Liver Biopsies
Ian Baird
I've been infected for ~20 years and had elevated LFT's for the past
few years, and the occasionally raised AFP count. I am co-infected with HIV
which is managed well with combination therapy. My ID Doc thinks it's time
to start thinking about treating my HCV infection as well and to this end he
would like a liver biopsy done. Unfortunately I suffer from Haemophilia A
and my centre has a NO policy on liver biopsies, so they will take some
convincing I think. What can a liver biopsy tell me that blood tests cannot?
What does the procedure entail?
I understand the combo for HCV is very unpleasant and I would like to
make sure that if I do start treatment it is warranted. I honestly don't
think I could manage two separate regimes and cope with both sets of side
effects, and be able to maintain the same functionality I have enjoyed over
the past four years. Any advice would be gratefully received and faithfully
applied.
Be Well,
Ian Baird
Consultancy
I cannot tell you much about co-infection with HIV/HCV - however I do have
some articles on the subject - I will look into them and eventually
post/repost them if you wish. I can give you a link that might be an
interesting starting point to look up some info on the net - about HIV - HCV
and also for people having both : http://www.hivandhepatitis.com/
For what's the biopsy-question : they will see the real state your liver is
in : is there any fibrosis, is there cirrhosis, is there even cancer or if
1 - 2 or 3 : in what stade are you... Normally the procedure is a needle
biopsy... but there are other ways to do it (alltough imo those give not
the conclusive results nedle-biopsies give).
And for what's the combo - it is a fact that treatment for HCV given to an
HIV + patient is different and much more delicate than if one is HIV - .
Will try to give you some more info on it coming day(s).
Meanwhile,
take care,
Ciao,
Nico.
"Ian Baird" <ianmac...@ibaird.fsnet.co.uk> wrote in message
news:8j3g4r$tt4$1...@newsg1.svr.pol.co.uk...
Firebird
ianmac...@ibaird.fsnet.co.uk (Ian Baird) wrote:
Before you can make any decisions you have to find out if your GP is
willing to pay for interferon. It's all part of the postcode lottery that
makes up the NHS.
Alan
Cmhdavid
>What can a liver biopsy tell me that blood tests cannot?
Ian,
The biopsy tells you how much liver damage you have. See if they will settle
for a MRI. It is limited in what it will tell you, but it's better than no
biopsy.
Research all you can on the treatment before you begin, make a conscious
decision. I don't know too much about co-infection. There are a few that post
here occasionally that are HIV as well as HCV. There is a web site that deals
strictly with HIV and HCV together. Maybe someone can post that for you. They
have good info, and stay pretty current.
Hope the best for you.
David
~ http://members.aol.com/cmhdavid ~
"Fear is faith in the Enemy." --author unknown
Consultancy
23% of 1,260 HIV positive patients had HCV co-infection; typical patient was
Caucasian, female, mean age of 42 years and became infected by injecting
drugs
by Harvey S. Bartnof, MD
Researchers at UCSD (** University of California at San Diego in La Jolla)
profiled their database of HIV positive patients followed during the 1990s
at their Owen Clinic to determine the rate and characteristics of those
co-infected with HCV (* hepatitis C virus). Due to similar routes of
transmission, HIV/HCV co-infection is becoming more common. US west coast
demographics for co-infection appear to have similarities and differences to
profiles of co-infected patients from other geographic locations. The report
was presented at Digestive Disease Week 2000 that was held in San Diego,
California between May 21-24, 2000.
Regarding all of the 1,260 HIV positive patients, 16% were women. The
race-ethnic profile was 57% Caucasian, 19% Hispanic, 15% African-American
and 9% other. Transmission risk factors for HIV infection were 52%
gay/bisexual male contact, 22% injection drug use, 16% heterosexual contact,
7% data missing and 3% blood/blood product transfusion. An HIV RNA level
greater than 400 copies per milliliter was present in 40%, while a level
less than that was present in 54%. HIV RNA data was missing for the other
5%. The percentages for each CD4 count level in cells per microliter were
11% (0-50), 21% (51-200), 40% (201-500), 26% (greater than 500) and 2%
missing information.
The information about HCV co-infection among their HIV positive patients was
as follows. HCV co-infection was present in 23% of those with HIV infection.
Women were more likely to be co-infected (32%) than men (21%). Co-infection
by race-ethnicity revealed that 34% of Blacks had HIV/HCV co-infection, 22%
of Caucasians, 19% of Hispanics and 18% other. Reported in a different way,
among all HIV/HCV co-infected patients, the majority was Caucasian (55%),
with 15% who were Hispanic, 23% who were Black and 7% who were other. The
rates of co-infection by transmission risk factor revealed that 69% of blood
product recipients were co-infected, 61% of injection drug users, 12% of
heterosexuals, 8% of gay/bisexual men and 19% of those with missing
transmission information. Reported in a different way, among all HIV/HCV
co-infected patients, 60% had a history of injection drug use, 17% had a
history of gay/bisexual male contact, 9% history of heterosexual contact, 8%
history of blood product transfusion and 6% with missing data.
The percentage of co-infection by age group was 16% (of those from ages
18-33 years), 14% (34-37 years), 30% (38-45 years) and 32% (46 years or
older). Co-infection by CD4 categories revealed 21% of those with a CD4
count between 0-50 cells per microliter, 25% of those with a count between
51-200, 24% of those with a count between 201-500 and 21% of those with a
count greater than 500 cells per microliter. Regarding HIV RNA, 42% of
co-infected patients had an HIV RNA level less than 400 copies per
milliliter, while 58% had a level greater than that (those percentages were
nearly equivalent for HIV mono-infected patients). However, anti-HIV therapy
that would affect CD4 and HIV RNA levels was not reported. Also, HCV RNA
information was not reported.
In a statistical "multiple logistic regression analysis," the following
factors were highly statistically significant for predicting HIV/HCV
co-infection: female gender (male 0.6 "odds ratio" or 60% of the rate in
women), age 34-45 years ("odds ratio" 2.7 where age 46 years and older is an
odds ratio of 1.0) and transmission risk factor (odds ratios: blood products
1.0, injection drug use 0.6, heterosexual 0.04, gay/bisexual men 0.03. and
missing 0.1). The following calculations in the same analysis did not reveal
significant differences by HCV co-infection status: race-ethnicity, HIV RNA
and CD4 count.
The authors concluded, "Although HIV/HCV co-infection is less prevalent
among men who have sex with men (MSM) than in injection drug users, the
prevalence among MSM is sufficiently high (8%) to justify current CDC
recommendations for routine screening." Also, "HCV prevalence is not
influenced by HIV disease stage."
The study is limited by the cross-sectional nature of the analysis during
the period 1990-1999. The authors did not indicate whether the laboratory
values, e.g., CD4 count, were the first ones entered for each patient, were
random or the most recent ones. Undoubtedly, some patients have laboratory
values for each of the ten years. Without indicating past or current HIV
treatments, it is not clear whether the CD4 counts and HIV viral loads
represent levels before, during or after therapy. Therefore, it is not clear
how the authors arrived at their second conclusion without this information.
Also, it would have been helpful to know the HCV viral loads and liver
biopsy results, if available. However, it is possible that they do not have
such information for all or the majority of HIV/HCV co-infected patients.
Another limitation is that HCV antibody tests performed between 1990-1992
were first generation and can be "false negative" in HCV-infected patients.
If some of their HIV positive patients were only tested for HCV during that
period, some that were truly co-infected with HCV might have been missed.
Moreover, one group of researchers recently has reported a 6% false negative
rate of HCV antibody tests among HIV/HCV co-infected patients, using the
current second-generation test.
At this Conference, Marion G. Peters, MD, at the University of California at
San Francisco said that if an HIV positive person with a high risk behavior
history for HCV infection (injection drug use, blood transfusion before
1990-1992) has a negative antibody test for HCV, it should be repeated to
rule out a false negative test. Dr. Peters made the comments during her
"Meet-the-Professor" session entitled "Hepatitis C and HIV Co-infection."
Collectively, all of the information in these last two paragraphs suggests
that this report's 23% rate of co-infection might be an underestimation.
Even considering these limitations, the report has value into providing
insights about HIV/HCV co-infected patients at UCSD, which reflects a
somewhat different profile in the San Diego region of southern California
from other geographic locations in the US. Some might be surprised by the
fact that among all of their HIV/HCV co-infected patients, 55% were
Caucasian and only 23% were Black and 15% Hispanic.
6/7/00
References:
George S and others. Antibody negative HCV infection in HIV-positive
individuals. Abstract 127 at the 10th International Symposium on Viral
Hepatitis and Liver Disease; April 9-14, 2000; Atlanta, Georgia.
Matthews C and others. Prevalence of HCV in a HIV cohort at a University HIV
clinic. Abstract and poster 211 at Digestive Disease Week 2000; May 21-24,
2000; San Diego, California.
Peters MG. Hepatitis C and HIV Coinfection. "Meet the Professor" session at
Digestive Disease Week 2000; May 21-24, 2000; San Diego, California.
"Ian Baird" <ianmac...@ibaird.fsnet.co.uk> wrote in message
news:8j3g4r$tt4$1...@newsg1.svr.pol.co.uk...
> Hello,
> I've been infected for ~20 years and had elevated LFT's for the
past
> few years, and the occasionally raised AFP count. I am co-infected with
HIV
> which is managed well with combination therapy. My ID Doc thinks it's time
> to start thinking about treating my HCV infection as well and to this end
he
> would like a liver biopsy done. Unfortunately I suffer from Haemophilia A
> and my centre has a NO policy on liver biopsies, so they will take some
> convincing I think. What can a liver biopsy tell me that blood tests
cannot?
Consultancy
Both measurements were insignificantly greater than among HCV-mono-infected
patients; co-infected patients had significantly more CD8 lymphocytes in
their livers
by Harvey S. Bartnof, MD
Due to similar routes of transmission, an increasing proportion of persons
have co-infection with HIV (human immunodeficiency virus) and HCV (*
hepatitis C virus). Without HAART (highly active antiretroviral therapy) for
HIV, co-infected patients have accelerated liver disease progression.
While HCV has been shown to increase hepatocyte (liver cell) apoptosis
(programmed cell death), specific effects of co-infection upon liver cells,
immune cells in the liver and "apoptosis" (programmed cell death) have not
been determined. Now, researchers from Cornell University have examined such
factors in co-infected patients. The report was presented at Digestive
Disease Week 2000 held in San Diego, California May 21-24, 2000. The lead
author was Dr. Andrew H. Talal.
The study included liver biopsy samples from seven patients with HCV
mono-infection, seven patients with HIV/HCV co-infection and three healthy
control patients. Thirteen of 14 patients with viral infection had abnormal
liver biopsies. The abnormalities were grade 1-2 "necroinflammation" (cell
death and presence of immune cells) and stage 1-2 fibrosis (scarring).
The results showed that the mean number of "apoptotic" ("caspase-3+") liver
cells (hepatocytes) was significantly greater among the mono-infected (0.7)
and co-infected patients (0.9) than among control patients (0.0). (Result
numbers are per high power field view under the microscope or times 40.)
Even though the co-infected patients had a greater number of apoptotic cells
than the mono-infected ones, the difference was not statistically
significant. Similarly, the mean number of proliferating liver cells
("Ki-67+") was significantly greater among the mono-infected (2.9) and
co-infected patients (3.9) than among control patients (0.4 per high power
field). And similar to the apoptotic profile, even though the co-infected
patients had a greater number of proliferating liver cells than the
mono-infected ones, the difference was not statistically significant. The
differences between co-infected and mono-infected patients regarding
apoptosis and proliferation of liver cells might have achieved statistical
significance with a greater number of patients.
Regarding immune lymphocyte cells seen on liver biopsies, the number of
"precursor" lymphocytes ("CD3+") was significantly increased in the
co-infected (32.5) and mono-infected patients (31.8), when compared to
control patients (15.9 per high power field). However, there was no
significant difference between mono- and co-infected patients. Regarding
"helper-inducer" ("CD4+") lymphocytes, the number per high power field was
insignificantly lower in the co-infected (2.5) and mono-infected patients
(3.2), when compared to controls (4.5 per high power field). Regarding
"suppressor-cytotoxic" ("CD8+") lymphocytes, co-infected patients and
mono-infected patients had a significantly greater number (19.6 and 12.8,
respectively) than control patients (10.1 per high power field). The
difference between co- and mono-infected patients was statistically
significant.
The authors concluded, "Dual infection with HCV and HIV-1 further increases
hepatic cellular turnover [compared to HCV-mono-infected patients] and may
partially explain the accelerated course of liver disease in the HCV/HIV-1
co-infected individuals." More studies like this one will help physicians
and patients to understand the difference in HCV disease progression in
co-infected patients. A more complete understanding of the mechanisms
involved in that accelerated course likely will lead to insights about new
therapeutic approaches against each viral infection.
The study is limited by not including information about the 14 patients with
viral infection(s). It would have been helpful to know the following at the
time of biopsy: HCV viral load, HIV viral load, CD4 count, current and past
anti-HCV therapy, current and past anti-HIV therapy and HBV (hepatitis B
virus) co-infection status. The viral load data should include measurements
from blood serum (no cells) and hepatocytes. Those data might have had a
direct relationship with the variables that were measured, particularly the
CD4 count for the co-infected patients. If the mono- or co-infected patient
groups were heterogeneous or homogeneous with regard to these factors, the
results in the current study might have been quite different. The authors
tried to control for liver disease state by choosing patients with similar
degrees of inflammation and fibrosis. However, without knowing these other
factors, the results have limitations. Nonetheless, the study represents a
first step in our understanding HIV/HCV co-infection effects in the liver.
6/5/00
Reference:
Talal AH and others. Effect of hepatitis C virus and HIV-1 on hepatic
parenchymal and mononuclear cell proliferation and apoptosis. Abstract 183
Consultancy
HIV Prevention Therapy
HIV antibody test became positive 13 months after exposure in one health
care worker who also became HCV positive
by Harvey S. Bartnof, MD
HIV/HCV (hepatitis C virus) co-infection is increasingly common, due to
similar routes of transmission. Health care workers, safety and emergency
response personnel are at risk for both infections after accidental
needlestick or other occupational exposure. Researchers at the Centers for
Disease Control and Prevention (CDC) have documented 6,524 occupational
exposures to HCV among health care workers during a 4-year period. In one
case of exposure to both HCV and HIV, HCV transmission occurred, and the HIV
antibody test became positive 13 months after exposure. The results suggests
that after co-exposure to HIV and HCV, follow-up HIV testing for longer than
12 months might be indicated if HCV transmission occurs. Even though HIV/HCV
transmission was after occupational exposure, those with non-occupational
co-exposure also might need longer follow-up for longer than one year. The
report was presented at the recent 10th International Symposium on Viral
Hepatitis and Liver Disease (April 9-13, 2000, Atlanta, Georgia).
From mid-1995 to mid-1999, 25 different US hospitals reported a total of
6,524 exposures to HCV among health care workers. Among those, 620 or 11%
involved a source patient who was co-infected with HIV/HCV. Another 92
source patients or 15% had an unknown HIV status. Among those 620 exposures,
80% involved blood or bloody fluids. Among those, 80% were "percutaneous"
(through the skin) and 20% were "mucocutaneous" or by exposure to moist
linings (mouth, nose, eyes). Unfortunately, the follow-up rate was low. Only
50% with blood exposure had at least one year of follow-up. Another 29% had
follow-up of at least 20 weeks.
There were five health care workers (HCWs) who became infected with HCV
after "percutaneous" blood exposure to a HCV positive source patient. There
were no HCV transmissions by "mucocutaneous" exposure. The HCV antibody test
became positive within six months after exposure for all of them. All five
also had detectable HCV RNA, including two who had a detectable level when
tested four weeks after exposure. In addition, all five had increased ALT
(alanine aminotransferase, liver enzyme), with a median peak of 870
international units per liter. For four of the five, the increased ALT was
detected at the same time that the HCV RNA test indicated dectectability.
The fifth patient had an increased ALT before detectable HCV RNA. Symptoms
or signs (abnormalities on physical examination) of acute hepatitis were
reported in three of the five HCWs.
Four of the five HCWs who became infected with HCV were exposed to a source
patient who was co-infected with HIV/HCV. All four of them took anti-HIV
"post-exposure prophylaxis" (PEP) or preventive therapy for 14-28 days. One
of those four patients first developed a positive HIV antibody test 13
months subsequent to exposure, after a negative one was documented six
months after exposure. This indicated occupational transmission of both HIV
and HCV from the same exposure event. Other specifics about that health care
worker were not presented, including type of anti-HIV PEP, HIV RNA and CD4
count. Specific information about the source patient at the time of
transmission also was not presented, including HIV RNA, history of anti-HIV
therapy, CD4 count, HCV RNA and history of anti-HCV therapy. The report also
did not indicate whether this one health care worker took the full four
weeks of PEP or at what point he/she developed HCV infection.
The lead author, Dr. S.R. Campbell and colleagues concluded that "health
care workers are at risk of acquiring HCV infection after occupational
exposure." Also, "exposures to source patients co-infected with HIV and HCV
require further study."
The results also suggest that after co-exposure to HIV/HCV, follow-up
testing for HIV might need to be performed for a duration longer than 12
months, particularly when HCV transmission occurs. The optimal duration of
follow-up testing is unknown. Whether a similar, longer duration of HIV
testing might be needed for those with non-occupational exposure to both
viruses is unknown, for those who become HCV positive.
The report also did not state when the HIV RNA viral load became detectable,
if performed prior to the positive antibody test. The HIV RNA tests are not
FDA-approved for diagnosis of HIV infection. "False positive" tests have
occurred when used to help diagnose infection, but the level of the results
is usually low, less than approximately 1,000 copies per milliliter.
The report does not state whether any treatment for HCV was prescribed for
the health care worker who became co-infected. That aspect is important
enough that the researchers most likely would have indicated if that were
the case.
Even though newer devices are available that decrease the risk of
occupational exposure to blood-born infections, many hospitals and clinics
do not use them due to increased cost. The state of California has passed
legislation requiring the availability of these devices for health care
workers.
5/15/00
Reference:
Campbell SR and others. Hepatitis C infection after occupational exposure.
Abstract C065 at the 10th International Symposium on Viral Hepatitis and
Liver Disease; April 9-13, 2000; Atlanta, Georgia.
Consultancy
Now HIV/HCV co-infected patients will have access to Rebetron, the
standard-of-care treatment for chronic hepatitis C
by Harvey S. Bartnof, MD
On March 2, the California AIDS Drug Assistance Program (ADAP) approved
Rebetron as a new addition to the state drug formulary for Californians with
HIV infection and chronic hepatitis C. Rebetron is two drugs: Rebetol
(ribavirin) plus Intron A (interferon alfa * 2b) and represents the
"standard-of-care" for the treatment of chronic hepatitis C.
An increasing percentage of patients with HIV are also infected with HCV
(hepatitis C virus), since the two viruses have similar routes of
transmission. Approximately 1/3 (350,000) or more of HIV positive patients
in the US are co-infected with HCV. Many HIV positive patients have "stable"
HIV disease due to the widespread use of HAART (highly active antiretroviral
therapy). Therefore, in the last 1-2 years, there have been reports that HIV
positive patients increasingly are dying from liver disease often due to
chronic hepatitis C and not from the "classical" AIDS opportunistic
infections (OIs). Yet, chronic hepatitis C is now considered an AIDS OI. In
the most recent update of the IDSA/CDC (Infectious Disease Society of
America/Centers for Disease Control and Prevention) 1999 Guidelines for the
treatment of opportunistic infections (OIs) in persons with HIV, chronic
hepatitis C is now listed as an AIDS-defining illness. The updated
Guidelines recommend that every HIV positive patient be tested for infection
with HCV.
Is There a Different Rebetron Dosing for the HIV/HCV Co-Infected Patient?
The FDA-approved dose of Rebetol is 1,000 mg (165 pounds or less) or 1,200
mg daily (more than 165 pounds), while that for Intron A is 3 million units
self-injected 3-times weekly. For chronic hepatitis C, many physicians are
using a more frequent and sometimes higher dose of Intron A, 3 to 5 million
units daily (or more), which (5 million units daily) is the dose that
happens to FDA-approved for treating chronic hepatitis B. The reason for a
higher dosing that is daily is that blood levels of the drug decrease
dramatically and are sub-therapeutic (too low) during the "off days" with
the 3-times weekly dosing. (The original dosing was designed by Hepatology
Fellows-in-training who did not want to be bothered with dosing issues on
the weekend!) There also are a few studies indicating a more rapid decline
in HCV RNA viral load with higher dosing. However, this has not been proven
to increase the rate of sustained response (HCV viral load undetectability
six months after therapy is stopped). The downside of higher dosing might be
increased side effects that can be problematic.
For HIV/HCV co-infected patients, many physicians also are using a lower
dose of Rebetol at 800 mg daily, which is not FDA-approved. This is due to
reports by experienced gastroenterologists (stomach-colon physician
specialists) and hepatologists (liver physician specialists) who, in
preliminary studies, have found that the lower dose appears to be just as
effective and decreases the high rate of "hemolytic anemia" (low red cell
count due to bursting of those cells) that commonly occurs in HIV/HCV
co-infected and to a lesser degree, in HCV-mono-infected patients.
In one preliminary study of 44 patients with HCV mono-infection (without
HIV), 600 mg of Rebetol daily was "at least as effective as higher
('standard') doses (1000-1200 mg per day), and are tolerated better [in
combination with alfa interferon]." The lead author of the poster presented
at the 50th Annual Meeting of the American Association for the Study of
Liver Diseases (AASLD) last November was Herbert Bonkovsky, MD, from the
University of Massachusetts in Worcester. Both Rebetol and alfa * interferon
have immune-modulatory and some antiviral properties.
Who Will Treat HIV/HCV Co-Infected Persons?
Previously, many uninsured Californians with HIV/HCV co-infection who were
not eligible for MediCal insurance coverage, could not afford the high price
of Rebetron. Now that the ADAP has added it to the HIV formulary, many of
these patients will have access to the drug. However, a major issue is who
will be treating the HIV/HCV co-infected patients who need Rebetron?
While an increasing number of community physicians have been treating
persons with HIV, the same is not true for those with HCV. Many
"generalists" (Family Medicine, Internal Medicine, General Practitioners) do
not have the requisite knowledge of and experience with treating persons who
have chronic hepatitis C. Many Infectious Disease physicians who treat
persons with HIV/AIDS would prefer to have Gastroenterologists or
Hepatologists treat the hepatitis disease. Yet, many gastroenterologists
prefer not to treat those with HIV infection. Moreover, many
gastroenterologists prefer not to treat chronic hepatitis C, much less
perform the liver biopsy that is often required as a part of hepatitis C
care. The reason is partly due to the stereotypic profile and stigmatization
of injection drug use that is associated with persons who have HCV
infection. Also, in part, it is due to the preference by many "GI"
(gastrointestinal) physicians not to be "burdened" with managing ongoing and
common side effects related to chronic therapy. (Note in many institutions,
the "Interventional Radiologist" ("X-ray" and Imaging specialist) is doing
liver biopsies.)
Due to a significant rate of increased liver enzymes when HAART (highly
active antiretroviral therapy) for HIV is taken by patients with chronic
viral hepatitis, current knowledge of both diseases is important for
physicians when treating patients with HIV/HCV, HIV/HBV or HIV/HBV/HCV
co-infection. For more information about increased liver enzymes in patients
with HIV/HCV co-infection after HAART, CLICK BELOW
http://www.hivandhepatitis.com/conferences/viralhep.html#day4.
http://www.hivandhepatitis.com/conferences/idsa.html#sulkowski
Also, the "state-of-the-art" of chronic hepatitis C is undergoing rapid
development. Therefore, it is an increasing challenge for physicians to
remain current, similar to how it has been for HIV/AIDS.
Fortunately, patients who live near a medical school usually have access to
physicians knowledgeable about HIV/AIDS and hepatitis viruses. For those
patients not in those geographic areas, access to physicians who remain
current is more of a problem.
Potential Problems When Combining
Treatments for Both Infections
A major issue in the area of treatment for HIV/HCV co-infection is whether
drugs to treat each infection have negative interactions with each other
when taken by patients. This is because of laboratory research that revealed
"antagonistic" (effects canceled) when Rebetol was combined with either
Retrovir (zidovudine, AZT, ZDV), Zerit (stavudine, d4T) or Hivid
(zalcitabine, ddC). In contrast, when Rebetol was combined with Videx, an
enhanced effect by the latter occurs. Yet, most patients with HIV are taking
two NRTI (nucleoside reverse transcriptase inhibitor) drugs as a part of
their HAART regimen. And, the vast majority of those are taking either
Retrovir or Zerit. Therefore, there has been reluctance by physicians to
prescribe Rebetol (as part of Rebetron) when patients were taking any of
those three anti-HIV NRTI drugs listed above. Only a few small studies have
been reported whereby the combination of drugs for HIV/HCV were taken by
patients. In very preliminary reports in a very small numbers of patients
followed for short periods, there were no adverse effects on HIV or HCV
viral loads. Co-infected patients generally had stable HIV disease
(undetectable HIV viral load and increased CD4 counts) with HAART and then
started Rebetron (many with reduced dose Rebetol, as described above). In
general, HCV viral loads were driven to undetectability, while the HIV blood
markers remained unchanged. However, blood levels of "intracellular
NRTI-triphosphates" (the active component of NRTI drugs) have not been
reported.
Also, liver biopsy results usually are not reported.
Treatment Guidelines for Patients with
HIV/HCV Co-Infection
In September 1999, a consortium of San Francisco Bay Area physicians and
national physician experts in hepatitis C or HIV/HCV co-infection met to
discuss treatment issues for the co-infected patient and to devise a set of
Treatment and Management Guidelines. Those Guidelines currently are in a
draft form and will be made public within the next few months (watch this
website-it will be posted here.)
Research About HIV/HCV Co-Infection
The body of research in the area of HIV/HCV co-infection is rather small,
when compared to that of HCV mono-infection and markedly smaller than that
of HIV/AIDS. Slowly, HIV/HCV-related research is starting to increase. For
example, the recent 7th Conference on Retroviruses and Opportunistic
Infections (7th CROI) that took place four weeks ago had an entire oral
session on Hepatitis C for the first time, during which Mark Sulkowski, MD,
from Johns Hopkins University, presented an overview of HIV/HCV
co-infection. Also, there was a half-row of posters on one day that was
devoted to HIV/HCV or HIV/HBV co-infection. Similarly, at last November's
37th Annual Meeting of the IDSA (Infectious Diseases Society of America),
there was an entire oral session devoted to Hepatitis C, during which Dr.
Sulkowski also presented an overview of HIV/HCV co-infection.
Long-Acting "Peg" Alfa * Interferon
A longer-acting "pegylated" form of Intron A called PEG-Intron is under
development by Schering, the manufacturer of Rebetron. Roche Pharmaceuticals
has its own Experimental version of pegylated alfa * interferon under
development called Pegasys. The dose for either is a once-weekly injection.
This allows for a steady blood level of alfa * interferon during a 7-day
period. Roche's alfa * interferon is called Roferon-A.
On Dec. 23, 1999, Schering-Plough submitted a Biologics License Application
(BLA) to the US Food and Drug Administration (FDA) seeking marketing
approval for PEG-Intron (peginterferon alfa-2b) for the treatment of chronic
hepatitis C in adults with compensated liver disease.
Just two weeks ago on February 22, it was announced that the Committee for
Proprietary Medicinal Products (CPMP) of the European Agency for the
Evaluation of Medicinal Products (EMEA) issued a "positive opinion"
recommending approval of PEG-Intron for the treatment of adult patients with
chronic hepatitis C. The CPMP opinion serves as the basis for a European
Commission approval, which is typically issued within approximately three
months. Commission approval of the centralized Marketing Authorization
Application for PEG-Intron will result in one single Marketing Authorization
with unified labeling that will be valid in all 15 European Union-Member
States.
* Note that all four generic versions use the spelling 'alfa' and not
'alpha' interferon.
3/6/00
References:
August, Ken. (Public Relations for the California Department of Public
Health). Personal communication on March 4, 2000.
Bonkovsky HL and others. Low doses (600 mg/day) of ribavirin are superior to
high doses (1000-1200 mg/day) with interferon for chronic hepatitis C:
results of a controlled, randomized, multicenter trial. Hepatology 30(4)
part 2 (supplement): 265A and Abstract and poster 418 at the 50th Annual
Meeting of the AASLD (American Association for the Study of Liver Diseases);
November 5-9, 1999; Dallas, Texas
Stansell, John D. Management of the HCV and HIV Co-Infected Patient.
Innovations in the Management of Hepatitis C. March 3, 2000; San Francisco,
California.
Sulkowski M. The treatment of chronic HCV infection in HIV-infected persons.
Abstract and oral presentation S11 at the 7th Conference on Retroviruses and
Opportunistic Infections (CROI); January 30-February 2, 2000; San Francisco,
California.
Sulkowski M and others. Combination therapy with peginterferon alfa-2a
(PEG-IFN) and ribavirin in the treatment of patients with chronic hepatitis
C (CHC): a phase II open-label study. Hepatology 30(4) part 2
(supplement):197A and Abstract and poster 145 at the 50th Annual Meeting of
the AASLD (American Association for the Study of Liver Diseases); November
5-9, 1999; Dallas, Texas
Consultancy
HAAC urges ADAPs to consider purchasing interferon from other manufacturers
and to buy ribavirin from one of several compounding pharmacies at 1/3 the
cost of Schering's Rebetol
by Ronald Baker, PhD
Hepatitis C activists reacted angrily to the announcement that the New York,
California and possibly other ADAPs (AIDS Drug Assistance Programs) have
added Schering's Rebetron to their formularies for the treatment of patients
co-infected with HIV and HCV (hepatitis C virus).
The Rebetron kit is an FDA-approved treatment for HCV infection that
contains two products: Schering's Intron A (interferon alfa 2b) and Rebetol
(ribavirin), which Schering has licensed for marketing from ICN
Pharmaceuticals. Members of the Hepatitis C Action & Advocacy Coalition
(HAAC) contend that adding Schering's "bundled" product Rebetron for the
treatment of HCV/HIV co-infection to ADAP formularies is too expensive,
raises safety issues, and diverts scarce financial resources away from ADAP
funding for primary treatments for HIV and HIV-associated opportunistic
infections.
HAAC coordinators Brian Klein and James Learned sent the following letter
outlining their concerns and alternative recommendations to ADAP
administrators in all 50 states, Puerto Rico and Washington, DC:
"We are writing to strongly oppose the inclusion of Schering-Plough's
Rebetron on ADAP formularies for the treatment of HIV/HCV co-infection.
Making HCV treatment available to co-infected individuals through ADAP is
certainly a laudable goal, but we do not believe that including Rebetron is
the best way to accomplish this goal.
"The Rebetron kit, a two-drug kit containing Intron A (injectable interferon
alfa-2b) and Rebetol (oral ribavirin capsules), is NOT the most efficient,
effective or safest way to use interferon and ribavirin. Most patients need
larger doses of interferon and/or lower doses of ribavirin than are packaged
in the Rebetron kit. Purchase of the Rebetron kit would result in the
accumulation of large amounts of unneeded ribavirin - a terrible waste of
scarce resources as well as a significant safety concern. Furthermore, the
price of the ribavirin in the kit is more than 325% above the price of
Ziagen (abacavir), the next most expensive nucleoside on ADAP formularies.
We are seriously concerned that this grossly overpriced and inappropriately
packaged kit would divert money from primary antiviral and OI treatments
needed by so many on ADAP. Our concerns are expressed in greater detail
below along with a suggested solution:
Safety and Efficacy
"Rebetron does not easily allow adjustments to treatment to maximize
individual safety and efficacy. In many circumstances, the Rebetron kit
provides interferon doses that are too low and ribavirin doses that are too
high.
"In the rosiest of scenarios, Rebetron has been shown to produce sustained
response (virologic undetectability six months post-treatment) in less than
40% of singly infected HCV individuals. When the data on genotypes 1a and 1b
are reviewed alone (60-80% of those with HCV in the US), this figure drops
to 28%. This figure drops even further when viewing the sustained response
of those with baseline HCV viral loads > 2 million copies/ml. The
overwhelming majority of co-infected patients are those with genotype 1a or
1b and higher viral loads.
"To maximize virologic response, most co-infected patients need higher doses
of interferon than the 3MIU tiw in the fixed Rebetron kit. Some respond
better to daily interferon dosing. Other patients may actually respond
better or have less adverse events with one of the other two interferons on
the market (Amgen's Infergen and Roche's Roferon).
"The Rebetol in the standard fixed Rebetron kit comes in 1000 or 1200mg/day
doses depending on body weight. Co-infected patients are particularly
susceptible to hemolytic anemia that can occur with ribavirin treatment.
Patients have to add in erythropoiten to counter the effects, reduce the
dosage of the ribavirin, or both. Yet ADAP and patients will still have to
purchase and be prescribed the full standard doses of Rebetol since that is
the way it is co-packaged in the Rebetron kit. This is a terrible waste of
resources as well as a safety concern, since patients will often accumulate
large amounts of unneeded Rebetol. Furthermore, research is showing that
lower doses of the ribavirin (at least down to 800mg/day if not lower) are
equally effective and less toxic than the standard doses. The Rebetron kit
is not the most efficient, effective or safest way to use interferon and
ribavirin.
Price and Bundled Packaging
"Even with the 15% discount below AWP of Rebetron that ADAP will receive,
this is an exorbitantly overpriced medication for ADAP to have to purchase.
The price of the nucleoside analogue Rebetol in the kit is about $1000/month
at AWP-if it were available separately. This is more than 325% above the
price of Ziagen (abacavir), the next most expensive nucleoside on ADAP
formularies. Most patients will have to go on treatment for one year,
meaning a cost to ADAP of approximately $15,300 per patient in addition to
their other treatments. The fixed dosing will likely be effective in less
than 25% of these patients, who will then end up having to be re-treated or
use something else. Patients and limited ADAP resources should not be held
hostage to this fixed dose packaging that is demanding an unwarranted
premium price. We are also concerned that this expensive treatment could
divert money from primary antiviral and OI treatments needed by so many on
ADAP.
Social Consequences
"HCV affects more than 4 million Americans, while HIV affects about
1million. Allowing those who are co-infected access to the expensive
treatment of Rebetron, while those who are singly infected with HCV cannot
get it, could set a troubling double standard of access to treatment.
However we cannot ignore that at least 40% of people infected with HIV are
co-infected with HCV. HCV, although a separate infection, is clearly
opportunistic in HIV. The progression of liver disease is often much faster
in co-infected individuals than in those with HCV alone; therefore treatment
needs must be addressed for these individuals.
A Suggested Solution
"There is a less expensive and more flexible HCV treatment alternative to
providing Rebetron on formulary. ADAP should get bids from the three current
interferon makers (Amgen, Roche, and Schering-Plough) to get the best price
on interferon alone and in a variety of doses for maximal efficacy.
"ADAP should also put out for bid to obtain ribavirin USP separately through
compounding pharmacies. Ribavirin has been available through compounding
pharmacies since July 1999. Doctors can legally write individual
prescriptions to the compounding pharmacy directly. ADAP should be able to
get a price of at least $1.25 per 200mg capsule of ribavirin, bringing the
standard dose price down to $225 from Schering's approximate $1000/ month
for Rebetol (if it were available separately)-an 80% reduction. In many
circumstances, patients will not need this standard dose, thus saving ADAP
even more money.
"This solution will serve not only those who are co-infected, but, as part
of a larger strategy to force a Rebetron price reduction, will ultimately
benefit people who are singly infected with HCV as well.
"ADAP can cut the price of a year of HCV treatment nearly in half using this
method, now being utilized by state correctional programs including Texas
and Utah as well as many HMOs across the country. We are happy to provide
you with any information you need to assist you in this decision. Please
contact us at your earliest convenience regarding this important matter. We
look forward to hearing from you in the near future."
Brian D. Klein, MA, LMSW
HAAC-SF, haa...@hotmail.com (415) 863-5172
James Learned
HAAC-NY, James_...@prodigy.net (718) 369-3779
cc: Joseph O'Neill, HIV/AIDS Bureau
Health Resources and Services Administration
Joe Kelly, Deputy Director
National Alliance of State and Territorial AIDS Directors
Richard Jefferys, Access Project Director
AIDS Treatment Data Network
Members of the HIV and HCV communities
0/6/00
Consultancy
All HCV quantitative viral load tests will be reported in "international
units" in one month; physician and patient confusion is very likely
by Harvey S. Bartnof, MD
A seminar that addressed treatment and management issues for the HIV/HCV (*
hepatitis C virus) co-infected patient was held in San Francisco on March 3,
2000. A small group of HCV and/or HCV-treating physicians participated in
the seminar that was sponsored by Schering Oncology Biotech by an
unrestricted educational grant.
Nezam H. Afdhal, MD, indicated that tests measuring HCV RNA viral load
(quantitative viral burden) would have a new standard of units within the
next month. Dr. Afdhal is Chief of Hepatology at the Beth Israel Deaconess
Medical Center at Harvard Medical School in Boston, Massachusetts. While
current HCV viral load tests are reported in "copies per milliliter," the
new standard will be in "international units." Dr. Afdhal said that the new
unit measurements would have numbers that are much lower than their
equivalence in copies per milliliter. Therefore, it is very likely that
patients and physicians who are accustomed to the current measurement will
have some degree of confusion until the newer measurement has been in use
for some time. The World Health Organization (WHO) ruled in 1997 that the
conversion to international units should take place.
Dr. Afdhal said that he is not aware of any "conversion equation," similar
to what was used to compare HIV viral load assay results using different
test kits soon after they were first available. As a "rule of thumb" for the
new HCV international units (IU), Dr. Afdhal said that at the "high end" of
results, multiplying the results in IU times a factor of four would give an
approximate estimate of what the results would have been in the old "copies
per milliliter" measurement. Results at the "low end" in IU could be
multiplied by two to give an approximate estimate of what the results would
have been in the old measurement. However, Dr. Afdhal indicated that the
cut-off between "high" and "low" was not specifically defined. (In the old
measurements, a result greater than 2 million copies per milliliter was
considered "high," while a result less than that was considered "low.") Dr.
Afdhal did give an example that 500,000 IU would approximately equal 2
million copies per milliliter.
Physicians and patients accustomed to thinking about HIV viral load results
usually have been surprised by the overall higher levels of HCV viral loads
in copies per milliliter that are very common. The higher levels are
associated with a daily virion production that is 100- to 1,000-fold higher
in chronic hepatitis C than in HIV disease.
The most commonly used tests to quantify HIV RNA viral load use either "PCR"
(polymerase chain reaction) from Roche or the "bDNA" (branched chain DNA)
from Bayer (formerly Chiron Diagnostics).
Unlike HIV viral loads that usually are relatively stable over a period of
months, HCV viral loads can be much more variable. Also, unlike HIV viral
loads that have significant prognostic information (about future HIV disease
course), the HCV viral load is not related to long-term disease outcome or
with the degree of hepatitis. Physicians and patients who are knowledgeable
about HIV viral loads often incorrectly assume that HCV viral loads carry
the same prognostic significance in chronic hepatitis C. However, HCV viral
loads do correlate with response to therapy, which in turn is related to
long-term liver disease outcome.
Managing Side Effects
During the Seminar, there also was a presentation entitled, "Side Effects
Management." Yvonne S. Baulch, RN, MS, OCN, a Patient Care Consultant with
Schering Oncology, was the speaker. Ms. Baulch reviewed some very practical
tips about managing side effects due to Rebetron or Intron-A. For example,
she said that the Rebetol (ribavirin) component of Rebetron should be taken
with breakfast and dinner and not at bedtime. This is because many patients
will have insomnia (inability to sleep) after Rebetol dosing. Also, she
recommended that the alfa * interferon be injected at dinnertime for the
opposite reason. Many patients will have the side effect of fatigue that
starts approximately four hours after a dose. This can be more troubling if
it occurs during the daytime; whereas at bedtime or nighttime, would not be
a problem.
Ms. Baulch also described the "Be In Charge" program offered by Schering for
patients taking Rebetron. This is a comprehensive patient support program
with ongoing nurse counseling, patient education, and support materials. It
is designed to assist physician offices with patient management and to
improve adherence. One part of this program involves a nurse counselor who
will call the patient monthly to see how he/she is doing, particularly about
side effects and to help with adherence issues. Physicians or patients may
call 1-888-437-2608 (1-888-HEP-2608) Monday through Friday, 9AM to 8 PM,
eastern standard time, for more information. The information also is
available on the Internet at www.beincharge.com
Ms. Baulch discussed the "Patient Care Consultant" program also offered by
Schering for Rebetron patients. This is a group of 31 advanced practice
nurses in the US who are available to assist with managing side effects
associated with Rebetron or Intron-A. Physicians may call 1-800-782-2347
extension 6003 for more information.
Schering also has a financial assistance program for patients called
"Commitment to Care." The telephone number for patients to call is
1-800-521-7157.
3/6/00
References:
Afdhal, Nezam H. Current strategies for the diagnosis and treatment of
hepatitis C. Innovations in the Management of Hepatitis C. March 3, 2000;
San Francisco, California.
Baulch, Yvonne S. Side Effects Management. Innovations in the Management of
Hepatitis C. March 3, 2000; San Francisco, California.
Consultancy
At 28 weeks, 35% undetectability rate; CD4 count increase of 210 cells per
microliter
A 5-drug, 2-drug class treatment combination during primary HIV infection
led to an 80% HIV RNA viral load undetectability rate (limit 50 copies per
milliliter) at 28 weeks. Agenerase (amprenavir), Ziagen (abacavir) and
Combivir (Retrovir or zidovudine plus Epivir or lamivudine, 3TC), led to a
35% undetectability rate at 28 weeks using an ultrasensitive test with a
limit of 5 (five) copies per milliliter. CD4 counts increased by
approximately 210 cells per microliter. A total of 98 patients were included
in the analysis; 151 have been recruited. Despite undetectable viral load
levels, there still was evidence of HIV DNA and mRNA (messenger RNA) within
blood mononuclear immune cells. Markers of "immune activation" were
decreased markedly, as measured by the decline in "CD8+CD38+" (suppressor)
cells. After 12 months of 5-drug HAART (highly active antiretroviral
therapy), patients will be randomized to HAART alone, HAART plus the ALVAC
vaccine, or HAART plus the ALVAC and Remune (inactivated HIV) vaccines. The
entire study will last for at least 24 months. The lead author was David
Cooper, MD, from St. Vincent's Hospital in Sydney, Australia.
2/17/00
Reference:
Cooper D and others. Intervention with quadruple HAART
(Combivir/abacavir/amprenavir) during primary HIV-1 infection (PHI) is
associated with rapid viraemia clearance and decrease of immune activation.
Abstract and poster presentation 552 at the 7th Conference on Retroviruses
and Opportunistic Infections; January 30-February 2, 2000; San Francisco,
California.
Consultancy
Hepatitis Viruses
HBV disease reactivation described as a "new entity" in those with past
infection; 84% of 37 patients were co-infected with HIV plus two or three
hepatitis viruses
by Harvey S. Bartnof, MD
Since the transmission routes are similar for HIV, HBV (hepatitis B virus),
HCV (hepatitis C virus) and HDV (hepatitis D virus), many patients with HIV
have co-infection with one or more hepatitis viruses. There are few reports
in the literature regarding the effects of HAART (highly active
antiretroviral therapy) for HIV among those patients who have co-infection
with two or more hepatitis viruses. Now, researchers from the Instituto de
Salud Carlos III in Madrid, Spain have reported results regarding 37 such
patients in a retrospective study. The data were presented at the recent 3rd
International Conference on Therapies for Viral Hepatitis (Maui, USA,
December 12-16, 1999). The lead author was R. Rodriguez-Rosado, MD. A
co-author was Victor Soriano, MD.
All 37 patients had HIV infection requiring HAART, in addition to chronic
hepatitis B. In this case, all were positive for hepatitis B surface
antigen, although at least four patients also had hepatitis B "e" antigen
(total not stated). In addition, eight or 21% of patients had triple
co-infection with HIV/HBV/HDV. (Hepatitis D is a "super-infection" that
occurs among those who have chronic hepatitis B.) Another 18 patients (49%)
had triple co-infection with HIV/HBV/HCV. And, five or 14% of patients had
quadruple co-infection with HIV/HBV/HCV/HDV. All 37 patients began HAART
between 1996 and 1999. HAART included Epivir (lamivudine, 3TC) for 87% of
patients. (Epivir has both anti-HIV and anti-HBV activity.) Other drugs that
were a part of HAART were not stated.
Selected descriptive results were reported in this cohort of patients. Among
those with detectable HBV DNA at baseline who had Epivir as a part of their
HAART, more than 80% became undetectable after at least six months of
therapy. There is an assumption that most patients, if not all, had
detectable HBV DNA at baseline. However, the baseline percentage was not
reported. Four patients (11%) seroconverted from "e" antigen positive to "e"
(core) antibody positive. (There is an assumption that many patients were
"e" antigen positive at baseline. However, the number who was positive was
not stated.) Also, another three patients (8%) seroconverted from surface
antigen positive to surface antibody positive. (Each of these
seroconversions is associated with a better clinical course of disease and a
lower rate of contagion or infectiousness to sexual and needle-sharing
partners.) The poster did not indicate whether these patients with HBV
seroconversions were those with double, triple or quadruple virus
co-infection.
Dr. Rodriguez-Rosado reported that one patient developed acute hepatitis
symptoms after starting HAART. Symptoms include nausea, weakness, loss of
appetite, abdominal pain, vomiting, jaundice (yellow coloring of the skin)
and/or icterus (yellow coloring of white of eyes), weight loss, and fever
(not all symptoms need to be present). Associated with these symptoms would
be an increase in liver enzymes (ALT, alanine aminotransferase and AST,
aspartate aminotransferase). However, the patient did not seroconvert from
antigen positivity to antibody positivity. Therefore, Dr. Rodriguez-Rosado
said that this patient had acute hepatitis symptoms due to "inflammatory
immune recovery syndrome." This syndrome is associated with an improved
immune system due to HAART and reactivation of one or more opportunistic
conditions. They generally occur within the first six to nine months after
HAART is started and include "shingles" (skin rash due to varicella zoster
virus), tuberculosis, and others. It was not stated whether this patient had
double, triple or quadruple virus co-infection.
Another patient developed symptoms of hepatitis with increased liver enzymes
after Epivir was discontinued. A rebound of HBV growth was the most likely c
ause, according to the authors. This development can also occur among those
patients with chronic hepatitis B (without HIV infection) after monotherapy
with Epivir-HBV is discontinued. A similar picture can develop in some HBV
mono-infected patients who develop resistance to Epivir-HBV. The poster did
not indicate whether this patient had double, triple, or quadruple virus
co-infection.
Dr. Rodriguez-Rosado described three other patients who developed acute
symptoms of hepatitis B after HAART for HIV, with past exposure to or
"recovered" HBV infection. (These patients could not have been a part of the
original 37 above, all of whom were surface antigen positive at baseline.)
These three patients had the following baseline profile markers for HBV:
positive for "e" or core antibody, negative for "e" antigen, (assumed)
negative for HBV DNA, and negative for surface antigen. During each of their
episodes of acute hepatitis, HBV DNA became detectable and their tests for
surface antigen became positive. Two of them even became positive for "e"
antigen. During their episode of acute hepatitis, all had CD4 counts of 200
cells per microliter or higher. Therefore, the authors conclude that the
acute B hepatitis symptoms were not due to immunodeficiency. The authors
hypothesized that each of these patients had "occult" hepatitis B at
baseline, rather than past exposure to or recovery from HBV. Their
explanation was that these patients likely had a low, but detectable HBV DNA
at baseline, with negative tests for surface antigen. However, baseline HBV
DNA tests were not reported or not performed. Dr. Rodriguez-Rosado concluded
that this occurrence represents a new clinical entity or description.
In the past, those who had negative tests for HBV antigen, positive tests
for core ("e") and surface antibodies and normal liver enzymes were assumed
to have past or recovered HBV infection. Acute hepatitis symptoms with
recurrent antigen (and DNA) markers were not believed to occur among those
patients. However, they were not tested for HBV DNA or, if they were, they
might have had "false negative" result due to test insensitivity. Yet,
according to the current report, reversion to active HBV disease may occur
in the setting of HAART for co-infection with HIV. Dr. Rodriguez-Rosado's
hypothesis about this new clinical entity would need to be confirmed with
positive baseline HBV DNA tests. However, newer generation tests that are
more sensitive might need to be developed. Also, there would need to be
other reports by other clinicians of the same occurrence. A simpler
explanation could be laboratory test errors at baseline.
In their conclusions, the authors say that there are now five causes of
acute symptomatic hepatitis among patients with HIV who are co-infected with
HBV (and possibly other hepatitis viruses) after HAART is started. They are:
Liver toxicity due to anti-HIV drugs that are a part of HAART;
Acute immune restoration syndrome;
After Epivir is withdrawn or resistance to Epivir develops;
Hepatitis "flare" that is associated with seroconversion to (development of)
testing positive for antibodies to HBV's core ("e") and/or surface; and
"Reactivation of HBV in [an] HIV positive person with markers of past HBV
exposure." The authors add that this fifth reason is a "new entity, which
merits further study."
There was much information that was not reported about the total of 40
patients in the poster presentation. They include: baseline and resulting or
interim laboratory measurements (HBV DNA viral loads, liver enzyme tests,
HBV antigens tests, HCV RNA viral loads, HIV viral loads, CD4 counts); liver
biopsy results (examination under the microscope); specific drugs in HAART
regimens; side or adverse effects from HAART; and drug discontinuation
rates. Also, the association of specific outcomes (e.g., seroconversions)
with the various subgroupings of hepatitis virus co-infections would have
been very useful. For example, there have been past reports of poorer
responses to anti-HCV therapy among patients co-infected with HBV/HCV
(without HIV). Future analyses and reporting of the 40 patients discussed in
the poster would be helpful for physicians, researchers and patients.
12/27/99
Reference:
Rodriguez-Rosado R and others. Impact of antiretroviral treatment on
hepatitis B virus infection in human immunodeficiency virus-infected
patients. Abstract and poster presentation 59 at the 3rd International
Conference on Therapies for Viral Hepatitis. December 12-16, 1999; Maui, USA
and Antiviral Therapy 1999; 4 (Supplement 4), 20.
Ian Baird
> willing to pay for interferon. It's all part of the postcode lottery that
> makes up the NHS.
I don't think this will be a problem. I've never had difficulty in obtaining
treatments for my Haemophilia or HIV, both of which are expensive to treat.
My Doc was talking of starting me on treatments if I cannot get a biopsy.
Besides, the NHS gave me both HIV & HCV so they can ****** well pay to fix
it.
Ian Baird
date?
Firebird
ianmac...@ibaird.fsnet.co.uk (Ian Baird) wrote:
> I don't think this will be a problem. I've never had difficulty in
> obtaining
> treatments for my Haemophilia or HIV, both of which are expensive to
> treat.
> My Doc was talking of starting me on treatments if I cannot get a
> biopsy.
> Besides, the NHS gave me both HIV & HCV so they can ****** well pay to
> fix
> it.
Then you have to balance your present state of health and how badly your
liver is damaged against the known side effects and the fact that combo is
60% successful at most.
Plus we all keep hoping that they will come up with a real cure soon.
Alan
Firebird
> I'm curious, what is this postcode lottery NHS?
There is some strange way of funding the NHS now.
> And GP (general
> practitioner?)
Correct!
> willing to pay? What?? Who pays? I'm confused.
They sort of budget a GP's money according to how many patients he/she
has. However if you live in an area full of fit healthy people the budget
goes further. If you live in an area of older or sicker people who need
more health care then the money doesn't stretch as far. So I was lucky in
that my GP was able to finance the interferon. Some people aren't.
The tax-payer always pay whatever happens.
> I thought that national healthcare meant that the government pays for
> your
> doctor visits and treatment from taxes.
Yes! They told me that too when I started paying taxes as a young man.
Basically, they lied!
> In fact, I've always wished we had national healthcare in this
> country.
When they created the system they didn't know how pharmaceutical giants
would become money sinks.
> I see now that I don't understand what I'm wishing for....
> I guess I don't even know how it really works.
> Saydee
Parts of it work fine. Other parts are problematical.
Alan
Alan
Firebird
> <!doctype html public "-//w3c//dtd html 4.0 transitional//en">
> <html>
> Thanks for enlightening me. It doesn't seem fair that the doctor's
> allotted money determines who gets treatment. Which leads me to
> two
> more questions - if your doctor didn't have the funds to pay for
> treatment
> could you switch doctors?
Yes, but it may require you to move address, hence the nickname Postcode
lottery. A classic example is one street in London, one side is in poorer
Fulham and the other side is in Battersea.
> Pay for the treatment yourself?
You can always do that!
> <p>At least you have national healthcare. Our system has been
> ranked
> below yours and many other nations; I read that in the paper last
> week.
> One in five Americans doesn't have health insurance. And even if
> you do have insurance, they often won't pay for things. They
> really
> like to get us on pre-existing conditions or they say the doctor charged
> too much so they won't pay the full amount. And if you work for a
> small company, you hope your fellow workers are healthy. Because
> if they're not and too many claims are made then the whole company gets
> canceled for insurance.
> <p>Our insurance companies here do not pay for medication. In
> fact,
> medicare for the old people doesn't pay for medications. The
> senior
> citizens that live near the Canadian border takes busses over to Canada
> and buy their medication there because it's cheaper. Sadly, some
> seniors go without food or other necessities to pay for medication.
It was like that where I lived in Africa.
> <p>I still think I wish we had your system. Now that I've talked
> about our system, I've depressed myself.
> <p>Saydee
Aw come on! Just one smile for me... <grin>
Alan
Firebird
> Well.... I'm not that depressed. Shoot, I'm happy to have
> insurance because things were a lot harder without it.
> See, I'm smiling.
> Saydee
Your smile lights up the whole newsgroup.
Alan
Firebird
> Thanks Alan. :-)
>Saydee
The pleasure was all mine. That was a lovely smile.
Alan
Pete Zakel
>What can a liver biopsy tell me that blood tests cannot?
>What does the procedure entail?
A liver biopsy can tell the state of the liver with regard to fibrosis and/or
cirrhosis. Neither blood tests nor non-invasive procedures (ultrasound,
x-ray, MRI, etc.) can adequately define the state of the liver.
A biopsy entails sticking a biopsy needle between your ribs and into your
liver and pulling a section out. It is typically done with a mild general
anaesthetic such as Versed and a local anaesthetic, and directed by
ultrasound. There can be pain afterward if a nerve is inflicted (nerves
can't be seen by ultrasound) and there is a small risk of serious bleeding
if a major blood vessel is inflicted (I know that's not the right verb, but
I can't think of the right verb at the moment...). My own biopsy was painless
(the worst pain was when the doctor was sticking her finger into my side
looking for the right spot to stick the needle) and without incident.
> I understand the combo for HCV is very unpleasant
Note that combo *can* be unpleasant, but the degree of unpleasantness varies
from person to person. You always have the option of stopping treatment if
you find you can't handle the side effects.
-Pete Zakel
(p...@seeheader.nospam)
"Successful and fortunate crime is called virtue."
-Seneca