Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The false diagnosis of "phlebitis" is extremely frequently made: 1) They often relate to the poor interpretation of aspecific clinical signs: oedema, tumefaction, erythema and especially Homan's sign, myalgia, tendinitis, haematoma, hypodermitis, insect bites, thrombosis and varicose sclerosis. 2) The haemostatic syndrome can indicate to the experienced phlebologist: cardiac decompensation, cirrhosis, atonia and post-traumatic muscle atrophy, compressive affections (aneurysms, hernia and especially malignant tumours) and automutilation. 3) Finally, false diagnoses are made more and more frequently because the results of para-clinical tests are taken into account without fitting them into the total clinical picture itself.
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PMID:[False diagnosis of phlebitis]. 745 5

A 48-year-old woman with type II diabetes developed fatigue, arthralgia and myalgia. A few weeks later she was found to have hepatomegaly. The erythrocyte sedimentation rate was raised (53/93 mm), as were liver enzyme activities (GOT 186 U/l; GPT 240 U/l; gamma-GT 199 U/l), the gamma-globulin levels (40.7%;IgG 4470 mg/dl, IgA 698 mg/dl, IgM 245 mg/dl), antinuclear antibodies and antibodies against double-strand DNA, smooth muscles and actin. Laparoscopy revealed small-nodular liver cirrhosis. The autoimmune hepatitis was treated with prednisolone (initially 60 mg daily, then reduced to 10 mg daily) and azathioprine (initially 100 mg daily, reduced to 50 mg daily). The symptoms markedly improved. But one year later, during follow-up examination, gastric polyps were found, excised and histologically found to be carcinoid. The gastrin level was raised to 765 pg/ml. Another year later the liver cirrhosis had advanced further and the type A gastritis was still present, but there was no sign of carcinoid recurrence.
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PMID:[Autoimmune hepatitis, autoimmune gastritis, hypergastrinemia and stomach carcinoid]. 788 17

Alpha-interferon has emerged as the most effective agent for the treatment of chronic hepatitis when active replication of virus B or D is present. Exogenous administration of human alpha-interferon, now possible through modern large-scale production methods, is associated with disappearance of virus from blood. Amelioration of liver disease occurs in 35% of patients with chronic hepatitis B (e-positive) with interferon doses of 10 MU thrice weekly for 16 weeks; after therapy persistent normalization of serum aminotransferases is observed in 30%. Improvement in liver disease has only occasionally been documented for chronic hepatitis D and for chronic hepatitis B e-minus mutant. Enhanced response rates (> 50%) may possibly 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. Patients with decompensated cirrhosis are particularly prone to bacterial infection and disease exacerbation and should receive lower-than-normal 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.
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PMID:Treatment of chronic hepatitis B. 820 5

A 49-year-old man, who had a 3-year history of liver dysfunction but had not been treated, was admitted to the hospital with a sudden onset of fever and generalized muscle pain. He subsequently developed generalized purpura with scattered hemorrhagic bullae of the skin and massive bloody stools. Aeromonas sobria was proven by culture of both blood and bullous fluid. In spite of the extensive treatment with antibiotics and other medications in the intensive care unit (ICU), the patient went into septic shock and died 2 days after admission. Pathological examination on autopsy revealed segmental necrotizing gastroenteritis with bacterial colonies and alcoholic liver cirrhosis, in addition to extensive severe soft tissue damage involving cellulitis and rhabdomyolysis and epidermolysis. Although the prognosis for Vibrio vulnificus infection with severe soft tissue damage in patients with liver cirrhosis, malignancy, diabetes mellitus or other pre-existing diseases is poor, the unfavorable progression of Aeromonas species, especially A. sobria infection is rare. This is thought to be the first report of an autopsied case.
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PMID:Aeromonas sobria infection with severe soft tissue damage and segmental necrotizing gastroenteritis in a patient with alcoholic liver cirrhosis. 1046 97

We experienced two patients having Aeromonas species infection with severe clinical manifestations. The one patient was a 15-year-old high school girl student, who had been healthy in her school life, was admitted to the hospital with a sudden onset of left thigh muscle pain and swelling. She subsequently went into septic shock and died one day after admission. Pathological examination on autopsy revealed massive gas formation, skin bullas and ulcers, and extensive severe soft tissue damage throughout the body. Also, all the specimens, including brain, liver, spleen, thigh muscle, and blood in cardiac cavity, were positive for A. veronii biovar sobria. The other patient was 35-year-old man, who suffered from multiple bone fractures during the work in the harbor. One day after admission, he became febrile and went into septic shock. With the presumptive diagnosis of sepsis and gas gangrene, amputation of left thigh was performed. The exudate and aspirate of the amputated portion were repeatedly positive for A. hydrophila. Through the surveillance in Okinawa, Kagoshima, Miyazaki, and Kumamoto Prefectures, a total of 426 isolates from blood cultures were collected in the period from August, 1999 to February, 2000. Of these, 14 isolates (3.3%) were the species of Aeromonas. Of 14 isolates of Aeromonas, 13 were reported from Okinawa and the remaining one was from Kumamoto. Most patients had underlying diseases, particularly liver diseases including liver cirrhosis. The mortality rate was extremely high at 62.5%, and the patients died in short terms after blood culture became positive. With these, Aeromonas species infection is unique to Okinawa, and positive blood culture for Aeromonas species potentially indicates a high-risk, particularly among the patients with underlying diseases.
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PMID:[Aeromonas species infection with severe clinical manifestation in okinawa, Japan -association with gas gangrene-]. 2679 Apr 86

In numerous studies of symptoms in patients with chronic hepatitis C there has been no systematic assessment of both fatigue and extrahepatic manifestations. Our objective was to assess the prevalence of fatigue in patients with hepatitis C virus (HCV) infection, and to identify associations between fatigue and clinical and biological hepatic and extrahepatic manifestations. We studied 1614 patients. Data were prospectively recorded during the first visit of patients infected with HCV and the prevalence of fatigue and its association with dermatological, rheumatological, neurological and nephrological manifestations; diabetes; arterial hypertension; auto-antibodies, and cryoglobulinaemia were assessed. Then, using multivariate analysis, we identified demographic, biochemical, immunological, virological, and histological factors associated with the presence of fatigue. Fatigue was present in 53% of patients (95% confidence interval 51-56). In 17% of patients (95% confidence interval 15-19) fatigue was severe, impairing activity. Five other extrahepatic manifestations had a prevalence above 10% including, in decreasing order: arthralgia, paresthesia, myalgia, pruritus, and sicca syndrome. In univariate and multivariate analyses, fatigue, in comparison with the absence of fatigue, was associated with female gender, age over 50 years, cirrhosis, depression and purpura. Independent of these associations, fatigue was associated with arthralgia, myalgia, paresthesia, sicca syndrome and pruritus. The prevalence of fibromyalgia (as defined by the association of fatigue with arthralgia or myalgia) was 19% (95% confidence interval 17-21). There was no significant association between fatigue and the following characteristics: viral load or genotype, alcohol consumption, abnormal thyroid function, and type and level of cryoglobulinaemia. Hence, fatigue is the most frequent extrahepatic manifestation in patients infected with HCV. Fatigue is independently associated with female gender, age over 50 years, cirrhosis, depression and purpura.
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PMID:Fatigue in patients with chronic hepatitis C. 1208 7

Peginterferon-alpha-2a (40KD) is a new 'pegylated' subcutaneous formulation of interferon-alpha-2a that has been developed to improve on the pharmacokinetic profile and therapeutic efficacy of interferon-alpha-2a. Peginterferon-alpha-2a (40KD) is produced by the covalent attachment of recombinant interferon-alpha-2a to a branched mobile 40KD polyethylene glycol moiety, which shields the interferon-alpha-2a molecule from enzymatic degradation, reduces systemic clearance and enables once-weekly administration. Peginterferon-alpha-2a (40KD) was significantly more effective than interferon-alpha-2a in interferon-alpha therapy-naive adults with chronic hepatitis C in three nonblind, randomised, multicentre trials. Virological responses (intention-to-treat results) were achieved in 44 to 69% of patients with or without cirrhosis after 48 weeks of treatment with peginterferon-alpha-2a (40KD) 180 microg/week; sustained virological responses 24 weeks after the end of treatment occurred in 30 to 39% of patients. Virological responses at the end of treatment and at long-term follow-up were significantly higher than those achieved with interferon-alpha-2a. Peginterferon-alpha-2a (40KD) was significantly more effective than interferon-alpha in patients with or without cirrhosis infected with HCV genotype 1. Sustained biochemical responses achieved with peginterferon-alpha-2a (40KD) 180 microg/week ranged from 34 to 45% and were significantly higher than with interferon-alpha-2a. Recipients of peginterferon-alpha-2a (40KD) also experienced histological improvements; 24 weeks after discontinuation of treatment with peginterferon-alpha-2a (40KD) 180 microg/week, 54% to 63% of patients had a >/=2-point improvement in histological activity index score. Peginterferon-alpha-2a (40KD) produced histological responses in patients (with or without cirrhosis) with or without a sustained virological response. Peginterferon-alpha-2a (40KD) produced better results than interferon-alpha-2a alone or interferon-alpha-2b plus oral ribavirin on various measures of quality of life in patients with chronic hepatitis C. The tolerability profile of peginterferon-alpha-2a (40KD) is broadly similar to that of interferon-alpha-2a in patients with chronic hepatitis C with or without cirrhosis. Headache, fatigue and myalgia are among the most common adverse events. In conclusion, peginterferon-alpha-2a (40KD) administered once weekly produces significantly higher sustained responses, without compromising tolerability, than interferon-alpha-2a administered thrice weekly in noncirrhotic or cirrhotic patients with chronic hepatitis C, including those infected with HCV genotype 1 - a group in whom interferon-alpha treatment has usually been unsuccessful. Peginterferon-alpha-2a (40KD) is a valuable new treatment option and appears poised to play an important role in the first-line treatment of patients with chronic hepatitis C, including difficult-to-treat patients such as those with compensated cirrhosis and/or those infected with HCV genotype 1.
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PMID:Spotlight on peginterferon-alpha-2a (40KD) in chronic hepatitis C. 1210 49

Excessive alcohol ingestion is damaging and gives rise to a number of pathologies that influence nutritional status. Most organs of the body are affected such as the liver and gastrointestinal tract. However, skeletal muscle appears to be particularly susceptible, giving rise to the disease entity alcoholic myopathy. Alcoholic myopathy is far more common than overt liver disease such as cirrhosis or gastrointestinal tract pathologies. Alcohol myopathy is characterised by selective atrophy of Type II (anaerobic, white glycolic) muscle fibres: Type I (aerobic, red oxidative) muscle fibres are relatively protected. Affected patients have marked reductions in muscle mass and impaired muscle strength with subjective symptoms of cramps, myalgia and difficulty in gait. This affects 40-60% of chronic alcoholics (in contrast to cirrhosis, which only affects 15-20% of chronic alcohol misuers).Many, if not all, of these features of alcoholic myopathy can be reproduced in experimental animals, which are used to elucidate the pathological mechanisms responsible for the disease. However, membrane changes within these muscles are difficult to discern even under the normal light and electron microscope. Instead attention has focused on biochemical and other functional studies. In this review, we provide evidence from these models to show that alcohol-induced defects in the membrane occur, including the formation of acetaldehyde protein adducts and increases in sarcoplasmic-endoplasmic reticulum Ca(2+)-ATPase (protein and enzyme activity). Concomitant increases in cholesterol hydroperoxides and oxysterol also arise, possibly reflecting free radical-mediated damage to the membrane. Overall, changes within muscle membranes may reflect, contribute to, or initiate the disturbances in muscle function or reductions in muscle mass seen in alcoholic myopathy. Present evidence suggest that the changes in alcoholic muscle disease are not due to dietary deficiencies but rather the direct effect of ethanol or its ensuing metabolites.
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PMID:Alcoholic muscle disease and biomembrane perturbations (review). 1462 92

Fenoverine is a derivative of phenothiazine. It is commonly used in the treatment of gastrointestinal and gynecological spasmodic disorders. Myalgia is a common side effect, but rhabdomyolysis has only been scarcely reported before. A 77-year-old patient without previous history of liver diseases received fenoverine therapy for four days due to abdominal pain. Acute onset of myalgia, proximal muscle weakness and high creatinine phosphokinase (CK) occurred. The foregoing symptoms and signs and abnormal biochemistry improved gradually after discontinuation of fenoverine use. The pathophysiology of fenoverine-induced rhabdomyolysis is unclear. Some predisposing factors, especially liver cirrhosis, had been reported. However, our patient had none of the well-known precipitating factors. Physicians should be aware of the possibility of rhabdomyolysis in patients receiving fenoverine, whether they are healthy or have musculoskeletal or liver dysfunction.
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PMID:Rhabdomyolysis induced by fenoverine: a case report and literature review. 1625 17


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