September 13-16, 1997. San Francisco, CA.
The first stand-alone Infectious Diseases Society of America (IDSA) annual conference
was held in San Francisco, September 13-16, 1997, at the Moscone Center. The following are selected reports from this meeting
adapted from reports authored by Kenneth Mayer, MD & Charles van der Horst, MD and are sourced from healthcg.com, thebody.com
and Aegis.
Searchable abstracts from the conference are available on the internet at:
http://207.78.88.28/IDSA97/mainfram.htm
or
http://www.idsa.org
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TRANSMISSION
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Bob Coombs presented the resistance data from a subset of the original ZDV Prevention
of Transmission Trial, ACTG 076. Of the original cohort, 85 women were evaluated for genotypic mutations at codon 70 and 215.
Thirteen of the women transmitted HIV and 72 did not transmit it to their babies. Ninety-two percent (92%) were ZDV naive. At
baseline only 1 of 61 women demonstrated a codon 70 mutation. By delivery, after receiving on ZDV monotherapy the last trimester
(approx. 18 weeks of therapy) one more women developed the codon 70 mutation. No subjects had a codon 215 mutation at baseline
or delivery. The 95% estimate for high level ZDV resistance was thus 6% at baseline and 9% at delivery. The rate for both naive
and non-naive women was low, but four fold higher for those individuals with prior ZDV. Thus, for this small cohort with little
prior experience with ZDV, few subjects developed a mutation and there was no association with transmission.
Seth Welles of the University of Minnesota presented the data on transmission from
the Women Infants Transmission Study (WITS). The researchers screened for mutations at codon 41, 67, 70, 210, 215, 219. In this
epidemiologic study, the baseline CD4+ count was 315 cells/mm3 and HIV RNA was 24,800 copies/mL. In contrast to the Coombs paper reviewed above,
32% of the women were treated with ZDV before pregnancy. Of the women who transmitted HIV to their babies 48% had a history of
previous ZDV therapy prior to pregnancy compared to 29% of the women who did not transmit HIV. Duration of membrane rupture was
9.4 hours in transmitting women versus 1.4 hours in non-transmitting women. Of 203 women treated with ZDV prior to delivery 152
were culture positive, 142 had virus recovered by PCR, and 24% of these women had at least one ZDV mutation.
The median HIV load in patients with wild type HIV was 19,800 copies/mL and in those
with any ZDV mutations it was 64,500 copies. Thus, the higher the viral load and the lower the CD4+ count the more likely that
the mother had a resistant virus.
Multivariate analysis suggested that having a reverse transcriptase enzyme mutation,
prolonged rupture of the membranes, or a higher peripheral blood lymphocyte count were each independently associated with maternal
transmission of HIV. The mother's viral load or CD4 count during pregnancy were not associated with HIV transmission. These
findings suggest that in women with prior ZDV experience who develop resistant strains and become pregnant and continue ZDV monotherapy,
the risk of transmitting HIV to their offspring is particularly high. The risk of transmitting HIV was not associated
with HIV-related immunosuppression in this study.
Some of the infants were infected with resistant strains of HIV, but not all. WITS
overall transmission rate is 7-8% since adopting the ACTG 076 treatment regimen and virtually 100% of the pregnant women in the
study are currently following that regimen (ZDV for the last two trimesters, intrapartum IV ZDV and oral ZDV for the new-born baby).
This paper illustrates the need for providing women, who have received prior ZDV or
have become infected with an ZDV resistant strain, a combination regimen of new non-cross resistant medications in order to reduce
transmission to their babies. This is a worrisome piece of information. As the population becomes increasingly more anti-retroviral
experienced and as these resistant HIV are transmitted to newly infected women there may be an increase in HIV transmission
back to the pre-ACTG 076 levels of 25%. ZDV resistance during limited monotherapy use in pregnancy appears to have a low risk
of developing and the single codon 70 mutation was the only change seen with ZDV use in this way.
The widespread practice of including 3TC with ZDV, in the absence of safety data for
3TC, in women with ZDV experience means many women effectively receive 3TC monotherapy, to which resistance develops rapidly
and which may damage the potential for the mother to benefit from future antiretroviral combinations seems clearly irrational. Studies
are now beginning in the UK at the Kobler centre and in the US and France to assess the role and safety of protease inhibitors
in pregnancy with the hope of establishing triple therapy in pregnancy. |
Dr. Harold Kessler of Chicago's Rush Medical College presented data from a collaboration
with colleagues at the University of Colorado in which they analysed HIV isolates they obtained from 22 source patients of
health care workers who sustained occupational exposures to evaluate the presence of antiretroviral resistance. They found that
genetic evidence of resistance to ZDV was present in 10 of the samples, and resistance to ddI in 5, but found no evidence of resistance
of d4T. The patients whose cells contained HIV with resistance mutants were more immunosuppressed (median CD4 count of
9 cells/mm3) compared to those for whom they found no resistance mutations (median CD4 count
169 cells/mm3). The data suggested a high prevalence of antiretroviral drug resistance in HIV isolates
from patients who were the source of health care worker occupational exposures. The importance of this finding is that current
CDC guidelines suggest that the front line therapy of occupational exposures should include ZDV+3TC +/- a protease inhibitor,
but may need to be individualised if the patient is drug experienced.
The current study suggests that resistance is common, so that often post-exposure
prophylaxis will need to use combinations of d4T with either 3TC or ddI, i.e. drugs that are different from those the source patient
was taking. Most progressive clinics have ZDV/3TC/IDV available in HIV clinics, casualty and theatres for treatment of needlestick
injuries. Importantly, most clinicians regularly dealing with PEP recommend modification of subsequent therapy based on
history of antiretroviral usage in the source patient (if known). At Hamburg, workers from Murex will report on using the LIPA assay,
available in the UK to evaluate the reverse transcriptase resistance profile as a means of rapidly individualising PEP. Theoretically
NNRTIs should also prove useful in PEP (given in active form, extremely potent) more studies
are needed to evaluate their potential role. |
|
ANTIVIRALS
|
Dr. Russell Petrak and colleagues at Metro Infectious Disease College of Hinsdale,
Illinois evaluated the efficacy of the combination of daily ddI (400 mg every morning), with d4T 40 mg bid, with indinavir 800
mg tid. An interim analysis was reported which involved 27 patients, of whom 22 were adherent to the study protocol. All the patients
were nucleoside analogue experienced, but all were protease inhibitor naive. The median plasma viral RNA load fell from 33,581
at baseline to undetectable levels for 94% of the participants at 6 months. For the 22 patients who were adherent to the study
protocol, the median CD4 count rose from 97 at baseline to 268 at month six. Although some of the non-adherent patients complained
of mild side effects including gastrointestinal distress and peripheral neuropathy, none of these symptoms persisted after
withdrawal of the drugs. For the majority of participants, the 6 month regimen was well-tolerated and impressive changes in surrogate
immune and virologic markers were noted. ddI, d4T and indinavir appear to be a promising combination regimen for reverse
transcriptase experienced patients.
This combination represents another potent triple therapy and appears useful in NA
experienced patients. ddI and indinavir should be dosed at least one hour apart to ensure that the ddI buffer does not inhibit
the absorption of indinavir. |
Dr. P. Keiser and colleagues from the Southwestern Medical centre in Dallas reported
on their findings in an open label trial comparing ddI given once or twice a day. The patients were nucleoside analogue experienced
and had median viral loads greater than 100,000 copies/mL. Changes in viral load were comparable between the two groups at
about one half log at 8 weeks. One person in the bid group developed pancreatitis, and 3 o.d. patients complained of gastro-intestinal
intolerance and stopped medication. 5/8 patients in each arm were judged to be adherent to the study regimen. In summary,
the once daily dosing of ddI seemed comparable to the twice daily regimen in terms of antiviral activity and tolerability in
this preliminary study.
Favourable data has also been presented on once-daily administration of ddI at the
ECCMID meeting earlier this year (see DocFax 24). Once daily dosing of ddI is now widely established at leading units. Reducing
the level of inconvenience may enhance compliance and thereby improve long-term antiretroviral efficacy. |
Ann Collier of the University of Washington presented an elegant study on indinavir
(IDV) levels in the cerebrospinal fluid (CSF) and the effect on HIV load in CSF. It has previously been identified that HIV load
in CSF does correlate with the degree of neurologic impairment in patients with HIV Dementia Complex. However, there is little
information about IDV levels in the CSF other than in four children who had from 246->1000 nM IDV in CSF.
The Seattle group studied ten patients who were on a blinded trial, including some
individuals on IDV who then were placed on open label IDV. Patients received IDV from 6-300 days, with five patients receiving
less than two weeks of open label IDV (Group A). Another group (nine subjects) who were not on protease inhibitors were placed on
IDV (Group B) and were tested before PI and eight weeks after being on IDV. Only patients with CD4+ counts less than 100 cells/mm3 received a CT head scan prior to lumbar puncture (LP). The target time for LP in
Group A patients was one hour after IDV dose. The lower limit of detection of IDV by HPLC was 3.3 nM or 2 ng/mL in CSF. The lower
limit of detection of HIV was 200 copies.
9/10 patients in group A had an undetectable HIV viral load in CSF while 6/8 of those
in group B became undetectable in CSF after 8 weeks of treatment (baseline median HIV viral load CSF 2.1 log).
The range of total IDV in the CSF was 51-466 nM. The ratio of CSF/Plasma IDV rose
late after dose. Since the IC95 for IDV is 25-100 nM, these levels should be sufficient to suppress HIV. Thus, contrary
to the current opinion that protease inhibitors, which have high protein binding (over 60% for IDV), will not enter the CSF,
IDV does enter the CSF and in sufficient quantities to suppress the CSF viral load to undetectable levels.
CSF concentration is widely used as a substitute for concentration of a substance
in the brain. It is reassuring, however, that CSF viral inhibition is achieved in almost all patients in this study. Data from previous
studies indicate that CSF viral load is generally lower than plasma VL thus lesser reductions in CSF VL may be needed to
establish VL <200 in CSF. The IC95 for IDV in vitro (in 10% plasma) is 100nM. Levels of indinavir are near the range of in vitro IC95 - however, protein binding in vivo may influence this inhibitory concentration. It
is also unclear how much inhibition of HIV outside the CNS influences viral production within the CNS. |
Mike Saag of University of Alabama presented the update on a randomised trial of nelfinavir
750 mg tid or 500 mg tid or placebo combined with ZDV or 3TC. Patients were on this regimen for 24 weeks and then the
placebo patients were randomised to one of the nelfinavir arms. Patients were antiretroviral naive with an HIV load of 15,000 copies/mL.
Twelve month data was available for 69 of the higher dose nelfinavir arm and 61 of
the lower dose arm. At 12 months the reduction in log HIV RNA by the standard Roche Amplicor was sustained from that at six months
at approximately 2 logs for both nelfinavir arms. At six months after becoming undetectable, only 20% of the placebo arm (ZDV/3TC
alone) remained undetectable.
CD4+ counts increased for both nelfinavir arms by approximately 140-150 cells/mm3 at six months and continued to rise over the next six months.
The ZDV/3TC arm added nelfinavir at six months and did not do as well. The percentage
of patients with undetectable viral load rose from approximately 20% at six months to only 50% six months after nelfinavir was
added.
A more interesting analysis was that of the duration of response or how long the patients
who became undetectable remained so in relation to baseline viral load and CD4+ count. Both nelfinavir arms performed better
than the ZDV/3TC arm for all viral loads and all CD4+ counts. However, the higher dose nelfinavir arm was clearly superior
to the lower dose arm when the viral load exceeded 100,000 copies/mL or the CD4+ count was less than 100 cells/mm3. Additionally, within the nelfinavir 750 mg arm patients with a viral load less than
50,000 copies did better than those with more than 100,000 copies. At 12 months after becoming undetectable patients with the
lower baseline viral load were still undetectable 90% of the time, whereas it dropped to 60% for those with the greater viral
load (p=0.027). This difference in duration of response within the high dose nelfinavir arm was not seen when analysed by different
CD4+ cohorts.
This study nicely illustrates all of the current proposed treatment guidelines. Triple
therapy including a protease inhibitor is better than dual therapy without a protease inhibitor. Changing one drug at a time
will not give much of a response, such as simply adding nelfinavir to ZDV/3TC. If a patient is failing therapy as many new medications
as possible need to be started. Finally, perhaps patients with high viral loads, such as >100,000, should be treated with
four drugs instead of three. |
Piliero et al at Albany Medical College examined the benefit of switching 32 patients
who were failing current PI therapy (23 on IDV, 11 on RTN, 5 on SAQ) to combined therapy with ritonavir and saquinavir. The
rationale for this study is a little confusing since to switch someone who is failing therapy from ritonavir to ritonavir plus saquinavir
makes no sense. It is basically adding only one new drug and the HIV will likely become quickly resistant to the new agent.
The same is true for those patients with prior saquinavir treatment. Nonetheless, there is scant information on the ritonavir/saquinavir
combination in protease inhibitor experienced patients, thus, this author is presenting the study data. Four patients
were excluded from analysis due to early therapy discontinuation and three had incomplete data. The median CD4+ was 61 cells/mm3 (range 6-439); the median viral load was 197,273 copies/mL (range 400-750,000). Two
patients were undetectable at baseline. Eight patients were treated only with RTN/SAQ. After a median follow-up of five weeks
only nine patients had a greater than 0.5 log decrease in HIV load and two were undetectable. Fifteen patients stopped therapy
because of persistently high viral load (six), drug toxicity (three) or both (six). In 11 patients who continued on therapy for
a median of 22 weeks the viral load declined from 116,000 to 35,000.
The rationale for a switch from failing ritonavir to RTV/SQV is not quite as nonsensical
as the author suggests. SQV may have some activity after RTV failure and continuing the RTV will ensure meaningful blood
levels of the SQV. A more rational choice, however, may be nelfinavir/saquinavir, 2 new PIs and again the interaction raises SQV to useful blood levels (approx. 5 times). |
In its current formulation, saquinavir has a bioavailability of only 4% giving an
antiretroviral potency at currently licensed doses which many believe is sub-optimal. Roche has modified the formulation of saquinavir
to create saquinavir soft-gel and is dosing this new formulation at twice the dose of the current hard gelatin capsule. This
increases the absorption and results in up to ten times the AUC seen with the current formulation of saquinavir. Charles Farthing
of the AIDS Healthcare Foundation in Los Angeles conducted an open label study of 41 antiretroviral naive patients of saquinavir
soft-gel; 1,200 mg tid together with ZDV 300 mg bid and 3TC 150 mg bid. In the 30 patients who reached 12 weeks, the mean
change in plasma HIV RNA was -2.74 log, 77% were undetectable (<400 copies, Roche Amplicor assay) and 23% had less than 50 copies
by the Ultra-Sensitive assay. Mean CD4+ count rose 143 cells/mm3 at 12 weeks. Adverse effects were mild and consisted of six patients with nausea,
four each with diarrhoea and vomiting, and three with headaches. Only two patients had to discontinue treatment for toxicity, including
one with Grade III/IV AST/ALT elevations and one with Hepatitis A.
A Dutch group at University Hospital in Utrecht presented preliminary results of an
on-going open-label randomised comparison of the soft-gel formulation versus indinavir 800 mg tid plus ZDV 200 mg tid plus 3TC
150 mg bid for 48 weeks. To date, 45 of the 60 planned patients have been enrolled with less than 12 months ZDV experience, no
prior history of 3TC or protease inhibitor and with one of the following: CD4+ < 500 cells/mm3, HIV > 10,000 copies or CDC class B or C.
All patients in both arms were undetectable (<400 copies by Roche Amplicor). Only
one patient on the saquinavir arm and two on the indinavir arm stopped therapy due to an adverse event. Six patients on the saquinavir
arm complained of diarrhoea and two of nausea (not mutually exclusive). One patient developed nephrolithiasis on indinavir.
This study and the earlier studies of saquinavir-hgc (InviraseTM) using 3,600mg and 7,200 mg daily, show that the currently recommended dosage (1,800
mg daily) is sub-optimal. The recently completed 16-week analysis of NV15355C (presented by Laurent Fischer, M.D.), which compared
the two formulations in combination with two RTIs of choice (in treatment na ve individuals), showed that only 43% of patients achieved plasma viral load <500
copies/ml on the hard-gel formulations. |
The major predictor of resistance developing to antiretroviral combination therapy
is persistence of detectable HIV RNA, according to Albany Medical College researchers. The risk is significantly lessened with
three-drug combination antiretroviral therapy.
Dr. Stein's group evaluated data from five trials comprising a total of 197 subjects
who received either monotherapy with indinavir or combination therapy with indinavir and two nucleoside analogues--ZDV, ddI or
3TC.
They found that "...the lower the HIV RNA PCR achieved, the lower the risk of emergence
of resistance." The lowest risk was achieved with suppression of viral load to less than detectable or quantifiable levels.
Patients on combination therapy had significantly longer times to emergence of resistance than those on monotherapy, even when
adjusted for the minimum HIV RNA level achieved.
Based on these findings, Dr. Stein's team recommends that patients receive combination
regimens "if at all possible," and that the therapeutic goal should be undetectable levels of HIV RNA. The data show "...that
it does not matter how much you decrease the viral load," Dr. Stein said. "Unless it reaches the point of being undetectable,
your risk of ultimately failing therapy is high."
The lower the viral load the more durable the therapy has previously been suggested
by data from ritonavir phase II studies. As ultrasensitive assays become available we should see a continuing shift towards realising
the need to achieve less than 50 copies/mL. The focus of research needs to shift towards achieving this response for more
people for longer periods of time. |
DMP-266 (Efavirenz) is a nonnucleoside reverse transcriptase inhibitor (NNRTI) developed
by Dupont-Merck currently in clinical development. It is a potent NNRTI that is highly protein bound (99.5%), however, free
drug levels following a 600 mg dose easily exceed the IC95 of most isolates, including those with single-point mutations. High level resistance
develops more slowly and requires more than one mutation, however, DMP-266 is cross-resistant with the other NNRTIs.
The pharmacokinetics and known safety profile of DMP-266 are favourable. The plasma
half-life is 40-50 hrs, hence the drug is dosed once daily. There is no significant food interaction and the only important drug
interactions are with clarithromycin and the protease inhibitors. Concomitant use with clarithromycin is not well tolerated and
results in a 44% decrease in the AUC of clarithromycin and a 21% increase the hydroxy metabolite. Since DMP-266 is an inducer
of the p-450 enzyme system, metabolism of many drugs that utilise that pathway, such as protease inhibitors, is accelerated. The
effect of DMP-266 on specific protease inhibitors is not intuitive: indinavir AUC is reduced by 36%, but nelfinavir AUC is increased
by 15%. It is even more confusing with saquinavir, where lower doses result in lower saquinavir levels while higher doses
increase concentrations. When the drug is used in combination with indinavir, the indinavir dose should be increased to 1000 mg
tid; for nelfinavir, no dose adjustment appears necessary. The drug appears safe, and there has been less problem with rash as
compared to what has been reported with delavirdine or nevirapine. The main adverse events are central nervous system related, typically
dizziness, insomnia, and light-headedness. Because of the nature of these side effects, the drug is usually given at bedtime,
and in the case of intolerable symptoms, the dosage can be divided and given twice daily.
The results from the largest clinical trial that has been completed were reported
during the Late Breaker Session. This was the Dupont-Merck Study 003, a trial in 101 patients of DMP-266 200 mg daily plus indinavir
800 mg tid compared with placebo plus indinavir 800 mg tid. As more information became available to the investigators, the
DMP-266 dose was increased to 600 mg daily, stavudine was added to both arms, and the indinavir dosage was increased to 1000 mg
tid. The baseline characteristics of the patients included 71% with prior treatment with nucleosides, a median CD4+ count of 283
cells/mm3, and a plasma HIV-1 RNA concentration of 5.04 log10 copies/mL. Although the results
are somewhat difficult to interpret because of the relatively small number of patients enrolled and the changing dosing schema,
the findings do suggest that the DMP-266-containing regimen was effective and well tolerated. At 48 weeks, the DMP-266 arm had
a median HIV-1 RNA decrease of 2.38 log10 copies/mL compared to 1.89 log10 copies/mL in the indinavir arm (p<0.01).
There was a greater increase in the CD4+ cell counts in the DMP-266 group, 245 cells/mm3 versus 150 cells/mm3. The study drugs were well tolerated and, interestingly, there was only one serious
rash in the entire study which occurred in the indinavir group.
Dr. S. Riddler of the University of Pittsburgh reported for the DMP-266 clinical development
team on the 48 week data for a cohort of asymptomatic patients treated with DMP-266 (200 mg/d), a nonnucleoside reverse
transcriptase inhibitor, with Indinavir (800 or 1000mg/tid). The patients had a mean baseline plasma HIV RNA of 5.06 log10 copies
of HIV RNA/mL and mean CD4 count of 283 cells/mm3. 71% had prior nucleoside therapy. In the course of the study, 42 of the 59 patients
who initially enrolled added D4T to their regimen at 12 weeks, and all patients had their DMP-266 dose increased to 600 mg/d
after 36 weeks of treatment. By 44 weeks, 89% of the patients who received DMP-266 plus indinavir had plasma viral load less than
400 copies/mL, and 77% of the patients who also were on d4T had VL that were below the limits of detection. The regimens were
generally well-tolerated, with only 2 persons in either treatment arm withdrawing because of side effects, which included infrequent
rashes, but none that were severe or persistent. DMP-266 appears to be a very well tolerated new NNRTI compound which can
be given once daily and adds to the potency of indinavir therapy.
This is encouraging data. Larger and better designed studies with DMP-266 are ongoing
in children and adults. It is expected that Dupont-Merck will seek accelerated approval of this agent in the first half of 1998
in the US if the clinical data remains favourable. |
An expanded access programme has just been announced in the US and Dupont-Pharma
are expected to announce a European wide compassionate use programme within the next month. The EMEA is the main delay for availability
in Europe pushing licensing more than six months behind the US. Do not expect licensing anytime before early 1999 if currently
appalling EMEA performance is anything to go on. No comparative studies with other NNRTIs (delavirdine or nevirapine) have been performed but current data favours DMP-266
on convenience and tolerability. |
|
OPPORTUNISTIC ILLNESS
|
Finkelstein and co-workers presented the results of ACTG 181 on the natural history
of CMV disease. Patients were monitored every 4 to 12 weeks for evidence of CMV shedding in the urine and blood by culture methods.
The researchers found 68 of 177 patients urine CMV positive and 22 of 177 patients blood CMV positive during the study, while 33 patients had CMV-related end-organ
disease. In a model adjusting for CD4+ cell count, the investigators reported that CMV positive blood or urine was associated with
an increased risk of end-organ disease (relative risk = 9.2 blood and 3.08 urine). CMV appeared in the urine first in the majority
of cases, followed by blood positivity. The rate of CMV disease after shedding was 5% at three months and 16% at six months.
Mallolas and colleagues reported data from a prospective cohort study conducted in
Spain. The investigators identified 21 patients who developed CMV disease after instituting therapy with protease inhibitor based
antiretroviral therapy. The majority, 19 of 21 cases, occurred within two months of starting PIs with a range of CD4+ counts
from 2 - 225 cells/mm3. Seven subjects had CD4+ counts greater than 50 cells/mm3. The investigators reported that after the two month interval, cases of CMV disease
have fallen dramatically in patients receiving PI therapy.
This poster supports the role of potent antiretroviral therapy in the prevention of
opportunistic infections. However, the results also demonstrate that CMV may occur after effective HIV treatment despite relatively
high CD4+ cell counts, particularly in the period immediately after initiating therapy.
The Royal Free is already monitoring for CMV by PCR to assess the potential for pre-emptive
therapy (treatment for CMV before clinical disease). Early use of potent antiretroviral therapy is likely to better delay
development of all OIs including CMV. |
Hoffman and co-workers provided further evidence that effective antiretroviral therapy
can impact the prognosis of patients with opportunistic infections (OIs). In this retrospective analysis of 25 patients with
proven PML, they found that patients receiving no antiretroviral therapy or nucleoside analogues only had a median survival of
123 and 127 days respectively, while patients receiving PIs had a median survival of over 403 days, with four of five patients
still alive.
|
OTHER REPORTS
|
Results from these two trials presented at conferences have been previously reported
in ATPs Doctor Fax (issue 18, 20 &28). The second study outlined above also looked at viral
load down to 50 copies/mL and foundÖmost patients in the three-drug group whose HIV RNA levels were reduced to less than
500 copies/mL also had less than 50 RNA copies/mL when the ultrasensitive investigational assay was used. The investigators also stateÖcontinued suppression of HIV RNA levels for one year without evidence of the emergence
of resistant virus suggests that there was little, if any, continuing HIV replication in the patients receiving three-drug
therapy. |
British AIDS charities have condemned uneven access to protease inhibitors in the
UK, saying the quality of care of infected patients should not depend on the area in which they live.
Charity officials said some patients were being denied life-prolonging combination
drug therapies, others were being prescribed the drugs too late, and in many areas of the country an important viral load test
that monitors the effectiveness of the treatment was not available.
They urged the government to set national guidelines on treatment to establish a standard
of care across Britain. "This situation amounts to a lottery of care for people with HIV," Derek Bodell, director of the
National AIDS Trust, told a news conference.
Ian Kramer the deputy chairman of the UK Coalition of People living with HIV and AIDS
said there was no longer any debate about the effectiveness of combination therapies so it was a scandal that some patients
were still not receiving them. "It means that hundreds of people will die much earlier than they need to. It is like condemning
a small town to death. This kind of geographical lottery is totally unacceptable."
Kramer said people with HIV attending a British AIDS conference last week highlighted
the disparity of care across the country and emphasised the lack of knowledge among health officials.
Doctors are not up to date with the latest developments and information and advice
about new treatments are not available. Some patients said they knew more about the latest drug combinations, which have delayed
the onset of AIDS in patients infected with HIV and improved the lives of many with the disease, than the people treating them.
People with HIV were also demanding a say in the decisions being taken that would
influence their health and well being. "People are becoming ill and dying as a result of this mess," said Jonathan Grimshaw, who
chaired the AIDS conference. "We need some kind of action to sort this mess out."
BHIVA guidelines were originally written to represent a minimum national standard.
However, Health Authorities are legally allowed to spend and prioritise their budget as they see fit. Unfortunately, patients transferring
care to centres which know the value of potent therapy and appropriate monitoring are placing financial strain on these
units. In HIV care the money has not followed the patient. The need for expertise in the management of HIV patients suggests
the need for regional centres of excellence, appropriately funded, as there are for a range of surgical and other specialities
(eg. oncology). As an interim measure, perhaps BHIVA could look into setting up a register to certify doctors on a voluntary basis
since many doctors involved in HIV care find it difficult to keep up with this increasingly complex field. |