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Serum transaminases

A serious and potentially fatal adverse reaction to tolcapone ishepatic injury. Regular blood testing to monitor liver function is usually prescribed. The phys dan may order testing of serum transaminase levels at frequent intervals(eg, every 2 weeks for the first year and every 8 weeks thereafter). Treatment is discontinued if the ALT (SOFT) exceeds the upper normal limit or sgns or symptoms of liver failure develop. [Pg.271]

When administering the HMG-CoA reductase inhibitors and the fibric acid derivatives, the nurse monitors the patient s fiver function by obtaining serum transaminase levels before the drug regimen is started, at 6 and 12 weeks, then periodically thereafter because of the possibility of liver dysfunction with the drugs. If aspartate aminotransferase (AST) levels increase to three times normal, the primary care provider in notified immediately because the HMG-CoA reductase inhibitor therapy may be discontinued. [Pg.412]

Hepatic Effects. Elevated serum transaminases (AST, ALT) were seen in a patient two days after ingesting an unknown amount of endosulfan mixed in with food (Blanco-Coronado et al. 1992). [Pg.151]

Hepatic Effects. Jaundice and abnormal liver function tests including increases in serum transaminase levels have been reported in individuals occupationally exposed to trichloroethylene by both dermal and inhalation exposure (Bauer and Rabens 1974 Phoon et al. 1984). [Pg.107]

Elevations of serum transaminase concentrations generally are not correlated with the residual capacity of the liver to metabolize drugs, so these markers cannot be used directly as guides for residual metabolic capacity. Hepatically cleared TB drugs include isoniazid, rifampin, pyrazinamide, ethionamide, and p-aminosalicylic acid.39 Ciprofloxacin is about 50% cleared by... [Pg.1114]

Pankaj B, Kamik AB, Venkatakrishna-Bhatt H. 1986. Influence of oral lead acetate on serum transaminases and alkaline phosphatase in albino rats. Proc Nati Acad Set India Sect B (Biol Sci) 56 1-4. [Pg.562]

The answer is a. (Hardman, pp 885-8870 Lovastatin should not be used in patients with severe liver disease. With routine use of lovastatin, serum transaminase values may rise, and in such patients the drug may be continued only with great caution. Lovastatin has also been associated with lenticular opacities, and slit-lamp studies should be done before and one year after the start of therapy There is no effect on the otic nerve. The drug is not toxic to the renal system, and reports of bone marrow depression are very rare There is a small incidence of myopathy, and levels of creatinine kinase should be measured when unexplained muscle pain occurs. Combination with cyclosporine or clofibrate has led to myopathy There is no danger in use with bile acid sequestrants. [Pg.126]

Verma, S.R., S. Rani, and R.C. Dalela. 1981a. Isolated and combined effects of pesticides on serum transaminases in Mystus vittatus (African catfish). Toxicol. Lett. 8 67-71. [Pg.827]

Baseline serum creatinine, hematology profiles, and serum transaminases with repeat levels at 6- to 12-month intervals are useful in identifying specific toxicities to the kidney, liver, GI tract, or bone marrow. [Pg.30]

The diagnosis of HCV infection is confirmed with a reactive enzyme immunoassay for anti-HCV. Serum transaminase values are elevated within 4 to 12 weeks after exposure. [Pg.292]

The more common adverse reactions seen with trimethoprim-sulfamethoxazole are rash, fever, leukopenia, elevated serum transaminases, and... [Pg.457]

Therapy with INH results in a transient elevation in serum transaminases in 12% to 15% of patients and usually occurs within the first 8 to 12 weeks of therapy. Risk factors for hepatotoxicity include patient age, preexisting liver disease, and pregnancy or postpartum state. INH also may result in neurotoxicity, most frequently presenting as peripheral neuropathy or, in overdose, seizures, and coma. Patients with pyridoxine deficiency, such as alcoholics, children, and the malnourished, are at increased risk, as are patients who are slow acetylators of INH and those predisposed to neuropathy, such as those with diabetes. [Pg.555]

A black box warning for life-threatening liver failure was added to the prescribing information for nefazodone. Treatment with nefazodone should not be initiated in individuals with active liver disease or with elevated baseline serum transaminases. [Pg.799]

Hepatic Effects. No studies were located regarding hepatic effects in humans after exposure to 3,3 -dichlorobenzidine. Information from animal studies on the liver effects of exposure to 3,3 -dichloro-benzidine suggests that exposme to sufficiently high levels of the compoimd could cause liver injury as indicated by modest elevation in serum transaminase activity, fatty liver (Stula et al. 1978), decrease in hepatic vitamin E, and lipid peroxidation (Iba 1987a Iba and Lang 1988 Iba and Thomas 1988). Some of these effects may contribute to the liver tumors induced. However, it is not known whether these liver injuries will occur in humans exposed to 3,3 -dichlorobenzidine at levels at which it occurs at hazardous... [Pg.72]

Statins should be avoided in active liver disease and unexplained raised serum transaminases. Some antihistamines, such as diphenhydramine and promethazine, should be used with caution in mild-to-moderate liver disease. Selective serotonin re-uptake inhibitors should be used at a reduced dose or avoided in hepatic impairment. [Pg.118]

In a long-term inhalation study in rats, exposure to 1,4-dichlorobenzene at air concentrations of 490-499 ppm 5 hours per day, 5 days per week for 76 weeks resulted in an increase in absolute liver weight throughout the study in males and at weeks 27 and 112 in females (Riley et al. 1980). This effect was not accompanied by histological alterations or by increased serum transaminase activities. No hepatic effects were noted at 75 ppm. None of the adverse hepatic effects reported at lower concentrations of 1,4-dichlorobenzene for shorter durations (Hollingsworth et al. 1956), as described above, were identified in the 76-week study. Based on the NOAEL of 75 ppm for lack of hepatic effects, a chronic-duration MRL of 0.1 ppm was calculated as described in the footnote to Table 2-1 and in Appendix A (Hollingsworth et al. 1956). [Pg.50]

F8. Foulk, W. T., and Fleisher, G. A., The effect of opiates on the activity of serum transaminase. Proc. Staff Meet. Mayo Clin. 22, 405-410 (1957). [Pg.37]

Elevated serum transaminase /eve/s- Treatment-emergent elevations of serum transaminases (AST and /or ALT) above the upper limit of normal... [Pg.287]

ULN), greater than 1.8 x ULN, and greater than 3 x ULN occurred. These elevations were asymptomatic, reversible, more common in females, and, in general, were not associated with other evidence of liver dysfunction. In addition, these serum transaminase elevations appeared to be dose related. [Pg.288]

Hepatic function impairment- Use with caution in patients with hepatic impairment. Do not initiate rosiglitazone therapy if the patient exhibits clinical evidence of active liver disease or increased serum transaminase levels (ALT more than 2.5 times the ULN) at start of therapy. Liver enzyme monitoring is recommended in all patients prior to initiation of therapy with rosiglitazone and periodically thereafter. [Pg.327]

Serum transaminase levels -0.2% of patients treated with rosiglitazone had reversible elevations in ALT greater than 3 times the ULN compared with 0.2% on placebo and 0.5% on active comparators. Hyperbilirubinemia was found in 0.3% of patients treated with rosiglitazone compared with 0.9% treated with placebo and 1% in patients treated with active comparators. [Pg.332]

Renal function Adequately hydrate all patients undergoing treatment. Exercise caution in using succimer therapy in patients with compromised renal function. Limited data suggest that succimer is dialyzable but that the lead chelates are not. Hepatic function Trans ent mild elevations of serum transaminases have been observed in 6% to 10% of patients during the course of therapy. Monitor serum transaminases before the start of therapy and at least weekly during therapy. [Pg.376]

The most common events were Gl symptoms or increases in serum transaminases (10%) and rashes (4%). Mild to moderate neutropenia has occurred in some patients... [Pg.376]

Lab test abnormalities Propranolol may elevate blood urea levels in patients with severe heart disease. Propranolol and metoprolol may cause elevated serum transaminase, alkaline phosphatase and LDH. [Pg.528]

Significant adverse reactions include fatigue headache drowsiness paresthesias difficulty in micturition diarrhea reversible increases in serum transaminases dyspnea bronchospasm asthenia muscle cramps nausea vomiting fever with aching and sore throat toxic myopathy rashes systemic lupus erythematosus vision abnormality hypoesthesia ventricular arrhythmias intensification of AV block mental depression scalp tingling. [Pg.532]

Hepatotoxicity Fever has occasionally occurred within the first 3 weeks of therapy, sometimes associated with eosinophilia or abnormalities in 1 liver function test or more. Jaundice with or without fever may occur, usually within the first 2 to 3 months of therapy. Incidence of elevated serum transaminase levels and impaired hepatic function ranges from 1% to 27%. [Pg.550]

Hepatic function impairment Marked persistent increases (greater than 3 times ULN) in serum transaminases occurred in patients treated with all agents ranging in frequency from less than 1% to 1.9%. When the drug was interrupted or discontinued or the dosage was reduced, transaminase levels usually fell slowly to... [Pg.619]

Monitoring For lovastatin, perform LFTs before initiating therapy, at 6 and 12 weeks after initiation of therapy or after dose elevation, and periodically thereafter (approximately 6-month intervals). For rosuvastatin, fluvastatin, and atorvastatin, it is recommended that LFTs be performed prior to and at 12 weeks following both the initiation of therapy and any elevation in dose, and periodically (eg, semiannually) thereafter. For pravastatin and simvastatin, perform LFTs prior to the initiation of therapy, prior to elevation of dose, and when otherwise clinically indicated. For patients titrated to the 80 mg dose of simvastatin, perform LFTs prior to titration, 3 months after titration to the 80 mg dose, and periodically thereafter (eg, semiannually) for the first year of treatment. Pay special attention to patients who develop elevated serum transaminase levels. If transaminase levels progress. [Pg.620]

Hepatic function impairment Fenofibrate is associated with significant increases in serum transaminases (AST or ALT). Increases to more than 3 times the upper limit of normal (ULN) occurred. Hepatocellular, chronic active and cholestatic hepatitis associated with fenofibrate therapy have been reported after exposures of weeks to several years. [Pg.629]

Perform liver function tests on all patients during therapy with nicotinic acid. Monitor serum transaminase levels, including ALT and AST, before treatment begins, every 6 to 12 weeks for the first year, and periodically thereafter (at approximately 6-month intervals). Discontinue the drug if the transaminase levels show evidence of progression, particularly if they rise to 3 times the upper limit of normal and are persistent or if they are associated with symptoms of nausea, fever, or malaise. Consider liver biopsy if elevations persist beyond discontinuation. [Pg.632]

The combination of ezetimibe with an HMG-CoA reductase inhibitor is contraindicated in patients with active liver disease or unexplained persistent elevations in serum transaminases. [Pg.634]

Hepatotoxicity A few cases of reversible clinical hepatotoxicity have occurred in some patients, asymptomatic rises in serum alkaline phosphatase or serum transaminase levels have been observed. If anorexia, weight loss or pruritus develop in patients on allopurinol, evaluation of liver function should be part of their diagnostic workup. Perform periodic liver function tests during early stages of therapy. [Pg.951]


See other pages where Serum transaminases is mentioned: [Pg.425]    [Pg.105]    [Pg.148]    [Pg.43]    [Pg.1265]    [Pg.109]    [Pg.816]    [Pg.252]    [Pg.43]    [Pg.130]    [Pg.45]    [Pg.744]    [Pg.42]    [Pg.285]    [Pg.287]   
See also in sourсe #XX -- [ Pg.100 , Pg.117 ]

See also in sourсe #XX -- [ Pg.100 , Pg.117 ]

See also in sourсe #XX -- [ Pg.100 , Pg.117 ]

See also in sourсe #XX -- [ Pg.27 , Pg.415 , Pg.417 , Pg.420 ]




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Of serum transaminase

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Serum glutamic-oxaloacetic transaminase SCOT)

Serum glutamic-pyruvic transaminase

Serum glutamic-pyruvic transaminase SGPT)

Serum transaminase activity

Serum transaminase isoniazid

Serum transaminase levels

Serum-glutamic-oxaloacetic-transaminase

Transaminases

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