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Ulcerative colitis (UC)

Inflammatory bowel disease (IBD) is the general term for a group of diseases of unknown etiology causing chronic inflammation or ulceration in the large or small intestine. In most cases, IBD signifies ulcerative colitis (UC) and Crohn's disease (CD). UC is characterized by inflammation in the innermost mucosal lining of the large intestine, causing erosions and ulcers. Symptoms typically include diarrhea, bloody stool, fever, abdominal pain, and weight loss.
Although the precise etiology of UC is unknown, it is thought to be related to abnormal immune system responses via autoimmune mechanisms. The immune system functions to exclude foreign substances from the body. When the immune mechanism malfunctions, for example, when it "recognizes" normal gastrointestinal bacteria as foreign, leukocytes are activated to release inflammatory cytokines, causing inflammation in the intestinal tract.
LCAP (leukocytapheresis) was developed as a therapy for inflammation in UC. It utilizes the Cellsorba leukocytapheresis filter in extracorporeal blood circulation to remove leukocytes responsible for inflammation from the peripheral blood. LCAP is a new therapeutic option for UC patients who do not or no longer benefit from conventional medications, or for patients who experience adverse effects from medications.

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Crohn's disease (CD)

Inflammatory bowel disease (IBD) is the general term for a group of diseases of unknown etiology causing chronic inflammation or ulceration in the large or small intestine. In most cases, IBD signifies ulcerative colitis (UC) and Crohn's disease (CD). CD is a chronic disorder manifesting as inflammation and/or ulceration of the entire digestive or gastrointestinal tract from the oral cavity to the anus, particularly in the small and large intestines. One characteristic is that the lesions are not continuous, with normal sections occurring between them. CD symptoms include diarrhea, bloody stool, fever, abdominal pain, weight loss, and anal ulceration.
Although the precise etiology of CD is unknown, it is thought to be related to abnormal immune system responses via autoimmune mechanisms. The immune system functions to exclude foreign substances from the body. When the immune mechanism malfunctions, for example, when it "recognizes" normal gastrointestinal bacteria as foreign, leukocytes are activated to release inflammatory cytokines, causing inflammation in the intestinal tract.
LCAP (leukocytapheresis) was developed as a therapy for inflammation in CD. It utilizes the Cellsorba leukocytapheresis filter in extracorporeal blood circulation to remove leukocytes responsible for inflammation from the peripheral blood. LCAP is a new therapeutic option for CD patients who do not or no longer benefit from conventional medications, or for patients who experience adverse effects from medications.

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Severe acute pancreatitis

Acute pancreatitis is a sudden-onset inflammation of the pancreas triggered by excessive alcohol intake, calculi, etc. Digestive enzymes secreted by the pancreas are activated and begin to digest the pancreatic tissue. In severe acute pancreatitis, complications develop involving critical organs such as the heart, lung, kidneys, and cranial nerves, resulting in multiple-organ failure.
Treatment includes the administration of protease inhibitors or antibiotics and nutritional management. CRRT is performed to remove excess fluid and protease.

Post-operative hepatic failure

Post-operative hepatic failure results from various types of dysbolism due to hypofunction of hepatic cells after surgery. Symptoms of hepatic failure include hepatic coma caused by elevated plasma ammonia concentrations due to failure to metabolize urea, and jaundice caused by elevated plasma bilirubin concentrations due to the failure to excrete the bile.
In addition to nutritional management, CRRT or plasmapheresis is performed to support the patient until liver function is recovered.

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Acute hepatic failure

Acute hepatic failure is the sudden destruction of hepatic cells in individuals with no history of hepatic disease. The harmful substance ammonia cannot be metabolized to urea, the plasma ammonia concentration increases, and hepatic coma results. Similarly, bile cannot be excreted, the bilirubin concentration increases, and jaundice and other symptoms related to liver failure occur.
In addition to nutritional management, CRRT or plasmapheresis is performed to support the patient until liver function is recovered.

Primary biliary cirrhosis (PBC)

Primary biliary cirrhosis (PBC) is characterized by inflammatory destruction of the small bile ducts within the liver. Bile flow is obstructed and bile pooled in the liver causes symptoms. Inflammation continuing over a period of years progresses to liver cirrhosis. The symptoms of PBC include itching, jaundice, esophageal varices, ascites, and hepatic encephalopathy. Some patients do not exhibit any symptoms. Although the etiology may be associated with an autoimmune disorder, the precise cause is unknown.
Plasma adsorption (PA) or plasma exchange (PE) is performed to remove excessive bilirubin and bile acid from the blood.

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Hyperbilirubinemia

Hyperbilirubinemia is characterized by elevated plasma bilirubin concentrations due to hemolytic anemia, alcoholic hepatitis, calculi, etc. When the plasma bilirubin concentration becomes greater than 3.0 mg/dl, the patient exhibits jaundice.
Plasma adsorption (PA) or plasma exchange (PE) is performed to remove excessive bilirubin and bile acid from the blood.

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Fulminant hepatitis

Fulminant hepatitis (FH) and acute hepatic failure exhibit symptoms of hepatic failure including hepatic encephalopathy due to severe liver dysfunction resulting from marked, widespread hepatocyte necrosis. These two critical, life-threatening conditions are still difficult to treat in emergency medicine.
Plasmapheresis and CRRT are performed for artificial liver support (ALS). ALS results in significant improvement in the patient's systemic condition including maintenance of consciousness. It is also effective as a bridge to liver transplantation.

Chronic hepatitis C

Chronic hepatitis C is caused by hepatitis C virus infection that produces liver inflammation for more than 6 months, resulting in cell destruction. In the early stage, few symptoms are observed, but if left untreated, the infection is likely to develop into cirrhosis and hepatoma over a prolonged course. Although in some cases chronic hepatitis C remains a mild form of hepatitis, approximately 70% of patients have progressive symptoms and approximately 30-40% of those develop cirrhosis and subsequently hepatoma. Cirrhosis not only carries the risk of hepatoma but also increases the likelihood of life-threatening complications including rupture of esophageal varices and hepatic encephalopathy.
There are two therapies for chronic hepatitis C: 1) therapy aimed at cure of the infection by eliminating hepatitis C virus from the body; and 2) symptomatic therapy to prevent progression to chronic hepatitis C by improving liver function. If cirrhosis and hepatoma develop, liver transplantation is performed. Currently, double filtration plasmapheresis after liver transplantation to prevent recurrence is being investigated.

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