hepcBC.bull January 98 Part 2
SQUEEKY’S CORNER
Me, Sex and the Other Guy
Recently there’s been a lot of flack going round about
sexual transmission of HCV and we ain’t talking Roberta.
Some people get so frightened when they find out they have the
virus that they stop having relations with their partners, and,
as a result, many wonderful marriages have come to an end in
bitterness and tears. But, there has been a lot of talk recently
on the HEPV-L list about sexual transmission, and several members
have written in with their stories, stories which state that
their hep was sexually transmitted. Not that I want to split
hairs here, or anything like that—this is way too serious a
subject to squeek about—but I think it’s important to
understand that by “sexual transmission” we may be
talking about an activity that is larger than the sexual act. Or
are we? Is HCV transmitted during the act of sexual congress, or
can it be spread from partner to partner through more “innocent”
activities, such as kissing, shared coffee cups, a lick of
somebody’s fork? I don’t know, I’m just asking.
Most recent studies suggest that although the HCV virus can be
found in bodily fluids, the form and quantity of the virus is
such that it is highly unlikely that contagion be an issue.
However, if this were the case (i.e., lateral transmission from
bodily fluids) then the incidence of HCV in families would be
much higher, as is the case with Hep B, where lateral
transmission is a serious concern. Is HCV spread laterally?
Should we have our children tested? All the studies available say
no. And yet, the medical profession is still at a loss to explain
the origins of many cases of HCV, publicly preferring to lay the
blame on drugs and ethnic lifestyles.
Speaking of which, recently, it was brought to my attention that
there are many HCV positive children in the Aboriginal
communities here on Vancouver Island. How did they get their Hep?
What is the mitigating factor? Does the medical community have an
answer? I’m working on it, and as soon as I find out, I’ll
let you know. Meanwhile, here’s some stuff hot off the press
about why you shouldn’t be worried about getting or
spreading HCV sexually.
1. "Safer Sex Practice for Chronic HCV Carriers:
Is It Necessary?"
According to an abstract submitted by the authors to the First
Australasian Conference on Hepatitis C, held March 16-18, 1997,
in Sydney, Australia, "The efficiency of sexual transmission
of hepatitis C virus (HCV) is an important issue for individuals
with HCV infection and the role of sexual transmission in the
epidemiology of HCV infection continues to be debated. In
particular, whether HCV-discordant couples in established
monogamous relationships should be advised to use condoms is
controversial. We have routinely offered testing of the current
heterosexual partner to Sydney donors identified anti-HCV
positive attending for follow-up since January 1994. As at
September 1996, the partners of 40 such donors had been tested.
Only one of the 40 partners tested anti-HCV positive. This
partner had an independent established parenteral risk factor for
HCV infection. The median duration of the couples sexual
relationships was five years (range four months to 42 years).
Thirty-eight couples reported rarely or never using condoms in
their sexual relationships; two couples reported using condoms
for the majority but not all of their sexual relationships. Our
findings support larger epidemiological studies in blood donors,
multiply transfused patients and recipients of contaminated Rh
anti-D immunoglobulin which suggest that heterosexual
transmission of HCV is extremely uncommon. We counsel couples in
established monogamous relationships that it is probably
unnecessary to modify their sexual practice, other than to
consider using condoms during menstruation, anal intercourseor
when
genital ulceration is present."
AUTHORS: A.R. Davis and A.M. Kowalik. Affiliations not provided.
SOURCE: Hepatitis Weekly, 9/29/97, p16, 1/2p
2. “Absence Of Hepatitis C Virus Transmission but
Frequent Transmission Of HIV-1 from Sexual Contact with
Doubly-Infected Individuals”
Hepatitis C virus (HCV) is transmitted through infected blood and
blood products, but evidence of other routes of transmission is
less clearly understood. In a study designed to examine human
immunodeficiency virus (HIV) transmission, the prevalence of HCV
has also been measured. Sixty-one couples were analysed, 30 in
which partners were at risk through sexual contact alone, of whom
12 (40%) became infected with HIV and none with HCV. Thirty-one
partners were exposed sexually and additionally through
intravenous drug use. Of these, 16 (52%) became infected with HIV
and 25 (80%) contracted HCV infection. These findings support the
evidence of others that HCV is only rarely transmitted by sexual
intercourse in heterosexual relationships and that HIV is not a
cofactor for HCV transmission.
Author: Jr Robertson, Muirhouse Med Grp, 1 Muirhouse Ave,
Edinburgh Eh4 4pl, Midlothian Source: Journal Of Infection, 1997
Sep;35(2):163-166
BIOPSIES: A COMPARISON
I have heard many biopsy stories from people in my support group
and from those on the internet. They have included a man whose
bile duct was perforated and a woman whose blood covered the
room. They also include people who engaged in all normal
activities within a few hours after the procedure.
My first biopsy, performed in December of 1995, took place in a
Victoria hospital. My local gastroenterologist recommended the
physician as being the best liver biopsy person in town. My
doctor told me to expect to stay overnight, and I did. I had
blood tests done early in the morning and took up temporary
residence in a private room. Eventually the nurse wheeled me off
to meet my fate. I requested, and was refused, any sort of
medication to ease either pain or anxiety. The nurses, who were
very caring, did cover me up with a heated blanket to stop my
shivering, and one held my hand during the biopsy. The doctor
told me he would take 3 specimens. The first was painless—after
the initial freezing procedure, which was easy to endure—and
I was remarking on that fact when he took the second specimen.
Perhaps it was because I wasn’t holding my breath that I
experienced severe pain across my abdomen and in my right
shoulder. The doctor immediately checked the ultrasound machine
for any complications and decided to forgo the third sample. I
had a big drop in my blood pressure and it hurt me to breathe or
move for a couple of days because of the pain, which I could
control with Tylenol. The hospital released me the following
morning.
I was not overjoyed to learn that I would have to endure yet
another biopsy at the end of my Interferon/Ribavirin trial.
The time arrived this last December 15th. I decided to have the
biopsy done over in Vancouver. At least that way, I wouldn’t
have to wait months for it. I asked to be pre-medicated, and the
doctor told me to take 1 mg. of Ativan one hour before. I rambled
happily into the hospital on the arm of a fellow Hep C- er. I was
able to find my way to the ultrasound department, where they
issued me a gown and escorted me—walking—into the room.
Dr. Yee was very nonchalant and chatty, and his air was very
reassuring. The nurse didn’t hold my hand, though. The
doctor said he only needed one sample, performed the freezing,
and the whole thing was over very quickly. The only pain I felt
was during the freezing, which is similar to the freezing done at
my dentist’s office. I had no shoulder pain, or any other
pain after the procedure. I felt as if I could have walked out of
the room and gone straight home. They had me wait outside the
ultrasound room, lying on my right side, for an hour, though,
just to be safe. I am still amazed at how smoothly everything
went, and I will not be so afraid if I have to have another
biopsy. I was able to drive myself back to Victoria the next day
(but I didn’t because “rent-a-hepper” came through
with a chauffeur).
I guess the points I would like to make are that most biopsies
are probably relatively painless. If you can, get support from
your friends in your support systems who have gone through the
procedure. I found it really helps. It may also be beneficial to
go to a centre where they perform biopsies often. Joan Diemecke
JIM LODGE STEPS DOWN
Recently recovering from a bout of pneumonia, Jim Lodge,
Victoria's vice- chairperson, has stepped down. Jim joined our
group shortly after his wife died of hepatitis C. He became a
member of our steering committee, and eventually, co-chair of the
Victoria Chapter. One of his projects has been setting up the BC
membership data base on the computer. If that weren't enough, he
has faithfully greeted those who attend our meetings each month,
and overseen the labeling and mailing of our newsletter. He has
been instrumental in obtaining many of our corporate donations,
and done most of our banking. The coordination of our volunteers
and the organization of our office have also fallen onto his
shoulders. In short, his labour has been invaluable, and we will
miss him more than words can tell. In mourning the passing of his
wife, Jim has given life to our group. How we shall survive
without him remains to be seen.
How E. Coli Can Affect HCV Cloning
>From the article: "How Escherichia coli can bias the
results of molecular cloning: Preferential selection of defective
genomes of hepatitis C virus during the cloning procedure."
Forns X, Bukh J, Purcell RH, Emerson SU, Proc Natl Acad Sci, USA,
1997 Dec 9;94(25):13909-13914
The HCV was cloned and attached to the bacterium, E. Coli. This
altered product was then used to infect a chimpanzee which in
turn got HCV. This result initially caused a lot of excitement
because until this time there was no effective animal model with
which to study HCV.
The original studies assumed that the clones were representative
of the entire virus population. However this study found that
there was a strong cloning selection for defective genomes and
that most clones generated initially were incapable of expressing
the HCV proteins. In fact a random look at the clones showed that
only 8% were fully functional when compared to human HCV.
Further alterations were necessary to increase the number of
functional clones. But nonrandom selection of clones during the
cloning procedure can produce a false spectrum of genomic
diversity. It can also be an impediment to the construction of
infectious viral clones.
What this really means to us is that the reliability of the
animal model is itself in question. Any therapies that might work
in the animal model may, nevertheless, not have the same effect
in humans because of slight genetic modifications. More work
needs to be done in this area before it can be said that we have
a good working model.
HepC BC http://www.geocities.com/HotSprings/5670 Email:
hepcbc@iforward.com Education and Support for Hepatitis C
including Canadian Information.
DIET and the HOLIDAYS
Darlene Morrow, BSc
During the holidays our careful diets may be forgotten due to the
festive social gatherings and overabundance of food that is
prevalent. Certainly it is acceptable for us to loosen up a bit
and indulge in foods that we wouldn't normally eat. But, before
you find yourself feeling the effects of that change in diet you
might want to keep several things in mind. The most important
things to watch are fat, protein and salt.
Fats are digested with bile which is produced by the liver. The
bile breaks apart the fat into smaller parts so that enzymes in
the gut can facilitate its absorption. Monitoring your fat is
particularly important for those of you with steatosis (fatty
deposits in the liver). Some ways that you can limit fats in your
own cooking and baking are as follows:
1. Use evaporated skim milk instead of heavy cream.
2. 1/2 cup of oil or margarine (in baking): substitute 1/2 cup of
applesauce OR 1/4 cup of applesauce + 1/4 cup of buttermilk OR
1/2 cup baby food prunes.
3. 1/2 cup of oil (in sauces or marinades): substitute 1/2 cup of
defatted chicken broth OR 1/2 cup unsweetened pineapple juice.
4. 1/2 cup margarine or butter (for icings): 1/2 cup marshmallow
creme.
5. 1 ounce of unsweetened chocolate: substitute 3 tablespoons of
unsweetened cocoa powder.
Proteins are necessary for tissue growth and repair.
Approximately 1.0 to 1.5 gm. of protein per kilogram of body
weight is recommended daily for regeneration of liver cells in
non-cirrhotic patients. The protein is broken down into amino
acids. The amino acids contain ammonia which must broken down by
the liver into urea which is then excreted by the kidneys. Some
experts believe that the ammonia can lead to encephalopathy in
susceptible patients with cirrhosis.
Encephalopathy, or impaired mental status, includes symptoms of
disorientation, short term memory loss and confusion. While the
exact cause is not fully understood, many people feel better when
they restrict their dietary protein. However there is no
consensus here. Some experts do not believe there is a link
between dietary protein and encephalopathy while others believe
in drastically reducing animal protein in order to help improve
mental status. If you find that you are experiencing some of
these symptoms, you may want to turn down that second helping of
turkey.
Salt restriction in patients with ascites (abnormal accumulation
of fluid in the abdomen) is also recommended. This condition can
occur with cirrhosis. Each gram of sodium that you consume can
result in the accumulation of 200 ml. of fluid. So watch out for
any packaged or pre- prepared foods and leave the salt shaker on
the table.
References:
1. DIET AND YOUR LIVER From the American Liver Foundation
2. DIET AND HEPATITIS C by Melissa Palmer, MD source:
<http://www.liverdisease.com/diet.html>
3. Healthy Homestyle Cooking by Evelyn Tribole, MS, RD
BOOK REVIEWS
Both of the following books were to be found in a BC bookstore
just before Christmas:
Living With Hepatitis C.
Richard English and Dr. Graham Foster. Robinson Press, 168 pp.,
$17.99 Can.
Richard English, a Hep C sufferer and a Master of Philosophy, has
teamed together with a liver specialist to produce a guide geared
to educating the patient about most aspects of this disease. Easy
to understand, the book gives the basics and includes up-to-date,
and accurate, if not simplistic, information. English illustrates
his points with personal stories, providing interesting, as well
as informative reading. Peering into the psychological labyrinth
of the mind of the patient dealing with the disease, he provides
an excellent section on day-to-day coping.
On the downside, I found the book lacking in its discussion of
treatment options, in both the allopathic and alternative areas.
The author is apparently neutral, and claims to support both
types of treatment; however, the lack of comprehensiveness—i.e.,
I found that neither Amantadine nor Thymosin was mentioned—leads
me to question his intentions.
Other topics the author deals with include an explanation of the
disease, tests, and avoiding the spread of Hep C. He also gives
us a straight-forward description of end-stage liver disease and
transplants. Compared to Peppermint Patti’s FAQ, the book is
much shorter, but also less informative.
Anne Animas
Hepatitis C: A Personal guide to Good
Health. Beth Ann Petro Roybal. Ulysses Press, 152 pp., $19.95
Can.
You know gals, I was never one to be a party pooper. And hey, I
got hep too so I know how it feels. But this book makes me feel
fat. Too sweet and low on nutritional value if you know what I
mean.
Sure, if you just got hep, you don’t have a computer and can’t
get a hold of Peppermint Patti’s FAQ, or you live in
Timbuctoo—or wherever—and never met another hepper FTF
or stuff like that, then this book is a good place to start. Don’t
get me wrong. I like it. But it’s better off as an article
in Good Housekeeping than a book. It’s like when we were 13
and wanted to make a good impression: way too much padding.
Anyways, I better tell you something about the book or you’ll
just think I’m bitching cuz I didn’t write one, or
maybe cuz I don’t have 4 names that sound like more like
“retro-toyball”. Sheesh! Get a life.
Seriously though: old Retro does tell you about the liver and
viruses and treatments and tests and procedures and has a really
good glossary at the back. So if you don’t know much or
anything you’ll get quite a bit out of this book.
What really irks me though is when she says things like: “If
the liver completely fails to function ... transplantation may be
an option to consider” (26). MAY BE AN OPTION!!! Is
breathing out an “option” after breathing in? Is “death”
an “option” {smouldering anger--ed.}. Or, like when she
recommends an exercise program for heppers and suggests a minimum
of 30 minutes of aerobics 3 times a week. Like, HELLO??? Like,
how many heppers do you know? Like, sometimes I can’t even
get out of bed, lady—nor can LOTS of heppers I know that I
met on the HEPV-L list and on email, etc.
So: if you think that HCV is a recreational disease, sort of like
going for a walk with your dog and your kids in a stroller, then
this is the book for you. But nobody should really get mad at Ms.
Toyball: she’s just passing along the misinformation she got
from the NIH consensus (Big Sister in the US of A) who would have
us believe that, afterall, HCV isn’t that serious--yur gonna
die from bubkas before the dragon gets you. And since the NIH can’t
find a cure (maybe because they spend less than nothing on
research) the focus is now on “management,” which, if
you think about it, is really convenient. This way, if you die
from the stuff, well, I guess it was only an “option.”
Sue Denham
HEP C TREATMENTS
>From the annals of this year's NIH Consensus Development
Conference on Management of Hepatitis C comes an interesting
article, "Other Options for Treatment of Hepatitis C,"
by Herbert L. Bonkovsky, M. D. This article stresses the need for
more effective therapy, a need demonstrated by the continuing
search for better treatments. The general concensus now is that
present treatments are far from perfect, where the goal of
treatment is seen as ridding the body of all detectable virus.
Unfortunately, it is becoming increasingly obvious that this goal
is difficult, if not impossible. Therefore, the medical world is
choosing less satisfactory, but useful, goals, such as lowering
the viral count (and thus the risk of passing on the disease),
reducing liver inflammation, and slowing down the rate of
progression, which would delay the onset of cirrhosis and liver
cancer.
Other methods of treatment other than Interferon and Ribavirin
have been tried, one of which is iron reduction. Iron is
necessary for almost all organisms to multiply. Patients with
infections or inflammatory conditions have low iron levels in
their blood. The body produces excess concentrations of iron help
the body to fight infection due to bacterial and fungal
infections, and perhaps in viral infections, as well. Researchers
have studied the role iron plays in viral hepatitis for at least
15 years, by observing patients with hepatitis B. Those with high
levels of iron in their blood had more of a chance of developing
chronic infections than those with lower levels. Other reports
associate stored iron in the liver with the development of
scarring and liver cancer in cases of hepatitis B.
Higher levels of iron in the blood correspond to a poorer
response to IFN therapy, as well, and complete responders usually
have lower levels than non- or partial-responders. Lack of
evidence of iron storage in samples from portal tracts seems to
correspond to a better response to IFN therapy.
Blood letting alone (phlebotomy), without IFN, leads to improved
ALT levels in perhaps 50% of subjects, and seems to lead to lower
viral levels, as well.
This article also discussed Antioxidant and anti-inflammatory
agents. Among them was N-acetyl cysteine (NAC). In chronic Hep C,
as well as in other liver diseases, oxidative stress increases
while plasma and liver GSH levels decrease. NAC alone doesn't
seem to have much effect, but when combined with IFN, it seems to
improve the response. Vitamin E seems to help avoid the
development of fibrosis, as do aspirin, other NSAIDS,
pentoxyfylline, and colchicine. (Ed. note: beware of bleeding
disorders associated with aspirin, etc.) Other treatments, such
as Chinese remedies and herbs, seem to improve blood tests, but
it isn't known yet whether this indicates improvement in the
progression rate of the disease, as well.
Supplemental (tauro-) ursodeoxycholic acid has improved ALT
levels, both alone and combined with IFN. These bile salts seem
to improve the state of liver inflammation.
Substances that effect the immune system, such as
granulocyte/monocyte colony stimulating factor (GM- CSF) have not
shown much promise. Not only are they expensive and not tolerated
well, but they seem to have little effect except to raise
neutrophil levels in patients who have severe neutropenia during
IFN treatment. On the other hand, thymosin alpha-I, given
together with IFN, produces very favourable results when
comparing ALT levels in trial patients.
Amantadine and isoprinosine are being investigated, as well.
Amantadine showed promise, and more tests are being done, but the
isoprinosine didn't. HCV protease and RNA polymerase inhibitors
are also under investigation at the present time.
Dr. Bonkovsky believes that several therapies, other than IFN and
ribavirin, have good effects on Hep C. Combination treatments
will probably be more effective than just one treatment alone. We
urgently need more clinical trials.
Hepatitis C and Alcohol
Eugene R. Schiff, M.D.
NIH Consensus Development Conference on Management of Hepatitis C
Introduction
The alcoholic patient is no less subject to the spectrum of
hepatobiliary disorders that may afflict the nonalcoholic patient
and, in some cases, may be predisposed to liver injury because of
specific socioeconomic, epidemiologic, or metabolic risk factors.
Prevalence of Anti-HCV Markers
Multiple studies have clearly demonstrated a high prevalence of
anti-HCV among alcoholic patients with liver disease. Testing
with supplemental assays (e.g., recombinant immunoblot assay
[RIBA]) confirmed that 8~5 percent of alcoholic patients with
liver disease have anti-HCV (RIBA+). The prevalence of anti- HCV
is sevenfold higher among alcoholics than in the population at
large (10 percent vs. 1.4 percent), but is even higher in those
with liver disease (30 percent). Most of those with liver disease
have detectable HCV RNA which may also be present in some
anti-HCV(-) patients. Anti-HCV(+) (RIBA+) patients are likely to
have HCV RNA detected, which is indicative of active viral
infection, usually associated with some degree of
necroinflammatory changes, with or without fibrosis, regardless
of alanine aminotransferase (ALT) levels.
HCV Correlation With Severity of Liver Injury The
prevalence of anti-HCV(RIBA+) correlates with the severity of
liver injury seen in alcoholic patients.
Anti-HCV positivity (RIBA+) correlated positively and
significantly with cirrhosis, cellular unrest, periportal
inflammation, and piecemeal necrosis, in contrast to anti-HBc,
which did not correlate with any of these histologic features, in
a large Veterans Administration (VA) study. In a study of 144
alcoholic patients, a prevalence of 20 percent anti-HCV
positivity in alcoholic fibrosteatosis, 21.4 percent in alcoholic
hepatitis, and 42.6 percent in alcoholic cirrhosis, as compared
to 2.2 percent in alcoholic patients without liver disease, was
noted. Histologic features, with the exception of sinusoidal
cellularity, were comparable in alcoholic patients with and
without anti-HCV. Nishiguchi et al. performed both immunoblot and
HCV RNA determinations among 80 alcoholic patients with liver
disease. Patients with cirrhosis and HCV RNA had higher ALT
activity than comparable patients without HCV RNA. The HCV RNA(+)
patients had higher histologic activity indices (Knodell) than
those without detectable HCV RNA. The presence of HCV RNA
conferred a more severe degree of periportal and bridging
necrosis, intralobular degeneration, focal necrosis. and Dortal
inflammation.
Effect of Abstinence on Alcoholic Patients with
Histologic Evidence of Chronic Hepatitis
In HCV RNA(+) alcoholic patients with histologic evidence of
chronic hepatitis, abstinence was not followed by resolution of
aminotransferase elevation, which has been observed in both
anti-HCV(+) HCV RNA(-) and anti-HCV(-), HBsAg(-) alcoholic
patients with similar histologic features. This suggests that
chronic hepatitis C infection perpetuates the liver damage in
these alcoholic patients who have abstained. Nevertheless, serum
HCV RNA levels will decrease with abstinence.
Epidemiology of Hepatitis C Among Alcoholic Patients
The epidemiology of hepatitis C among alcoholic patients with
bonafide viral C infection has not been definitively
characterized. Intravenous drug abuse (IVDA) is the most common
risk factor. Yet there has not been a good explanation for the
disproportionately high prevalence of HCV among alcoholic
patients with liver disease without a history of IVDA. Caldwell
et al. found the prevalence of anti-HCV similar among patients
with alcoholic liver disease who had high risk factors as
compared to those without identifiable modes of parenteral
transmission.
Effect of Alcohol on HCV Replication
A critical question is whether or not alcohol and hepatitis C
infection are synergistic in a combined liver injury. In some
patients, there are both histologic features of alcoholic liver
injury and chronic viral hepatitis, but in most studies the
predominant pattern is chronic hepatitis. Alcohol may enhance the
replication of hepatitis C and produce a more severe injury
independent of the direct alcohol-induced toxic injury. There is
a correlation between HCV RNA levels and amount of alcohol
consumed. Alcoholic patients with HCV infection have higher
hepatic iron concentrations, which may be germane to increased
HCV replication. Clinical evidence of hepatic activity and viral
levels is significantly greater in those consuming greater than
10g of alcohol per day.
Effect of Alcohol on Progression of Chronic Viral C
Hepatitis to Cirrhosis and Hepatocellular Carcinoma
There is a more rapid development of cirrhosis and hepatocellular
carcinoma in the alcoholic with chronic HCV infection. The period
from transfusion to the diagnosis of cirrhosis is shorter in the
heavy drinker. The risk for the development of hepatocellular
carcinoma in alcoholic cirrhotics is 8.3 times higher in the
HCV(+) patients than HCV(-) patients, and the prevalence of
anti-HCV among alcoholics with HCC is 50-70 percent. Therefore,
alcohol may modify the replication of HCV as well as the
oncogenicity of HCV in hepatocellular carcinoma.
Interferon Therapy in Alcoholic Patients with Chronic Hepatitis C
Among alcoholic patients with chronic hepatitis C who remained
abstinent during therapy with interferon, there was a
significantly lower rate of HCV RNA clearance in those who
consumed >70g/day of ethanol as compared to <70g/day
drinkers or nondrinkers. A similar experience noted zero HCV RNA
clearance in those consuming >70g/day up to the time of
interferon therapy.
Conclusion
The most common type of nonalcoholic liver disease seen in
alcoholic patients is chronic viral hepatitis C. Evidence
accumulated thus far supports the concept that superimposed
hepatitis C infection confers a more severe liver injury in
alcoholic patients, possibly by enhancing viral replication. The
progression of the liver disease is more rapid and the risk for
the development of hepatocellular carcinoma, once cirrhosis has
developed, is high. It remains to be proven whether or not
successful antiviral therapy will change the natural history and
improve the prognosis in such patients who abstain. Regardless,
part of the mystery of why some alcoholics develop liver disease
while most do not can be explained by the presence of chronic
viral C hepatitis.
Ed. note: References upon request. Call Joan Diemecke (250)
479-5290
Does hepatitis C affect women differently?
Hormonal effects of hepatitis C can involve menstrual
irregularities, particularly if you are experiencing significant
hepatitis C symptoms. It is important that your general health is
checked as well as your hepatitis C monitored. Birth control: If
you are experiencing significant hepatitis C symptoms, using the
oestrogen-based contraceptive pill may be inadvisable. In these
cases, the progesterone-only pill or Depo-Provera may be
preferable. In any case, you should consult a woman’s health
practitioner. Hormone Replacement Therapy: If you have severe
hepatitis C symptoms you may need to discuss with your doctor or
specialist whether hormones should be used for menopausal
symptoms. If this is the case, external vaginal creams and skin
patches are probably better than pills.
http://www.span.com.au/hepatitis_c/info.html#vir
COMBINATION THYMOSIN ALPHA(1) AND
LYMPHOBLASTOID INTERFERON TREATMENT IN CHRONIC HEPATITIS C
Background-Monotherapy for chronic hepatitis C using interferon
(IFN) results in a very small proportion of patients exhibiting a
sustained response. Clinical trials assessing the benefit of
combination drug therapy may provide evidence of improved
treatment response over that seen with single drug treatment.
Aim-To assess the response in patients with chronic hepatitis C
to one year of combination treatment: thymosin alpha(1) (T
alpha(1)), 1 mg twice weekly, and lymphoblastoid (L)-IFN, 3 MU
thrice weekly. Patients and Methods-Fifteen patients with serum
HCV RNA positive chronic hepatitis C were studied. Eleven
patients were treatment naive and four had failed previous
standard IFN therapy. Thirteen patients were HCV RNA serotype 1b.
All patients were given combination T alpha(1) and L-IFN therapy
for one year with a six month follow up period. Results-Six
months after initiation of treatment seven patients (47%) were
sera HCV RNA negative and at completion of the one year treatment
11 (73%), including two who had failed previous standard IFN
treatment, had negative serum HCV RNA. Six months after
treatment, six patients (40%), including five with HCV type 1b,
showed a sustained response characterised by a negative serum HCV
RNA. Conclusions-The results of this open label trial suggest
that there may be a potential benefit to combining an immune
modulator (T alpha(1)) with an antiviral (IFN) in the treatment
of chronic hepatitis C. Verification of the observations in this
study require completion of a randomised controlled study.
Author: MG MUTCHNICK, WAYNE STATE UNIV, HARPER HOSP, DIV
GASTROENTEROL, 3990 JOHN R, DETROIT, MI 48201 Source: GUT 1996
NOV;39(5):679-683