| |
|
Symptoms of Cirrhosis
The early stages of cirrhosis often produce no symptoms.
As scar tissue replaces healthy cells, the liver begins to fail and
symptoms may become evident. The severity of symptoms depends on the
extent of liver damage.
Because the liver is crucial for so many metabolic
activities, cirrhosis impacts a wide range of the bodies functions,
including nutrient and hormone metabolism, blood clotting, and
processing of ammonia and other toxic wastes. Many of the symptoms of
cirrhosis are directly related to disruption of these functions.
However, most of these symptoms can also be caused by other conditions,
so it is important to consult with your health care provider if you
experience any of these symptoms, particularly if you have risk factors
that increase your likelihood of developing cirrhosis.
Early symptoms of cirrhosis include:
- Fatigue and weakness “ related to anemia and altered nutrient
metabolism
- Poor appetite
- Nausea
- Weight loss
- In men:
- Impotence
- Reduced testicle size
- Enlarged, tender breasts
- Loss of interest in sex “ due to altered liver metabolism of sex
hormones
- Small, red spider-like blood vessels under the skin “ caused by
increased pressure in the tiny blood vessels due to liver congestion
- Increased sensitivity to drugs “ due to reduced ability of the
liver to inactivate them
Symptoms become more pronounced as cirrhosis progresses.
In addition, complications may develop that produce other, frequently
life-threatening, symptoms of the disease.
Later symptoms, some of which are due to complications,
include:
- Reddened or blotchy palms
- Loss of body hair
- Sleep disturbances
- Insulin resistance
- Ulcers
- Fever and other signs of infection “ due to altered immune
function
- Gallstones “ if cirrhosis prevents bile from reaching the
gallbladder
- Pale or clay-colored stools “ caused by a reduction in excreted
bile pigments
- Frequent nosebleeds, skin bruising or bleeding gums “ resulting
from decreased liver synthesis of clotting factors
- Ascites “ water retention and swelling in the legs and abdomen
caused by obstructed blood flow through the liver and reduced
synthesis of the protein albumin
- Bacterial peritonitis “ infection of ascites causing abdominal
pain and fever
- Itching “ caused by deposition of bile products in the skin
- Jaundice “ yellowing of the skin or eyes due to build-up of bile
pigments (bilirubin)
- Vomiting blood “ due to swollen veins in the esophagus that burst
- Encephalopathy and coma “ mental changes, including forgetfulness,
trouble concentrating, confusion, and agitation, caused by the
build-up of ammonia in the blood
- Decreased urine output and dark urine “ caused by kidney
dysfunction or failure
- Liver cancer
Etiology
of Cirrhosis
Cirrhosis of the liver is a chronic, diffuse (widely
spread throughout the organ), degenerative disease in which the
parenchyma (the functional organ tissue) deteriorates; the lobules are
infiltrated with fat and structurally altered; dense perilobular
connective tissue forms; and often areas of regeneration develop. The
surviving cells multiply in an attempt to regenerate and form "islands"
of living cells that are separated by scar tissue. These islands of
living cells have a reduced blood supply, resulting in impaired liver
function. As the cirrhotic process continues, blood flow through the
liver becomes blocked; portal hypertension may occur (high blood
pressure in the veins connecting the liver with the intestines and
spleen); glucose and vitamin absorption decrease; the manufacturing of
hormones and stomach and bowel function are affected; and noticeable
facial veins may appear. Most patients die from cirrhosis in the fifth
or sixth decade of life (Wolf 2001).
Approximately one-third of cirrhosis cases are
"compensated," meaning there are no clinical symptoms. Compensated cases
are usually discovered during routine tests for other problems or during
surgery or autopsy. Cirrhosis is irreversible. Unless the underlying
cause of cirrhosis is removed and the person takes measures to treat the
condition, the liver will continue to incur damage, eventually leading
to liver failure, ammonia toxicity, gastrointestinal hemorrhage, kidney
failure, hepatic coma, and death. For some people, the only chance for a
long-term cure is a liver transplant.
According the Centers for Disease Control (CDC), in
the year 2000, preliminary data compiled by the Division of Vital
Statistics revealed that even though cause of death from cirrhosis and
chronic liver disease had fallen a rank from 7th to 12th, the number of
people who died from liver disease was 26,219, almost the same as when
cirrhosis was ranked 7th (Minino et al. 2001).
In cirrhosis, healthy, functioning liver cells are destroyed, and
scarring and distortion of the liver eventually takes place. As fewer
liver cells function, smaller amounts of albumin (a protein) are
manufactured. Lower albumin levels facilitate water retention (edema) in
the legs and abdomen (ascites). Excessive bile product deposits cause
intense skin itching, often accompanied by jaundice (yellowed skin).
Other symptoms are testicular atrophy (Swelling of Testicles) ,
gynecomastia (enlargement of the male breast), and loss of chest and
armpit hair.
Psychotic mental changes such as extreme paranoia can also occur in
cases of advanced cirrhosis.
Systemic Complications from Cirrhosis
In the cirrhotic liver, when blood flow is restricted, blood can back
up in the spleen, causing an enlarged spleen and sequestered blood
cells. In this situation, the platelet count typically falls and
abnormal bleeding results. In extreme cases, blood actually flows
backward from the portal circulation to systemic circulation. In
addition to esophageal varices, varicose veins can develop in the
stomach (gastric varices) and rectum (hemorrhoids). Ruptured varices
cause massive bleeding and are often fatal. Bilirubin levels may also
build up in the blood, causing jaundice and bright yellow to dark brown
urine. Additionally, insulin resistance and diabetes mellitus, kidney
dysfunction, and congestive heart failure, as well as osteomalacia (the
adult form of rickets, resulting in bone softening that often leaves
them brittle) and osteoporosis (reduction in bone mass) are associated
with cirrhosis (NIDDK 2000).
If cirrhosis prevents bile, a green-brown fluid that is produced by
the liver, from reaching the gallbladder, a person may develop
gallstones (NIDDK 2000). It is then secreted through tiny channels
within the liver into a duct to the gallbladder. Bile is stored in the
gallbladder until it is needed for digestion of fats. Most gallstones
are formed from cholesterol. If the liver is healthy, the bile contains
the proper constituents to dissolve cholesterol excreted by the liver,
but in a cirrhotic liver, the bile cannot adequately dissolve
cholesterol. The cholesterol then forms crystals, which settle to the
bottom of the gallbladder and eventually become stones (ALF 2002; MFMER
2002; WebMD 2002).
A cross-sectional study was conducted in 1010 patients with cirrhosis
related to alcohol abuse, chronic viral infection, or miscellaneous
causes (42%, 48%, and 10%, respectively). Gallstone development was
monitored by ultrasound in 618 patients who were free of gallstones at
enrollment. The overall prevalence of gallstones was 29.5% and increased
significantly with age without differences according to sex or cause of
cirrhosis. During a mean ± SD follow-up of 50 months ± 9 months, 141
(22.8%) of 618 patients developed gallstones, with an estimated
cumulative probability of 6.5%, 18.6%, 28.2%, and 40.9% at 2, 4, 6, and
8 years, respectively. Multivariate analysis showed that degree of
cirrhosis and high body mass index carried a significantly greater risk
of gallstone formation, leading the researchers to conclude: "Cirrhosis
per se represents a major risk factor for gallstones whose prevalence
and incidence were far higher than those reported in a general
population from the same area" (Conte et al. 1999).
-
Note: Cholesterol in the bile
has no relation to the cholesterol in the blood. Therefore
cholesterol-lowering drugs do not prevent gallstones.
Toxins that the liver normally removes build up in the blood, dulling
mental function and leading to personality changes. The condition of the
liver also affects how drugs are filtered from the body. Drugs the
patient is taking that are normally filtered out by the liver and
disposed of in the urine may remain in the bloodstream for a much longer
period, acting longer than expected or even building up in body tissue.
A cirrhotic liver is usually much larger than a healthy liver (Clayman
1989; Glanze 1996; NIDDK 2000; Wolf 2001).
Treating the Complications
In patients who have cirrhosis, complications from the disease must be
treated. In particular, acute variceal bleeding is a very serious,
life-threatening medical emergency. Infections such as spontaneous
bacterial peritonitis must be promptly treated with appropriate
antibiotics. Coagulation disorders will sometimes respond to vitamin K.
However, drugs that are metabolized in the liver must be used with
caution.
Ascites
Mild cases of ascites are treated with a salt-restricted diet (2000 mg
of sodium daily or less in some cases). Cirrhosis patients often need
guidance in planning a diet that has low sodium content without
compromising caloric and nutritional requirements (NIDDK 2000). If salt
restriction is not effective, diuretic drugs are the next treatment
consideration (e.g., Aldactone or Lasix). In patients who continue to be
resistant to drug therapy, peritoneovenous and portosystemic shunts
(plastic tubing) are inserted subcutaneously to connect the peritoneal
cavity or the portal system to an internal jugular or subclavian vein
(Wolf 2001).
Hepatic Encephalopathy
Blood ammonia will be checked because an elevated serum ammonia level is
a classic laboratory finding in hepatic encephalopathy. Lactulose is
helpful in some patients to assist in removal of ammonia (Wolf 2001).
Lactulose is a synthetic sugar that is not absorbed by the body and is
used a laxative. Neomycin and other antibiotics are also used to
decrease bacteria in the intestine that produce ammonia. Depending on
nutritional status, dietary protein may be restricted in patients who
are having an acute flare-up of hepatic encephalopathy (Wolf 2001).
Esophageal Varices
Restricted blood flow in the portal vein causes blood from the
intestines and spleen to back up into stomach and esophagus blood
vessels. These vessels are not intended to carry large amounts of blood
and become enlarged. As these veins enlarge (varicose veins or varices),
the walls become thin and are likely to burst as pressure increases.
Variceal hemorrhaging is very serious and requires immediate medical
attention. As part of routine monitoring, a diagnostic endoscopy will be
done to determine if a patient has asymptomatic esophageal varices. If
varices are present, treatment can include reducing salt intake; taking
diuretics to eliminate excess salts and fluids from the body; taking a
beta-blocker (propranolol, nadolol); injection of a clotting agent;
injection of a scarring chemical (sclerotherapy); or rubber-band
ligation (a surgical procedure using a device to compress the varices
and stop bleeding) (Pugh et al. 1973; NIDDK 2000; Wolf 2001). In
addition, there is a radiological procedure called transjugular
intrahepatic protosystemic shunt (TIPS) that shows some promise.
Hepatoma
In the United States, hepatocellular carcinoma is observed in 10-20% of
patients who have cirrhosis (Wolf 2001). The liver cells develop a
malignant change leading to a type of cancer called hepatocellular
carcinoma (HCC). As with other cancers, early detection and number and
size of tumors influence survival. Treatment for HCC ranges from
surgical removal of the HCC if the patient has good liver function to
transplantation (NIDDK 2000; Columbo 2001; Wolf 2001). If the patient
cannot have surgery (advanced age, other health conditions, poor liver
function, large tumors, or tumors in strategic locations), possible
treatment includes ultrasound-guided injection of solutions that cause
necrosis of tumor cells in the cancerous area; using a catheter to
eliminate blood supply to the tumor; injecting antitumor agents directly
into the tumor; systemic chemotherapy; and radiation (Columbo 2001).
Portal Hypertension
A healthy liver can accommodate a wide range of changes in portal blood
flow without alteration of portal blood pressure. However, when the
portal vein is obstructed, portal hypertension (very high blood
pressure) occurs (Clayman 1989; Wolf 2001). Factors causing increased
resistance to blood flow are fibrotic changes in the liver caused by
cirrhosis, compression of the nodules that are regenerating liver
tissue, and increased collagen deposition and levels of chemicals that
act to constrict the blood vessels in the liver. Other causes are a
blood clot in the portal vein or congenital narrowing (Clayman 1989).
Treatment can consist of controlling ascites with salt restriction and
diuretics; treating varices; or surgically implanting a shunt to divert
blood from the portal vein to another blood vessel to relieve some of
the pressure on the portal vein (Clayman 1989).
Cirrhosis and the Hepatitis C Factor
Until recently, the most common cause of cirrhosis of the liver in
the United States was attributed to alcohol abuse. Because of the rapid
increase of hepatitis C virus infection, hepatitis C has now taken over
first place (26%), with alcohol abuse falling to second place, but only
slightly behind at 21% (NIDDK 2000). There are vaccines for some of the
hepatitis viruses, but at this time, there is no vaccine to prevent
transmission of the hepatitis C virus. Preventive and deterrent
practices are the only means to avoid it (Alter et al. 1998; Buggs 2002;
NIDA 2002). The most common routes of infection with the hepatitis C
virus are via needles, sexual contact, and blood transfusions, and from
an infected pregnant female to her newborn (NIDA 2002) (see
the protocol on
Hepatitis C for a complete discussion of the hepatitis C virus).
Hepatitis C is one of six viruses known to cause liver disease (Buggs
2001; NIDA 2002, Strickland 2002). Hepatitis C is very difficult for the
immune system to overcome and often becomes chronic, leading to serious
and permanent liver damage. Typically hepatitis C infection is mild in
the early stages and rarely recognized until it has caused significant
damage to the liver. From infection to noticeable or significant liver
damage can take 20 years or more. The symptoms of hepatitis C are also
very mild in the early stages. Fatigue, the most common symptom, may not
appear for many years. Other symptoms are mild fever, muscle and joint
aches, nausea and vomiting, poor appetite, and vague abdominal pains.
Hepatitis C often goes undiagnosed because the symptoms come and go and
are so suggestive of a flu-like illness. Its presence is usually
identified during a routine blood test or because the hepatitis C
antibody is positive at the time of a blood donation.
A low level of infection with practically no symptoms can continue
for years. The hepatitis C infection causes inflammation of the liver,
with chronic infection resulting in cirrhotic-like scarring.
Unfortunately, more than 80% of infected individuals eventually progress
to the chronic stage of hepatitis C which results in cirrhosis (severe
scarring of liver tissue). Persons with the late stages of hepatitis C
can also develop liver cancer. When the hepatitis C virus is a cofactor,
there is an increased risk of cirrhosis in those who also consume
alcohol in excess (NIDA 2002). |
“How will I know
if I get cirrhosis?
Kara Wright, PA-C
One of the most common questions from a patient
with hepatitis C is: “How will I know if I get cirrhosis?” People always
want to know what to look for. In reality, many patients with cirrhosis
may not even know they have significant liver disease until further
evaluated by a medical provider. Many patients may have cirrhosis and
have no signs or symptoms at all. In this article, we will discuss the
physical and laboratory signs of cirrhosis.
Cirrhosis is late stage liver disease. It is characterized by actual
distortion of the liver architecture due to scarring of the liver and is
generally considered irreversible. Once the liver cells become scarred,
liver function declines which produces a number of physical as well as
laboratory findings. Although these findings often indicate cirrhosis,
they are not specific only to liver disease.
Physical signs
Ascites is the accumulation of fluid in the abdominal cavity.
In many cases, several liters of fluid can build up and cause severe
abdominal distention. This is the most common complication of cirrhosis.
Nearly 60% of all patients with compensated cirrhosis will develop
ascites in 10 years.
Spontaneous bacterial peritonitis (SBP) is an infection of
ascitic fluid. Manifestations of SBP include fever, abdominal pain,
abdominal tenderness, and altered mental status. In the event of SBP, a
provider must do a diagnostic paracentesis (draining of the fluid from
the abdomen).
Hepatomegaly is enlargement of the liver. The cirrhotic liver
may be large, normal sized, or small. When it can be felt, it will have
a firm and nodular consistency.
Splenomegaly is enlargement of the spleen and is common in
patients with cirrhosis.
Caput medusa is noted when the veins in the abdomen are very
prominent. This appearance has been said to resemble the head (caput) of
the mythical Gorgon Medusa.
Hepatic encephalopathy is a potentially reversible disturbance
in consciousness and behavior. Disturbance of sleep pattern is a common
early feature that typically precedes overt neurologic features.
Patients often feel very confused. Physical findings include asterixis.
Asterixis is the bilateral but non-uniform flapping motions of
outstretched hands.
Fetor hepaticus is a sweet, pungent smell to the breath of
cirrhotic patients. It is caused by increased concentrations of a
chemical, which is not being detoxified by the liver.
Variceal hemorrhage is a devastating complication that occurs
in 25-40 percent of patients with cirrhosis. This occurs when a blood
vessel has very high-pressure blood flow, which causes it to break and
bleed.
Jaundice is the yellow coloring of the skin and mucus membranes
that results from increased serum bilirubin.
Spider angiomata, also known as spider telangiectasias,
are markings on the body, which, as indicated in the name, look like
spiders. They have a central circular artery with smaller vessels
radiating from the center like spokes, or legs of a spider. The lesion
is typically red or purple in color and the central part of the lesion
may pulsate when compressed with a glass slide. Spider angiomata are
most frequently found on the trunk, face and arms. As a general rule,
the number and size of the spider angiomata correlate with the severity
of liver disease.
Palmar erythema is an exaggeration of the normal spotty redness
on the palms of the hands. It is characterized by a deep redness on the
fleshy part of the palm.
Nail changes are sometimes found. Muehrcke’s nails are
characterized by paired horizontal white bands separated by normal color
in the nail. Another nail disorder, Terry’s nails, is seen in
patients with cirrhosis. In this case, the two-thirds of nail plate
closest to the hand appears white whereas the furthest one-third is red.
Gynecomastia is benign growth of the tissue of the male breast.
The tissue typically feels firm and rubbery. Up to two-thirds of
patients with cirrhosis have gynecomastia. Men may also develop other
features such as loss of chest or underarm hair and inversion of the
normal male pubic hair pattern.
Constitutional symptoms such as weakness, fatigue, anorexia,
and weight loss also occur. The fever of cirrhosis is typically low
grade and continuous.
Laboratory findings
Liver enzymes may provide the first clue to liver dysfunction.
Aspartate aminotransferase (AST) and alanine aminotransferase
(ALT) are usually moderately elevated in cirrhotic patients. AST is
often more elevated than ALT, but levels can be normal in cirrhotics.
Alkaline phosphatase is usually elevated but less than 2-3
times the upper normal limit.
Bilirubin is often normal in well-compensated cirrhosis, but
will rise as cirrhosis progresses.
Albumin is synthesized exclusively in the liver. Albumin levels
fall as the synthetic function of the liver declines due to worsening
cirrhosis. Serum albumin levels can help to grade the severity of
cirrhosis.
The liver synthesizes many proteins required for normal clotting. The
prothrombin time (PT) reflects the degree of liver dysfunction.
The PT increases as the ability of a cirrhotic liver to synthesize
clotting factors diminishes.
Anemia may occur in cirrhotic patients due to a number of
causes.
Thrombocytopenia (low platelets) is very common in cirrhotic
patients and is often caused by an enlarged spleen, which can sequester
up to 90% of circulating platelets.
If a patient has any of these signs, he or she should discuss them with
a medical provider. These signs do not always indicate cirrhosis, but
can help establish that diagnosis.
http://www.hcvadvocate.org/news/newsLetter/advocate1103.html#3 |
Risk Factors for
Developing Cirrhosis from Hepatitis C.
Between 20% and 30% of people with hepatitis C develop cirrhosis after
twenty years. (It should be noted that even in patients with cirrhosis,
survival rates in one study were nearly 80% at 10 years in these patients.)
The following conditions put people with hepatitis C at higher risk for
liver damage:
-
Having a specific genetic type of hepatitis C (genotype
1). This is the strongest risk factor for severity and risk for cirrhosis.
-
Being male may pose a higher risk for severity than
being female.
-
Developing hepatitis C at an older age.
-
Heavy alcohol use.
-
Co-infection with HIV or hepatitis B.
-
A history of transfusions. (One study reported that they
are twice as likely as intravenous drug users to develop cirrhosis.)
-
Being overweight, particularly if fat is distributed in
the abdomen (an apple-shape). This condition may pose a higher risk for a
fatty liver, which in turn is more apt to become scarred and cirrhotic.
-
Having large iron stores in the liver.
Risk Factors for Developing Cirrhosis from Hepatitis B. The great
majority of people with chronic persistent hepatitis B have a good long-term
outlook, but between 5% and 10% become carriers of the virus and 5% to 10%
of these individuals eventually develop cirrhosis. The addition of hepatitis
D is a particular danger and increases the risk for cirrhosis. [ See also
Well-Connected, Report #59, Hepatitis.]
To read full article on Cirrhosis :
http://www.reutershealth.com/wellconnected/doc75.html
Natural
History of Cirrhosis
Two recent studies examined the natural history
of liver cirrhosis in individuals with viral hepatitis. In the May issue of
Gut, L. Benvegnu and colleagues investigated the progression and
outcome of initially compensated cirrhosis in a cohort of 312 Italian
patients with hepatitis B (43 patients), C (254 patients), or both (15
patients), followed for an average of about eight years. Tests were
performed every six months to assess liver disease progression and identify
major complications. During the follow-up period, 102 patients (about 33%)
developed at least one complication. The most common were hepatocellular
carcinoma (HCC, a type of liver cancer; about 21%), ascites (about 20%),
gastrointestinal bleeding (about 5%), and encephalopathy (about 2%). About
20% experienced liver disease progression as evidenced by an increased
Child-Pugh cirrhosis score. About 19% died from liver disease during
follow-up, most (70%) due to HCC. The authors concluded that HCC was “the
most frequent and life-threatening complication, particularly in HCV
positive cases.”
The same month in the Journal of Hepatology, Ramon Planas and
colleagues from Spain reported on the natural history of decompensated
cirrhosis in patients with hepatitis C. Two hundred patients were followed
from their first hospitalization for hepatic decompensation; average
follow-up was about three years. The most common initial complications
related to decompensation were ascites (48%), gastrointestinal bleeding
(about 33%), severe bacterial infection (about 15%), and encephalopathy
(5%). During follow-up, about 17% developed HCC and about 43% died. “Once
decompensated HCV-related cirrhosis was established,” the researchers
concluded, “patients showed not only a very high frequency of readmissions,
but also developed decompensations different from the initial one.”
http://www.hcvadvocate.org/news/newsRev/2004/HJR-1.11.html#3
NATURAL HISTORY OF COMPENSATED CIRRHOSIS
| |
|
The natural history of
compensated cirrhosis due to hepatitis C virus
06 June 2006 |
| Hepatitis C-related cirrhosis is a slowly
progressive disease and may be accelerated by other potential causes
of liver disease, find scientists in the June issue of Hepatology. |
| |
| It is necessary to follow large groups of
patients for long periods to establish the rates, chronology, and
hierarchy of complications of cirrhosis, and other potential causes of
liver disease.
In this study, scientists followed a cohort of 214 patients with
compensated cirrhosis due to hepatitis C virus (HCV) for 17 years.
Study subjects were HCV RNA-seropositive with Child-Pugh class A
cirrhosis.
They had no previous clinical decompensation.
The team found that hepatocellular carcinoma (HCC) developed in
32%of patients during follow-up.
Ascites developed in 23%, jaundice in 17%, upper gastrointestinal
bleeding in 6%, and encephalopathy in 1%. |
| |
|
They found that clinical status remained unchanged in 72%, progressed to
Child-Pugh class B in 21% and class C in 7%.
The scientists determined that HCC was the cause of death in 44% of
patients and also the first complication to develop in 27%.
Overall, the annual mortality rate was 4% per year.
Dr Angelo Sangiovanni's team concluded, "Hepatitis C-related
cirrhosis is a slowly progressive disease that may be accelerated by other
potential causes of liver disease".
"HCC was the first complication to develop and the dominant cause for
increased mortality".
Hepatology 2006; 43(6): 1303-10
06 June 2006
http://www.gastrohep.com/
NATURAL HISTORY OF COMPENSATED CIRRHOSIS
This study was presented at the EASL liver
meeting in Madrid by a Greek research group from the University of Crete.
The aim of this study was to define the natural history of compensated
cirrhosis and analyze age, sex and cirrhosis etiology at diagnosis to
identify prognostic factors available at diagnosis which might influence
the time or decompensation or survival.
The authors retrospectively analyzed data of 306 compensated cirrhotic
patients from diagnosis to decompensation and, death, using the log rank
test and univariate Cox PH models.
RESULTS: 54.9% of the patients were males, 47.06% were <64
years old. 56 had alcoholic cirrhosis, 17 had alcoholic cirrhosis with a
viral infection, 45 had HBV cirrhosis, 145 had HCV cirrhosis and 43 had
cryptogenic cirrhosis. 150 patients (49.02%) became decompensated within
the study period. Median time to decompensation was 58 months (95% CI 51
and 65 months). Patients with HCV cirrhosis had longer times to
decompensation than the other groups (81 months).
65% of all patients remain compensated 3 years after diagnosis,
reduced to 34% after 7 years. 70 patients (22.88%) died within the study
period. The median survival time was 126 months (95% CI 103 to 149
months). The prognostic factors available at diagnosis that were found to
have a significant effect on decompensation and survival time were sex (p
= 0.0024 and p = 0.0007) and etiology of cirrhosis (p < 0.0001 and p =
0.0024). The authors found that females with HCV cirrhosis have the
longest time until decompensation and the longest survival times.
http://www.natap.org/2002/easl/day9.htm
Compensated cirrhosis: natural history and prognostic
factors.
Gines P, Quintero E, Arroyo V, Teres J, Bruguera M, Rimola A, Caballeria
J, Rodes J, Rozman C.
To investigate the natural history of compensated cirrhosis, 293 consecutive
patients without previous major complications (ascites, jaundice,
encephalopathy or gastrointestinal hemorrhage) were studied in terms of
morbidity (probability of developing decompensated cirrhosis during
follow-up) and survival. Patients were diagnosed by liver histology between
1968 and 1980. Median follow-up was 63 months. Decompensation of cirrhosis
was considered when a patient first developed one of the major complications
of the disease. Ten years after diagnosis, the probability of developing
decompensated cirrhosis and the survival probability rate were 58 and 47%,
respectively. A multivariate survival analysis (Cox's regression model)
using clinical, biochemical and histological data obtained at diagnosis
disclosed seven factors that predicted prognosis: serum bilirubin; serum
gamma-globulin concentration; hepatic stigmata; prothrombin time; sex; age,
and alkaline phosphatase. According to the contribution of each one of these
factors to the final model, a prognostic index was constructed that allows
calculation of the estimated survival probability. The predicting value of
this index was validated by a split sample testing technique.
PMID: 3804191 [PubMed - indexed for MEDLINE]
Natural history of
decompensated hepatitis C virus-related cirrhosis. A study of 200 patients.
Hepatol. 2004 May;40(5):823-30.
Planas R, Balleste B, Antonio Alvarez M, Rivera M, Montoliu S, Anton
Galeras J, Santos J, Coll S, Maria Morillas R, Sola R.
Department of Gastroenterology, Hospital Universitari Germans Trias i Pujol,
Universitat Autonoma de Barcelona, Badalona, Spain.
BACKGROUND/AIMS: Since few data are available concerning the clinical course
of decompensated hepatitis C virus (HCV)-related cirrhosis, the aim of the
present study was to define the natural long-term course after the first
hepatic decompensation. METHODS: Cohort of 200 consecutive patients with HCV-related
cirrhosis, and without known hepatocellular carcinoma (HCC), hospitalized
for the first hepatic decompensation. RESULTS: Ascites was the most frequent
first decompensation (48%), followed by portal hypertensive gastrointestinal
bleeding (PHGB) (32.5%), severe bacterial infection (BI) (14.5%) and hepatic
encephalopathy (HE) (5%). During follow-up (34+/-2 months) there were 519
readmissions, HCC developed in 33 (16.5%) patients, and death occurred in 85
patients (42.5%). The probability of survival after diagnosis of
decompensated cirrhosis was 81.8 and 50.8% at 1 and 5 years, respectively.
HE and/or ascites as the first hepatic decompensation, baseline Child-Pugh
score, age, and presence of more than one decompensation during follow-up
were independently correlated with survival. CONCLUSIONS: Once decompensated
HCV-related cirrhosis was established, patients showed not only a very high
frequency of readmissions, but also developed decompensations different from
the initial one. These results contribute to defining the natural course and
prognosis of decompensated HCV-related cirrhosis.
PMID: 15094231 [PubMed - in process]
|
