Optimal dose rate

Treatment should begin as early as possible in patients with a diagnosis of AD.30 Figure 32-2 provides a recommended treatment algorithm for AD.31 Patients should be switched to another ChE inhibitor from their initial ChE inhibitor if they show an initial lack of efficacy initially respond to treatment, but lose clinical benefit or experience safety/tolerability issues. This switch should not be attempted until the patient has been on a maximally tolerated dose for a period of 3 to 6 months. The switch should also be based on realistic expectations of the patient and/or caregiver.32 ChE inhibitor therapy should be discontinued in patients who experience poor tolerance or compliance, who show a lack of clinical improvement after 3 to 6 months at optimal dosing, who continue to deteriorate at the pretreatment rate, or who demonstrate dramatic clinical deterioration following initiation of treatment.33... 

Once a tolerated agent is found, continue that therapy until poor tolerance or compliance occurs, no clinical improvement is seen with 3 to 6 months of optimal dosing, or the pretreatment deterioration rate continues. Inform the patient and the caregiver that the treatments available for Alzheimer s disease are not curative, but may slow the deterioration rate of the patient. 

From a technical point of view, intensity-modulated radiation therapy (IMRT) optimizes several parameters selection of multiple beams and, for each beam, optimization of dose, dose rate, size and shape, etc. Tomotherapy optimizes the dose distribution by IMRT in successive sections with immediate verification gamma knife, cyberknife, and radiosurgery concentrate high radiation doses in well-defined small volumes. 

CYP2C19 genotype status is determined before treatment, an optimal dose of a PPI may be prescribable on the basis of phar-macogenetic or pharmacogenomic status. This predetermined strategy should increase the eradication rates of H. pylori achieved by the initial treatment... [11]. 

As discussed later in this chapter, optimal dosing of these medications requires TDM at least once early in treatment to adjust for the substantial, primarily genetically determined differences in the elimination rate of these drugs, even in physically healthy individuals. Generally, repeat monitoring is only done for cause, such as the following ... 

Controlled dissolution/release By these means, it is possible to optimize the rate of delivery of the drug to improve therapy, to reduce the frequency of dosing, and to aid patient compliance. 

Figure 7.13 shows similar dependence for a fixed dose rate but varying the temperature (F centre mobility). As it is expected from equation (7.2.14), the higher the temperature, the more intensive defect recombination is and thus the lower the saturation concentration. Curve 3 in Fig. 7.13(b) confirms once more that T 100°C is the optimal aggregation temperature for a given dose rate of 1017 cm-3 s-1 whereas at higher temperatures a portion of F2 centres decreases. 

Typical doses are in the range of 2.5-5 i.u. per mouse. Optimal dose varies by strain, age, and weight of the mouse. Extending the oocyte collection window beyond 14 h post-hCG may reduce fertilization rates and compromise embryo quality due to oocyte aging. 

Mobilization of edema (weight loss) and lowering of heart rate are simple but decisive criteria for achieving optimal dosing. If ATPase activity is inhibited too much, K+ and Na+ homeostasis is disturbed the membrane Luellmann, Color Atlas of Pharmacology All rights reserved. Usage subject to terms... 

The mean values of and within the population are 4mg/L and 7mg/kg/day, respectively. The variation within the population is also depicted in Fig. 6, where 50% of the population has K a and Em values within the innermost circle, 75% within the second circle, and so on. With the help of this graph, the suitable dosing rate of phenytoin for an individual patient can be determined. With two plasma concentrations at two different dosing rates of phenytoin in one patient, his/her individual and values can be obtained to further optimize the dosing schedule. 

As with ALL, the goal of remission induction for AML is to rapidly induce a CR. Compared to ALL, however, fewer patients with AML achieve CR. Since the CR rate in AML is related to the intensity of the remission induction regimen, the drugs used in AML are given at doses that uniformly cause severe marrow hypoplasia (except tretinoin). One reason for the lower CR rate in AML as compared to ALL is the inability to give optimal doses of chemotherapy because of marrow toxicity. With continued improvement of supportive care for patients... 

---