in ulcerative colitis and irritable bowelsyndrome. Gastroenterology. 2004;126:1657.
and diarrhea. Am J Gastroenterol. 2001;96:1499.
syndrome. Clin Gastroenterol Hepatol. 2009;7:68.
for development of the irritable bowelsyndrome: postalsurvey of patients. BMJ. 1997;314:779.
study. J Gastroenterol Hepatol. 2007; 22:2261.
review. Am J Gastroenterol. 2008;103:765.
Camilleri M. Management of the irritable bowelsyndrome. Gastroenterology. 2001;120:652.
Saito YA et al. Familial aggregation of irritable bowel syndrome: afamily case-control study. Am J
Bertram S et al. The patient’s perspective of irritable bowelsyndrome. J Fam Pract. 2001;50:521.
treatment outcomes? Clin Gastroenterol Hepatol. 2010;8:125.
and chronic idiopathic constipation. Am J Gastroenterol. 2014;109:S2–S26.
Longstretch GF et al. Functional bowel disorders. Gastroenterology. 2006;130:1480–1491.
Arch Intern Med. 2001;161:2081.
52. doi: 10.1055/s-0032-1301759.
syndrome: a psychological component is the rule. Am J Gastroenterol. 2009;104:1772.
also have a concurrent psychiatric disorder? Aust N Z J Psychiatry. 2005;39:807.
controlled trial. BMJ. 2009;339:b3154.
randomized placebo-controlled trial. Am J Gastroenterol. 2011;106:508–514.
of symptoms in irritable bowelsyndrome. J Gastroenterol Hepatol. 2010;25:1366–1373.
irritable bowelsyndrome. Aliment Pharmacol Ther. 2006;23:191.
irritable bowelsyndrome with constipation. Aliment Pharmacol Ther. 2002;16:1877.
Amitiza [package insert]. Deerfield, IL: Takeda Pharmaceuticals; 2013.
—results of two randomized, placebo-controlled studies. Aliment Pharmacol Ther. 2009;29:329.
Linzess [package insert]. Cambridge, MA: Ironwood Pharmaceuticals; 2014.
placebo-controlled trial to evaluate efficacy and safety. Am J Gastroenterol. 2012;107:1702–1712.
Tack J et al. Systematic review: the efficacy of treatments for irritable bowel syndrome—a European
perspective. Aliment Pharmacol Ther. 2006;24:183.
Talley NJ. SSRIs in IBS:sensing a dash of disappointment. Clin Gastroenterol Hepatol. 2003;1:155.
Talley N. Serotoninergic neuroenteric modulators. Lancet. 2001;358:2061.
Lotronex [package insert]. San Diego, CA: Prometheus Labs; 2014.
syndrome: a randomized trial. Ann Intern Med. 2006;145:557.
Xifaxan [package insert]. Salix pharmaceuticals: Raleigh, NC; 2015.
Gastroenterology. 2013;145(2):329–338.
Viberzi [package insert]. Cincinnati, OH: Pantheon Pharmaceuticals; 2015.
Cirrhosis is defined as the fibrosis of the hepatic parenchyma, resulting in
altered hepatic function, restricted venous outflow, and portal
hypertension. Cirrhosis results in an overall vasodilated state, activation
of the renin–angiotensin–aldosterone system, altered hepatic synthetic
function, and development of complications such as ascites and other
Physical findings of ascites can include the presence of an enlarged
fluid-filled abdomen, increased abdominal girth, a positive fluid wave,
increased body weight and is often accompanied by peripheral edema.
The goals of treatment for ascites are to mobilize ascitic fluid, diminish
abdominal discomfort, as well as to prevent complications such as
bacterial peritonitis and respiratory distress.
The treatment for ascites involves sodium restriction (2 g/day), water
restriction for severe dilutional hyponatremia, and the use of
spironolactone and furosemide (100:40 mg ratio). Management and
monitoring of ascites includes ensuring adequate weight loss,
maintaining electrolyte balance, and preventing complications of diuretic
In cases of refractory ascites (diuretic-resistant), large-volume
paracentesis, along with albumin replacement, is often indicated.
Transjugular intrahepatic portosystemic shunt (TIPS), surgicalshunts,
and liver transplantation are the options for the treatment of refractory
ascites when paracentesis is deemed ineffective, or in patients who are
intolerant or who have a contraindication to paracentesis.
Spontaneous bacterial peritonitis (SBP) is a common complication of
ascites. Prophylactic regimens include the long-term administration of
also include the administration of antibiotic prophylaxis for prevention of
SBP in patients with variceal hemorrhage.
Because esophageal varices are directly related to the severity of portal
hypertension, the treatment is aimed at primary prevention of bleeding
by reduction of portal pressure with the use of nonselective β-blockers,
and/or elimination of the varices with endoscopic variceal ligation
(EVL). Treatment approaches depend on the risk of hemorrhage.
Secondary prophylaxis to prevent recurrent bleeding episodes includes
the combination of nonselective β-blockers and EVL. TIPS may be an
option in patients who experience recurrent variceal hemorrhage despite
combination of pharmacologic and endoscopic therapy.
Acute variceal bleeding is considered a medical emergency and should
be treated immediately. Treatment goals include volume resuscitation,
acute treatment of bleeding, and prevention of recurrence of variceal
bleeding. For the control and management of acute hemorrhage, the
combination of pharmacologic therapy and variceal ligation is the
preferred approach. In cases of acute variceal bleeding uncontrolled by
pharmacologic and endoscopic therapy, TIPS can be an effective
Hepatic encephalopathy is a metabolic disorder of the central nervous
system that occurs in patients with either advanced cirrhosis or
fulminate hepatic failure. The clinical features include altered mental
state and asterixis. Several theories exist about the pathogenesis of
hepatic encephalopathy; however, it is likely multifactorial. Precipitating
causes can include GI bleeding, diuretic-induced hypovolemia and/or
electrolyte abnormalities, metabolic alkalosis, as well as sedating drugs.
After identifying and removing precipitating causes of hepatic
encephalopathy, therapeutic management is aimed primarily at reducing
the amount of ammonia or nitrogenous products in the circulatory
system by limiting protein intake and by the use of lactulose. Other
therapeutic options include rifaximin and neomycin.
Monotherapy with lactulose should be tried first. If satisfactory results
do not occur, switching to another option (rifamixin or neomycin) or
combination therapy should be considered.
Hepatorenalsyndrome (HRS) is a complication of advanced cirrhosis
and is diagnosed by exclusion of other known causes of kidney disease.
The definitive treatment for type 1 and type 2 HRS is liver
transplantation, which is the only treatment that assures long-term
survival. The main goal of pharmacologic therapy is to reverse HRS
sufficiently so that appropriate candidates for liver transplantation can
survive untilsuitable donor organs can be procured.
According to the National Vital Statistics Report published by the Centers for
Disease Control and Prevention, chronic liver disease and cirrhosis is the 12th
leading cause of death in the United States, accounting for approximately 38,170
1 Cirrhosis, or end-stage liver disease, can be defined as fibrosis of
the hepatic parenchyma resulting in nodule formation and altered hepatic function,
which results from a variety of causes. Although there are other common causes of
cirrhosis, most cases of cirrhosis worldwide result from chronic viral hepatitis or
2 This chapter describes the pathogenesis of cirrhosis
and the associated complications of portal hypertension (esophageal varices, gastric
varices, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, and
hepatorenal syndrome) and their treatment.
The liver consists of the hepatic parenchyma (hepatocytes) and a large proportion of
nonparenchymal cells, including sinusoidal endothelial cells, Ito cells, and
macrophages. Most of the liver’s role in detoxification takes place within the
hepatocytes. Also within the liver is the biliary tree in which bile drains from the
liver and some substances are actively transported into the bile.
strong capacity to regenerate; however, ethanol and hepatitis viruses can impair this.
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