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Tion losses and rendering them too cumbersome for routine clinical use 5, 6 ; . In most published HPLC methods 7, 10 ; liquid-solid chromatography normal phase ; on silica columns is used, with an aliphatic amine in the eluent to decrease chemisorption, which causes peak tailing. This leads to early deterioration of column efficiency owing to gradual dissolution of the silica packing at pH values above 7. Also, the predominantly hydrophilic endogenous plasma components and extraneous polar substances in the crude extracts have a high affinity for the polar packing material, causing background interferences and necessitating long intervals for column recovery in between injections, or heated column compartments 10 ; . For these reasons the use of reversed-phase HPLC is preferred for clinical routine applications. The few reversed-phase methods suitable for application in the clinical laboratory are generally limited to the analysis of one specific tricyclic drug and its metabolite s ; 11, 12 ; .The applicablility of high-speed ionpair partition chromatography to the separation of tricyclic tranquilizers and antidepressants was first studied by Knox and Jurand 13 ; , who paired the tricyclic amines with perchlorate ion adsorbed to the surface of a silica stationary phase and eluted the ion-pairs with eluents containing dichloromethane and a higher aliphatic alcohol. We have developed a reversed-phase method with use of ion-pairing with pentanesulfonic acid, permitting the simultaneous quantitative analysis of doxepin, amitriptyline, nortriptyline, imipramine, and desipramine under routine clinical conditions, and have applied this procedure for monitoring the concentrations of tricylic drugs and their metabolites in the serum of depressed in-hospital patients. Small crossover trial N 38 ; , desipramine was compared with amitriptyline for treatment of DPNP.18 Mean dosages of each drug were 105 mg d for amitriptyline and 111 mg d for desipramine. Moderate or greater relief of pain was reported by 28 74% ; of 38 patients during treatment with amitriptyline and 23 61% ; of 38 patients during treatment with desipramine. The difference between the 2 treatments was not significant, and desipramine was better tolerated. Nortriptyline, another TCA, combined with fluphenazine was found to be equivalent to the anticonvulsant carbamazepine for treatment of DPNP in a crossover study with 16 patients.19 The adverse effects of TCAs are fairly predictable and mostly anticholinergic in nature; they include dry mouth, constipation, dizziness, blurred vision, cardiac arrhythmias, and urinary retention. The tertiary amine TCAs amitriptyline, imipramine, and clomipramine ; are associated with more severe effects, including extreme sedation and orthostatic hypotension, limiting their usefulness in many patients. Amitriptyline has the highest affinity for the muscarinic cholinergic ; receptors, followed by clomipramine, doxepin, imipramine, nortriptyline, and desipramine.14 Amitriptyline is contraindicated for older patients and patients with any cardiovascular disease because it has been shown to prolong QT intervals. A retrospective cohort study that included 1.28 million person-years of follow-up for subjects aged 15 to 84 years identified an excess number of sudden cardiac deaths associated with TCAs, particularly at higher doses which may result if more medication than is prescribed is taken but not necessarily at the lower doses used for the management of pain ; .20 The rate ratio for patients taking the equivalent of 300 mg d of amitriptyline was 2.53 compared with 0.97 for patients taking less than 100 mg d. The analgesic efficacy of TCAs for patients with DPNP must be weighed against the adverse events associated with these agents. Little difference in efficacy was seen among the agents in a systematic review, and agents with the lowest risk of adverse events eg, desipramine ; should be considered before agents that produce more adverse effects are used eg, amitripty.

Context.--Depression and ischemic heart disease often are comorbid conditions and, in patients who have had a myocardial infarction, the presence of depression is associated with increased mortality. Patients with heart disease need a safe and effective treatment for depression. Objective.--To compare the efficacy, cardiovascular effects, and safety of a specific serotonin reuptake inhibitor, paroxetine, with a tricyclic antidepressant, nortriptyline hydrochloride, in depressed patients with ischemic heart disease. Design.--Two-week placebo lead-in followed by a double-blind randomized 6week medication trial. Setting.--Research clinics in 4 university centers. Patients.--Eighty-one outpatients meeting Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria for major depressive disorder and with documented ischemic heart disease. Interventions.--Treatment with either paroxetine, 20 to 30 mg d, or nortriptyline targeted to a therapeutic plasma level, 190 to 570 nmol L 50-150 ng mL ; , for 6 weeks. Main Outcome Measures.--For effectiveness of treatment, a decline in the score of the Hamilton Rating Scale for Depression by 50% and final score of 8 or less; for cardiovascular safety, heart rate and rhythm, supine and standing systolic and diastolic blood pressures, electrocardiogram conduction intervals, indexes of heart rate variability, and rate of adverse events. Results.--By intent-to-treat analysis, 25 61% ; of 41 patients improved during treatment with paroxetine and 22 55% ; of 40 improved with nortriptyline. Neither drug significantly affected blood pressure or conduction intervals. Paroxetine had no sustained effects on heart rate or rhythm or indexes of heart rate variability, whereas patients treated with nortriptyline had a sustained 11% increase in heart rate from a mean of 75 to beats per minute P .001 ; and a reduction in heart rate variability, as measured by the SD of all normal R-R intervals over a 24-hour period, from 112 to 96 P .01 ; . Adverse cardiac events occurred in 1 2% ; of patients treated with paroxetine and 7 18% ; of 40 patients treated with nortriptyline P .03 ; . Conclusions.--Paroxetine and nortriptyline are effective treatments for depressed patients with ischemic heart disease. Nortriptylone treatment was associated with a significantly higher rate of serious adverse cardiac events compared with paroxetine.
Blood levels of amitriptyline plus nortriptyline greater than 95 to 160 ng mL are ineffective. 5. Secondary amines a. Desipramine Norpramin ; is an active metabolite of imipramine. Desipramine differs from the tertiary amines in that it is much more selective in its properties of norepinephrine blockade than in its properties of serotonin reuptake blockade. It tends to have much less sedative and anticholinergic side effects. It does, however, share the side effect of orthostatic hypotension. The usual starting dose of desipramine is 25 mg daily. b. Noryriptyline Aventyl ; is an active metabolite of amitriptyline. Like desipramine, nortriptyline has significantly more effects on norepinephrine than on serotonin receptors. Although nortriptyline has fewer sedative and anticholinergic side effects than the tertiary amines, it has slightly more than desipramine. It is distinctly different from desipramine in that it has very little orthostatic hypotensive effects. Nortriptylkne is twice as potent as the other cyclic antidepressants. The starting dose is typically 25 mg daily. 6. Cardiac testing. Before initiating treatment with any of the cyclic antidepressants, patients must be screened for cardiac conduction system disease, which precludes the use of these medications. Patients over age 40 years should have a baseline electrocardiogram ECG ; . D. Venlafaxine Effexor ; is a phenylethylamine and is structurally distinct from existing antidepressants. It is a potent inhibitor of serotonin reuptake and an inhibitor of norepinephrine reuptake. Venlafaxine is metabolized in the liver to O-desmethylvenlafaxine, an active metabolite. The t 1 2 the parent compound plus the active metabolite is 11 hours. There is a slow-release form that allows for once-daily dosing. Venlafaxine is excreted by the kidney, and food does not affect its absorption. Venlafaxine is a weak inhibitor of the p450 2D6 enzyme, but it tends to not interact with most coadministered medications except MAOIs ; . 1. Dosing for the immediate-release form of venlafaxine typically begins at 37.5 mg twice daily. The medication can be increased by 75 mg every four days to a maximum dose of 375 mg daily in three divided doses. The extended-release form of venlafaxine is given as a single-morning dose of 37.5 mg. If this is well tolerated, the dose is increased to 75 mg in a single daily dose. The medication can be increased by 75 mg every four days to a recommended maximum of 225 mg daily in a single-daily dose. 2. The most common side effects of venlafaxine are nausea, dizziness, insomnia, sedation, and constipation. It can also induce sweating in some patients. Venlafaxine may cause blood pressure increases. Three to 7 percent of patients have mild blood pressure elevations average 1 to 2 Medications that inhibit CYP2D6 can increase the plasma level of venlafaxine. This is sometimes encountered when switching a patient from an SSRI with CYP2D6 inhibiting properties eg, fluoxetine, paroxetine ; to venlafaxine. Venlafaxine overdose is more serious than overdose with SSRIs. Venlafaxine is more likely to cause seizures than tricyclic antidepressants. Rates of serotonin toxicity were also higher with venlafaxine than with tricyclic antidepressants. Venlafaxine should be avoided in patients who are at high risk for deliberate overdose. 3. Patients who do not respond to other antidepressants may respond better to venlafaxine, and venlafaxine may be less likely to lose efficacy over time than other antidepressants. Venlafaxine may be more likely to lead to a remission of depression. E. Duloxetine Cymbalta ; is an inhibitor of both serotonin reuptake and norepinephrine reuptake. 1. Duloxetine is metabolized in the liver and should not be administered with hepatic insufficiency. Metabolites are excreted in the urine, and the use of duloxetine is not recommended in end-stage renal disease. Food delays the absorption of duloxetine, and the t 1 2 hours. Duloxetine is a moderate inhibitor of CYP2D6. 2. Dosage is 20 mg twice daily or 60 mg daily either as a single dose or as 30 mg twice daily. Start at 30 mg daily and increase to 60 mg daily; there may be added benefit to using up to 120 mg daily. 3. Nausea, dry mouth and constipation are common. Diarrhea and vomiting are seen less often. Insomnia, dizziness, somnolence, and sweating occur. Sexual side effects occur, but may be less common than with the SSRIs. Duloxetine is marketed as a treatment for physical pain associated with depres.
The maximum quantity for pharmacy purchased medications is 34-day supply at retail pharmacy, 90-day supply through mail order. Some medications may be limited by quantity rather than day supply. Some medications may require preauthorization by the health plan. Compound medications are only covered when one ingredient is a federal legend or state restricted medication and pamelor.
K0277 K0278 K0279 K0280 Skin barrier; solid 4x4 or equivalent, standard wear, with built-in convexity, each Deleted eff. 12 31 1999 ; Skin barrier; with flange solid, flexible or accordion ; , standard wear, with built-in convexity, any size, each Deleted eff. 12 31 1999 ; Skin barrier; with flange solid, flexible or accordion ; , extended wear, with built-in convexity, any size, each Deleted eff. 12 31 1999 ; Extension drainage tubing, any type, any length, with connector adaptor, for use with urinary leg bag or urostomy pouch, each Deleted eff. 12 31 2000 ; Lubricant, individual sterile packet, for insertion of urinary catheter, each Deleted eff. 12 31 2000 ; Water, distilled, 1000 ml, used with large volume nebulizer Deleted eff. 12 31 1994 ; Saline solution, per 10 ml, metered dose dispenser, for use with inhalation drugs Deleted eff. 12 31 2000 ; External infusion pump, mechanical, reusable, for extended drug infusion Deleted eff. 12 31 1999 ; Repair of prosthetic device, labor component, per 15 minutes Deleted eff. 12 31 1996 ; Adhesive skin support attachment for use with external breast prosthesis, each Deleted eff. 12 31 1999 ; For diabetics only, deluxe feature of off-the shelf depth inlay shoe or custom molded shoe, per shoe Deleted eff. 12 31 1999 ; Gauze, non-impregnated, sterile, pad size 16 sq. in. or less, without adhesive border, each dressing Deleted eff. 12 31 1996 ; Gauze, non-impregnated, sterile, pad size more than 16 but less than or equal to 48 sq. in., without adhesive border, each dressing Deleted eff. 12 31 1996 ; Gauze, non-impregnated, sterile, pad size more than 48 sq. in., without adhesive border, each dressing Deleted eff. 12 31 1996 ; Gauze, elastic, sterile, all types, per linear yard Deleted eff. 12 31 1996 ; Gauze, non-elastic, sterile, per linear yard Deleted eff. 12 31 1996 ; Urinary catheter anchoring device, adhesive skin attachment Deleted eff. 12 31 2000 ; Urinary catheter anchoring device, leg strap Deleted eff. 12 31 2000 ; Sterile water irrigation solution, 1000 ml Deleted eff. 12 31 2000.

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