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Efficacy and Toxicity

4 Cell Specific Delivery of Anti-Inflammatory Drugs to Hepatic Cells [Pg.110]

9 Targeting of Anti-inflammatory Drags for the Treatment of Liver Fibrosis [Pg.110]

A pronounced alteration in the intrahepatic distribution of Nap was observed when Nap was coupled to mannosylated HSA as compared to Nap coupled to HSA. Coupling to Mauio-HSA resulted in a major shift in intrahepatic distribution from mainly SECs to mainly KCs [184]. [Pg.112]

One study has described the use of NSAID-loaded liposomes for the targeting of inflammatory lesion sites for the treatment of postoperative pain and pain related to various types of cancer [186]. In this study they showed strong and immediate analgesic effects in relieving pain with NSAID-loaded liposomes, but did not compare this with the analgesic effects of free NS AID. [Pg.112]


Identify a monitoring plan to assess for efficacy and toxicity of the recommended drug therapy. [Pg.58]

Monitor a patient taking hormone-replacement therapy for efficacy and toxicity. [Pg.765]

Select an appropriate drug to reduce serum uric acid levels in patients with gout, and outline a plan for monitoring efficacy and toxicity. [Pg.891]

Closely monitor patients for efficacy and toxicity while they are receiving hydroxyurea. Monitor mean corpuscular volume (MCV) because it increases as the level of HbF increases. If the MCV does not increase with hydroxyurea use, the marrow may be unable to respond, the dose may not be adequate, or the patient may be noncompliant.27 HbF levels also can be monitored to assess response. Assess blood counts every 2 weeks during dose titration and then every 4 to 6 weeks once the dose is stabilized. Temporary discontinuation of therapy is warranted if the hemoglobin level is less than 5 g/dL (50 g/L or 3.1 mmol/L), the absolute neutrophil count is less than 2000/mm3 (2 x 109/L), platelets are less than 80,000/mm3 (80 x 109/L), or reticulocytes are less than 80,000/mm3 (80 x 109/L) if the hemoglobin is less than 9 g/dL (90 g/L or 5.6 mmol/L). Monitor for increases in serum creatinine and transaminases. Once the patient has recovered, hydroxyurea may be restarted with a dose that is 2.5 to 5 mg/kg less than the dose associated with the patient s toxicity. Doses then may be increased by 2.5 to 5 mg/kg daily after 12 weeks with no toxicity. [Pg.1013]

Monitor for therapeutic response by assessing efficacy and toxicity of the antimicrobial regimen. [Pg.1031]

Develop a treatment plan including medication and a monitoring plan for both efficacy and toxicity. [Pg.1366]

Prepare a monitoring plan to evaluate the efficacy and toxicity of pharmacotherapy for oncologic emergencies. [Pg.1467]

A variety of species of laboratory animal are employed to study aerosol deposition for both efficacy and toxicity. It is important to recognize that the breathing parameters [17], not to mention the anatomy [18], of these animals differ substantially from humans. Table 3 shows a range of breathing parameters for several species of laboratory animal. Clearly there is a matter of scale involved in that small animals cannot generate the same airflow volumes as humans and to some extent compensate by increasing their respiratory rate. [Pg.485]

Ward et al. [130] studied the pharmacokinetics of (+)- and (—)-primaquine in the isolated perfused rat liver preparation. The perfusate plasma concentrations of primaquine in the isolated, perfused rat liver, declined biexponentially following the addition of either (+)- or (—)-primaquine at doses 0.5-2.5 mg in the perfusate reservoir. There were no differences between pharmacokinetic profiles of the two isomers at the 0.5 mg dose. By contrast, the elimination of (—)-primaquine was greater than (+)-primaquine when either was added in a dose of 2.5 mg also, the clearance of the (—)-isomer was greater, the half-life was shorter, and the area under the plasma concentration curve was shorter. The volume of distribution was similar for the two isomers. These results are relevant to both the therapeutic efficacy and toxicity of primaquine. [Pg.199]

Rininger JA et al. Differential gene expression technologies for identifying surrogate markers of dmg efficacy and toxicity. DDT 2000 5 560-568. [Pg.125]

Tokiyoshi K, Ohnishi T, Nii Y. 1991. Efficacy and toxicity of thromboxane synthetase inhibitor for cerebral vasospasm after subarachnoid hemorrhage. Surg Neurol 36 112-118. [Pg.90]


See other pages where Efficacy and Toxicity is mentioned: [Pg.132]    [Pg.33]    [Pg.332]    [Pg.190]    [Pg.103]    [Pg.140]    [Pg.470]    [Pg.293]    [Pg.1266]    [Pg.170]    [Pg.341]    [Pg.4]    [Pg.82]    [Pg.129]    [Pg.370]    [Pg.489]    [Pg.9]    [Pg.42]    [Pg.44]    [Pg.46]    [Pg.156]    [Pg.212]    [Pg.9]    [Pg.13]    [Pg.357]    [Pg.27]    [Pg.35]    [Pg.666]    [Pg.321]    [Pg.560]    [Pg.7]    [Pg.276]    [Pg.24]    [Pg.55]    [Pg.57]    [Pg.63]    [Pg.64]   


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