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)

Interferon-alpha-n1 (lymphoblastoid interferon-alpha) is a nonrecombinant 'natural' interferon derived from lymphoblastoid cells exposed to Sendai virus. In common with endogenous and recombinant interferon-alpha molecules, interferon-alpha-n1 has antiviral, immunomodulatory and antiproliferative properties. Interferon-alpha-n1 shows some efficacy in immunocompetent adults with well-compensated chronic viral hepatitis B. Rates of complete virological response (defined as an absence of detectable hepatitis B virus-DNA in the serum) ranged from 5 to 79% of adults who received various dosage regimens of interferon-alpha-n1 in monotherapy trials. Clearance of hepatitis B 'e' antigen was reported in 5 to 70% of patients treated with the drug. Spontaneous virological responses occurred in 0 to 48% of untreated patients. The clinical efficacy of interferon-alpha-n1 in patients with chronic hepatitis B is not improved by concomitantly administered deflazacort, zidovudine or levamisole, but may be increased by a course of corticosteroid pretreatment in some patients. Interferon-alpha-n1 also shows therapeutic benefit in adults with chronic hepatitis C. Complete biochemical responses (defined as normalisation of serum ALT levels) were achieved in 27 to 60% of adult patients treated with the drug, whereas spontaneous normalisation of serum ALT levels occurred in up to 11% of untreated patients. Responses to interferon-alpha-n1 were temporary in 27 to 78% of treatment responders but were sustained in 6 to 40% of patients. Emerging data delineating baseline factors predictive of a positive response to interferon-alpha-n1 treatment may aid in the selection of patients with hepatitis B or C most likely to benefit from treatment with this drug. Most patients receiving interferon-alpha-n1 experience a transient 'influenza-like' syndrome during the first week of treatment. The syndrome, which is dose related and alleviated by paracetamol (acetaminophen), is characterised by fever, chills, and arthralgia. Dose-limiting adverse effects occurring during longer term interferon-alpha-n1 therapy include fatigue, myalgia, headache, depression, pruritus and seizures. Neutropenia and thrombocytopenia may also occur during interferon-alpha-n1 treatment. Autoimmune thyroid disease may develop in up to 9% of patients treated with interferon-alpha-n1 for >or=6 months. At present, interferon-alpha-n1 and the recombinant forms of interferon-alpha are the only drugs available for the treatment of adults with well-compensated hepatitis B or C. Interferon-alpha-n1 produces moderate response rates in adults with well-compensated chronic hepatitis B or C. Thus, it is positioned alongside recombinant interferon-alpha products as a useful first-line treatment option for patients with chronic hepatitis B or C.
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PMID:Interferon-alpha-n1: a review of its pharmacological properties and therapeutic efficacy in the management of chronic viral hepatitis. 1802 May 50

Abnormal liver tests occur in 3%-5% of pregnancies, with many potential causes, including coincidental liver disease (most commonly viral hepatitis or gallstones) and underlying chronic liver disease. However, most liver dysfunction in pregnancy is pregnancy-related and caused by 1 of the 5 liver diseases unique to the pregnant state: these fall into 2 main categories depending on their association with or without preeclampsia. The preeclampsia-associated liver diseases are preeclampsia itself, the hemolysis (H), elevated liver tests (EL), and low platelet count (LP) (HELLP) syndrome, and acute fatty liver of pregnancy. Hyperemesis gravidarum and intrahepatic cholestasis of pregnancy have no relationship to preeclampsia. Although still enigmatic, there have been recent interesting advances in understanding of these unique pregnancy-related liver diseases. Hyperemesis gravidarum is intractable, dehydrating vomiting in the first trimester of pregnancy; 50% of patients with this condition have liver dysfunction. Intrahepatic cholestasis of pregnancy is pruritus and elevated bile acids in the second half of pregnancy, accompanied by high levels of aminotransferases and mild jaundice. Maternal management is symptomatic with ursodeoxycholic acid; for the fetus, however, this is a high-risk pregnancy requiring close fetal monitoring and early delivery. Severe preeclampsia itself is the commonest cause of hepatic tenderness and liver dysfunction in pregnancy, and 2%-12% of cases are further complicated by hemolysis (H), elevated liver tests (EL), and low platelet count (LP)-the HELLP syndrome. Immediate delivery is the only definitive therapy, but many maternal complications can occur, including abruptio placentae, renal failure, subcapsular hematomas, and hepatic rupture. Acute fatty liver of pregnancy is a sudden catastrophic illness occurring almost exclusively in the third trimester; microvesicular fatty infiltration of hepatocytes causes acute liver failure with coagulopathy and encephalopathy. Early diagnosis and immediate delivery are essential for maternal and fetal survival.
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PMID:Liver disease in pregnancy. 1826 10

An asymptomatic 70-year-old Hispanic woman with type 2 diabetes was found in 2004 to have an AST of 132 U/L, ALT 146 U/L, alkaline phosphatase 1107 U/L, total serum bilirubin 3.5 mg/dL, and albumin 2.9 g/dL. Viral hepatitis testing was negative. Serum IgG, IgA, and IgM were all elevated, antimitochondrial antibody was weakly positive, and antinuclear antibody was negative. Liver biopsy was reported to show "evolving cirrhosis with marked lymphoid hyperplasia." Although the indication was nowhere stated, she was prescribed ursodeoxycholic acid 500 mg b.i.d, on which her biochemical tests initially improved. One year later she developed itching and jaundice. Imaging studies revealed multiple gallstones. An MRCP was suggestive of cirrhosis with a questionable common bile duct stricture, and she underwent ERCP with removal of gallbladder and common bile duct stones and placement of a biliary stent. A periampullary mass, which proved to be a somatostatinoma, was excised in 2006 via an open laparotomy, at which the stent was removed and a second liver biopsy performed. It was reported as showing chronic active hepatitis, activity stage 2, and fibrosis grade 3 with bridging. Her subsequent course was complicated by recurrent bleeding from small bowel arteriovenous malformations. Seen for the first time at Columbia University Medical Center in January 2007, she complained of continuing pruritus. AST was 69 U/L, ALT 43 U/L, alkaline phosphatase 491 U/L, and total bilirubin 3.3 mg/dL. Serum albumin was 2.6 g/dL. Antinuclear antibodies, negative in 2004, were now positive at 1:320, and antimitochondrial M2 antibodies were strongly positive. Serum IgG and IgA, but NOT IgM, were elevated. Review of her outside liver biopsies revealed features of primary biliary cirrhosis (PBC) in the first, and of both PBC and autoimmune hepatitis (AIH) in the second. The patient exhibits an overlap syndrome, in which both histologic and serologic features of AIH evolved in a setting initially most suggestive of PBC alone. The phenomenon of autoimmune overlap syndromes is discussed.
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PMID:Evolution from primary biliary cirrhosis to primary biliary cirrhosis/autoimmune hepatitis overlap syndrome. 1829 83

A 46-year-old female patient was referred to our department with presenting symptoms of asthenia, jaundice, and pruritus. There was no medical history or clinical evidence of viral hepatitis, autoimmune hepatitis, hemochromatosis, or Wilson's disease. The patient revealed that 14 days prior to admission she had begun self-medicating with conjugated linoleic acid (CLA) to reduce body fat, leading to the suspicion of CLA hepatotoxicity, which was subsequently confirmed by a liver biopsy. After the patient ceased to ingest CLA, liver enzymes levels normalized. To the best of our knowledge, this is the first report of hepatotoxicity due to CLA ingestion.
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PMID:Conjugated linoleic acid-induced toxic hepatitis: first case report. 1872 3

Abnormal liver function tests occur in 3 - 5% of pregnancies for different reasons. Apart from pre-existing liver diseases liver diseases occurring during pregnancy, such as gall stones or viral hepatitis, most liver dysfunctions in pregnancy are caused by one of the five pregnancy-related liver diseases. The five known pregnancy-related liver diseases can be classified in two main categories depending on their association with or without preeclampsia. The preeclampsia-associated liver diseases are the preeclampsia itself, the HELLP-syndrome ("Hemolysis" (H), "Elevated Liver Tests" (EL), "Low Platelet Count" (LP)) and the acute fatty liver of pregnancy. Hyperemesis gravidarum and intrahepatic cholestasis of pregnancy are not associated with preeclampsia. Hyperemesis gravidarum is characterised by intractable vomiting in the first trimester of pregnancy. 50% of patients with this condition have liver dysfunction. Intrahepatic cholestasis of pregnancy presents with pruritus and elevated bile acids in the second half of pregnancy. Patients have often mild jaundice and highly elevated liver enzymes. Treatment of choice is ursodeoxycholic acid to relieve the mother's symptoms. With this condition mainly the fetus is at risk. Severe preeclampsia is the most common cause of liver dysfunction in pregnancy, and is in some cases further complicated by HELLP syndrome. The prompt delivery of the baby is the only definitive therapy. However, many life-threatening maternal complications like liver hematoma or rupture and abruptio placentae can occur. Acute fatty liver of pregnancy is also a severe illness occuring mostly in the third trimester; microvesicular fat deposition in the liver can cause liver failure with coagulopathy and encephalopathy. Only the immediate delivery of the fetus can save mother and child.
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PMID:[Liver diseases in pregnancy]. 1894 56

Albendazole binds to parasite's tubulin inhibiting its glucose absorption. Its common adverse effects are nausea, vomiting, constipation, thirst, dizziness, headache, hair loss and pruritus. Although mainly metabolized in the liver, abnormal liver function tests were a rare adverse effect during clinical trials and we found no literature about albendazole-induced hepatitis requiring admission. This patient had a previous history of albendazole ingestion in 2002 resulting in increase of liver function tests. And in 2005, the episode repeated. We evaluated the patient for viral hepatitis, alcoholic liver disease, and autoimmune hepatitis, but no other cause of hepatic injury could be found. Liver biopsy showed periportal steatosis and periportal necrosis. The initial abnormal liver function test improved only with supportive care. These findings and the Roussel Uclaf Causality Assessment Method of the Council for International Organizations of Medical Sciences (RUCAM/CIOMS) score of 9 are compatible with drug-induced hepatitis so we report the case of this patient with a review of the literature.
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PMID:Acute drug-induced hepatitis caused by albendazole. 1895 2

Pruritus is a common complication of end-stage renal disease (ESRD), affecting about one-third of dialysis patients. It is a chronic, unpleasant symptom with a strong negative impact on patients' quality of life, often inducing sleeplessness and mood disorders. Recent data show that it is also associated with increased mortality. The pathogenesis of uraemic pruritus (UP) is multifactorial. Triggering factors may include uraemia-related abnormalities (particularly involving calcium, phosphorus and parathyroid hormone metabolism), accumulation of uraemic toxins, systemic inflammation, cutaneous xerosis, and common co-morbidities such as diabetes mellitus and viral hepatitis. Recent findings suggest that the neurophysiology of itch is similar to that of pain; this has led to the hypothesis that the two phenomena also closely interact in ESRD patients, who often also experience uraemic neuropathy. The management of UP needs to address several different issues, such as optimization of dialysis efficacy and skin hydration, and correction of calcium-phosphorus metabolism abnormalities. A wide range of antipruritic drugs have been suggested for the treatment of UP, although most of them have only been tested in small, uncontrolled trials, which have yielded conflicting results. Antihistamines are now known to have little or no efficacy, although they are still often prescribed. Novel neurotropic drugs such as gabapentin, along with opioid receptor modulators such as nalfurafine, appear to be effective and well tolerated, but their efficacy has not yet been directly compared. Finally, physical therapies, including UV radiation, may also have a role in patients with refractory symptoms.
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PMID:Uraemic pruritus: clinical characteristics, pathophysiology and treatment. 1927 70

Pruritus is a common and unpleasant symptom in the dialysis setting, affecting about half of all hemodialysis and peritoneal dialysis patients. It has a great impact on patients' quality of life and is also associated with increased mortality. The pathogenesis of uremic pruritus (UP) is clearly multifactorial and still poorly understood. At least four main hypotheses have been put forward: dermatological abnormalities, an immune-system derangement that results in a proinflammatory state, an imbalance of the endogenous opioidergic system, and a neuropathic mechanism. The neurophysiology of itch has been shown to be quite similar to that of pain, supporting the hypothesis that the two phenomena may be closely related in dialysis patients, who often also experience uremic neuropathy. Moreover, an array of other triggering factors may include uremic toxins, systemic inflammation, cutaneous xerosis, and common comorbidities such as diabetes mellitus, endocrinopathies and viral hepatitis. The first step in the treatment of UP focuses on some general strategies that include the optimization of the dialysis schedule using biocompatible membranes such as polymethyl methacrylate, and the control of the divalent ion metabolism. The second step may be local therapy with skin emollients and capsaicin creams. More specific treatments that appear promising but have not been proven to be definitively efficacious include UVB light, gabapentin and the novel k-opioid-agonist nalfurafine. Nephrologists, who still tend to neglect this disabling symptom, need to be aware that UP is associated with poorer patient outcomes and that a stepwise therapeutic approach is now available.
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PMID:[Uremic pruritus: an unresolved challenge]. 1980 4

Pruritus is a well-known manifestation of various cholestatic disorders. Increased opioidergic tone is one of the mechanisms for this. This prospective, uncontrolled study was done to determine the efficacy of intravenous naloxone in pruritus of acute cholestasis. Twenty-two patients with severe pruritus (based on visual analogue scale [VAS] score of 0-100 and associated symptoms) were treated with intravenous naloxone (0.4 mg every 8 hours) for at least 48 hours. Viral hepatitis E was found to be the most common etiology for cholestatic pruritus (n=12). Eighteen patients (81.8%) patients had significant reduction in VAS after 48 hours of starting naloxone; these patients also showed reduction in alkaline phosphatase and gamma glutamyl transpeptidase. There was no side-effect or 'breakthrough' phenomenon noted in any patient over next 6 weeks. Naloxone is safe and efficacious in symptomatic improvement in cholestatic pruritus.
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PMID:Role of intravenous naloxone in severe pruritus of acute cholestasis. 2010 67

We describe two cases with acute hepatitis of patients who live at Lima, Peru and have a high socio-economic status. The first case, is a 58 years old female with asthenia, jaundice, coluria and pruritus. The physical exam revealed jaundice and laboratory exams revealed transaminasemia (AST= 1754, ALT= 2680) and hyperbilirubinemia (total bilirubin= 7.98, direct bilirubin=7.03). Furthering serologic tests, revealed a positive test for anti-Hepatitis E virus IgM and IgG. All the symptoms were remitted by the 3rd week of disease. The second case described, is a 64 years old female with asthenia, hyporexia and abdominal pain, without jaundice. The physical exam was normal and initial laboratory tests revealed an AST= 2999 and ALT= 4370. All the symptoms were remitted by the 3rd week of disease. The ELISA testing for anti-Hepatitis E virus IgM, was positive. In both cases other viral hepatitis serologic tests were negative. We make a description of these 2 cases and a literature review, because these both, are the first cases of Hepatitis E described in our city, and for the relevance of this virus in current medical knowledge for patients with non A, non B, non C acute hepatitis.
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PMID:[Acute hepatitis secondary to hepatitis E. Report of two cases from a population of high socioeconomic level Lima]. 2126 64


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