ICAAC Updates
Videx Bioequivalence
HCV/HIV Co-Infection:
ALT & Biopsy
Methadone &
Amprenavir
Interrupting Therapy
while on NNRTIs
Videx Bioequivalence
Abstract # 1663 &
1664:
New
Formulation of Videx.
These
two posters dealt with the bioequivalence studies of enterically coated Videx. Videx
currently is co-formulated with an antacid because Videx is unstable in the
presence of stomach acid. This has
made Videx more challenging to take and adhere to then the other available
nucleosides. Bristol Myers Squibb (BMS), the makers of Videx have for
sometime been attempting to improve the delivery mechanism for this drug.
They compared an enterically coated tablet that did not dissolve in the
stomach but rather in the small intestine to an encapsulated beadlet formulation
of Videx. The encapsulated beadlet
formulation of Videx more rapidly dissolved and entered the systems of the
participants thus that formulation was chosen for further development.
When this beadlet formulation of Videx was compared with the currently
available antacid tablets the AUC was similar.
Authors concluded: VidexÆ EC is equivalent to
the chewable tablet in extent of exposure, but the formulations differ in rate
of absorption. Dissolution of the coat was rapid once the BEADS emptied from the
stomach. The performance of VidexÆ EC, relative to the tablet, is the same in
healthy and HIV-infected subjects.Commentary:
Patients who are unable to tolerate the currently available form of
Videx can ask their health care provider to contact the expanded access program
for the beadlet formulation (877) 418-3889.
In order to qualify patients must need Videx to construct a viable
antiretroviral regimen and be intolerant to the currently available formulation.
The FDA is expected within weeks to rule on the approval of this beadlet
formulation.
HCV/HIC
Co-Infection: ALT normal but 8/10 Persons had Fibrosis
Abstract
# 175:
HCV and Liver Biopsies.
In yet another of the now many examples of why ALT is not an adequate
marker for determining extent of liver damage, Hoffman-Terry and colleagues
performed liver biopsies on 24 HIV co-infected patients.
14 of the 24 had elevated ALTís. On
biopsy, 14 out of 14 with elevated ALT showed moderate to severe fibrosis and 8
out of the 10 without elevated ALT also showed fibrosis.
2/8 had severe inflammation +/- fibrosis. Author concluded: While our study population was not large enough to achieve statistical
significance, biopsy proven inflammation/fibrosis was evident in all patients
with abnormal ALTs but also 8/10 of those with normal ALTs. Once again
directing patients and clinicians to suggest liver biopsy for everyone who is
co-infected with HIV and HCV. In
their conclusions the authors made an interesting observation among this small
number of patients. They noted that
those who did not have elevated ALTís were those who had lower CD4ís.
They stated that this might be due to a decrease in immune activity
against HCV leading to less hepatocyte destruction and thus less release of ALT
into the bloodstream. This will have to be confirmed in larger studies but it worth
noting. Link to detailed NATAP web site report:
http://www.natap.org/sept2000/ICAAC/ICAAC_rpt_1_hcv_liver_enzyme_test_alt91900.htm
Methadone
& Amprenavir
Abstract
# 1649: Amprenavir
& Methadone interactions (Hendrix, Johns Hopkins Univ).
17 patients took part in an observational study to examine the effect of
Amprenavir on Methadone levels in patients who were taking Methadone.
There was a 13% reduction in the active enantiomer of Methadone by the
Amprenavir. However no patient
experienced symptoms of methadone withdrawal.
Commentary: This is yet another study showing a decrease in methadone
levels by a protease inhibitor. Previous
studies of nelfinavir and saquinavir have showed even greater reductions with
those agents. Still none of the
proteases, in my clinical experience, lead to patients experiencing clinically
significant opioid withdrawal. The
opioid withdrawal is still relegated to Nevirapine and Efavirenz.
Reports
on individual response to PI-methadone experiences vary. I have heard for some
individuals there are no withdrwal symptoms while for others there are
withdrawal symptoms. So, I think one individual may experience a different
response than another individual. Abstract: conclusion- Despite the modest decreases in the active (R)-MD AUC24
and Cmax, the lack of change in opioid PD effects indicate there is not a
clinically significant interaction of APV with MD suggesting no alteration in MD
or APV dosing is recommended when the drugs are coadministered. Results:
Preliminary data (geometric LS mean ratio [90% CI]) for 12 subjects found that
plasma (R)-MD and (S)-MD AUC24 decreased by 12 (1-21)% and 37 (28-46)%,
respectively, and plasma (R)-MD and (S)-MD Cmax decreased by 24 (12-35)% and 45
(32-55)%, respectively. None of the 4 opioid PD measures changed from baseline
in a repeated measures analysis (p>0.05). Within day peak/trough differences
were detectable in pupil diameters and agonist symptoms throughout the study,
regardless of APV dosing (p<0.01). APV Cmax and AUC24 were consistent with
historical controls
Interrupting
Therapy while on NNRTIs
Abstract
# 1545: Stopping
Efavirenz and resistance mutations?
Recently fear has been expressed regarding patients who are virologically
suppressed on Sustiva and go on a drug holiday, stop or interrupt therapy for
adverse events. It has been
hypothesized that they may be at high risk of developing clinically significant
resistance due to the long halflife of Sustiva. David Baker and Lee Bacheler of DuPont looked at patients who
were participating in their pivitol 006 trial and compared the resistance
profiles of those who virologically failed Sustiva versus those who ceased
taking the drug while virologically suppressed. As expected 10 out of the 10 patients who virologically
failed Sustiva had the K103N mutation at the time of virologic failure.
However in 6 out of 7 patients who self discontinued Sustiva while
virologically suppressed, they did not show evidence of the K103N mutation when
they stopped Sustiva and their virus rebounded.
The patient who did show the K103N was sporadically adherent to Sustiva
while taking the drug prior to interruption.
The method used was the VGI kit, which is sensitive down to about 10% of
the viral species. Commentary:
This is an important matter in this era of patients taking more drug
holidays or STIís. While this doesnít settle the question surrounding
interruptions, resistance, and Sustiva, it does at least give us an initial
hopeful report. What is needed next
are studies with larger number of individuals who cease Sustiva and then
subsequently re-start therapy. This
will allow us to evaluate whether clinically significant resistance can develop
through interruptions of Sustiva. The
NIH in their STI studies using Sustiva currently stops the Sustiva a few days
prior to stopping other drugs with shorter half-lives.
Commentary
from Jules Levin: This issue is complex and needs consideration of several
issues. In theory, if a person has had <50 copies/ml for an extended period
of time and has been completely adherent (not missed a dose), the risk appears
less or little if stopping a triple regimen atonce (e.g. Sustiva-AZT./3TC).
Virus is well suppressed in such a situation and ought not be expected to
rebound into replication so easily and quickly. In theory, although EFV drug
levels are decreasing incrementally over a few days it ought not to be a
difference in such a situation described above. But that is theoretical. In
reality, there is no way to know for sure if a person has been missing doses and
how many. There is no way to know for sure if a person has experienced real
viral load blips. No there is no way to know if viral load blips a person may
have experienced is real. Sometimes blips can occur due to lab errors. that But
if a person had had some non-adherence and some viral blips, in theory it's
possible that upon interruption virus replication could occur more quickly and
easily. Although these questions need to be answered with some studies, these
are complex situations that are difficult to sort out. Predicting response after
interruption depends on individual experiences. In sum, until studied further,
there appears to be some risk when interrupting nevirapine or efavirenz,
depending on an individual's experience.
In a
second study reported on at ICAAC, 23 individuals on nevirapine+2 nukes with
undetectable viral load interrupted therapy one or more times. Upon
re-initiation, VL fell BLQ (<400) in 21 of 23 interruptions (91.3%).
Non-adherence was associated with one failure, while viral isolates resistant to
NVP were detected in the other.
Abstract
1546, Interrupting Nevirapine
(Yozviak et al, Philadelphia Coll. of Osteopathic Med., Philadelphia, PA 2 Bornemann
Internal Med., Reading, PA). Retrospective
chart review of all patients (N=536) seen 9/96 to 4/00 yielded 135 patients on
NVP and dual NRTIs. Charts were abstracted for: NVP regimen, treatment duration,
VL before/during ART-interruption, ART-i duration, and viral load after
re-initiation. ART-i was defined as simultaneous cessation of entire regimen for
>7 days. Undetectable was defined as <400 copies of HIV RNA per ml plasma
(<50, if available). Results: Seventeen of 135 had viral load undetectable
with documented ART-i followed by initiation of the same regimen. 2/17 had a 2nd
ART-i and 2/17 had a 3rd ART-i yielding 23 total ART-i for analysis. Mean
baseline VL was 108,276 (5.03 log10). Mean initial ART duration was 193 days.
Mean ART-i duration was 58 days. Upon re-initiation, VL fell to ubdetectable
(<400) in 21 of 23 interruptions (91.3%). Non-adherence was associated with
one failure, while viral isolates resistant to NVP were detected in the other.
Author concluded more study is needed.