Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Liver disease follow

Cohen C, Frank AL Liver disease following occupational exposure to 1,1,1-trichloroethane A case report. Am J Ind Med 26 237-241, 1994... [Pg.694]

As stated at the beginning of this article, the liver is the most intensively studied animal tissue in biochemistry. In the context of the role of free radicals in human diseases, the liver is not obviously at centre stage, since heart disease and cancer are more important in the industrialized world than, for example, cirrhosis. Free-radical biochemistry of the liver will remain a fertile area of work, however, not least because so many original ideas and techniques are developed there and then applied to the study of other tissues. The increasing use of liver transplantation, following the acceptance of kidney and heart transplants as almost routine, will surely increase the interest in the study of ischaemia-reperfusion injury in... [Pg.243]

In contrast to chlordiazepoxide and diazepam, lorazepam and oxazepam are not metabolized into active compounds in the liver. Instead, they are excreted by the kidneys following glucuronidation. This is important because many alcohol-dependent patients have compromised liver function. Therefore, when treatment is initiated before the results of blood tests for liver function are known, as is often the case in outpatient clinics, lorazepam and oxazepam may be preferred. Patients with liver disease may still be treated with diazepam and chlordiazepoxide, but at lower doses. This can be accommodated with the loading technique, although hourly dosing with 5 mg of diazepam or 25 mg of chlordiazepoxide may be sufficient. [Pg.537]

Several clinically distinct forms of Wilson s disease have been described. Thus, a relatively mild, late-onset form of the disease, has been described in Jewish patients from Eastern Europe. These patients usually present with the neurologic signs of the disease. In contrast, the more common early-onset (childhood) forms of the disease often present first with liver problems, followed by neurologic manifestations. [Pg.774]

The most commonly used screening method for HIV is an enzyme-linked immunosorbent assay, which detects antibodies against HIV-1 and is both highly sensitive and specific. False positives can occur in multiparous women in recent recipients of hepatitis B, HIV, influenza, or rabies vaccine following multiple blood transfusions and in those with liver disease or renal failure, or undergoing chronic hemodialysis. False negatives may occur if the patient is newly infected and the test is performed before antibody production is adequate. The minimum time to develop antibodies is 3 to 4 weeks from initial exposure. [Pg.450]

Potentially, individuals with low activities of the enzymes phenol sulfotransferase and glucuronyl-transferase may be more susceptible to phenol toxicity. Persons with ulcerative colitis may have an impaired capacity to sulfate phenol (Ramakrishna et al. 1991), which may increase the amount of unchanged phenol that is absorbed following oral exposure. Neonates may also be more susceptible to toxicity from dermally-applied phenol because of increased skin permeability and proportionately greater surface area. A study in which 10-day-old rats were more sensitive to lethality following oral exposure to phenol than 5-week-old or adult rats (Deichmann and Witherup 1944) further suggests that the young may be more sensitive to phenol. (For a more detailed discussion please see Section 2.6.) Because phenol is a vesicant, individuals with sensitive skin or pulmonary incapacity may be more sensitive to phenol. Individuals with kidney or liver diseases that impair metabolism or excretion of phenol and phenol metabolites may be more susceptible to phenol. [Pg.140]

Hepatic function impairment Patients started on pyrazinamide should have baseline liver function determinations. Closely follow those patients with pre-existing liver disease or those at increased risk for drug-related hepatitis. Discontinue pyrazinamide and do not resume if signs of hepatocellular damage appear. [Pg.1721]

Chronic HCV- In combination with interferon alfa-2b injection for the treatment of chronic HCV in patients 3 years of age (oral solution) or 5 years of age (capsules) and older with compensated liver disease previously untreated with alpha interferon or in patients who have relapsed following alpha interferon therapy. Note Ribaspheres is only indicated in combination with interferon alfa-2b in patients 18 years of age and older. [Pg.1772]

Renai/Hepatic function impairment The safety and pharmacokinetics of rimantadine in renal and hepatic insufficiency only have been evaluated after single dose administration. In a single dose study of patients with anuric renal failure, the apparent clearance was approximately 40% lower and the elimination half-life was 1.6-fold greater than that in healthy controls. In a study of 14 people with chronic liver disease (mostly stabilized cirrhotics), no alterations in the pharmacokinetics were observed after a single dose of rimantadine. However, the apparent clearance of rimantadine following a single dose to 10 patients with severe liver dysfunction was 50% lower than that reported for healthy subjects. Because of the potential for accumulation of rimantadine and its metabolites in plasma, exercise caution when patients with renal or hepatic insufficiency are treated with rimantadine. [Pg.1785]

Patients with psoriasis or RA who have any of the following alcoholism, alcoholic liver disease, or other chronic liver disease overt or laboratory evidence of immunodeficiency syndromes preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia). [Pg.1972]

Clinical pharmacology. Following absorption, peak plasma concentrations occur 1-3 hours after oral administration (Franc et al. 1991). Following extensive hepatic metabolism, the bioavailability of nefazodone is between 15% and 23%, after which it is 99% protein bound. Nefazodone reaches steady-state plasma levels in 3 days and is eliminated from the body within 24 hours, reflecting its half-life of 2-4 hours (Franc et al. 1991). Therapeutic doses in young adults have been found to range from 100 to 300 mg twice daily (E. Fontaine 1994). Lower doses are recommended in patients with concomitant liver disease and the elderly, as plasma concentrations can be double those seen in younger patients. [Pg.216]

Hepatitis C virus (HCV) is an RNA virus that is a common cause of parenterally acquired viral hepatitis chronic infection follows acute infection in 80% to 85% of cases. Although liver disease resulting from chronic HCV infection is only slowly progressive, HCV is the most common cause of chronic liver disease in the United States, the most common etiology for hepatocellular carcinoma, and the leading indication for liver transplantation [34-36]. [Pg.181]

The initial steps in BA synthesis are characterised by the introduction of a hy-droxylic group in the la position, or in position 27, followed by another in the la position into the cholesterol nucleus. Both synthetic pathways (the neutral and the acidic pathways) possess a distinct microsomal 7-oxysterol hydroxylase, which is regulated by different genes. The most recently described disorder of BA synthesis is cholesterol 7a-hydroxylase deficiency, in which their decreased production through the classical pathway is partially balanced by activation of the alternative pathway. Cholesterol levels increase in the liver, with a consequent low-density lipoprotein hypercholesterolemia, and cholesterol gallstones may result, although there is no liver disease. In contrast, a defect in the conversion of 27-hydroxy-cholesterol to la,27-dihydroxy-cholesterol due to deficiency of the oxysterol 7a-hydroxylase specific for the alternate pathway, causes severe neonatal liver disease [8]. [Pg.610]

Selection from among several drugs depends upon host factors which include the following (1) concomitant disease states (eg, AIDS, severe chronic liver disease) (2) prior adverse drug effects ... [Pg.1170]


See other pages where Liver disease follow is mentioned: [Pg.898]    [Pg.1552]    [Pg.126]    [Pg.55]    [Pg.55]    [Pg.898]    [Pg.1552]    [Pg.126]    [Pg.55]    [Pg.55]    [Pg.601]    [Pg.277]    [Pg.425]    [Pg.747]    [Pg.1243]    [Pg.111]    [Pg.148]    [Pg.1386]    [Pg.10]    [Pg.79]    [Pg.79]    [Pg.629]    [Pg.547]    [Pg.20]    [Pg.303]    [Pg.26]    [Pg.443]    [Pg.455]    [Pg.267]    [Pg.139]    [Pg.1386]    [Pg.18]    [Pg.109]    [Pg.245]    [Pg.147]    [Pg.553]    [Pg.249]    [Pg.256]    [Pg.485]    [Pg.465]    [Pg.311]    [Pg.27]   
See also in sourсe #XX -- [ Pg.1808 ]




SEARCH



Liver diseases

© 2024 chempedia.info