Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In three patients, the first manifestation of Wilson's disease was a syndrome in which acute intravascular hemolysis and acute liver failure were associated. This syndrome developed in three periods; the first, lasting 3 to 14 days, was characterized by fatigue, fever, and jaundice; the second, lasting 1 or 2 days, by severe intravascular hemolysis; and the third, lasting 2 to 6 days, by hepatic encephalopathy. All of the patients died from liver failure 7 to 21 days after the onset of the syndrome. The association of acute intravascular hemolysis and acute live failure is a characteristic manifestation of Wilson's disease; it is rarely associated with other liver diseases. This association might result from hepatic cell necrosis due to accumulation of copper, the consequences being acute liver failure and destruction of erythrocytes by the large amounts of copper released from the necrotic hepatic cells to the plasma.
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PMID:Acute intravascular hemolysis and acute liver failure associated as a first manifestation of Wilson's disease. 84 89

We studied 50 patients (36 males and 14 females) with chronic hepatitis C who were admitted consecutively to our medical department during the period 1987-91. Eight patients (16%) had had a blood transfusion, 17 (34%) had used intravenous drugs and 25 (50%) were "sporadic cases" with no identifiable risk factor except that at least five had been tattooed. Most of the patients had moderate symptoms, including tiredness and asthenia. Few were jaundiced. A percutaneous liver biopsy was performed in 27 patients and showed chronic persistent hepatitis in 12 of them, chronic active hepatitis in six and cirrhosis in nine. Three patients with cirrhosis died; one from hepatoma, one from an endstage cirrhosis with bleeding and coma hepaticum, and one from septicaemia.
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PMID:[Chronic hepatitis C. Experience with 50 patients]. 132 64

To evaluate the possible contribution of bioenergetic failure in the particular brain regions to the pathomechanism of hepatic encephalopathy (HE), local cerebral metabolic rate for glucose (LCMRglue) was evaluated from [3H]-deoxyglucose uptake in frontal, visual and auditory cortex, striatum, cerebellum and medulla oblongata of rats with acute HE induced with a hepatotoxin--thioacetamide (TAA). HE caused a decrease of LCMRglue in all the regions studied. The strongest decrease (about 65%) was noted in hippocampus and cerebral cortex--the two regions rich in glutamatergic neurons. The results indicate a possible link between decreased energy metabolism and impaired excitatory, glutamatergic neurotransmission--the two factors whose contribution to HE has so far been implicated separately.
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PMID:Decreased glucose utilization in discrete brain regions of rat in thioacetamide-induced hepatic encephalopathy as measured with [3H]-deoxyglucose. 188 55

Dietary measures have achieved mixed results in the management of liver disorders. Although a high energy diet may shorten the course of viral hepatitis by a relatively small amount, dietary restriction is usually of no benefit in compensated cirrhosis. Restriction of sodium intake to 22 to 60 mol/day leads to resolution of cirrhotic ascites in approximately 20% of patients, and reduces the requirement for diuretics in the remainder. In advanced liver disease, diet plays an important role in the avoidance of portal-systemic encephalopathy (PSE), with the tolerance of most nutrients, most importantly protein, being sharply reduced. Despite the frequent presence of carbohydrate intolerance in liver disease, carbohydrate supplementation may be required to ensure adequate utilisation of the reduced dietary protein intake. Zinc supplementation may also be required in liver cirrhosis to compensate for a deficiency. Bed rest is an important component of the management of acute and chronic liver disorders, together with the avoidance of fatigue. Abstinence from alcohol is required in alcoholic liver disease patients, who should receive parenteral thiamine 100 mg and other vitamin and mineral supplementation as required. Agents acting on the ascending loop of Henle [such as furosemide (frusemide)] or the distal tubule (such as spironolactone) are the diuretics most frequently employed to mobilise ascites in cirrhosis, the latter drug being the more effective in nonazotaemic patients. In the absence of oedema, the diuresis should be restricted to a maximum of 750 ml/day; however, patients with oedema may safely undergo a diuresis of less than or equal to 1.5 L/day. Diuretic therapy is often associated with renal complications, such as azotaemia (usually reversible) and severe hyponatraemia in cirrhotic patients with ascites; spironolactone may produce antiandrogenic adverse effects. Lactulose, used in the treatment of acute and chronic PSE, acts by inhibiting gastrointestinal absorption of ammonia and other toxic nitrogenous substances, and by reducing urea degradation. Other pharmacological treatments, such as branched-chain amino acids and benzodiazepine antagonists have a limited role in the management of PSE. Chronic cholestasis has been treated with cholestyramine and fat-soluble vitamins, whereas ursodeoxycholic acid appears to be a promising agent in the treatment of primary biliary cirrhosis. In chronic hepatitis, the prevention of development of cirrhosis is a primary treatment goal which has been attempted with variable success using antifibrotic drugs such as penicillamine and colchicine.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Traditional management of liver disorders. 208 80

We conducted a clinical trial to study the effects of a 10-week course of prednisone therapy and its withdrawal on serum aminotransferase levels and on hepatitis B virus (HBV) markers in patients with hepatitis B surface antigen (HBsAg) positive chronic active hepatitis (CAH-B). Eighteen patients with CAH-B were treated with prednisone, while another 18 patients matched for age, sex, race and sexual preference were followed simultaneously without treatment for the same duration. Nine of 18 prednisone-treated patients became transiently DNA polymerase positive. All nine patients developed a transient rise in serum alanine aminotransferase (ALT) levels of greater than 300 U/L above baseline values, which was associated with a drop in HBsAg levels from a mean of 186 micrograms/ml prior to therapy to 92 micrograms/ml at 6 months following treatment. Six of these patients developed fatigue, anorexia and dark urine, and four also developed either ascites or hemorrhage from esophageal varices, which was accompanied by hepatic encephalopathy. All six of these patients had histologic evidence of CAH with cirrhosis. In comparison, none of the control, untreated patients with CAH-B had any change in either HBV markers or serum ALT levels. Therefore, even a short course of prednisone in patients with CAH-B with cirrhosis is detrimental and its use should be discouraged.
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PMID:Effects of short-term, high-dose prednisone treatment of patients with HBsAg-positive chronic active hepatitis. 388 51

The authors report two cases of hepatic encephalopathy with chronic hepatic failure. Case 1 was a 78-year-old woman with liver cirrhosis, admitted because of general fatigue and loss of appetite. Her electroencephalogram showed frequent slow waves in the theta range with intermittent triphasic waves T1-weighted MR images showed increased signal intensity in the globus pallidus and the putamen. Case 2 was a 71-year-old woman with chronic hepatitis, admitted because of depression. Her electroencephalogram showed frequent slow wave activities in the theta-delta range with intermittent trisphasic waves. Her serum ammonia level was 84 micrograms/dl (normal 12-54 micrograms/dl). T1-weighted MR images showed increased signal intensity in the globus pallidus, the putamen and the hypothalamus. On the basis of these findings, both patients were diagnosed as having hepatic encephalopathy, although disturbance of consciousness was not obvious. The observed MR image abnormalities might be due to the metabolic and pathological changes of chronic hepatic failure. Such MRI findings may be useful for the diagnosis of hepatic encephalopathy.
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PMID:[Two cases of hepatic encephalopathy associated with a high-intensity area in the basal ganglia on T1-weighted MR images]. 823 Jul 86

Intrahepatic shunts are rarely diagnosed as a cause of neurocognitive abnormality. A complaint of fatigue led to the diagnosis of a right portal vein-hepatic vein aneurysmal communication in a 23-yr-old, otherwise healthy woman. Neuropsychological testing, imaging, and MR spectroscopy revealed changes similar to those described in patients with cirrhosis and subclinical hepatic encephalopathy. T1-weighted MRI showed a hyperintense globus pallidus, a feature seen in subjects with and without portal-encephalopathy. Portal-systemic shunting in the absence of parenchymal liver disease reproduces neurological features described in cirrhosis.
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PMID:Intrahepatic portal-hepatic venous anastomosis: a portal-systemic shunt with neurological repercussions. 1089 98

A 55-year-old Turkish man with a history of chronic hepatitis B for 35 years, presented with incapacitating fatigue and worsening shortness of breath. He was hospitalized several times because of hepatic encephalopathy. He underwent liver transplantation for a clinical diagnosis of Child's C cirrhosis complicated by hepatopulmonary syndrome. The explanted liver, however, was not cirrhotic and demonstrated features of hepatoportal sclerosis. Although treatment for hepatoportal sclerosis is relief of portal hypertension; in rare cases such as in this patient with liver failure, liver transplantation is indicated.
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PMID:Portal hypertension and hepatopulmonary syndrome in a middle-aged man with hepatitis B infection. 1107 5

Altered central neurotransmission contributes to behavioural complications of chronic liver disease, such as pruritus and hepatic encephalopathy. Another behavioural complication of chronic liver disease, including chronic hepatitis C, is profound fatigue. Evidence that altered serotoninergic neurotransmission contributes to fatigue of central origin, and relief of profound fatigue in a patient with chronic hepatitis C associated with long-term ondansetron therapy, support the hypothesis that altered central serotoninergic neurotransmission contributes to fatigue complicating chronic hepatitis C. Drugs that specifically modulate serotoninergic neurotransmission may be effective in ameliorating fatigue in patients with chronic hepatitis C.
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PMID:Altered central serotoninergic neurotransmission: a potential mechanism for profound fatigue complicating chronic hepatitis C. 1146 Nov 59

The best known example of an interaction between the liver and the brain is hepatic encephalopathy. In the 90s a central nervous system origin of the pruritus of cholestatic liver disease and more recently of fatigue of liver disease has been suggested. Hence, three important manifestations of liver disease may be of central origin. Evidence is accumulating that the central opioid system is involved in the development of these manifestations. This short review summarizes current knowledge on the role of the opioid system in development of these liver disease manifestations.
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PMID:The central opioid system in liver disease and its complications. 1172 91


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