HEALTHY HEPPER: Preventing Cirrhosis

[Guest guest]

HEALTHY HEPPER MAILING LIST 3/1/01

RE: Preventing Cirrhosis

Hello to everyone,

I get a lot of requests for information about how to treat cirrhosis and prevent cirrhosis with natural medicine. Since I am in the middle of writing a detailed report on the subject I thought I would share with you an interesting piece of information I came accross on Dr. Zhang's website:

How can Cirrhosis be prevented?

http://www.dr-zhang.com/

If no proper treatment is given, about 25% of patients with chronic hepatitis will develop cirrhosis in 20 to 30 years. If the liver disease is properly treated and the inflammation controlled, even though the HCV is still present, the median time for the development of cirrhosis is about 80 years. In short, controlling liver inflammation is the first step in preventing cirrhosis. The second step is to facilitate bile secretion, the third is to improve microcirculation, and the fourth is to remove the CIC and regulate immunity.

In China, herbs used for silicosis (miner's lung) to suppress the fibroblastic activities have been used for treating early-stage cirrhosis. Controlled animal studies found that in cirrhotic animal models treated with these herbs, liver collagen content was much lower than in the untreated control group.

Cordyceps sinensis, Persicae Semen, Salvia miltiorrhizae, and Glycyrrhizin can decompose collagen and soften the liver, while at the same time promote liver-cell regeneration.

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According to Dr. Zhang the key to preventing cirrhosis is in controlling inflammation of the liver. Fortunately, many people have been successful at doing this very thing by taking herbs and other natural supplements. This topic of controlling liver inflammation is covered in my E-books, with each supplement and herb that has been noted to achieve this therapeutic goal.

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Have a great weekend!

Rockenbaugh

http://www.objectivemedicine.com

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[Guest guest]

About preventing Cirrohsis,...someone had emailed me and told me that

Interferon had halted Cirrohsis and reversed the scarring on his

liver...I've never heard of this before...I though that once a liver

had scars, it would be the same as scars on the outside of the

body...they don't go away, do they? (unless it's a miracle, and I do

believe those happen).

[Guest guest]

Hi, ,

Here's a copy of an article that might answer your question about scarring

etc.

Love,

ARTICLE:

The New England Journal of Medicine -- February 8, 2001 -- Vol. 344, No. 6

Is Liver Fibrosis Reversible?

Cirrhosis represents a late stage of progressive scarring in chronic liver

disease. It begins with subendothelial or pericentral fibrosis (hepatic

fibrosis) and progresses to panlobular fibrosis with nodule formation

(cirrhosis). Once established, fibrosis has generally been considered to be

irreversible. This belief was established more than half a century ago,

when the diagnosis of cirrhosis was made clinically on the basis of signs

of end-stage liver disease, such as ascites, muscle wasting, variceal

bleeding, jaundice, and encephalopathy. These features continue to indicate

a poor prognosis in the absence of liver transplantation and are still used

to classify the severity of liver disease in patients who are awaiting

transplantation.

The point at which cirrhosis or extensive fibrosis becomes irreversible has

not been well defined. Cirrhosis is now frequently diagnosed at an early

stage by percutaneous liver biopsy. In many cases, patients with cirrhosis

are asymptomatic, with normal findings on physical examination, and the

disorder is detected initially because of elevated serum liver enzyme

levels or a positive serologic test for hepatitis B or C virus. Advances in

the treatment of liver diseases have made it increasingly apparent that

medical treatment may be beneficial even for patients with advanced

histologic changes, including cirrhosis. Furthermore, in some cases

fibrosis and even frank cirrhosis have appeared to regress with treatment.

In this issue of the Journal, Hammel et al. describe a group of patients

with liver fibrosis who underwent surgical decompression of an obstructed

biliary system. (1) Liver-biopsy specimens obtained before and after

surgery were compared. In some patients, the liver fibrosis significantly

regressed after decompression. These findings are important because the

natural history of histologic changes after biliary decompression has not

been well described in humans. The implication of this study is that the

fibrosis caused by biliary obstruction is reversible in some instances.

The study did not include a control group. Hammel et al. describe only a

small number of patients who were selected from a larger group that

underwent biliary decompression for chronic pancreatitis and stenosis of

the common bile duct. Thus, there may have been some selection bias.

However, a systematic bias seems unlikely, since the patients had

underlying chronic pancreatitis that had worsened, requiring repeated

surgery.

Another concern is the possibility that the changes could have been

accounted for by variation in sampling on liver biopsy. Although this

possibility cannot be completely excluded, 19 of the 22 specimens were

large wedge specimens taken from the third segment of the left hepatic lobe

under direct vision at the time of surgery.

Despite these limitations, the apparent improvement in fibrosis after

biliary decompression reported by Hammel et al. adds another example to the

growing list of liver diseases in which specific interventions have been

associated with histologic improvement, including regression of fibrosis.

These observations are further supported by animal models that have shown

that even extensive fibrosis is reversible.

Reports of the reversibility of liver fibrosis in humans have in common the

elimination of the cause of the underlying liver disease or the

implementation of an effective treatment. Examples include abstinence from

alcohol, surgical reversal of jejunoileal bypass, (2) immunosuppressive

therapy for autoimmune hepatitis, (3) phlebotomy for hemochromatosis, (4)

long-term treatment with lamivudine for chronic hepatitis B, (5) treatment

of hepatitis C (3,6,7,8) and hepatitis D (9) with interferon, and treatment

of primary biliary cirrhosis with ursodiol plus methotrexate. (10)

Like the study by Hammel et al., the other studies included only small

numbers of patients. In addition, there is no way to exclude the

possibility that the changes observed were due only to sampling variation

on liver biopsy. However, two lines of evidence support their validity.

First, histologic regression of fibrosis was usually accompanied by

clinical and biochemical improvement, including a decrease in noninvasive

measures of hepatic fibrogenesis (those that do not require a liver biopsy)

in some studies. Second, in large controlled trials of interferon and

ribavirin for the treatment of hepatitis C and of lamivudine for the

treatment of chronic hepatitis B, fibrosis was decreased in the patients

who received these treatments but not in the controls. (7,8,11)

Over the past 15 years, substantial progress has been made in understanding

the cellular and molecular regulation of hepatic fibrosis. This knowledge

provides a rational explanation for the potential reversibility of the

process. (12) It is now clear that the accumulation of extracellular

matrix, or scarring, in fibrotic diseases of the liver is not a static or

unidirectional event but a dynamic and regulated process that is amenable

to intervention. Activation of hepatic stellate cells (formerly known as

Ito cells) is a central event in hepatic fibrosis. (12) In all forms of

liver injury, these perisinusoidal cells undergo a conversion from

quiescent cells that store vitamin A to cells that are contractile,

proliferative, and fibrogenic.

Key mediators of the activation of hepatic stellate cells include a host of

cytokines and their receptors, reactive oxygen intermediates, and other

paracrine and autocrine signals. In animal models of early liver injury,

the accumulation of extracellular matrix as a result of the activation of

stellate cells is offset by a proportional increase in the degradation of

matrix through the action of so-called interstitial collagenases. The

cellular sources of these collagenases are still uncertain, but their

activity is tightly regulated by the amount of active protein and the

concentration of specific inhibitory molecules, called tissue inhibitors of

metalloproteinases (TIMPs). In animal models, as liver injury resolves,

activated stellate cells are cleared by apoptosis, and the expression of

TIMPs decreases, allowing active enzymes to resorb extracellular matrix.

(13) Although these observations in animals need to be validated in humans,

they point to the potential for exploiting the factors that regulate

collagenase activity in order to develop effective antifibrotic therapies.

Key aspects that remain unclear are the cellular sources of interstitial

collagenases and the point (in histologic, cellular, or molecular terms) at

which fibrosis becomes truly irreversible.

This growing body of clinical and scientific evidence suggests that

extensive fibrosis or cirrhosis in patients with well-preserved liver

function should no longer be considered untreatable. Both current and

future therapies have the potential for preventing the progression of

disease and facilitating endogenous mechanisms that lead to the degradation

of extracellular matrix and the regression of fibrosis.

Several issues remain to be addressed, however. Liver fibrosis does not

develop at the same rate in all patients, and responses to treatment vary.

Therefore, we need to identify host- or disease-specific factors that are

associated with both a slower progression of fibrosis and a favorable

response to treatment. Furthermore, the possible roles of treatment

strategies designed to reverse fibrosis should be analyzed critically. As

an example, long-term therapy with interferon alfa may improve fibrosis in

patients with chronic hepatitis C, even in the absence of a virologic

response. (7) This finding might justify the use of long-term interferon

alfa therapy, under certain circumstances, in patients without virologic

responses to treatment. The report by Hammel et al. should spur efforts to

develop new treatments for patients with extensive liver fibrosis or

cirrhosis.

A.L. Bonis, M.D.

Tufts-New England Medical Center

Boston, MA 02111

L. Friedman, M.D.

Mount Sinai Medical Center

New York, NY 10029

Marshall M. Kaplan, M.D.

Tufts-New England Medical Center

Boston, MA 02111

[ ] Re: HEALTHY HEPPER: Preventing Cirrhosis

> About preventing Cirrohsis,...someone had emailed me and told me that

> Interferon had halted Cirrohsis and reversed the scarring on his

> liver...I've never heard of this before...I though that once a liver

> had scars, it would be the same as scars on the outside of the

> body...they don't go away, do they? (unless it's a miracle, and I do

> believe those happen).

>

>

>

>