 6 after the use of fenfluramine.
15 specific serotonin releaser-uptake inhibitor dexfenfluramine and alterations in the expression of sev
16  agents and updates the evidence associating dexfenfluramine and fenfluramine with valvulopathy.
17 ntitate brain levels of the fluorinated drug dexfenfluramine and its active metabolite dex-norfenflur
18                                 In contrast, dexfenfluramine and MDMA depleted brain serotonin and pr
19                                              Dexfenfluramine and MDMA, on the other hand, markedly de
20 e and phentermine, dexfenfluramine alone, or dexfenfluramine and phentermine had a significantly high
21 e alone, 24.5 (5.9 to 102.2) with the use of dexfenfluramine and phentermine, and 26.3 (7.9 to 87.1)
22 atients who had taken dexfenfluramine alone, dexfenfluramine and phentermine, or fenfluramine and phe
23                Our data indicate that use of dexfenfluramine and phentermine/fenfluramine is associat
24 s, 1473 were eligible (479 and 455 had taken dexfenfluramine and phentermine/fenfluramine, respective
25 and 13 to 26 months after discontinuation of dexfenfluramine and phentermine/fenfluramine.
26 trial comparing dexfenfluramine with regular dexfenfluramine and placebo.
27 en the dietary suppressants fenfluramine and dexfenfluramine and valvular heart disease was first des
28          Appetite suppressants fenfluramine, dexfenfluramine, and phentermine have been used alone or
29    Anorexigens such as aminorex fumarate and dexfenfluramine are associated with the development of s
30                                        Using dexfenfluramine as unconditional stimulus (US), the auth
31 veloped flavor avoidance with either LiCl or dexfenfluramine as US.
32                      Patients received 15 mg dexfenfluramine BID for 90 days.
33 Valve regurgitation has been associated with dexfenfluramine, but its prevalence and severity are unc
34                                              Dexfenfluramine causes reversible membrane depolarizatio
35 itral regurgitation in patients treated with dexfenfluramine compared with placebo.
36           Measured brain dexfenfluramine/nor-dexfenfluramine concentrations were well below levels pr
37 n, with an investigational sustained-release dexfenfluramine (Dexfen SR), or with a placebo, with ech
38 hree to five months after discontinuation of dexfenfluramine (Dexfen) therapy.
39 he brain concentration of the anorectic drug dexfenfluramine (DF) in human subjects receiving clinica
40     The acute appetite suppressant effect of dexfenfluramine (DF) in rats, which may depend upon its
41 The first agent is the serotonergic agonist, dexfenfluramine (DFEN) and the second is the pancreatic
42  of fluoxetine, sibutramine, sertraline, and dexfenfluramine for 4 days on brain serotonergic nerve t
43  among those who took either fenfluramine or dexfenfluramine for less than four months (95 percent co
44 s phentermine (fen-phen) and the approval of dexfenfluramine gave rise to widespread, long-term use o
45 exigen-treated patients and were 8.9% in the dexfenfluramine group (RR, 2.18; 95% confidence interval
46 .8 percent of those in the sustained-release dexfenfluramine group, 5.4 percent of those in the two a
47 curred in 5.0 percent of the patients in the dexfenfluramine group, 5.8 percent of those in the susta
48 0 (3.3) months (range, 1-18.4 months) in the dexfenfluramine group, and 11.9 (10.4) months (range, 1.
49 ased aortic regurgitation (P = 0.003 for the dexfenfluramine group, P = 0.02 for the sustained-releas
50 up, a greater proportion of patients in both dexfenfluramine groups had decreased aortic regurgitatio
51 gurgitation were considered and when the two dexfenfluramine groups were combined, there was a higher
52 p to 30% to 38% of users of fenfluramine and dexfenfluramine had valvular disease, these drugs were w
53                                One of these, dexfenfluramine, has been withdrawn because of fenfluram
54                             Fenfluramine and dexfenfluramine have been demonstrated to damage brain s
55 n important clinical problem, and the use of dexfenfluramine hydrochloride for weight reduction has b
56 rfused rat lung, aminorex, fenfluramine, and dexfenfluramine induce a dose-related increase in perfus
57 e, we found that aminorex, fenfluramine, and dexfenfluramine inhibit potassium current in smooth musc
58 ginine methyl ester, the pressor response to dexfenfluramine is greatly enhanced.
59 reatment with phentermine, fenfluramine, and dexfenfluramine is now becoming clarified with the publi
60  came to be associated with fenfluramine and dexfenfluramine, leading to their eventual withdrawal fr
61 aised that the d-enantiomer of fenfluramine, dexfenfluramine, may also cause this problem.
62                               Measured brain dexfenfluramine/nor-dexfenfluramine concentrations were
63                   The use of fenfluramine or dexfenfluramine, particularly for four months or longer,
64 had decreases; 1 [0.2%] had an increase); 29 dexfenfluramine patients (23 [6.4%] had decreases; 6 [1.
65 o more frequent mild aortic regurgitation in dexfenfluramine patients (6.3% versus 1.6% in controls;
66 gitation) was significantly more frequent in dexfenfluramine patients (7.6% versus 2.1% for controls;
67 subjects meeting the same entry criteria (51 dexfenfluramine patients and 17 controls).
68 he total sample of 412 subjects included 172 dexfenfluramine patients and 172 unexposed controls matc
69  of drug to follow-up echocardiogram for 371 dexfenfluramine patients was 17.5 months (range, 13-26 m
70                                              Dexfenfluramine-related valve regurgitation may regress
71 , the appetite suppressants fenfluramine and dexfenfluramine, the dopamine agonists pergolide and cab
72  or progress 1 year after discontinuation of dexfenfluramine therapy has not been determined.
73                                        After dexfenfluramine therapy is taken for 2 to 3 months and d
74 d, double-blind, placebo-controlled study of dexfenfluramine to include echocardiographic examination
75                                              Dexfenfluramine use is associated with an increase in th
76                                              Dexfenfluramine was approved in the United States for lo
77 itral regurgitation in patients treated with dexfenfluramine was small, and the degree of regurgitati
78                             Fenfluramine and dexfenfluramine were voluntarily withdrawn from the mark
79 late serotonin release and reuptake, such as dexfenfluramine, were withdrawn from sale because of CLH
80 tion by modifying an ongoing trial comparing dexfenfluramine with regular dexfenfluramine and placebo

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