Liver disease cholestatic

There is very little evidence relating to the role of ROMs in cholestatic liver disease. Serum selenium and glutathione peroxidase activity are decreased in humans with intrahepatic cholestasis of pregnancy (Kauppila et al., 1987). Low levels of vitamin E have been reported in patients with primary biliary cirrhosis, and in children with Alagille s syndrome or biliary atresia (Knight et al., 1986 Jeffrey etal., 1987 Lemonnier etal., 1987 Babin etal., 1988 Kaplan et al., 1988 Sokol etal., 1989). Serum levels of Mn-SOD are increased in patients with all stages of primary biliary cirrhosis compared with patients with other forms of chronic liver disease, although whether this causes or results from the disease process is unclear (Ono etal., 1991). 

In the bile-duct-ligated rat, hepatic mitochondrial lipid peroxides are increased and correlate with serum levels of alkaline phosphatase, bilirubin and alanine aminotransferase (Sokol et al., 1991). Dietary vitamin E deficiency resulted in relatively higher lipid peroxide and bilirubin 

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Cholestatic liver disease/cirrhosis (e.g., primary biliary cirrhosis)... 

Cholestatic liver diseases Primary biliary cirrhosis... 

Alkaline phosphatase levels and GGT are elevated in plasma with obstructive disorders that disrupt the flow of bile from hepatocytes to the bile ducts or from the biliary tree to the intestines in condition such as primary biliary cirrhosis, sclerosing cholangitis, drug-induced cholestasis, gallstone disease, and autoimmune cholestatic liver disease. 

The levels of GGT in plasma correlate well with elevations of alkaline phosphatase and are a sensitive marker for cholestatic liver disease. 

Intermittent EN is similar to bolus EN except that the feeding is administered over 20 to 60 minutes, which improves tolerability but requires more equipment (e.g., reservoir bag and infusion pump). Like bolus EN, intermittent EN mimics normal eating patterns. As compared with continuous EN, bolus or intermittent EN minimizes the development of cholestatic liver disease. 

Requirements for trace elements during organ failure are not clearly defined. Manganese and copper should be restricted or withheld in patients with cholestatic liver disease. Chromium, molybdenum, and selenium should be restricted or withheld in patients with renal failure. 

Deems, R. O., and M. I. Friedman. Macronutrient selection in an animal model of cholestatic liver disease. Appetite 1988 11(2) 73-80. 

Liver disease is commonly associated with oq-antitrypsin deficiency and may develop at any age. Approximately 10% to 20% of oq-antitrypsin-deficient infants with the phenotype PIZZ are first seen for neonatal cholestatic liver disease, as was the child in this case report. Conjugated hyperbilirubinemia and he-... 

Dincsoy HP, Saelinger DA. Haloperidol-induced chronic cholestatic liver disease. Gastroenterology 1982 83(3) 694-700. 

Primary sclerosing cholangitis is characterised by inflammation, fibrosis and destruction of the intrahepatic and/or extrahepatic bile ducts. It results in a chronic cholestatic liver disease that may lead to liver cirrhosis. Cholangiocarcinoma occurs in approximately 10-30% of patients. PSC occurs more frequently in men between the ages of 20 and 40, with a male female ratio of 2 1. It is often associated with inflammatory bowel disease, particularly chronic ulcerative colitis. 

CYP2E1 or Nt Effect may depend on aetiology of cirrhosis-only subjects with severe cholestatic liver disease have reduction in CYP2E1. Another confounding factor is effects of alcohol [38, 39, 53]... 

Niacin and acipimox should be relatively safe to use in the absence of varices, gastritis, coagulopathy, thrombocytopenia or a history of decompensation. Both can cause pruritus, which is common in cholestatic liver disease. The extended release formulation of niacin (Niaspan Prolonged Release) may cause hepatitis and LFTs should be monitored. 

Reduction in bone density is an important complication and cause of morbidity in chronic liver disease. This can lead to osteoporosis and osteomalacia with resulting bone fractures, pain, deformity and immobility. The problem is greatest in cholestatic liver diseases such as... 

HRT has also been shown to cause favourable changes in serum lipid levels in normal postmenopausal women [13]. This effect could be particularly beneficial in women with cholestatic liver disease who may have elevated serum cholesterol. 

The levels of GGT in plasma correlate well with elevations of alkaline phosphatase and are a sensitive marker for cholestatic liver disease. Elevations of serum bilirubin are common in end-stage liver disease and obstruction of the common bile duct, but other causes of hyperbilirubinemia are numerous. 

Zinc, copper, chromium, manganese, and possibly selenium and molybdenum are the only trace elements that require supplementation during PN. Requirements for trace elements during organ failure are not clearly defined. Manganese and copper should be restricted or withheld in patients with cholestatic liver disease. Chromium, molybdenum, and selenium should be restricted or withheld in patients with renal failure. Sodium, potassium, calcium, magnesium, phosphorus, chloride, and acetate are necessary components of PN for maintenance of numerous cellular functions. 

Hormone preparations. Use of contraceptives should be monitored carefully in patients with cholestatic liver disease, because jaimdice may be exacerbated continued use of oral contraceptives during an attack of acute hepatitis can have the same effect. Low oestrogen preparations carry less risk of this complication. 

This chronic cholestatic liver disease affects 1 in 4000 people in the United Kingdom. Pruritus is a common early symptom, and can be helped by colestyramine. Qu-onic cholestasis leads to malabsorption of fat-soluble vitamins, particularly vitamin D, and deficiency of which must be corrected to avoid osteomalacea. 

Xanthomas xanthoma tuberosum) display a straw-like yellow through to greyish yellow hue. These are round, well circumscribed, plaque-like raised or papuloid deposits in the skin, which predominantly occur on the extensor sides of the extremities, the elbow and knee area, the external ear, parts of the buttocks and back, occasionally also on the hands and soles of the feet. They can appear in cholestatic liver diseases, particularly in biliary cirrhosis as a result of CDNC. Their occurrence depends on the lipid and cholesterol content of the blood, (l) These changes are considered to be late symptoms, (s. p. 235) (s. figs. 4.15, 4.16)... 

Tab. 13.7 Possible antibody constellations in chronic cholestatic liver diseases...

Hofmann, AJ. Cholestatic liver disease Pathophysiology and therapeutic options. Liver 2002 22 (Suppl. 2) 14—19... 

Jain, R., McLaren, B., Bejarano, P., Sherman, K.E. Diagnostic problem in clinical hepatology. A 69-year-old man with cholestatic liver disease. Semin. Liver Dis. 1996 16 445-449... 

Cupruria In pronounced liver cell decay, there is not only a rise in the copper value in serum, but more particularly in the amount of copper excretion in the urine. Cupruria of < 50 pg/day rules out the presence of Wilson s disease (differential diagnosis e.g. kidney disease). The penicillamine test has proved successful after administration of 600 mg penicillamine, copper excretion increases to > 300 pg/6 hr (> 600 pg/24 hr). However, it should be noted that this test may show similar positive results in cholestatic liver diseases. 

Modes of action The mechanisms of UDCA and its effects in cholestatic liver diseases are not yet fully understood - even though a number of different effects have been demonstrated. These include (i.) hepatopro-tective (92, 97, 98), (2.) cytoprotective (89), and (3.) biliary-metabolic effects (84, 93, 104, 105), as well as (4.) an influence on the immune system. In ligature of the bile duct in rats, UDCA was found to reduce the occurrence of histological changes and biliary cirrhosis as well as of portal hypertension. (98) (s. tab. 40.7)... 

Fal malabsorption syndromes Fat malabsorption syndromes such as cystic fibrosis and cholestatic liver diseases (lack of bile salts) can impair the absorption of vitamin D. 

Cholestatic liver disease may occur in infancy. One particularly severe symptom is the inability to walk. The neurological symptoms can be treated with weekly injectiorrs of 100 mg a-tocopherol over half a year. Vitamin E deficiency in newborns has been associated with hemolytic anemia. Anemia is a decreased eoncen-trahon of red blood cells in whole blood as well as a drop in the hemoglobin level... 

A 46-year-old woman with rheumatoid arthritis developed cholestatic liver disease while taking chlormezanone and paracetamol (2). 

Fox JC, Szyjkowski RS, Sanderson SO, Levine RA. Progressive cholestatic liver disease associated with clarithromycin treatment. J Clin Pharmacol 2002 42(6) 676-80. 

Menghini VV, Arora AS. Infliximab-associated reversible cholestatic liver disease. Mayo CUn Proc 2001 76(l) 84-6. 

In patients on home parenteral nutrition, hypermangane-semia can be facilitated through (1) cholestatic liver disease and thereby reduced manganese biliary excretion, (2) high nutritional requirements (responsible for increased manganese supply), and/or (3) altered manganese metabolism or body distribution (12). 

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