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Acute viral hepatitis

For example, the elevated serum GPT seen in acute viral hepatitis is useful because it is many times greater than the normal range. [Pg.186]

There is no specific pharmacologic treatment for acute viral hepatitis A, B, C, D, or E only supportive care is available. [Pg.345]

Managing viral hepatitis involves both prevention and treatment. Prevention of hepatitis A and B (and indirectly for hepatitis D) can be achieved with immune globulin or vaccines. There is no specific pharmacologic treatment for acute viral hepatitis A, B, C, D, or E only supportive care is available. Individuals with mild to moderate symptoms rarely require hospitalization. Occasionally, hospitalization is required in individuals experiencing significant nausea, vomiting, diarrhea, and encephalopathy. Liver transplantation may be required in rare instances if fulminant hepatitis develops. [Pg.350]

There are no specific treatments for acute viral hepatitis and management is essentially supportive. Immuno-prevention is considered elsewhere. [Pg.632]

Moroz L, Paliy I (2006) Study of influence of detoxicant Enterosgel on chnical and laboratory indexes in acute viral hepatitis. In Medico-biological aspects of enterosorbent Enterosgel Use for therapy of different diseases, Kyiv (In Russian), pp 71-76... [Pg.217]

Glucocorticoid treatment in the early phase of acute viral hepatitis carries the risk of transition to chronic active hepatitis (SEDA-3, 308). [Pg.22]

Milk thistle has been used to treat acute and chronic viral hepatitis, alcoholic liver disease, and toxin-induced liver injury in human patients. Milk thistle has most often been studied in the treatment of alcoholic hepatitis and cirrhosis. In both of these disorders, outcomes have been mixed and reports include significant reductions in markers of liver dysfunction and in mortality, as well as no effect. In acute viral hepatitis, studies have generally involved small sample sizes and have shown mixed outcomes of improved liver function (eg, aminotransferase values, bilirubin, prothrombin time) or no effect. Studies in chronic viral hepatitis and toxin-induced injury have also been of small size but have reported mostly favorable results. Parenteral silybin is marketed and used in Europe as an antidote in Amanitaphalloides mushroom poisoning, based on favorable outcomes reported in case-control studies. [Pg.1543]

The liver function was also studied in patients with viral hepatitis. During the acute phase of the infection, the ASGP-receptor concentration was markedly decreased, but during the course of the disease receptor concentrations increased to normal values. This correlated well with other laboratory tests for liver function and thus again demonstrates the potential of this imaging technique in evaluating the condition of patients with acute viral hepatitis [271],... [Pg.226]

Francioni S, M Pastore, Alpha-fetoprotein and acute viral hepatitis type B, J. [Pg.535]

Blaschke TF, Meffin PJ, Melmon KL, et al. (1975) Influence of acute viral hepatitis on phenytoin kinetics and protein binding. Clin Pharmacol Ther 17 685-691. [Pg.127]

The half-life of paracetamol has been shown to be prolonged during acute viral hepatitis and in patients with severe chronic liver disease. Most studies were single-dose studies. One study looked at the pharmacokinetics of paracetamol (1 g) in ten patients with acute viral hepatitis (ALT increased at least tenfold and acute onset of symptoms) and 20 controls. In the hepatitis patients the paracetamol dose was given in both the acute phase and in the convalescence phase (approximately one month after complete biochemical recovery). At the time of the acute attack, peak concentrations of paracetamol did not differ significantly compared to the recovery phase, nor to the 20 controls. However, during acute hepatitis the half-life of paracetamol was significantly increased compared to the convalescent phase (3.2 h vs... [Pg.177]

Cirrhotic patients and those with acute viral hepatitis have experienced a doubling of the half-life of pethidine and a corresponding reduction in clearance compared to healthy subjects. [Pg.189]

Patients with cirrhosis and acute viral hepatitis may have a 50% reduction in pethidine clearance [63, 64]. In a single-dose study, 0.8 mg/kg of pethidine were given intravenonsly to eight healthy volunteers and ten patients with liver cirrhosis (nine alcohol induced, all with a history of varices and/or ascites). There was an approximate doubling of the half-... [Pg.196]

Another study using the same dose assessed pharmacokinetic parameters in 15 healthy volunteers and 14 patients with an acute exacerbation of viral hepatitis. None had significantly altered prothrombin times, but all had significantly raised transaminase levels. Similar alterations in pharmacokinetics were observed. Acute viral hepatitis increased the half-life from 3.37 hours to 6.99 hours (p<0.001) (range ... [Pg.197]

If the patient had acute viral hepatitis with significantly raised transaminases and a raised PT, an increase in the dosage interval of paracetamol should be considered as the clearance of paracetamol has been shown to be reduced by approximately 50% in these types of patients. [Pg.198]

Paracetamol could be considered in a patient with acute liver failure caused by something other than a paracetamol overdose. Normal therapeutic doses of paracetamol can be used, but it may be prudent to extend the dosing interval in all patients with acute liver failure because a reduced clearance has been demonstrated in patients with acute viral hepatitis and a prolonged PT. [Pg.206]

McHorse TS, Wilkinson GR, Johnson RF, et al. (1975) Effect of acute viral hepatitis in man on the disposition and elimination of meperidine. Gastroenterology 68 775-780. [Pg.210]

Acute viral hepatitis Other drugs/toxins Metabolic disorders Hypoxia/ischaemia... [Pg.304]

Principles of Clinical Pharmacology TABLE 7.1 Pharmacokinetics of Some Drugs during and after Acute Viral Hepatitis ... [Pg.78]

Difference in studies during and after recovery from acute viral hepatitis was significant at P < 0.05 by paired t-test. Protein binding results for individual patients were not given, so was estimated from average values. [Pg.78]

Pain on palpation mainly points to capsular tension as a result of an enlarged liver (acute viral hepatitis, fatty liver, congested liver). In general, the metastatic liver is likewise painful. Liver abscesses may cause (frequently severe) pain on tapping. The liver parenchyma itself is insensitive to pain, although pain receptors are found... [Pg.78]

Exanthemas are observed as prodromal skin symptoms in acute viral hepatitis (5-20% of cases). They can be manifested as urticaria, scarlatinoid or morbilliform exanthemas as well as varicella and erythematous multiform rashes. [Pg.84]

Acrodermatitis papulosa eruptiva infantum Gianotti-Crosti syndrome) can occur in children with acute viral hepatitis B. This is a lichenoid-papuloid skin rash on the face and limbs, which breaks out suddenly. These skin stigmata generally take 2-8 weeks to disappear.(s. p. 430)... [Pg.84]

Elevated iron, which usually corresponds to increased ferritin, is found primarily in idiopathic haemochromatosis and secondarily in acute viral hepatitis, liver cell necrosis and necrotic episodes, alcoholic liver diseases, porphyria cutanea tarda, oestrogen administration, etc. [Pg.99]

Acute viral hepatitis, acute hepatic damage T N... [Pg.102]

In acute viral hepatitis A, there is a marked increase in IgM during the course of 6-8 weeks and a subsequent slight increase of IgG. As of the 2 week of disease, the IgM level declines faster than the slightly elevated IgG level, with normalization of IgM after 4 weeks. A persistent elevation of IgM and IgG or a marked elevation of IgG is suggestive of persistent (protracted) hepatitis. Apart from an increase of IgM, acute viral hepatitis B and C are associated with a stronger and earlier increase in IgG than in viral hepatitis A. Normalization of IgG and IgM values occurs more slowly than in hepatitis A. Normal values of IgG are mostly reached only after 6 months. There are no differences between the icteric and the anicteric form. [Pg.111]


See other pages where Acute viral hepatitis is mentioned: [Pg.1130]    [Pg.73]    [Pg.208]    [Pg.330]    [Pg.93]    [Pg.23]    [Pg.88]    [Pg.245]    [Pg.43]    [Pg.524]    [Pg.104]    [Pg.177]    [Pg.41]    [Pg.77]    [Pg.77]    [Pg.95]    [Pg.95]    [Pg.96]    [Pg.97]    [Pg.97]   
See also in sourсe #XX -- [ Pg.112 , Pg.404 , Pg.413 ]




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