Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033774 (pruritus)
 14,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Based on uncontrolled observations, we have proposed ursodeoxycholic acid (UDCA) as a novel therapeutic approach in primary biliary cirrhosis (PBC). To confirm and extend our original findings, we have designed a double-blind multicentre randomized clinical trial. An interim analysis was planned at 6 months, involving all subjects included in the trial, with a final analysis at 2 years. The UDCA-PBC trial began in June 1987 and will be completed in March 1990. Seventy patients were randomized to receive UDCA and 68 a placebo. The two groups were well matched with respect to age, sex, duration and prevalence of symptoms and histologic severity (50% of the UDCA group had stage III-IV disease vs. 37% of the placebo group). During the first 6 months of follow-up, six patients withdrew from the trial. At 6 months, the proportion of patients with jaundice was significantly lower (p less than 0.01) in UDCA recipients than in the placebo group. There was a similar decrease in the proportion of patients with pruritus and fatigue in both groups. The following laboratory test values were significantly lower in UDCA recipients than in the placebo group after 6 months of therapy: serum bilirubin, alkaline phosphatase, alanine aminotransferase (ALAT), aspartate aminotransferase (ASAT), gamma-glutamyltranspeptidase activities (p less than 0.001), cholesterol (p less than 0.003) and IgM levels (p less than 0.03). The results of this interim analysis confirm and extend the biochemical data provided by our previous pilot study. However the final analysis of the trial is necessary for a definitive assessment of the safety and efficacy of UDCA therapy in PBC.
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PMID:Ursodeoxycholic acid for the treatment of primary biliary cirrhosis. Interim analysis of a double-blind multicentre randomized trial. The UDCA-PBC Study Group. 197 19

A multi-center double-blind controlled trial of ursodeoxycholic acid (UDCA) for treatment of primary biliary cirrhosis (PBC) was carried out. Twenty two and 23 patients were treated with 600 mg/day UDCA and placebo, respectively, for 24 weeks. In UDCA-treated patients, fall of serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma-glutamyltranspeptidase activities started within 4 weeks after start of the trial and continued throughout the trial period. The serum IgM level fell in 7 UDCA-treated patients examined but not in 10 placebo-treated patients examined. Serum bilirubin concentration showed no significant change at the end of the study in either of UDCA- and placebo-treated group of patients. There was no significant difference between these two groups with respect to the frequency of improvement of pruritus. In UDCA-treated patients, serum bile acid composition changed markedly, though its concentration showed no significant change. The percentage of total bile acid which ursodeoxycholic acid took up increased, whereas those which cholic acid, chenodeoxycholic acid and deoxycholic acid took up were decreased.
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PMID:A multi-center double-blind controlled trial of ursodeoxycholic acid for primary biliary cirrhosis. 198 Jun 54

Six patients were studied to evaluate the efficacy and safety of plasma exchange (PE) in the treatment of primary biliary cirrhosis (PBC). All patients were affected by PBC at stage III-IV and presented symptoms refractory to pharmacologic therapy. Patients underwent PE for a mean period of 40 weeks (range 10-88). A mean of 33 liters (range 17-64) of plasma per patients was removed. Patients reported less fatigue (4/6), pruritus (5/5), nausea (3/3), Sjogren's syndrome (2/6), and painful neuropathy (2/3). A reduction of xanthomata was noted in one of the three affected patients. Definitive improvement was seen in the patient with Raynaud's phenomenon. A significant reduction was noted for serum cholesterol and gammaglobulins. ALT, AST, gamma-GT, alkaline phosphatase, bilirubin, prothrombin activity, AMA titers were not affected by PE. All patients suffered some mild adverse effects during PE. Two patients (IV stage) developed late edema and ascites after 34 and 44 weeks of treatment. We conclude that PE can be considered effective chronic treatment for advanced symptomatic PBC refractory to pharmacological therapy.
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PMID:Effects of plasma exchange (PE) in primary biliary cirrhosis (PBC). A pilot study. 231 37

Clinical and experimental investigations have suggested that ursodeoxycholic acid (ursodiol) may have cytoprotective or choleretic action and therefore be beneficial in patients with intrahepatic cholestasis or chronic liver disease. In an open-label study, we treated 45 patients with chronic hepatitis with 300 mg of ursodiol three times daily for six months. At four months, gamma-glutamyl transpeptidase (gamma-GTP) and leucine aminopeptidase levels had decreased. SGOT and SGPT levels also decreased significantly. Evaluation of histologic changes has not yet been completed. No significant differences in improvement of liver function tests were found in a comparison with 19 historical controls. We also studied eight patients with primary biliary cirrhosis, treated for more than one and a half years with 600 mg of ursodiol per day. At one month, itching diminished in five patients who had pruritus. ALPase and gamma-GTP levels decreased significantly, and GOT and GPT levels were also reduced. IgM levels did not change, but the titer of antimitochondrial body decreased by half in two patients. Levels of glycoursodeoxycholic acid increased, and in three patients follow-up liver biopsy showed marked improvement. These preliminary results suggest that ursodiol is safe and effective for the treatment of chronic hepatitis and primary biliary cirrhosis, but a large-scale, controlled trial is needed.
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PMID:Effect of ursodeoxycholic acid in chronic hepatitis and primary biliary cirrhosis. 257 57

Altogether 108 patients with acute alcoholic hepatitis (AAH) were examined. Of these, 14 patients (13%) presented with the cholestatic pattern of AAH, 45 with extrahepatic cholestasis, and 45 were healthy. As compared with the total patients' group with AAH, the patients with the cholestatic form consumed alcohol in greater amounts. Due to intensive jaundice, 50% of the patients were admitted by error to the infectious clinic and 32% to the surgical one. The disease runs a comparatively grave course, the general conditions gets deteriorated, the body temperature rises, the patient senses pains in the right hypochondrium, skin pruritus is lacking. As compared with other patterns of cholestasis, cholestatic AAH is characterized by a higher thymol test, higher levels of cholesterol, low density lipoproteins, activation of gamma-glutamyl transpeptidase and aspartate aminotransferase and by a lower level of leukocytes, bilirubin, free fatty acids and alkaline phosphatase. Verification of the diagnosis demands the use of certain up-to-date instrumental methods. To identify the cause of cholestasis, great diagnostic significance is attached to echography.
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PMID:[Clinico-laboratory characteristics of the cholestatic form of acute alcoholic hepatitis]. 263 92

The study includes 108 patients with acute alcohol hepatitis, 45 patients with cholestasis and 124 healthy controls. In 14 patients (13%) cholestatic acute alcohol hepatitis was found. The patients with cholestatic acute alcohol hepatitis consumed considerably more alcohol than the other patients with acute alcohol hepatitis. The intensive jaundice led half of the patients with cholestatic acute alcohol hepatitis to the infectious diseases clinic and 32% of them to the surgical clinic. The course of the disease was heavy, with disturbed general condition, high temperature, pain in the right subcostal region but without itching. The patients showed higher levels of timol test, cholesterol, LDL-cholesterol, coefficient LDL/HDL-cholesterol, beta-lipoproteins, total lipids, gamma-GTP, ASAT and lower levels of leucocytes, bilirubin, SMC, alkaline phosphatase and LAP than the other patients with cholestasis. The patients with cholestatic acute alcohol hepatitis showed a higher level of total lipids and gamma-GTP than the other patients examined. The confirmation of the diagnosis implies the application of contemporary instrumental and invasive methods. The ultrasound examination is of special importance.
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PMID:[The clinico-laboratory characteristics of the cholestatic form of acute alcoholic hepatitis]. 263 77

The effects of ursodeoxycholic acid (UDCA, 13-15 mg/kg body weight daily) were prospectively evaluated in fifteen patients with primary biliary cirrhosis (PBC). The mean concentration of UDCA in serum expressed as the percentage of total bile acids rose from 0% at baseline to 58% (SEM 9%) after 2 years' treatment, whereas total serum bile acid levels did not change significantly. The proportion of patients with pruritus necessitating the use of cholestyramine was significantly lower at 2 years than at baseline. Standard liver function tests improved in all the patients. At 2 years the average activities of gamma-glutamyltranspeptidase, alkaline phosphatases, and alanine aminotransferase and bilirubin levels were reduced (respectively 78%, 65%, 68%, and 36% of pretreatment values). In three patients who agreed to interrupt the ingestion of UDCA for 3 months after 2 years' treatment there was clear deterioration in liver function tests, which again improved after reinstitution of UDCA. These results suggest that long-term UDCA might be a safe and effective treatment for PBC, but a randomised, controlled, double-blind trial is urgently needed.
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PMID:Is ursodeoxycholic acid an effective treatment for primary biliary cirrhosis? 288 36

Seven patients developed acute hepatitis after receiving Plethoryl for obesity for 4 to 16 weeks. Jaundice was generally associated with or preceded by asthenia, nausea and pruritus. Serum aminotransferase activities were markedly increased whereas alkaline phosphatase and gamma-glutamyltransferase activities were moderately elevated. There was no hepatic failure. In all cases, Plethoryl administration was promptly discontinued. In 6 cases, jaundice disappeared within 2 to 4 weeks, and recovery occurred within 2 to 5 months. In one case, however, jaundice disappeared within 12 weeks and recovery took 10 months.
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PMID:[Hepatitis probably caused by Plethoryl. Apropos of 7 cases]. 337 97

The first case of hepatic injury induced by Venoplant, extracts of Aesculus Hippocastanum, having antiinflammatory activities, was described. A 37 yr-old man was admitted for treatment of pathological fracture of the left brachial bone. He had been received 65 mg Venoplant at another hospital several hours before admission. 17 days later, a liver function test showed mild abnormality and 60 days after injection, he complained of pruritus and jaundice. Laboratory studies revealed moderate elevation of total bilirubin, ALP, gamma-GTP and mild eosinophilia. CT studies and ERC showed no signs of extrahepatic obstructive jaundice. The lymphocyte stimulation test was positive. The liver biopsy demonstrated marked cholestasis with zonal necrosis in the centrilobular areas but showed little or no changes in the portal tracts. These features are consistent with drug-induced hepatic injury.
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PMID:A case of Venoplant-induced hepatic injury. 369 1

A relapsing papulo-vesicular rash with or without pruritus was observed in 54 out of 148 patients (36%) with posttransfusion or sporadic, acute or chronic, non-A, non-B (NANB) hepatitis. The predominant location was the trunk and the anterior surfaces of the upper extremities. The face was affected less often. The eruptive phase was accompanied by general symptoms and increases in aminotransferases and gamma-GT values. The nature of the eruption was consistent with cutaneous reactions as frequently seen in enterovirus infections. No predominance was found for special groups of patients when the skin lesions were correlated to either sex, mode of infection or pattern of transaminase elevation (i.e. monophasic or bi-, and multi-phasic).
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PMID:Cutaneous papulo-vesicular eruptions in non-A, non-B hepatitis. 392 44


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