Hepatic disease hepatotoxicity

Suicide risk even in patients without psychiatric disease Avoid in uncontrolled narrow-angle glaucoma (causes mydriasis) Hepatotoxic avoid in alcoholics even if signs/symptoms of hepatic disease are absent. 

Rare cases of hepatic failure, some leading to death or liver transplant, have occurred with the use of terbinafine for the treatment of onychomycosis in individuals with and without pre-existing liver disease. In the majority of liver cases reported in association with terbinafine use, the patients had serious underlying systemic conditions and an uncertain causal relationship with terbinafine. Terbinafine is not recommended for patients with chronic or active liver disease. Before prescribing terbinafine, assess pre-existing liver disease. Hepatotoxicity may occur in patients with and without preexisting liver disease. Pretreatment serum transaminase (ALT and AST) tests are advised for all patients before taking terbinafine. 

Liver Methotrexate causes hepatotoxicity, fibrosis, and cirrhosis, but generally only after prolonged use. Acutely, liver enzyme elevations are frequent, usually transient and asymptomatic, and also do not appear predictive of subsequent hepatic disease. Liver biopsy after sustained use often shows histologic changes, and fibrosis and cirrhosis have occurred these latter lesions often are not preceded by symptoms or abnormal liver function tests (see Precautions). For this reason, periodic liver biopsies are usually recommended for psoriatic patients who are under long-term treatment. Persistent abnormalities in liver function tests may precede appearance of fibrosis or cirrhosis in the RA population. 

Hepatic disease Use with caution in patients with hepatic disease or in conjunction with hepatotoxic drugs. 

Comparable reports have prompted a questionnaire investigation of 770 patients with type 2 diabetes at the start of acarbose therapy (51). Patients with one or more susceptibility factors for liver damage underwent ultrasonography and autoantibody assays. There was silent hver disease in 13% and 20 patients had a fatty liver without hepatic disease. In 15% of these patients there were slight reversible changes in transaminase activity after acarbose. This supports the supposition that severe hepatotoxic reactions to acarbose are idiosyncratic. 

With phenytoin, carbamazepine, phenobarbital, primidone, and lamotrigine, hepatotoxicity usually occurs as part of a hypersensitivity reaction, with skin rashes and fever in the early weeks of treatment. More rarely, hepatic disease can develop after many years without signs of hypersensitivity. Once hepatotoxicity develops, mortality... 

Of eight patients who were given an infnsion of gemtnznmab 9 months after hemopoietic stem cell transplantation, seven had normal semm biUmbin concentrations, and all eight had transaminase and alkaline phosphatase activities that were less than 1.5 times the npper limit of the reference range (4). Six had no evidence of hepatotoxicity. One developed abdominal pain, ascites, and mildly raised transaminases. A CT scan showed no evidence of hepatic disease. This patient did not meet the criteria of veno-occlnsive disease. Patient 8 did meet the criteria of veno-occlnsive disease 3 days after infnsion... 

Levamisole is mostly metabolized to pora-hydroxylevami-sole (52). It should not be used in severe hepatic disease, nor should it be combined with hepatotoxic anti-helminthic drugs or other drugs presenting risks to the hver. 

This was the third published case of fatal valproate liver toxicity in an adult with Friedreich s disease, suggesting that this condition is a predisposing factor. Although the risk of valproate hepatotoxicity in adults is much lower than in children, adults still represented over 15% of the cases known to the authors. Overall, a total of 26 other adults (age range 17-62 years) with fatal valproate-induced Uver failure have been reported of these, 3 were taking monotherapy and 12 had no underlying disease or a clearly non-metabolic and non-hepatic disease. The duration of treatment before the first symptoms varied between 6 days and 6 years. 

Flowever, ampelopsin C and the mixture of (-i-)-vitisin A (698) and (+)-cw-vitisin A (702) were found to be powerful hepatotoxins. The coexistence of hepatoprotective and hepatotoxic agents in the same plant is very interesting, and the plant has been used to cure hepatic diseases such as hepatitis and liver cirrhosis [519]. 

The clinical utility of thiabendazole in adults is compromised by its toxicity, which has diminished its clinical use. Frequent side effects include GI upset, fatigue, drowsiness, and headache. Occasional fever, rash, erythema multiforme, hallucinations, and sensory disturbances have been reported. Angioedema, shock, tinnitus, convulsions, and intrahepatic cholestasis, and crystalluria are rare complications. Transient leukopenia has been noted. Thiabendazole is hepatotoxic and should be used with caution in patients with hepatic disease. The effects of thiabendazole in pregnant women have not been studied adequately, so it should be used in pregnancy only when the potential benefit justifies the risk. 

Didanosine may cause pancreatitis or hepatic disease, and zidovudine may also rarely cause hepatic disease. It has been suggested that the hepatotoxicity of didanosine and paracetamol are augmented when they are given together. ... 

Yellow phosphorus was the first identified liver toxin. It causes accumulation of lipids in the liver. Several liver toxins such as chloroform, carbon tetrachloride, and bromobenzene have since been identified. I he forms of acute liver toxicity are accumulation of lipids in the liver, hepartxiellular necrosis, iii-trahepatic cholestasis, and a disease state that resembles viral hepatitis. The types of chrome hepatotoxicity are cirrhosis and liver cancer. 

Medication use must be monitored carefully for potential hepatotoxicity. Hepatically metabolized medications have the potential to accumulate in patients with liver disease. Little guidance is available on drug dosing in hepatic impairment because these patients are often excluded from drug trials. Daily acetaminophen use should not exceed 2 g. Dietary supplements have not been well studied in hepatic impairment and cannot be recommended. 

Oral testosterone-replacement regimens can cause hepatotoxicity, ranging from mildly elevated hepatic transaminases to serious liver diseases (e.g., peliosis hepatitis, hepatocellular and intrahepatic cholestasis, and benign or malignant tumors). 

Liver disease may decrease hepatic metabolism resulting in enhanced responses to parent chemicals however, for many compounds, metabolism is only slightly impaired in moderate to severe liver disease. Disease-induced alterations in clearance and volume of distribution often act in opposite directions with respect to their effect on half-life. Bioavailability may be markedly increased in liver disease with portal/systemic anastomosis (the connection of normally separate parts so they intercommunicate) so that orally administered chemicals bypass hepatic first-pass metabolism. Altered receptor sensitivity has been observed for some chemical substances in liver cirrhosis. When liver tissue repair is inhibited by chemical co-exposure, even an inconsequential level of liver injury may lead to fulminating liver failure from a nonlethal exposure of hepatotoxic-ants. (Several articles, as reviewed by Dybing and Spderlund 1999.)... 

Naltrexone is contraindicated in acute hepatitis or liver failure. Carefully consider its use in patients with active liver disease in light of its hepatotoxic effects. 

Hepatotoxicity Itraconazole has been associated with rare cases of serious hepatotoxicity, including liver failure and death. Some of these cases had neither pre-existing liver disease, nor a serious underlying medical condition. If liver function tests are abnormal, discontinue treatment. In patients with raised liver enzymes or an active liver disease or who have experienced liver toxicity with other drugs, do not start treatment unless the expected benefit exceeds the risk of hepatic injury. In such cases, liver enzyme monitoring is necessary. 

The most commonly observed side effects are GI disturbances and nervous system symptoms, such as nausea, vomiting, headache, dizziness, and fatigue. Hepatitis is a major adverse effect, and the risk is highest in patients with underlying liver diseases and in slow isoniazid acetylators the rate of hepatotoxicity is increased if isoniazid and rifampin are combined. 

Gene expression inhibition. Chloroform/ methanol extract (1 1) of the dried leaf, in cell culture, was active on hepatoma-Cos-7, IC50 600.0 pg/mL vs TAT-dependent activation of HIV promoter hioassay - . Hepatotoxic activity. The leaf, taken orally by a female adult, was active - . A patient consumed 15 tablets of the leaf per day for 4 months. Approximately 1 year after stopping consumption, liver enzymes returned to normal and fatigue was no longer a complaint - ". Infusion of the dried leaf, taken orally by a female adult at variable doses, was active. The 60-year-old woman who took Lama tridentata for 10 months developed severe hepatitis for which no other cause could be found. Despite aggressive supportive therapy, the patient s condition deteriorated and required orthotropic liver transplantation - " . Dried leaves, administered orally to adults at variable doses, were active. A public warning has been issued by the US Centers for Disease Control based on reports of liver toxicity after use of Lama tridentata tea - " k Dried leaves, administered orally to adults of both sexes at variable doses, were active - ". The plant, administered orally to adults at variable doses, was active - ". Dried leaves, administered orally to adults at variable doses, were active. One case of hepatotoxicity induced by Larrea tridentata taken as a nutritional supplement was reported - ". Thirteen patients were identified for whom Larrea tridentata tincture for internal use was prescribed. Additionally, 20 female and three male patients were identified from whom an extract of Larrea tridentata in castor oil for... 

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