Re: Digest Number 1144

September 27, 2000

" http://www.pslgroup.com/dg/1da4ea.htm "

People With Depression At Increased Risk Of Stroke

WASHINGTON, DC -- July 21, 2000 -- People who experience symptoms of

depression are at an increased risk of developing stroke, suggest the

results of a two-decade study conducted by the Centers for Disease

Control and Prevention (CDC).

There was a 73 percent increase in stroke risk among study participants

with high levels of depression symptoms according to the researchers

from the CDC. They also found a 25 percent increase in stroke risk

associated with moderate levels of depression symptoms. The relationship

of stroke risk and high depression also varied by race and gender. There

was a 68 percent increase for white men, a 52 percent increase for white

women, and a 160 percent increase for African-Americans.

" The suggestion of an increasingly strong relationship between level of

depressive symptoms and stroke indicates that reducing depression may be

important for everyone, not just those whose symptoms may have clinical

implications, " said lead author Bruce S. Jonas, ScM, PhD, of the CDC's

National Center for Health Statistics in Hyattsville, MD.

The researchers followed a nationally representative sample of 6,095

stroke-free adults 25 to 74 years old in the early 1970s as part of the

first National Health and Nutrition Examination Survey. Participants

were followed for a maximum of 22 years by completing a series of

questionnaires probing their health history and psychological symptoms.

The increased risk of stroke for individuals with symptoms of depression

persisted even after controlling for other stroke risk factors including

baseline age, gender, race, education, smoking status, body mass index,

alcohol use, physical activity, serum cholesterol level, systolic blood

pressure, history of diabetes, and history of heart disease.

" Risk factors such as baseline age, gender, smoking status, systolic

blood pressure, serum cholesterol level, history of diabetes and history

of heart disease remain strong predictors of developing stroke " said Dr.

Jonas. " However, this study indicates that elevated depression levels

may also play an important role. "

Overall, 9.1 percent of all participants reported high levels of

depression and 32.7 percent reported moderate levels at the beginning of

the study. Among African-Americans, 15.7 percent reported high levels of

depression, compared with 10.4 percent of white women and 5.6 percent of

white men according to the study.

The exact mechanism by which depression may increase stroke risk is not

understood, noted the researchers. Previous research suggests

depression's effect on the nervous or immune systems may play a role.

Depression may also increase the risk of diseases such as hypertension,

that in turn increase stroke risk.

" Intervening hypertension might explain, at least in part, the pathway

from depression to stroke as well as the higher risk of stroke among

depressed African-Americans, " said Dr. Jonas. African Americans are

known to suffer from higher rates of hypertension and, based on previous

research by Dr. Jonas and others, depressed African Americans have

higher risks of hypertension compared to other groups.

__________________________________

Is Fibrosis Reversible? Part 1

Liver fibrosis and cirrhosis result from the majority of

chronic liver insults and represent a common and difficult clinical

challenge of worldwide importance. At present, the only curative

treatment for end stage cirrhosis is transplantation, but even in the

developed world, the number of donor organs available and the clinical

condition of the potential recipient limit the applicability of this

technique. The alternative clinical course is one familiar to

gastroenterologists - that of a progressive damage limitation exercise

in which the complications of fibrosis and cirrhosis are treated with

greater or lesser success. The development of fibrosis, and particularly

cirrhosis, is associated with a significant morbidity and mortality.

Thus, there is a considerable imperative to develop antifibrotic

strategies that are applicable to liver fibrosis. Such an approach is

attractive precisely because it is aimed at the final common

pathological pathway of chronic liver disease, regardless of aetiology.

However, because fibrotic liver disease may not present clinically until

an advanced or cirrhotic stage, the possibility of reversing the

fibrosis is an essential issue for developing therapeutic approaches.

Liver fibrosis represents the wound healing response of the

liver, as such it demonstrates generic aspects that characterise tissue

healing elsewhere in the body a wound healing response that is dynamic

and has the potential to resolve without persistent scarring. This may

seem at odds with the clinical impression that advanced fibrosis and

cirrhosis are at best irreversible and at worst progressive. However,

recent developments in our understanding of the process of hepatic

fibrogenesis confirm that the process is dynamic with respect to both

cell and extracellular matrix (ECM) turnover and suggest that a capacity

for recovery from advanced cirrhosis and fibrosis is possible. Moreover,

with the advent of effective antiviral therapies, biopsy documented

examples of improvements in fibrosis and in some examples resolution,

including that of cirrhotic change, are accumulating in the

literature.1-4 To utilise these observations and establish the

attributes required of an effective antifibrotic therapy, we need to

understand the nature and origin of the fibrotic ECM, the methods by

which the ECM is degraded and the essential processes which occur when

fibrosis undergoes recovery with restoration of the normal liver

architecture.

Nature and origin of fibrosis

Development of liver fibrosis entails major alterations in

the both quantity and quality of hepatic ECM and there is overwhelming

evidence that activated hepatic stellate cells (HSC, Ito, fat storing

cell, or lipocyte) are the major producers of the fibrotic neomatrix.5 6

Hepatic stellate cells reside in the space of Disse and in normal liver

are the major storage sites of vitamin A, stored in the cytoplasm as

retinyl esters. Following chronic liver injury, HSC proliferate, lose

their vitamin A and undergo a major phenotypical transformation to

smooth muscle

-actin positive myofibroblasts (activated HSC) which produce

a wide variety of collagenous and non-collagenous ECM proteins.

Cirrhotic liver contains approximately six times more ECM overall than

normal liver, and in the space of Disse collagen types III and V and

fibronectin accumulate in early injury.7 In chronic injury here is

increasing deposition of collagen types I and IV, undulin, elastin, and

laminin.8 Hyaluronan, normally a minor component of the space of Disse,

is increased more than eightfold9 and dermatan and chondroitin sulphate

and heparan sulphate proteoglycans also increase. Although collagen

types I, III, and IV are all increased, type I increases most and its

ratio to types III and IV therefore increases.7 10-12 Culture studies

have suggested that the neomatrix laid down in the space of Disse may

itself contribute to the disease associated alterations in the phenotype

of HSC, sinusoidal endothelial cells, and hepatocytes.13-16 With

progressive injury ECM spurs link the vascular structures, ultimately

resulting in the architecturally abnormal nodules that characterise

cirrhosis.

Complete recovery from liver fibrosis would involve

remodeling and breakdown of these multiple ECM components, with

degradation of the predominant component, collagen I, being particularly

important for recovery of normal liver histology. At present, the

identities of the enzyme(s) that degrade the fibrillar collagens

(collagens I and III) in the liver are unclear. The matrix

metalloproteinases (MMP), a family of zinc dependent endoproteinases,

have the capability to degrade these various ECM components and are

expressed particularly by HSCs and Kupffer cells.17 The first discovered

and best characterised interstitial collagenase in humans is MMP-1,

which is widely expressed in human tissues including liver, but other

human interstitial collagenases with a more limited cell expression

include neutrophil collagenase (MMP-8) and collagenase 3 (MMP-13). The

enzymes MMP-2 and MMP-14 have also recently been ascribed interstitial

collagenolytic activity.18 19 However, studies in animal models and

human liver fibrosis indicate that interstitial collagenolytic activity

decreases in liver extracts in advanced fibrosis,20-24 which would

promote net collagen deposition. There is increasing evidence that

collagenase inhibition may arise from increased expression in fibrotic

liver of endogenous MMP inhibitors, the tissue inhibitors of

metalloproteinases (TIMPs). Expression of both TIMP-1 and -2 is

increased in human and rat model fibrotic liver25-31 and in human liver

the degree of TIMP-1 expression correlates with extent of fibrosis25

assessed by hydroxyproline content. Studies by our group and others25 27

31-33 indicate that activated HSC may be an important source

of these TIMPs in injured liver. In rat models of liver fibrosis, TIMP-1

is expressed early in fibrogenesis before apparent collagen

deposition.26 In contrast to the TIMPs, mRNA for interstitial

collagenase (MMP-1 in humans, MMP-13 in rats) remains unaltered in human

and rat liver as fibrosis develops.25 26 34 The resulting increase in

TIMP:MMP ratio in liver may promote fibrosis by protecting deposited ECM

from degradation by MMPs. However, other MMP inhibitory mechanisms might

contribute to fibrosis. MMPs are released as inactive pro-enzymes, and

an important regulatory step involves cleavage of the inhibitory

N-terminal peptide to confer enzymatic activity.35 The means of

proenzyme activation varies between different MMPs, but the protease

plasmin is required for efficient activation of proMMP-1.36 Activated

HSC may however inhibit plasmin synthesis in fibrotic liver through

synthesis of plasminogen activator inhibitor-1 (PAI-1).37 38 Plasmin may

have an important antifibrotic role, as studies of fibrosis in lung and

kidney utilising PAI-1 and urokinase plasminogen activator knockout mice

suggest that an increased PAI-1:urokinase ratio in tissues promotes

fibrogenesis.39 In summary, activated HSC might produce a fibrogenic

environment within the liver through a combination of ECM

overproduction, diminished MMP activation and inhibition of active MMPs

by TIMPs. The removal or inactivation of activated HSC from the liver is

therefore likely to be a key process before recovery from fibrosis can

occur.

<

Resolution of fibrosis Part 2

In clinical circumstances where an effective treatment for

the underlying insult is available, remodeling of the scar tissue can

occur and a return towards architectural normality has been documented

even in advanced fibrosis and cirrhosis. This has been most clearly

documented in autoimmune disease, but is paralleled by observations of

haemochromatotic patients after venesection and patients with hepatitis

B and C after successful interferon therapy.1-4 These observations are

highly encouraging and suggest that the liver has a capacity to remodel

scar tissue which, if harnessed and manipulated, would offer a novel

therapeutic approach to the treatment of liver fibrosis. It is

difficult, if not impossible to follow the cellular mechanisms mediating

recovery in humans, as ethical considerations prevent serial biopsy

samples from being taken from patients with liver disease and fibrosis

which seems to be resolving clinically. However, recovery from fibrosis

has been studied in rat models, which permit frequent sampling and

control over the chronology and extent of the fibrotic lesion.

Abdel-Aziz and colleagues40 examined reversibility of fibrosis in

experimentally induced cholestasis in rats.

Following bile duct ligation for three weeks, the typical

features of bile duct proliferation and periportal fibrosis developed

with a notable increase in hepatic mRNA for collagens I and IV. However,

three weeks after relief of bile duct ligation (by reanastamosis of the

bile duct to a jejunal loop), there was resorption of periportal

fibrosis and the liver ECM returned virtually to normal, except for a

persistence of collagen IV in sinusoids. Moreover mRNAs for collagen I

and IV became virtually undetectable. We have recently examined

spontaneous recovery from liver fibrosis in carbon tetrachloride treated

rats.41 Rats treated for four weeks with intraperitoneal carbon

tetrachloride developed established liver fibrosis with extensive

intervascular bridging with collagen fibres. Carbon tetrachloride dosing

then stopped and livers were examined at various times up to four weeks

of recovery. After this time, histological analysis showed a noticeable

dissolution of the collagenous fibrotic matrix and a return of liver

structure to virtual normality. The hepatic mRNA content of TIMP-1 and

-2 and procollagen I all dropped greatly in livers the first week of

recovery which coincided with the most rapid phase of collagen

degradation, as assessed by hydroxyproline content. A key finding was

that interstitial collagenase activity increased in the liver

homogenates during this time. The data support the hypothesis that TIMPs

play a predominant role in regulating fibrosis by protecting fibrotic

ECM from degradation by collagenase and possibly other MMPs.

Another important observation was that there was prominent

apoptosis of activated HSC during recovery, particularly in the first

three days concomitant with the largest drop in hepatic TIMP and

procollagen I mRNA. Apoptosis therefore effectively removed the

activated HSC, which were overproducing ECM and TIMPs. This mechanism

may also effect removal of " professional " ECM producing cells in other

organs during wound healing and resolution of fibrosis. For example,

Baker and colleagues42 showed that apoptosis removed surplus mesangial

cells from glomeruli during resolution of mesangial proliferative

nephritis and apoptosis also removes myofibroblasts during skin wound

healing.43 44 Our more recent studies suggest that during progressive

fibrotic liver injury both HSC mitosis and apoptosis increasethat is,

turnover of these cells is increased, although proliferation

predominates such that there is net increase in HSC numbers. During

recovery, apoptosis becomes the overriding process with resulting net

HSC loss from the liver.

There are relatively few studies of how apoptosis of HSC is

controlled in the liver. HSC activated in culture undergo spontaneous

apoptosis in vitro, which can be greatly increased by serum deprivation

and fas ligand.41 45 46 Our recent studies show that a further cytokine

present in injured liver, nerve growth factor, induces HSC apoptosis in

culture. Mast cells, which become more abundant in fibrotic liver, are a

rich source of nerve growth factor.47 The proapoptotic receptor fas and

its ligand are also expressed by activated HSC.45 It is possible that

persistence of HSC in fibrotic liver might therefore require undefined

survival factors to offset the effects of these apoptotic stimuli, and

removal of survival factors when liver injury ceases would then allow

relatively rapid removal of HSC. Apoptotic signals in the liver might

not be confined to soluble factors and the fibrotic neomatrix itself

might render activated HSC susceptible to apoptosis. The role of

cell-matrix interactions in regulating cell survival has most

extensively been studied in epithelial cells in which absolute

deprivation of contact with the ECM is a potent proapoptotic mechanism,

a process that has been termed anoikis.48 A recent study has shown that

blocking HSC attachment to plastic induces apoptosis,49 whereas data

from our laboratory show that HSC cultured on plastic or collagen I are

more susceptible to apoptosis induced by serum deprivation than HSC

cultured on Matrigel, a basement membrane-like matrix which reduces HSC

proliferation and activation. These final data raise the interesting

idea that ECM degradation may result in HSC apoptosis rather than HSC

apoptosis facilitating ECM degradation.

Although liver fibrosis in rats is reversible, the

implications for recovery from cirrhosis in humans remain to be

clarified. In our studies41 and those of Abdel-Aziz and coworkers,40

liver cirrhosis had not been achieved before recovery was initiated.

Clearly a key question which can be tackled using rat models is: does

liver fibrosis reach a point where it becomes irreversible, and if so

what are the qualitative and quantitative differences in the liver

structure compared with recoverable fibrosis? Several factors might

dictate whether liver fibrosis can recover. Firstly, it is clear that

recovery requires degradation of the existing ibrotic matrix, but this

matrix may be modified to resist degradation as fibrosis progresses.

Newly secreted collagen fibrils can be cross-linked by both tissue

transglutaminase and lysyl oxidase pathways; the activity of both

pathways is increased during liver fibrogenesis.50-52 Such cross-linking

during maturation of collagen might reduce its susceptibility to

collagenase.53 A recent report also suggests that tissue

transglutaminase can be released onto ECM from apoptotic hepatocytes

which are found in increased numbers in fibrotic liver.54 Mature ECM is

also relatively rich in elastin; to date there are very limited data on

the turnover of this important matrix protein in fibrosis. Secondly,

recovery is unlikely if collagenolytic enzymes remain inactive following

cessation of liver injury. The full range of enzymes having interstitial

collagenase activities in liver still require identification. However,

interstitial collagenase mRNA expression (MMP-1 in humans, MMP-13 in

rats) is similar in normal compared with cirrhotic livers, and does not

change during recovery in the rat model, even in the face of overt ECM

degradation.25 26 41 Previous studies suggest that collagenase activity

becomes deficient during evolution of liver fibrosis in animal models

and in humans,20-24 and the studies described earlier suggest that this

may be caused by TIMP overexpression. Continued inhibition of ECM

degradation by TIMPs may block the ability to recover from fibrosis,

even after removal of the injury. As activated hepatic stellate cells

are an important source of both ECM and TIMPs, recovery from fibrosis

might require either removal of the activated HSC population, as shown

in rat models, or possibly the phenotypical reversal of stellate cell

activation, a process yet to be observed in vivo. In non-recovering

liver fibrosis activated HSC might persist as a result of a " memory "

effect, possibly mediated by collagenous and non-collagenous components

of the deposited fibrotic neomatrix, which either promote HSC activation

or protect them from apoptotic stimuli.16 48 49 55

In summary, accumulating evidence suggests that liver

fibrosis is reversible and that recovery from cirrhosis may be possible.

Moreover, the application of cell and molecular techniques to models of

reversible fibrosis are helping to establish the events and processes

that are critical to recovery. It is anticipated that ultimately these

approaches will lead to the development of effective antifibrotics,

which harness or mimic the liver's capacity for reversal of fibrosis

with resolution to a normal architecture.<

______________________________________________

Message: 11

Date: Tue, 26 Sep 2000 13:59:56 EDT

From: gehud119@...

Subject: diagnosing and treatment of cirrhosis

Diseases

Springhouse

Corporation, Springhouse, Pennsylvania, 1997

(A Nurses Manual)

DIAGNOSING CIRRHOSIS & TREATMENT

A through workup consisting of diagnostic and laboratory tests is

required to confirm the diagnosis, establish the type of cirrhosis, and

pinpoint complications.

* LIVER BIOPSY. The definitive test for cirrhosis, biopsy detects

hepatic tissue destruction and fibrosis.

* ABDOMINAL X-RAYS. Films show liver size and cysts or gas within

the biliary tract or liver; liver calcification and massive ascites.

* COMPUTED TOMOGRAPHY AND LIVER SCANS. These studies determine

liver size, identify liver masses, and visualize hepatic blood flow and

obstruction.

* ESOPHAGOGASTRODUODENOSCOPY. This study reveals bleeding

esophgeal varices, stomach irritation or ulceration, or duodenal

bleeding and irritation.

* BLOOD STUDIES. Liver enzymes (alanine aminotransferase {formerly

SGPT}, aspartate aminotransferase {formerly SGOT}, total serum

bilirubin, and indirect bilirubin levels are elevated. Total serum

albumin and protein levels decrease; prothrombin time is prolonged.

Hemoglobin, hematocrit, and serum electrolyte levels decrease. Vitamins

A, C, and K are deficient.

* URIN AND STOOL STUDIES. Urine levels of bilirubin and

urobilinogen increased; fecal urobilinogen levels fall.

Therapy aims to remove or alleviate the underlying cause of

cirrhosis, prevent further liver danage, and prevent or treat

complications. Vitamins and nutritional supplements promote healing of

damaged hepatic cells and improve the patients's nutritional status.

Sodium consumption is usually restricted to 500 mg/day and liquid intake

is limited to1,500 ml/day to help manage axcites and edema.

Drug therapy requires special caution because the cirrhotic liver

can't detoxify harmful substances efficiently. Antacids may be

prescribed to reduce gastric distress and decrease the potential for GI

bleeding. Postassium-sparing diuretics, such as furosemide, may be used

to reduce ascites and edema. However, diuretics require careful

monitoring because fluid and electrolyte imbalance may precipitate

hepatic encephalopathy. Vasopressin may be indicated for esophageal

varices. Alcohol is prohibited and sedatives should be avoided.

In patients with ascites, paracentesis may be used as a palliative

treatment to relieve absominal pressure. However, surgical intervention

may be required to divert ascites into venous circulation; if so, a

peritoneovenous shunt is used. Shunt insertion results in weight loss,

decreased abdominal girth, increased sodium excretion from the kidneys,

and improved urine output.

To control bleeding from esophageal varices or other GI

hemorrhage, nonsurgical measures are attempted first. These include

gastric intubation and esophageal balloon tamponade. In gastric

intubation, a tube is inserted and the stomach is lavaged until the

contents are clear. If the bleeding is assessed as a gastric ulcer,

antiacids and histamine astagonists are administered.

In esophageal balloon tamponade, bleeding vessels are compressed

to stanch blood loss from esophageal varices. Several forms of balloon

tamponade are available, including the Sengstaken-Blakemore method, the

esophagogastic tube method, and the Minnesota tube method.

Sclerotherapy is performed if the patient continues to experience

repeated hemorrhagic episodes despite conservative treatment. A

sclerosing agent is injected into the oozing vessels. This agent

traumatizes epithelial tissue, which caused thrombosis and leads to

sclerosis. If bleeding from the varices does not stop within 2 to 5

minutes, a second injection is given below the bleeding site.

Scherotherapy also may be perfrormed prophylactically on nonbleeding

varices.

As a last resort, portal-systemic shunts may be used for patients

with bleeding esophageal varices and portal hypertension. Surgical

shunting procedures decrease portal hypertension by diverting a portion

of the portal vein blood flow away from the liver. These procedures are

seldom performed because they can result in bleeding, infection, and

shunt thrombosis.

Massive hemorrhage requires blood transfusion. To maintain blood

pressure, crystalloid or colloid volume espanders are administered until

the blood is available________________

__________________________________

Source: Liver Diseases & Gallstones-The Facts

& Triger, 1992,

England

" People with cirrhosis should be advised to eat a well-balanced

diet with plenty of calories. People with very advanced liver disease

are often thin and malnorished, either because they are not eating

enough or because the damaged liver affects their ability to absorb

food. Like calories, vitamins are an important part of the diet. People

with cirrhosis may not have the ability to absorb food properly and may

become deficient in one or more vitamins. Patients are often prescribed

vitamin supplements. A dietary limitation concerns proteinand this

applies to people with very advanced liver disease. Much protein may

affect the brain causing confusion and loss of concentration

(encephalopathy or brain disease). Patients with cirrhosis complicated

by ascites (fluid retention in the abdomen are advised to moderate their

salt intake.

Encephalopathy {or brain disease} This is a condition which

affects the brain. Patients with this condition develop a variety of

different symptoms ranging from minor lapses in memory and inability to

concentrate, to slurred speech, and confusion episodes which may be

transient or permanent. As it progresses patients become sleepy or even

unconscious. Encephalopathy is believed to be caused by toxic substances

(ammonia) which are formed when protein in the diet is broken down by

the action of many millions of bacteria in the intestine.

The toxins are absorbed into the portal vein and normally removed

from the blood by the liver, but when the liver is damaged, they pass

through it and go into the bloodstream to the brain, where they have

direct harmful effect. Since we know that protein is the source of these

toxic substances, many of the symptoms can be improved by simply

restricting dietary protein-to about 40-60 grams a day.

{CONSULT WITH YOUR DOCTOR ABOUT DOSE AMOUNTS}

Also drug therapy-Neomycin-is the antibotic normally chosen

because it is a powerful drug that is taken by mouth and is not absorbed

from the intestine. Another drug-Lactulose-has also been shown to have

results which work in two different ways. First, it increases the

acidity of the bowel contents. The bacteria which inhibit the bowel only

thrive under certain conditions and quickly succumb to a change in

acidity. Secondly, it also works as a laxative. We know that

enciphalopathy is made worse by constipation-because the bowel contents

pass through very slowly, bacteria have a much greater opportunity to

break down protein.

{This is a good place to mention the need to give up red meats,

which take too long to digest in the intestinal tract!} The dose of

Lactulose is increased gradually until diarrhea develops-gradual

adjustment to the dosage will soon give patients just loose, bowel

actions. "

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Source: Teaching Patients with Chronic Conditions

Springhouse Corporation,

Springhouse, Penn, 1992

" Because cirrhosis is associated partly with nutritional

deficiencies, emphasize the importance of following dietary instructions

to achieve

remission of symptoms. The diet will depend on the severity of the

disorder. If the patient has uncomplicated cirrhosis, the doctor may

prescribe a diet

high in calories, carbohydrates and protein to promote liver

regeneration and provide energy for muscle repair and rebuilding.

If patient has elevated levels of serum ammonia, he will be

instructed to follow a LOW-PROTEIN diet to minimize the risk of

developing uremia.

Patient should take supplemental vitamins as ordered-A, B complex,

D and K (to compensate for the livers inability to store them) and Vit

B12, folic acid, and thiamine to correct anemia.

The patient should avoid fats if they cause indigestion or

diarrhea. It is advised to restrict sodium to prevent or reduce ascites.

Above all stress

abstention from alcohol.

If anorexia's a problem (inability to eat) reinforce the

importance of an adequate diet for liver cell regeneration. Advise

small, frequent meals, liberal snacking (of nutritious food), favorite

foods if allowed, and special importance of mouth care.

Medication-Take medications carefully-because of the liver's

inability to detoxify all substances is very much impaired. Patient may

be prescribed aniemetics (for nausea and vomiting), diuretics (for edema

or water retension), and antiacids for reducing the risk of GI bleeding.

Patients should know guidelines for taking all drugs, and their

potential adverse effects. "

Dietary Do's and Don'ts-Patient Teaching Aid

" Because you have cirrhosis, you need to pay special attention to

your diet. Healthful eating habits will help damaged hepatic cells to

regenerate and

prevent harm to the remaining cells. Follow this list of do's and

don'ts.

DO'S

* Ask your doctor or dietitian for help in planning your diet.

They can advise you about how many calories you need and how to best

meet your nutritional requirements. If you are used to eating fast

foods, they can help you choose the most nutritious ones on a

fast-food menu.

* Eat small, frequent meals. Instead of the traditional three

square meals, try eating five or six lighter ones. This may relieve

the bloated or sick feeling that cirrhosis can cause.

* Keep a food diary. After each meal, jot down the foods you ate,

the time of day, and how you feel. After a week, study your food

diary for patterns. Use the diary to make smarter choices about what

and when to eat.

* Weigh yourself daily, and keep a chart. If you weight goes up

more then five pounds, call your doctor-you may have retaining

fluid.

* Set an attractive table. To perk up your appetite, use nice

tableware, add a colorful garnish to your plate, and set an

appropriate mood with relaxing music or conversation.

DON'TS

* Avoid drinking alcoholic beverages-even occasionally. Alcohol

destroys live cells, so abstain COMPLETELY.

* Stay away from coffee or tea. Avoid all caffeine-containing

beverages foods, which can cause indigestion.

* Steer clear of spicy foods, which may upset your stomach.

* Eliminate salt while cooking, and do not salt your food. Too

much salt may make you retain fluid. Ask your doctor if you should

follow a salt-restricted diet.

* Do not go on a quick weight-loss diet. If you have gained weight

because of fluid build-up in your body, eating less will not help

you. Remember, good nutrition is essential to repair your liver.

Other Care Measures

Because impaired hepatic production of prothrombin may cause a

bleeding tendency, watch for the warning signs of bleeding-weakness,

hemoptysis (spitting up of blood from the lungs or bronchial tubes),

or blood in the stools (dark feces) or urine. Avoid the risk of

causing bleeding by avoiding aspirin, bruising, and straining during

defecation.

Patient should avoid blowing his nose, sneezing or coughing

vigorously. Also advisable is using an electric razor and a soft

toothbrush.

Avoid contact with people who are ill, obtain adequate rest, and

maintain any treatment regimen. Contact doctor immediately if patient

becomes ill.

Seek counseling for any alcohol or drug dependency. Counseling or

support groups are also available for emotional support. GINGER

______________________________________________

" Dietary Considerations for Impaired Liver Function, "

by L. Beyer, MS, RD,

Associate Professor Dietetics and Nutrition,

University of Kansas Medical Center.

Liver Functions

The liver is the body's recycling, manufacturing, and

waste management plant. This glandular organ's more than 400 functions

affect the performance of every other body system. Normal liver

functions include the:

1. Secretion of Bile

2. Synthesis and storage of glycogen

3. Synthesis and breakdown of fats

4. Conversion of ammonia to urea

5. Synthesis of cholesterol

6. Synthesis of clotting factors

7. Detoxification of drugs, alcohol and xenobiotics

8. Synthesis of glucose and lipids from other

substrates

9. Storage of some vitamins

10. Disposal of " worn-out " blood cells

Even when the liver is damaged, these functions

continue until about 80% of the liver is destroyed.

Chronic Liver Disease

This page is too big to be shown completely.

" You may be right, I may be crazy, but it just may be a lunatic your

looking for "

August 2, 2002

>________________________________________________________________________

>

>Hi Everyone,

> I have been out of state on vacation & was wondering if anyone attended

>Dr. Rutledge's seminar in Bay City, MI. I am from Bay City, but couldn't

>attend because of our vacation plans. I was so dissapointed, but would love

>to hear from anyone who went.

>

> Bonnie S. from MI

>

>this is a test

>_________________________________________________________________

>Send and receive Hotmail on your mobile device: http://mobile.msn.com

>

>________________________________________________________________________

>

_________________________________________________________________

Send and receive Hotmail on your mobile device: http://mobile.msn.com

January 26, 2003

In a message dated 1/26/03 8:39:24 AM Central Standard Time,

Hepatitis C writes:

> Vicky McKay

>

AND exactly what is NASH?? besides a liver disease? WHat are the sides and

does it make cirrhosis move faster??I need info.. I went from stage 3 grade 4

to end stage in less than 2 years... wondering if another disease has some

how worked into dis here damn Hep C. Pete G

" Chance favors the prepared mind "

Louis Pasteur

** If you can't be a good example then you have to be a horrible warning**

Da YOOPER

January 26, 2003

In a message dated 1/26/03 8:39:24 AM Central Standard Time,

Hepatitis C writes:

> Vicky McKay

>

AND exactly what is NASH?? besides a liver disease? WHat are the sides and

does it make cirrhosis move faster??I need info.. I went from stage 3 grade 4

to end stage in less than 2 years... wondering if another disease has some

how worked into dis here damn Hep C. Pete G

" Chance favors the prepared mind "

Louis Pasteur

** If you can't be a good example then you have to be a horrible warning**

Da YOOPER

January 29, 2003

Charlene you need to move to Ferndale Michigan home of the miracle worker PPI

teacher as I call her.LOL

Pennie

January 29, 2003

Feel the love in this room. LOL

January 29, 2003

My husbands hours have just been drastically cut, but my boss is looking for

anothe part time person. Youknow anything about watch repair or Jewelery? LOL

January 29, 2003

Nothing a maragarita wouldnt cure. LOL

Pennie

Heck I would be happy with a pepsi without " floaties "

LOL

January 29, 2003

Just wanted to say Thanks too all who e-mailed me with your support. Also the

charlene you just posted that's why I love most of you guys! Yes, we tend to

get a little opionated sometimes. Maybe its just an Ohio thing! Oh, well my

daughter is Autisic from what don't know , but is making great progress , and

if she never makes anymore progress or if she makes more great gains she's

just simply a gift from God who helps me learn from everyday life. Maybe has

not taught me to be quiet sometimes, but hey she does'nt either. Heck maybe

we all have some sort of Autism in us oh, well! Thanks to a great group of

people! le (mother of Noelle)

January 29, 2003

No not really I worked airforce then airguard, mcdonalds , pizza

time and walmart LOL

is a great talker and can convience anyone hes a great employer

Hes retired military then worked halliburton

-- Re: Digest Number 1144

My husbands hours have just been drastically cut, but my boss is looking for

anothe part time person. Youknow anything about watch repair or Jewelery?

LOL

January 30, 2003

love is not a feeling! It is a choice, remember?!

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January 30, 2003

Charlene-

Thanks for your post. I will put the info in the mail as soon as I get

the chance to send it. Have you tried typing Chromosome 15duplication in

your search engine, in the meantime?

On this post, I am mainly just looking for frienship and support, not a

place to voice my opinion. What I shared was a medically known fact about

my daughter. I do not want to argue with anyone, but it is hard not to

be on the defensive when one puts you on the spot for a cure just

because you know the cause of your child's Autism!! As far as any one

knows, there is no " cure " for Autism, no matter what caused it!!!

I was also wondering what you meant when you referred to a great school

program? What help Amber gets I am most thankful for and do not deserve

any more than any one else does. I just praise the Lord for His

wonderful provision and work that He is doing through all of Amber's

therapies.

Amy

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January 30, 2003

A great school program????? Would be at least half of your childs

needs met. In my case if I got 2 hours of speech therapy and 2 hours of

occupational therapy a week and school that would accept him I would be

happy. In my case Trinidad colorado didnt want as I had a problem

with cog preschool which is controlled by the las animas county government

as they said my son wasnt autistic that I was abusive. Headstart here said

we make too much money yet they keep children from 7am to 4:30pm ( I do not

want to start a topic of low income stuff been there done that and had lots

of arguements about it) Aguilar school said they were too full and Primero

school said they would never accept a child like mine so I had to fake

residency and go to neighboring Raton new mexico for services. As for my

daughter well I wished to get a small class with someone who is patient and

helps her through the day in socializing. All of this does not and never

will exist in southern colorado. If we would of stayed in Pemberton NJ

would of got 30 hours a week preschool based on his disability and not

income (we are not rich middle classed) would of got to be in the

multiple learning disabled class as she was previously in. New Jersey. I

would want a child study team that actually admits to the autism instead of

accusing the pediatric neurologist a liar!

I realize there is no cure for autism but it can be worked with so

the child can lead a normal healthy life.

Charlene