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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The transvenous electrophrenic respiration (EPR) is one of the effective and relatively simple method for artificial respiration. Twenty seven mongrel dogs were subjected to the experiment which were subdevided into 4 groups. Stimulation is 44 times in group 1, 22 times in group 2 and 3. Ventilation is carried out by Harverd Respirator in group 4. The normal arterial pressure, the normal minute ventilatory volume and the normal arterial blood gases were unchanged for a 5 hour period of experiment in group 2. However, the frequent stimulation such as 44 times/min. in group 1 yielded the hypotension, the decreased ventilatory volume and brought the congestion of the portal venous area and rendered the subjects to death. The systemic pressure remained in slightly lowered levels in group 2, 3 and 4 at the end of a 24 hour of experiment. The ventilatory volume decreased one third of initial values in group 2 and 3 at the end of a 24 hour of experiment. The pulmonary arterial pressure decreased in group 3 significantly, whereas it increased in positive pressure respiration in group 4. Intermittent clinical application of EPR was performed in three patients. The arterial pressure, minute ventilatory volume, arterial gases and central venous pressure were maintained normal. The following conclusions were obtained: 1) EPR is more physiologic than positive pressure respiration in ventilatory and circulatory aspects. 2) Undesiable conditions of stimulation cause complications such as neural fatigue, portal hypertension, etc. 3) Intermittent clinical application of EPR has been quite successful in supporting the ventilation of the patients.
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PMID:[Experimental and clinical studies of transvenous electrophrenic respiration (author's transl)]. 103 76

To determine the clinical, laboratory and hemodynamic profile in patients with primary pulmonary hypertension and associated portal hypertension, 7 new cases and 71 previously reported cases were analyzed. There was no gender predilection and the average age at diagnosis was 41 years. Liver cirrhosis was the most frequent cause of hypertension (82%) and a surgical portosystemic shunt was present in 29%. Almost invariably, portal hypertension either preceded or was diagnosed concurrently with pulmonary hypertension, favoring the hypothesis that in portal hypertension, the pulmonary vasculature may be exposed to vasoactive substances normally metabolized or produced by the diseased liver, possibly inducing vasoconstriction or direct toxic damage to the pulmonary arteries. Clinically, exertional dyspnea was the most frequent presenting symptom (81%); other symptoms, such as syncope, chest pain and fatigue, were present in less than 33%. An accentuated pulmonary component of the second heart sound (82%) and a systolic murmur (69%) were the most common physical findings. At least 75% of these patients had evidence of pulmonary hypertension on electrocardiography (right ventricular hypertrophy) or roentgenography (cardiomegaly or dilated main pulmonary arteries, or both). Hemodynamic findings included severe pulmonary hypertension (mean pulmonary artery pressure 59 +/- 19 mm Hg) with normal pulmonary capillary wedge pressure and cardiac output. Treatment was basically palliative and the mean and median survival times were 15 and 6 months, respectively. In brief, on the basis of clinical presentation and laboratory features, patients with combined primary pulmonary hypertension and portal hypertension seldom represent a diagnostic challenge. Further research is needed on treatment, which remains palliative. The survival rate is poor and worse than that seen in isolated primary pulmonary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association between primary pulmonary hypertension and portal hypertension: analysis of its pathophysiology and clinical, laboratory and hemodynamic manifestations. 199 8

Primary biliary cirrhosis is a chronic cholestatic disease which usually affects middle-aged women and is characterized by portal vein inflammation and by segmental and focal necrosis of small intrahepatic bile ducts. The prevalence of the disease is estimated at 8 to 12 cases for 100,000 inhabitants. Genetic, infectious and/or immunological factors acting together may be responsible for small bile duct destruction. The main consequence of this destruction is cholestasis. As in all types of mechanical cholestasis, so-called lobular lesions such a fibrosis or even cirrhosis may then develop. Clinically, primary biliary cirrhosis evolves in three phases: (1) a preclinical asymptomatic phase where the disease is revealed by the accidental discovery of antimitochondrial antibodies or of a moderate rise in gammaglutamyltranspeptidase or serum alkaline phosphatase activity; (2) a clinical phase, usually lasting 5 to 10 years, characterized by fatigue, pruritus and later, clinical signs directly related to the hepatic lesions; (3) a terminal phase marked by major cholestasis with lesions of fibrosis or cirrhosis and sometimes ascites and portal hypertension responsible for gastrointestinal haemorrhages. In the last few years the prognosis of primary biliary cirrhosis has been considerably improved by the introduction and development of liver transplantation (the first choice treatment in the terminal phase) and by the introduction of ursodeoxycholic acid.
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PMID:[Primary biliary cirrhosis]. 206 16

Primary biliary cirrhosis is a progressive disease of the liver characterized by the immunologic destruction of bile ducts; effective therapy is lacking. We therefore evaluated the safety and efficacy of low-dose cyclosporine in 29 patients with primary biliary cirrhosis without evidence of damage to the lobular architecture (precirrhotic disease) or portal hypertension. The patients were randomly assigned to receive either cyclosporine (4 mg per kilogram of body weight per day) or placebo. After one year 17 of the 19 patients assigned to cyclosporine had improvement or stability in their degree of fatigue, and 18 in their degree of pruritus. In contrast, among the 10 patients assigned to placebo, fatigue increased in 4 (P less than 0.06) and pruritus worsened in 6 (P less than 0.001). Those assigned to cyclosporine also had significant decreases in serum levels of bilirubin, alanine aminotransferase, alkaline phosphatase, gamma globulin, and the titer of antimitochondrial antibodies. For the 20 patients who have completed two years in the study, liver biopsies (coded specimens) showed evidence of histologic progression in only 1 of 13 patients in the cyclosporine group, as compared with 5 of 7 in the placebo group (P less than 0.003). No patient has permanently discontinued cyclosporine because of side effects; however, signs of nephrotoxicity developed in 12 of 19, and 9 of 19 had increased blood pressure. We conclude that in patients with precirrhotic primary biliary cirrhosis, immunosuppressive therapy with cyclosporine is promising and deserves further evaluation.
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PMID:A controlled trial of cyclosporine in the treatment of primary biliary cirrhosis. 221 26

Caroli's disease is one of the rare congenital conditions associated with the cystic dilatation of intrahepatic bile ducts. This is a case report of a 41-year-old Japanese male who complained of jaundice and general fatigue at the age of 34 for the first time. He was clinically diagnosed as having Caroli's disease by physical examination and image analyses study. The patient died after seven years and three months from the onset of the disease on account of renal function impairment. An autopsy was performed, revealing cystic dilatation of the intrahepatic bile duct, associated with a cirrhotic liver and also evidence of portal hypertension, substantiated by esophageal varices and splenomegaly. The liver weighed approximately 2,200 g. A histological investigation revealed typical morphological evidence of cirrhotic glomerulopathy and tubular degeneration with the presence of calcium casts in the dilated tubuli. The lung revealed diffuse alveolar damage with partial organization associated with remarkable polymorphonuclear and macrophagic infiltration. In this paper, the pathogenesis of the cirrhotic change, biliary duct abnormality and potential malignant transformation in the liver are discussed in relation to Caroli's disease.
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PMID:Caroli's disease associated with liver cirrhosis. An autopsy case. 225 97

Primary biliary cirrhosis (PBC) is likely an autoimmune disease that destroys the interlobular bile ducts. Although the term PBC implies cirrhosis, this is not always present. The condition may be entirely silent clinically, save for the hallmark mitochondrial antibodies in serum. The clinical spectrum of PBC ranges from asymptomatic anicteric cholestasis with or without extrahepatic manifestations to severe cholestasis with decompensated cirrhosis. It is uncertain whether or not the course of this disease is universally fatal. Currently, no specific features have been identified which predict progression from asymptomatic to symptomatic disease, although once hyperbilirubinemia is present, a rising level indicates a poor prognosis. The liver-specific complications include pruritus, abdominal pain, xantholasma, and portal hypertension. The latter is often an early feature, as the portal hypertension is presinusoidal in nature and, when present, does not always reflect the presence of cirrhosis. There are many extrahepatic features of PBC, the most common being metabolic, chiefly hypothyroidism and metabolic bone disease. Other common associations are rheumatologic, renal, pulmonary, neuromuscular, and dermatologic. The non-specific yet distressing symptom of fatigue affects up to two-thirds of PBC subjects, but its etiology remains obscure.
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PMID:The clinical expression of primary biliary cirrhosis. 908 8

The results of liver transplantation in patients with PSC are excellent and the quality of life is markedly improved. Indeed, liver transplantation is the therapy of choice for patients with end-stage PSC. However, in an age of cost containment, it appears that there are several advantages to offering transplant to patients with PSC a little bit earlier rather than later in the course of their disease. It appears that we can further improve survival, decrease morbidity, decrease blood usage, and avoid the risk of developing a cholangiocarcinoma, which occurs sporadically but not infrequently in the PSC patient. In addition, avoidance of right upper quadrant surgery, such as biliary or shunt surgery, appears to offer several advantages by decreasing resource utilization and possibly decreasing mortality. Although the UNOS selection guidelines recommend transplantation of the sickest patient, there appears to be accumulating evidence that transplantation in patients earlier in the course of their end-stage liver disease may improve survival, decrease morbidity, and also importantly, decrease the cost associated with this expensive procedure. Ideally, we would recommend consideration for liver transplantation all PSC patients who have (1) a Mayo risk score of > 4.8 in whom malignancy is ruled out, (2) cirrhosis and complications of portal hypertension such as variceal bleeding, refractory ascites, or portosystemic encephalopathy, or (3) disabling symptoms such as fatigue, pruritus, or recurrent bacterial cholangitis. We believe that biliary surgery to treat dominant strictures should be avoided and that such strictures should be approached either endoscopically or radiographically, which should include brushings, biopsies, and histology to reasonably exclude the diagnosis of cholangiocarcinoma. Finally, we continue to search for risk factors and for early markers of cholangiocarcinoma so these patients can be identified early and this devastating complication can be avoided by early transplantation.
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PMID:Liver transplantation for primary sclerosing cholangitis: impact of risk factors on outcome. 934 9

Cholestatic liver disease is primarily caused by impaired bile production on the level of hepatocytes and cholangiocytes. Clinically cholestasis can be divided into intrahepatic and extrahepatic forms based on the presence or absence of dilated bile ducts (sonography). Intrahepatic cholestasis is most frequently caused by end stage liver cirrhosis followed by primary cholangiopathies and canalicular transport defects in hepatocytes. The causes of the most important cholangiopathies, such as Primary Biliary Cirrhosis (PBC) and Primary Sclerosing Cholangitis (PSC) are so far not known. Therefore, drug therapy of cholestatic liver disease focuses on the improvement of symptoms such as fatigue, pruritus, abdominal discomfort, jaundice, xanthoma, hypercholesterolemia, portal hypertension, blood count abnormalities, osteoporosis/osteomalacia, and the prevention of complications such as bile-duct strictures in PSC and development of cholangiocarcinoma. The first choice drug in the treatment of cholestatic liver disease of various causes is urosodeoxycholic acid (UDCA), that has been shown to decrease bile acid toxicity in general and prolong the transplant free survival of patients with PBC. If cholestasis persists cirrhosis of the liver is the major complication and liver transplantation may be the definitive treatment in advanced cases of cholestatic liver disease.
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PMID:[Cholestatic liver diseases]. 945 66

Primary sclerosing cholangitis (PSC) is a chronic, progressive cholestatic liver disease whose aetiopathogenesis is unknown. PSC is frequently associated with inflammatory bowel disease, in particular chronic ulcerative colitis, is most commonly observed in young males and is clinically characterized by fatigue, pruritus and jaundice. The diagnosis is supported by a cholestatic biochemical profile and histological abnormalities, and confirmed by visualization of an abnormal biliary tree. The natural history of the disease is currently being evaluated but is generally recognized to be slowly progressive, leading to complications of chronic cholestasis, portal hypertension and biliary cirrhosis. There is no specific medical treatment, and orthotopic liver transplantation remains the only definitive treatment for patients with end-stage PSC. A more rational approach to medical therapy will ensue upon a better understanding of the aetiopathogenesis of this disease.
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PMID:Sclerosing cholangitis. 951 10

The diagnosis of primary biliary cirrhosis (PBC) is most often made in the asymptomatic phase, sometimes before the development of abnormal liver biochemistry. The antimitochondrial antibody remains the predominant hallmark, although not all patients test positive, even when the most sensitive techniques are used. The etiology of PBC remains elusive; studies suggest that the interlobular bile duct destruction is immune based, and associated autoimmune diseases are common. There are no surrogate markers that predict outcome in asymptomatic patients, whose chance of survival is less than that of age- and sex-matched populations but much better than the median survival of eight years in patients with symptomatic PBC. Symptoms common in this disease are fatigue, pruritus and xanthelasma, as well as complications of portal hypertension and osteoporosis. Treatment includes symptomatic and preventive measures, as well as specific therapeutic measures. Immunosuppressive therapy has yielded disappointing results in the long term management of PBC, and the only therapy shown to improve survival is the hydrophobic dihydroxy bile acid ursodeoxycholic acid. Treatment at a dose of 13 to 15 mg/kg/day is optimal, given in separate doses or as a single dose at least 4 h from giving the oral anion exchange resin cholestyramine, which may be used to control pruritus. However, liver transplantation remains the only cure for this disease, and the best postoperative survival is seen in patients whose serum bilirubin does not exceed 180 micromol/L at the time of liver transplantation. Recurrence takes place but is rarely symptomatic and does not deter from the benefits of transplantation.
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PMID:Update on primary biliary cirrhosis. 1065 26


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