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1 retroviral drugs (zalcitabine, didanosine or stavudine).
2 more convenient (specifically didanosine and stavudine).
3 minotransferase levels among patients taking stavudine.
4 d to 5-fold) to didanosine, zalcitabine, and stavudine.
5 sted of zidovudine plus either didanosine or stavudine.
6 sed resistance to AZT, ddI, zalcitibine, and stavudine.
7  received 0.1, 0.5, 1.0, or 2.0 mg/kg/day of stavudine.
8 stance, the primary candidates for replacing stavudine.
9 , 2',3'-dideoxycytidine, dideoxyinosine, and stavudine.
10 a conformational mimic of the anti-HIV agent stavudine (1, D4T) is described.
11 /day), 3TC (Lamivudine 50 mg/kg/day) or D4T (Stavudine 10 mg/kg/day) for 5 days, and cortices, hippoc
12 aboratory) occurred in 104 (67%) children on stavudine, 103 (65%) on zidovudine, and 105 (64%), on ab
13  occurred more frequently in those receiving stavudine (12% in the stavudine group compared with 4% i
14              K65R was frequently selected by stavudine (15.0%) or tenofovir (27.7%).
15 , 2011, 480 children were randomised: 156 to stavudine, 159 to zidovudine, and 165 to abacavir.
16                      The antiviral effect of stavudine (2', 3'-didehydro-3'-deoxythymidine) against h
17 or ritonavir, 350 mg/m2 2 times per day, and stavudine, 4 mg/kg 2 times per day (n = 97).
18 F and 253 (84%) of 301 in patients receiving stavudine (95% confidence interval, -10.4% to 1.5%), exc
19                                Drugs such as stavudine and didanosine are associated with serious met
20 exhibited low-level cross-resistance to both stavudine and lamivudine in drug susceptibility assays.
21 100 mg twice daily, each in combination with stavudine and lamivudine twice daily, for 48 weeks.
22 ived lopinavir/ritonavir or nelfinavir, plus stavudine and lamivudine, for up to 96 weeks.
23 ir with nelfinavir, each coadministered with stavudine and lamivudine, in 653 antiretroviral therapy-
24 ir versus nelfinavir, each administered with stavudine and lamivudine, in 653 antiretroviral-naive, h
25 reverse-transcriptase inhibitors, especially stavudine and lamivudine, was associated with possible m
26 ween specific drugs and HIV lipohypertrophy, stavudine and zidovudine have been implicated in the dev
27 two daily regimens: 600 mg of zidovudine (or stavudine) and 300 mg of lamivudine, or that regimen wit
28 avir every 8 h with 200 mg nevirapine, 40 mg stavudine, and 150 mg lamivudine, each given twice daily
29 ation [three HAART drugs (3-plex; indinavir, stavudine, and ddI)] at their clinical plasma concentrat
30 nti-HIV nucleoside drugs such as zidovudine, stavudine, and didanosine.
31  a first regimen failure, 0.55); didanosine, stavudine, and efavirenz (hazard ratio, 0.63); or zidovu
32 io for regimen failure, 1.24) or didanosine, stavudine, and efavirenz (hazard ratio, 1.01).
33 ilpivirine, in 27% for tenofovir, in 18% for stavudine, and in 10% for zidovudine.
34         Cross-resistance between zidovudine, stavudine, and lamivudine was studied, using purified re
35 tients were on therapy (lopinavir/ritonavir, stavudine, and lamivudine) with plasma HIV RNA <50 copie
36 e three-drug regimens containing didanosine, stavudine, and nelfinavir (hazard ratio for a first regi
37 ree-drug regimens beginning with didanosine, stavudine, and nelfinavir (hazard ratio for regimen fail
38  for cross-resistance between zidovudine and stavudine, and they suggest a possible effect of zidovud
39 ur previous observations of NRTIs, abacavir, stavudine, and zalcitabine increased HIV-1 mutation freq
40 enofovir, abacavir, lamivudine, zalcitabine, stavudine, and zidovudine.
41 t not efavirenz combined with didanosine and stavudine) appeared to delay the failure of the second r
42 0.61 log(10)copies/mL (4.1 copies/mL) in the stavudine arm (P=.24).
43  stavudine placebo twice daily) (n = 286) or stavudine at standard doses twice daily (plus emtricitab
44 l Treatment Guidelines recommend phasing-out stavudine because of its risk of long-term toxicity.
45 in resistance to zidovudine and >250-fold to stavudine) but not to other nucleoside reverse transcrip
46                     Monotherapy with peroral stavudine capsules or peroral zidovudine capsules.
47  increase at 3 years compared to patients on stavudine-containing regimens (2.1 vs 11.7 mg/dL, P < .0
48 ddC) > didanosine (ddI metabolized to ddA) > stavudine (d4T) >> lamivudine (3TC) > tenofovir (PMPA) >
49                                              Stavudine (d4T) and zidovudine (AZT) are thymidine analo
50 drug substitutions and regimen switches from stavudine (d4T) and zidovudine (AZT) regimens have been
51 e was found to regain sensitivity to AZT and stavudine (D4T) as a consequence of a pharmacologically
52 e safety, tolerance, and pharmacokinetics of stavudine (d4T) in human immunodeficiency virus (HIV)-in
53 ing zidovudine were randomized either to add stavudine (d4T) or didanosine (ddI) to their current reg
54 alcitabine (ddC), didanosine (ddI), 3TC, and stavudine (d4T) were determined, using an enzymatic assa
55                  The NRTIs zidovudine (AZT), stavudine (d4T), didanosine (ddI), and lamivudine (3TC),
56 ZDV)/lamivudine (3TC), ZDV/didanosine (ddI), stavudine (d4T)/3TC, d4T/ddI, and ddI/3TC.
57 rminating 2'-3'-didehydro 3'-deoxythymidine [stavudine (D4T)] and 2'-3'-dideoxyinosine [didanosine (d
58 avir, lopinavir, zidovudine (AZT), abacavir, stavudine, didanosine (ddI), and lamivudine] individuall
59 dine or emtricitabine, abacavir, zidovudine, stavudine, didanosine, and tenofovir and a specific GSS
60 e susceptibilities of PERV RT to lamivudine, stavudine, didanosine, zalcitabine, and zidovudine were
61 idence interval, 1.91-6.20]) or who received stavudine-didanosine combination therapy (odds ratio, 2.
62 lamivudine-nevirapine, stavudine-zidovudine, stavudine-didanosine, stavudine-saquinavir, stavudine-ne
63  of PYFU), stavudine/lamivudine (17.6%), and stavudine/didanosine (5.4%).
64 roviral therapy (ART) (P = .02), duration of stavudine exposure (P < .01), low-density lipoprotein ch
65 prior to combination antiretroviral therapy, stavudine exposure was independently associated with hyp
66 -1 resistance mutations following first-line stavudine failure from 35 publications comprising 1,825
67                                        After stavudine failure in African populations, zidovudine rat
68 sistance patterns associated with first-line stavudine failure.
69  were previously untreated (ART naive) or on stavudine for more than 2 years with viral load less tha
70 rological response < or =50 copies/mL vs the stavudine group (85% vs 76%, P =.005).
71  in the tenofovir DF group compared with the stavudine group (9 [3%] of 299 vs 58 [19%] of 301, P<.00
72 % for the emtricitabine group vs 54% for the stavudine group (P<.001).
73 4% in the emtricitabine group and 12% in the stavudine group (P<.001).
74 tly in those receiving stavudine (12% in the stavudine group compared with 4% in the zidovudine group
75                              Patients in the stavudine group had a greater probability of an adverse
76 he risk for death alone was 26% lower in the stavudine group than in the zidovudine group, but the co
77  cell counts were 30 cells/mm3 higher in the stavudine group than in the zidovudine group; this diffe
78 ion error, 156 children were analysed in the stavudine group, 158 in the zidovudine group, and 164 in
79  in 8 and 2 patients in the tenofovir DF and stavudine groups, respectively (P =.06).
80 vir, compared with 29% of patients receiving stavudine, had undetectable residual viremia (P=.07).
81                  These data demonstrate that stavudine has a substantial and durable antiviral effect
82 s compared with starting with didanosine and stavudine (hazard ratio, 0.68), and significantly delaye
83 05 (64%), on abacavir (p=0.63; zidovudine vs stavudine: hazard ratio [HR] 0.99 [95% CI 0.75-1.29]; ab
84 io [HR] 0.99 [95% CI 0.75-1.29]; abacavir vs stavudine: HR 0.88 [0.67-1.15]).
85 ir and abacavir have replaced zidovudine and stavudine in antiretroviral regimens, thymidine analog r
86 vudine or a regimen including didanosine and stavudine in combination with either nelfinavir or efavi
87 ganization guidelines on the substitution of stavudine in first-line ART in resource-limited settings
88 sition, involving both abdominal obesity and stavudine-induced peripheral lipoatrophy, might contribu
89                                              Stavudine is a promising antiretroviral agent, but its c
90                                              Stavudine is an important agent to consider for trials o
91 arms that included different combinations of stavudine, lamivudine (3TC), nevirapine (Nvp), nelfinavi
92 enz was highly effective and comparable with stavudine, lamivudine, and efavirenz in antiretroviral-n
93                   All patients also received stavudine, lamivudine, and indinavir.
94 IV-1) group O-infected patients treated with stavudine, lamivudine, and indinavir.
95    For patients on the first-line regimen of stavudine, lamivudine, and nevirapine the benefits of vi
96 th the WHO-recommended first-line regimen of stavudine, lamivudine, and nevirapine to second-line ant
97 hat significantly more children who received stavudine, lamivudine, nevirapine, and nelfinavir had pl
98 the initiation of therapy and treatment with stavudine, lamivudine, nevirapine, and nelfinavir were a
99 binations: lamivudine-zidovudine, lamivudine-stavudine, lamivudine-saquinavir, lamivudine-nevirapine,
100 erase domain were associated with failure of stavudine-lamivudine-nevirapine (d4T/3TC/NVP; P < .01),
101 ed were zidovudine/lamivudine (66% of PYFU), stavudine/lamivudine (17.6%), and stavudine/didanosine (
102 er 12 months in HIV-positive adults starting stavudine/lamivudine/nevirapine in Malawi, using Sanger,
103  to receive either tenofovir DF (n = 299) or stavudine (n = 303), with placebo, in combination with l
104 ther tenofovir disoproxil fumarate (n=55) or stavudine (n=45), by use of an HIV RNA assay with a limi
105 for tenofovir DF [n = 170] vs +134 mg/dL for stavudine [n = 162], P<.001), total cholesterol (+30 mg/
106 the four-drug regimen containing didanosine, stavudine, nelfinavir, and efavirenz and the groups that
107  stavudine-didanosine, stavudine-saquinavir, stavudine-nevirapine, lamivudine-zidovudine-saquinavir,
108 ith TAMs to lamivudine and abacavir, but not stavudine or didanosine.
109 ir in combination with either didanosine and stavudine or zidovudine and lamivudine with therapy invo
110  ART-naive individuals to receive didanosine-stavudine or zidovudine-lamivudine, combined with efavir
111 uggest an additional reason for accelerating stavudine phase out.
112 her 200 mg of emtricitabine once daily (plus stavudine placebo twice daily) (n = 286) or stavudine at
113                     Efavirenz (600 mg/d) and stavudine plus lamivudine were administered in addition
114 o women with HIV-1 infection who were taking stavudine presented with lactic acidosis and elevated le
115                           Patients receiving stavudine reached clinical end points at a rate of 26 pe
116 rial dysfunction among children who received stavudine regardless of exposure to other medications (o
117         There are two mutational pathways of stavudine resistance with different implications for zid
118  stavudine-zidovudine, stavudine-didanosine, stavudine-saquinavir, stavudine-nevirapine, lamivudine-z
119 zidovudine-saquinavir, lamivudine-zidovudine-stavudine, stavudine-zidovudine-nevirapine, lamivudine-z
120 ant to the nucleoside analogs lamivudine and stavudine, suggesting that mutations conferring resistan
121 susceptibility to group 1 drugs (zidovudine, stavudine, tenofovir, and adefovir) increased when M184V
122            Here, handling of HIV antivirals (stavudine, tenofovir, lamivudine, acyclovir, and zidovud
123 tase inhibitor (NRTI) backbones (zidovudine, stavudine, tenofovir, or abacavir, plus lamivudine or em
124 udine treatment; these patients could resume stavudine therapy at a lower dose.
125                               The benefit of stavudine therapy was seen in all CD4+ cell strata (< or
126 in many patients (63%) after interruption of stavudine treatment; these patients could resume stavudi
127 ed inhibition by zidovudine triphosphate and stavudine triphosphate and, to a lesser extent, lamivudi
128                                              Stavudine use was associated with lower EF and higher TF
129                 Resistance to lamivudine and stavudine was also significantly higher in nelfinavir-tr
130                                              Stavudine was well tolerated and delayed progression of
131     Exposure to lamivudine and to lamivudine-stavudine were also associated with an increased risk of
132 , and tolerability compared with twice-daily stavudine when used with once-daily didanosine and efavi
133 ial resistance to AZT, ddI, zalcitibine, and stavudine, whereas a combination of four mutations confe
134 and three-drug combinations of lamivudine or stavudine with other antiretroviral drugs were evaluated
135 (80%) and 95 (81%) ART-naive children in the stavudine, zidovudine, and abacavir groups, respectively
136                          We aimed to compare stavudine, zidovudine, or abacavir as dual or triple fix
137                  The NRTIs were lamivudine + stavudine, zidovudine, or tenofovir.
138 ee-drug combinations, but the combination of stavudine-zidovudine was antagonistic.
139 amivudine-saquinavir, lamivudine-nevirapine, stavudine-zidovudine, stavudine-didanosine, stavudine-sa
140 saquinavir, lamivudine-zidovudine-stavudine, stavudine-zidovudine-nevirapine, lamivudine-zidovudine-n
141 apine, lamivudine-zidovudine-nevirapine, and stavudine-zidovudine-saquinavir.
142               The main ART regimens included stavudine/zidovudine plus lamivudine plus nevirapine/efa

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