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)

This study, designed to evaluate fenoprofen in patients with osteoarthritis, consisted of two phases: I. A double-blind crossover comparison of fenoprofen, 200 to 600 mg every six hours, to aspirin, 325 to 975 mg every six hours; II. Longterm use of fenoprofen in an open study design. During the first part of the study, both fenoprofen and aspirin were significantly better than placebo in relieving the severity and duration of pain, and in reducing stiffness. In most of the variables fenoprofen was also slightly better than aspirin. The most frequently observed side effects were abdominal discomfort, headache, pruritus, nervousness, and tinnitus. Longterm administration demonstrated the safety of fenoprofen or periods exceeding two years. Fenoprofen did not precipitate or aggravate chronic disorders, nor did it mask the symptoms of any developing disease. No interaction with concomitant drug therapy was observed.
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PMID:Fenoprofen therapy in large-joint osteoarthritis: double-blind comparison with aspirin and longterm experience. 78 Dec 34

A 56-yr-old woman with long-standing rheumatoid arthritis exhibited jaundice, pruritus and abdominal discomfort after 8 yr of periodic gold sodium thiomalate injections amounting to a cumulative dose in excess of 2.5 gm. Histopathological examination of the liver biopsy specimen showed submassive loss of parenchyma, collapse of reticulin and mixed cellular inflammatory infiltrates. Macrophages contained dark granules, which displayed the characteristics of aurosomes when examined by transmission electron microscopy and electron microprobe analysis. It is likely that hepatocellular injury occurred when the lysosomal storage capacity for gold was exceeded.
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PMID:Light- and electron-microscopical study of a case of gold salt-induced hepatotoxicity. 190 34

Papillotubular adenoma of the ampullary region in a rare tumor which has the potential for malignant transformation. Although reported more frequently nowadays, ampullary tumors are difficult to diagnose before operation unless they cause obstructive jaundice. Occasionally they are detected by ultrasonography, computed tomography or ERCP in patients who complain of nonspecific upper abdominal discomfort. We report a case of a periampullary papillotubular adenoma causing generalized pruritus and weight loss but no jaundice. The tumor was extirpated by pancreaticoduodenectomy, and the patient has remained healthy for over five years.
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PMID:Papillotubular adenoma of the ampullary region. 248 74

This review summarizes adverse reactions probably or possibly attributable to oral ciprofloxacin therapy in worldwide clinical experience involving over 6500 patients. In Europe and Japan the overall incidence of adverse reactions amongst patients receiving ciprofloxacin is reported to be 3.0% and 6.5%, respectively. An increased incidence (13.4%) has been reported from the U.S.A., possibly relating to the use of higher dosages. Very few reactions have necessitated withdrawal of treatment. The most common adverse effects involve the gastro-intestinal system (2-8% of patients treated) and usually comprise nausea, vomiting, diarrhoea and abdominal discomfort. CNS effects are seen in 1-4% of patients but are usually minor dizziness or mild headache only. Hypersensitivity reactions, most commonly skin rashes or pruritus, affect about 1% of patients. There is little evidence of significant haematological or biochemical toxicity, other than a few reports of transient neutropenia and the finding, in a minority of clinical studies, of equally transient, usually trivial and invariably reversible elevations of serum aminotransferases. Serious, ciprofloxacin-related toxicity has been observed in only three patients: one who developed pseudomembranous colitis, another who developed interstitial nephritis and a third who had a grand-mal convulsion during concomitant administration of theophylline. Ciprofloxacin appears to have an excellent safety profile.
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PMID:Ciprofloxacin: an overview of adverse experiences. 354 45

Ten patients with frequent attacks of non-hereditary angioedema were treated with tranexamic acid or placebo in a double blind manner, each period lasting 3 months. During the tranexamic acid period nine patients became symptom-free, or substantially improved, while one was unaffected (P less than 0.05). In four patients itching was a major accompanying complaint which was relieved in three. Diarrhoea and abdominal discomfort were more pronounced during tranexamic acid treatment (P less than 0.05), but only necessitated dose reduction in one patient. Four years later contact was obtained with eight of the nine responders and six were still taking tranexamic acid regularly, while in two patients the attacks were so infrequent that the drug was not taken regularly.
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PMID:Non-hereditary angioedema treated with tranexamic acid. A 6-month placebo controlled trial with follow-up 4 years later. 388 74

Fansimef is a combination of 250 mg of mefloquine, 500 mg of sulfadoxine, and 25 mg of pyrimethamine per tablet. A total of 150 adult male Zambian patients who had symptomatic Plasmodium falciparum parasitaemia were treated in a double-blind randomized fashion with either one, two or three tablets of Fansimef. All patients in the three treatment groups showed an S-type response. The rates of clearance of parasitaemia and fever were similar in all treatment groups. Tolerance was good at all dose levels. The main side-effects were abdominal discomfort, weakness and lassitude, dizziness, and pruritus, but these were mild, transient and required no specific treatment. Vomiting occurred only in 4% of patients given the highest dose of three tablets. The results of various haematological and biochemical investigations and urinalysis were not adversely altered by the administration of Fansimef.
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PMID:A double-blind clinical trial of a combination of mefloquine, sulfadoxine and pyrimethamine in symptomatic falciparum malaria. 389 78

A 52-year-old female was hospitalized with malaise, pruritus, jaundice, abdominal discomfort and vomiting. For 20 weeks she had been taking enalapril (Reniten) for hypertension. Serum aminotransferases and bilirubin were highly elevated with prolonged thromboplastin time. There was no evidence for extrahepatic cholestasis in ultrasonography. Serological investigations for a viral etiology of the liver failure were negative and the patient had no risk factors for viral hepatitis or exposure to hepatotoxic substances. Liver puncture revealed hepatitis of the fulminant viral hepatitis type, a picture that can be seen in a drug-induced hepatitis. The complete recovery of liver function after cessation of enalapril administration suggests acute toxic hepatitis due to enalapril. A metabolically mediated idiosyncratic reaction is the most plausible. Potential mechanisms of enalapril-induced hepatotoxicity are discussed and the current literature is surveyed.
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PMID:[Enalapril (Reniten)-associated toxic hepatitis]. 806 14

Dyslipidaemia may be treated with a number of safe and effective pharmacological agents that target specific lipid disorders through a variety of mechanisms. The bile-acid sequestrants--cholestyramine and colestipol--primarily decrease LDL cholesterol by binding bile acids, thereby decreasing intrahepatic cholesterol, and by increasing the activity of LDL receptors. Nicotinic acid lowers LDL cholesterol and triglyceride by decreasing VLDL synthesis and by decreasing free fatty acid mobilization from peripheral adipocytes. The HMG-CoA reductase inhibitors--fluvastatin, lovastatin, pravastatin and simvastatin--lower LDL cholesterol by partially inhibiting HMG-CoA reductase (the rate-limiting enzyme of cholesterol biosynthesis) and by increasing the activity of LDL receptors. The fibric-acid derivatives--bezafibrate, ciprofibrate, clofibrate, fenofibrate and gemfibrozil--primarily decrease triglyceride by increasing lipoprotein lipase activity and by decreasing the release of free fatty acids from peripheral adipose tissue. Probucol decreases LDL cholesterol by increasing non-receptor-mediated LDL clearance; as an anti-oxidant, probucol also decreases LDL oxidation; oxidized LDL which is thought to lead to atherogenesis. Although these agents have been proven safe in clinical trials, like any drug, they carry the risk for adverse effects. The bile-acid sequestrants may cause constipation, reflux oesophagitis, and dyspepsia, and may bind coadministered medications such as digitalis glycosides, beta blockers, warfarin, and exogenous thyroid hormone. Nicotinic acid use is commonly associated with flushing and pruritus and may also cause non-specific gastrointestinal complaints, hepatotoxicity (hepatic necrosis, hepatitis, or elevated liver enzymes), gout, myolysis, decreased glucose tolerance and increased fasting glucose levels, and ophthalmological complications including decreased visual acuity, toxic amblyopia, and cystic maculopathy. The HMG-CoA reductase inhibitors may produce liver enzyme elevations, creatine kinase elevations and rhabdomyolysis. The combination of a reductase inhibitor and a fibrate increases the risk for rhabdomyolysis. Possible adverse effects of the fibric-acid derivatives include abdominal discomfort, nausea, flatulence, increased lithogenicity of bile, liver enzyme elevations and creatine kinase elevations. Probucol may increase the QTc interval and may cause non-specific gastrointestinal complaints.
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PMID:Currently available hypolipidaemic drugs and future therapeutic developments. 859 27

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

The efficacy of chloroquine for treating uncomplicated Plasmodium falciparum malaria was evaluated in 98 children in Nigeria. Forty-three children failed chloroquine treatment (21 RI, 20 RII, 2 RIII) and were allocated at random to receive multiple doses of a combination of chloroquine and chlorpheniramine or a single dose of mefloquine orally. The parasite and fever clearance times were 2.7 +/- 1.0 d and 1.6 +/- 0.6 d, respectively, in children treated with the combination and 1.6 +/- 0.5 d and 1.1 +/- 0.3 d, respectively, for mefloquine treatment. The cure rate on day 14 was 81% among children receiving chloroquine/chlorpheniramine and 100% on days 14 and 28 with mefloquine. Three children who failed treatment with the combination responded promptly to mefloquine, with clearance of parasitaemia and fever within 48 h. Adverse effects following therapy were minimal, comprising drowsiness and pruritus in the combination group and abdominal discomfort in the mefloquine group. Isolates obtained from children who failed initial treatment with chloroquine were resistant to chloroquine but sensitive to mefloquine in vitro. The efficacy of this combination of chloroquine and chlorpheniramine confirmed previous reports of enhanced activity and it was effective in the management of mild to moderate chloroquine-resistant malaria. Although mefloquine is more effective in this respect, the combination, when developed, will be a valuable addition to the list of drugs for the management of chloroquine-resistant malaria.
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PMID:Comparative efficacy of chloroquine/chlorpheniramine combination and mefloquine for the treatment of chloroquine-resistant Plasmodium falciparum malaria in Nigerian children. 950 81


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