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)

Non-A, non-B hepatitis has been diagnosed in 12 blood donors in a plasmapheresis unit. The course of the disease has been symptomatic, accompanied by jaundice, fatigue, and nausea in 8 cases, and subclinical in the remaining 4 patients. Nine patients were followed-up to 2 years and only 2 patients liver biochemical tests were normalized permanently. The biopsies performed, a year after the acute phase of hepatitis period revealed chronic active disease in patients, chronic persistent hepatitis in 2 patients, acute hepatitis in one, and normal liver in one patient. Repeated liver biopsies, performed one year later, have basically shown similar lesions except one patient in whom chronic active hepatitis progressed to incipient liver cirrhosis. No symptoms of the disease have been usually noted in patients with chronic form of the disease, and liver function tests have occasionally been normal.
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PMID:[Epidemic focus of non-A, non-B viral hepatitis in a plasmapheresis unit]. 143 24

We have evaluated the clinical and histopathological outcomes of patients who contracted chronic non A, non B hepatitis as a result of transfusions administered during heart surgery at the National Institutes of Health. Posttransfusion hepatitis developed in 65 of 1,070 (6.1%) patients and became chronic in 45 (69%) of those cases. Antibody to hepatitis C virus was detectable in 53 patients (82%) with posttransfusion non A, non B hepatitis. Thirty-three patients with chronic non A, non B hepatitis agreed to liver biopsy (group 1). In addition, six other patients with chronic posttransfusion non A, non B hepatitis were evaluated (group 2). These 39 patients were followed between 1 and 24 yr (mean = 9.7 yr). Cirrhosis developed in 8 patients (20%) between 1.5 and 16 yr after blood transfusion. Of the 33 patients in group 1, 11 (33%) died during follow-up. In two cases (6%), this was related to liver failure. At this writing, two additional patients (6%) have decompensated cirrhosis and one (3%) had debilitating fatigue. Twenty of 33 patients (61%) with histological evidence of chronic active hepatitis or cirrhosis are asymptomatic and have no clinical evidence of liver disease. Thus chronic non A, non B posttransfusion hepatitis appeared to be due to hepatitis C virus infection in most cases. It was associated with the development of cirrhosis in approximately 20% of cases and end-stage liver disease in 12% of patients followed prospectively. Most patients with histological evidence of cirrhosis or chronic active hepatitis, however, had minimal clinical evidence of liver disease within the time frame of this study.
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PMID:Long-term clinical and histopathological follow-up of chronic posttransfusion hepatitis. 195 84

The prevalence, risk factors, and incidence of hepatitis C virus (HCV) infection were studied in a cohort of drug users in Amsterdam. In intravenous drug users, the seroprevalence was 74% (224/304) versus 10% (4/42) in nonintravenous drug users. Risk factors independently associated with HCV antibody seropositivity were history and duration of intravenous drug use and frequency of injections. Daily smoking of heroin in the previous 6 months was independently associated with the absence of HCV antibodies. Periods of fever, tiredness, and diarrhea in the preceding 6 months were associated with HCV antibodies even after correction for human immunodeficiency virus infection. The incidence rate of HCV infection appeared high and stable over the years 1986 to 1989. Thus, HCV infections are common among intravenous drug users and are mainly due to the intravenous use of drugs.
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PMID:Prevalence, incidence, and risk factors of hepatitis C virus infection among drug users in Amsterdam. 211

Alpha-interferon has emerged as the most effective agent for the treatment of chronic hepatitis when active replication of virus B, C, or D is present. Exogenous administration of human alpha-interferon, now possible through modern large-scale production methods, is associated with suppression of virus in blood. Amelioration of liver disease occurs in 35% of patients with hepatitis B virus and in 50% with hepatitis C virus with interferon doses of 30 and 10 MU per week, respectively, for 16-26 weeks; after therapy, persistent normalization of serum alanine aminotransferase is observed in 35% and 27%, respectively. Similar results have now also been reported for chronic hepatitis D. Enhanced response rates (greater than 50%) may be obtained by prolonged intermittent interferon therapy. Combination of interferon with another 'antiviral' agent (vidarabine, acyclovir, prednisone) has not increased therapeutic efficacy. Alpha-interferon induces side effects such as fatigue, flu-like syndrome, myalgia, and changes in mood and granulocytes. Patients with decompensated cirrhosis are particularly prone to bacterial infection and disease exacerbation and should receive lower doses. Interferon, when applied skillfully, induces the highly beneficial transition of active viral replication into viral latency, thereby greatly reducing infectivity, symptoms, and activity of the liver disease. Prevention of death from liver failure or hepatocellular carcinoma is to be expected.
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PMID:Treatment of chronic viral hepatitis anno 1990. 212 46

A patient with chronic inflammatory demyelinating polyneuropathy (CIDP) associated with type B and type C hepatitis virus infection is reported. A 54-year-old female who had a blood transfusion at the age of 31 years was diagnosed as a carrier of hepatitis B virus at the age of 43. Liver dysfunction was first noted in 1987 and gradually grew worse year by year. Beginning in early June 1992, the patients general fatigue became worse, her serum GOT and GPT levels became elevated, and she complained of a tingling sensation in her arms and legs. Neurological examination revealed moderate sensory disturbance of the glove-and-stocking type in all of her extremities. Deep tendon reflexes were all diminished. Hepatitis C antibody was detected in the serum at this time. On June 12, 1993, progression of her sensory disturbance was found to be associated with generalized muscle weakness. Cerebrospinal fluid studies showed increased protein without pleocytosis. Motor nerve conduction studies revealed marked prolongation of terminal latencies, reduction of conduction velocities, and abnormal temporal dispersion of the motor potentials. No sensory potentials could be evoked at any of the sites stimulated. Sural nerve biopsy showed segmental demyelination and severe loss of large myelinated fibers as well as some onion bulb formation. A diagnosis of CIDP was made. Treatment with corticosteroids was started, but there was little improvement in neurological function. The liver dysfunction progressed further and ultimately the patient died of hepatic failure. An autopsy demonstrated liver cirrhosis, but no malignant tumors were evident.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chronic inflammatory demyelinating polyneuropathy associated with chronic liver disease due to type B and type C hepatitis virus]. 766 15

We review the charts of the hospital with diagnostic of acute viral hepatitis. We classified them using serologic markers in hepatitis B (60 patients), hepatitis A (27 patients) and C (4 patients). Fatigue, anorexia, fever, chills and lymphadenopathy where more common in hepatitis A. Arthralgias, pruritus and rash where more common in hepatitis B. Bilirubin levels where higher in patients with hepatitis B (10.3 = -6.04 S.E:0.80) and C (9.7 +/- 4.09 S.E:1.24) compared with hepatitis A (6.7 +/- 6.04 S.E:0.80) p < 0.01 and p < 0.05. Alamine-Aminotransferase (ALT) levels where higher in patients with hepatitis B (1.918 +/- 1.099 S.E:215.5) and hepatitis A (1879 +/- 1.099 S.E:215.5) and lower in hepatitis C (988 +/- 764 E.E:382) p < 0.05. Abdominal Ultrasound reveal splenomegaly in 45% and 50% of patients with hepatitis A and C and only in 15% of patients with hepatitis B. Changes in gallbladder wall where found in 50% of patients with hepatitis A. 3.3% of patients with hepatitis B and 75% of patients with hepatitis C developed chronic infection.
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PMID:[Clinical, laboratory, and ultrasonography features of acute viral hepatitis]. 776 17

A six-year history of repeated attacks of fatigue, fever, arthralgias, skin changes, Raynaud's phenomenon, and neuropathy is reported in a patient with chronic liver disease. The following diagnoses were made: (1) leukocytoclastic vasculitis; (2) acute urticaria; (3) cryoglobulinemia type II with Raynaud's phenomenon and low serum level of C4; (4) peripheral polyneuropathy; (5) sicca syndrome; and (6) chronic hepatitis C virus infection. Despite therapy with corticosteroids symptoms increased gradually over years. In the first PCR of the nested PCR analysis, HCV-RNA was exclusively detected in the cryoglobulin fraction but not in the serum supernatant, suggesting that antibodies bind HCV particles, forming circulating immune complexes. As diagnoses 1-5 are well-known organ manifestations of cryoglobulinemia, we speculated whether treatment of hepatitis C with IFN-alpha (3 million IU IFN-alpha 2b three times a week) would inhibit HCV replication, decrease the cryocrit level and thereby ameliorate organ manifestations such as neuropathy and vasculitis. During treatment with IFN-alpha only a very weak or no signal could be detected for HCV-RNA in the cryoglobulin fraction as well as in the serum supernatant. This held true also for the serum supernatant in the second PCR. In parallel, cryoglobulin level, immunoglobulins, and liver enzymes decreased substantially to normal or near normal levels. Clinical symptoms-leukocytoclastic vasculitis and neuropathy-disappeared. We conclude that chronic HCV infection is involved in the pathogenesis of cryoglobulinemia and that IFN-alpha might be an effective treatment in these patients.
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PMID:A role for chronic hepatitis C virus infection in a patient with cutaneous vasculitis, cryoglobulinemia, and chronic liver disease. Effective therapy with interferon-alpha. 778 36

Recent advances have been made in the treatment of chronic viral hepatitis, mainly with recombinant interferon (IFN) alpha. However, the present treatment of chronic viral hepatitis is not entirely satisfactory because the efficacy is inconstant and/or incomplete. In chronic hepatitis B IFN-alpha induces a sustained interruption of hepatitis B virus (HBV) replication, with a HBeAg to anti-HBe seroconversion in about 30% of patients. Patients most likely to respond are those with no immunosuppression, HBV infection acquired during adulthood or active liver disease with low HBV replication. Responders usually show a significant decrease in serum HBV DNA levels during the first 2 months of therapy, followed by a significant increase in the level of aminotransferases. New nucleoside analogues might be useful in combination with IFN-alpha in the treatment of those who do not respond to IFN therapy. In chronic hepatitis B-D, the rate of sustained response to IFN-alpha therapy is low. To be effective, IFN-alpha must be used at a high dosage (9-10 mega units) with a long duration (1 year). In chronic hepatitis C, IFN-alpha at a dosage of 3 mega units over 6 months, induces a sustained response in about 20% of patients. A higher dosage of IFN (5-10 mega units) and a longer duration of treatment increases the rate of sustained response but is associated with poor tolerance. Non-responders to a first course of IFN do not respond to a second course of treatment. In patients who respond but relapse after treatment, the rate of sustained response after a second course of IFN needs to be assessed. Ribavirin, which has a significant antiviral effect on hepatitis C virus, might be useful in combination with IFN-alpha. At the dosage (3-6 mega units) usually used, IFN-alpha is relatively well tolerated. In about 10% of the patients therapy is interrupted, mainly because of severe fatigue, thyroid dysfunction or depression.
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PMID:Treatment of chronic viral hepatitis. 794 57

Autoimmune chronic active hepatitis is a rare type of chronic active hepatitis which occurs with a bimodal age distribution (10 to 30 or > or = 50 years) most frequently in women. It is characterized by negative markers for other possible (e.g. viral) etiologies, hypergammaglobulinemia and a number of circulating autoantibodies. According to the latter, several subgroups can be discriminated today. Histology shows chronic active hepatitis with chronic, sometimes plasma-cell-rich infiltration of portal tracts and piece-meal necroses. Symptoms and signs are classically non-specific and include general malaise, lethargy and fatigue. Accompanying autoimmune diseases may be present. The disease is today, however, also frequently diagnosed in an early, asymptomatic stage. Cause(s) and pathogenetic mechanism(s) of the increasingly heterogeneous appearing disease remain unknown. Recent observations seem to indicate that as yet undetermined (exogenous) substance(s) and the hepatitis C virus may, at least in certain subgroups, trigger autoimmune reactions, which may then perpetuate on the basis of a permissive (immuno)genetic background. Untreated, the disease is, in general, progressive, leads to cirrhosis and shows a mortality of up to > or = 50% in 2 to 4 years. Signs potentially indicating a nonfavorable prognosis include high inflammatory activity and the presence of cirrhosis at diagnosis. Typically, immunosuppressive therapy with corticosteroids (with or without azathioprine) results in remission of inflammatory, but usually not fibro-genetic activity with its potential for cirrhosis. Exacerbations after cessation of treatment are not infrequent (> or = 50%), and indefinite therapy is required in a number of patients, despite its potential for unwanted effects (e.g. osteopenia). Such therapy may increase the 5-year survival rate to > 80%. Liver transplantation remains the sole therapeutic option in end stage disease.
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PMID:[Autoimmune chronic active hepatitis]. 845 13

We determined the course of hepatitis C infection in 125 patients with a history of injection drug use. The mean age at presentation was 43.5 years, and the mean age of initiating injection drug use was 23.1 years. Fatigue and hepatomegaly were present in as many as 60% of patients. All had antibodies to the hepatitis C recombinant protein C25, and 99% were positive for hepatitis C virus RNA. After the initial workup, 33 (26%) patients had chronic hepatitis, 46 (37%) had chronic active hepatitis, 45 (36%) had cirrhosis, and 1 (0.8%) presented hepatocellular carcinoma. During follow-up, hepatocellular carcinoma developed in 2 other patients. In 74 patients with a 1-year history of injection drug use, the mean number of years to the development of chronic hepatitis, chronic active hepatitis, cirrhosis, and hepatocellular carcinoma were 15.6, 17.6, 19.4, and 26.3 years, respectively. In this subgroup of patients, heavy alcohol abuse did not appear to influence the progression of liver disease. The 2-year case-fatality rate was 2%. Our findings indicate that hepatitis C is a progressive disease, but only a few died during the average 20.4 years after the initiation of injection drug use. Antiviral treatment to eradicate the virus and halt the progression of disease is indicated in this group of patients.
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PMID:Clinical sequelae of hepatitis C acquired from injection drug use. 876 37


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