Can anyone out there tell me the difference between a "persistent" disease
and a "chronic" one? For example, persistent hepatitis vs chronic
hepatitis.

Thanks,
Horace

I don't think there is a general distinction.  Rather, there are
two classes of chronic hepatitis: chronic active hepatitis and chronic
persistent hepatitis.  I can't think of any other disease where the
term persistent is used with or in preference to chronic.

Much as these two terms "chronic active" and "chronic persistent"
sound fuzzy, the actual distinction between the two conditions
is often fairly fuzzy as well.
--
David Rind

:>Can anyone out there tell me the difference between a "persistent" disease
:>and a "chronic" one? For example, persistent hepatitis vs chronic
:>hepatitis.
:
:I don't think there is a general distinction.  Rather, there are
:two classes of chronic hepatitis: chronic active hepatitis and chronic
:persistent hepatitis.  I can't think of any other disease where the
:term persistent is used with or in preference to chronic.
:
:Much as these two terms "chronic active" and "chronic persistent"
:sound fuzzy, the actual distinction between the two conditions
:is often fairly fuzzy as well.

I beg to differ.  Chronic *active* hepatitis implies that the disease
remains active, and generally leads to liver failure.  At the very
minimum, the patient has persistently elevated liver enzymes (what some
call "transaminitis").  Chronic *persistant* hepatitis simply means that
the patient has HbSag in his/her {*filter*} and can transmit the infection, but
shows no evidence of progressive disease.  If I had to choose, I'd much
rather have the persistant type.

--
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=  Kenneth Gilbert              __|__        University of Pittsburgh   =
=  General Internal Medicine      |      "...dammit, not a programmer!" =
=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-|-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=

Being a chronic HBsAg carrier does not necessarily mean the patient has chronic
persistent anything. Persons who are chronic carriers may have no clinical,
biochemical, or histologic evidence of liver disease, or they may have chronic
persistent hepatitis, chronic active hepatitis, cirrhosis, or hepatocellular
carcinoma.

Most cases of chronic persistent hepatitis (CPH) are probably the result of
a viral infection, although in a good number of cases the cause cannot be
determined. The diagnosis of CPH is made on the basis of liver biopsy. It
consists of findings of portal inflammation, an intact periportal limiting
plate, and on occasion isolated foci of intralobular necrosis. But in contrast
to chronic active hepatitis (CAH) there is no periportal inflammation,
bridging necrosis, or fibrosis.

CPH has, indeed, an excellent prognosis. If I had to choose between CAH and
CPH there is no question I would also choose CPH. However, as David pointed
out, the distinction between the two is not as neat as some of us would have
it. The histology can sometimes be pretty equivocal, with biopsies showing
areas compatible with both CPH and CAH. Maybe it is a sampling problem. Maybe
it is a continuum. I don't know.

=================================

Howard Doyle

:Being a chronic HBsAg carrier does not necessarily mean the patient has chronic
:persistent anything. Persons who are chronic carriers may have no clinical,
:biochemical, or histologic evidence of liver disease, or they may have chronic
:persistent hepatitis, chronic active hepatitis, cirrhosis, or hepatocellular
:carcinoma.
:
:Most cases of chronic persistent hepatitis (CPH) are probably the result of
:a viral infection, although in a good number of cases the cause cannot be
:determined. The diagnosis of CPH is made on the basis of liver biopsy. It
:consists of findings of portal inflammation, an intact periportal limiting
:plate, and on occasion isolated foci of intralobular necrosis. But in contrast
:to chronic active hepatitis (CAH) there is no periportal inflammation,
:bridging necrosis, or fibrosis.
:
:CPH has, indeed, an excellent prognosis. If I had to choose between CAH and
:CPH there is no question I would also choose CPH. However, as David pointed
:out, the distinction between the two is not as neat as some of us would have
:it. The histology can sometimes be pretty equivocal, with biopsies showing
:areas compatible with both CPH and CAH. Maybe it is a sampling problem. Maybe
:it is a continuum. I don't know.

Darn.  Just when I think I understand something someone who knows the
pathology has to burst my bubble :-(  We'd better not start talking about
glomerular diseases, then I'll really get depressed.

Seriously though, I wonder how someone with CPH would end up getting a
biopsy in the first place?  My understanding (and feel free to correct me)
is that the enzymes are at worst mildly elevated, with overall normal
hepatic function.  I would think that the only clue might be a history of
prior HepB infection and a positive HepB-sAg.  Or is it indeed on a
continuum with CAH, and the distinction merely one of pathology and
prognosis, but otherwise identical clinical features?

--
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=  Kenneth Gilbert              __|__        University of Pittsburgh   =
=  General Internal Medicine      |      "...dammit, not a programmer!" =
=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-|-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=

Chronic persistent hepatitis is usually diagnosed when someone does a liver
biopsy on a patient that has persistently elevated serum transaminases months
after a bout of acute viral hepatitis, or when someone is found to have
persistently elevated transaminases on routine screening tests. The degree of
elevation (in the serum transaminases) can be trivial, or as much as ten times
normal. Other {*filter*} chemistries are usually normal.
As a rule, patients with CPH have no clinical signs of liver disease.
Chronic active hepatitis can also be asymptomatic or minimally symptomatic, at
least initially, and that's why it's important to tell them apart by means of
a biopsy. The patient with CPH only needs to be reassured. The patient with
CAH needs to be treated.

======================================

Howard Doyle

:Chronic persistent hepatitis is usually diagnosed when someone does a liver
:biopsy on a patient that has persistently elevated serum transaminases months
:after a bout of acute viral hepatitis, or when someone is found to have
:persistently elevated transaminases on routine screening tests. The degree of
:elevation (in the serum transaminases) can be trivial, or as much as ten times
:normal. Other {*filter*} chemistries are usually normal.
:As a rule, patients with CPH have no clinical signs of liver disease.
:Chronic active hepatitis can also be asymptomatic or minimally symptomatic, at
:least initially, and that's why it's important to tell them apart by means of
:a biopsy. The patient with CPH only needs to be reassured. The patient with
:CAH needs to be treated.

I just went back to the chapter in Cecil on chronic hepatitis.  It seems
that indeed most cases of CPH are persistant viral hepatitis, whereas
there are a multitude of potential and probable causes for CAH (viral,
{*filter*}, {*filter*}, autoimmune, etc.).  Physicians seem to have a variety of
"thresholds" for electing to biopsy someone's liver.  Personally, I think
that if the patient is asymptomatic, with only slight transaminitis and
normal albumin and PT, one can simply follow them closely and not add the
potential risks of a biopsy.  Others may well biopsy such a patient, thus
providing these samples for study.  It would be interesting to see if
anyone's done any decision analysis on this.

--
=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-|-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=
=  Kenneth Gilbert              __|__        University of Pittsburgh   =
=  General Internal Medicine      |      "...dammit, not a programmer!" =
=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-|-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=

The problem with this approach, potentially, is that by the time someone
has an abnormal albumin or PT the liver is basically shot, so if there
is some treatable cause of CAH, it is too late to find out about it.

It's worth noting that at least in the case of Hepatitis C, recent
evidence suggests that there is virtually no relationship between
the level of transaminases and the degree of ongoing liver inflammation.
Some patients with normal transaminases turn out to have CAH and will
presumably go on to have higher risks of cirrhosis and hepatoma.
--
David Rind

:>"thresholds" for electing to biopsy someone's liver.  Personally, I think
:>that if the patient is asymptomatic, with only slight transaminitis and
:>normal albumin and PT, one can simply follow them closely and not add the
:>potential risks of a biopsy.
:
:The problem with this approach, potentially, is that by the time someone
:has an abnormal albumin or PT the liver is basically shot, so if there
:is some treatable cause of CAH, it is too late to find out about it.
:
:It's worth noting that at least in the case of Hepatitis C, recent
:evidence suggests that there is virtually no relationship between
:the level of transaminases and the degree of ongoing liver inflammation.
:Some patients with normal transaminases turn out to have CAH and will
                    ^^^^^^^^^^^^^^^^^^^^
:presumably go on to have higher risks of cirrhosis and hepatoma.

That may well be the case, but how do you go about finding those patients?
 If the enzymes are normal, and they are presumably otherwise
asymptomatic, then what do you base the diagnosis on?
Case in point:
  I saw a young male (25) today who denies any history of IV drug use or
{*filter*} activity of any kind.  Nevertheless, his father recently had a
liver transplant for CAH  and the young son was worried about hepatitis.
Normally I would not have even ordered the {*filter*}work, but I wanted to set
his mind at ease.  His HAV-Ab was postive, HBsAg was negative, HBsAb was
positive, HBcAb was positive, and HCVAb was positive.  This was a surprise
to both of us.  Nevertheless, his enzymes were normal, as was the rest of
his {*filter*}work, and he was asymptomatic.  Should I have sent him for
biopsy?  I think not.  In fact, I just reasurred him and suggested that he
have his LFTs checked again in a year.  On the other hand, if his enzymes
were elevated I would have referred him for biopsy, given his family
history.  Would anyone have done anything differently?

WRT the decision analysis, I did a literature search and this has not been
done, as far as I can tell.  Looks like a great research project for an
enterprising GI fellow.

--
=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-|-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=
=  Kenneth Gilbert              __|__        University of Pittsburgh   =
=  General Internal Medicine      |      "...dammit, not a programmer!" =
=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-|-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=

There are hepatologists who currently advocate considering liver
biopsy for anyone who is Hep C + regardless of their transaminase
levels.  I haven't yet encountered the scenario you describe, and
so I haven't had to decide what I would tell a patient to do.  

I do believe the evidence suggests that you can't rely on normal
transaminases.  However, the efficacy of therapy for Hep C CAH
is relatively poor, and the natural history of the disease is not
yet well described.
--
David Rind

I think we are going to see more of these cases of health individuals with
positive HCV serology with normal transaminases.  Last week I saw a young
woman referred in due to + HCV Ab found when she donated {*filter*}.  I told
here to have her internist check LFT yearly and see what happens, both
to the transaminases and to the literature of HCV infection.

I think it is safe to leave these people alone for now.  The risk of NANB
hepatitis from {*filter*} transfusion used to be over 10% and I do not know of
any autopsy series with anywhere near that rate of cirrhosis.  Hep C is
probably rather benign in its course.  With the toxicity of therapy
we are probably best leaving these folks alone.

Steve Holland

                                      ^^^^^^

This is not a flame, so please don't take it as one...  I'm just interested
in the way medical people use language compared with common usage of the same
word...  I know I've read in my files stuff like "pt denies [something or
other]", when my recollection of the conversation with the doc was something
like "Unh unh" in response to a question...  "Denies" has such an emphatic
connotation.  But it's such a nice, short word...

Physicians who have pts that read their files: has anyone gotten huffy
because of similar sorts of word choices?  I remember being _very_
surprised when I worked as a corrective therapy aide one summer, and
read in a pt's file "Pt became SOB and was taken back to ward."...
I was picturing someone that was going to be really tough to work with---
and was introduced to a nice guy who had a rough time breathing (SOB =
short of breath).  !!!

Kay Klier  Biology Dept  UNI

I read a newspaper article warning people to not
use foam cups.  The article stated that foam not only
harms the ozone layer (because of CFC's) but foam
is made from benzene.  And benzene is a known carcinogen.

Are there any truth to these claims?
Should I toss my newly purchased designer stryofoam china
collection?

--

 From the beautiful and historic New York State Mid-Hudson Valley.