Fluoxetine continued

SSRIs Citalopram 10-30 mg fluoxetine 10-20 mg fluvoxamine 50 mg paroxetine 10-30 sertraline 25-150 mg all agents are given by mouth daily and can be dosed continuously or during the luteal phase only26 Sexual dysfunction (reduced libido, anorgasmia), insomnia sedation, hypersomnia, nausea, diarrhea... 

The first-line therapeutic options for PMDD include the selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, fluvoxamine, sertraline, paroxetine, and citalopram. These agents can be given either continuously or only during the luteal phase of the menstrual cycle, i.e., initiated at the time of ovulation and discontinued on the first day of menses. 

Antidepressants. Short-term studies of desipramine and fluoxetine indicate that both medications reduce binging in patients with BED. In addition, fluoxetine-treated patients may also experience a modest reduction in weight during short-term treatment. However, this early weight loss with fluoxetine may not be sustained despite continued treatment. 

Michelson D, Pollack M, Lydiard RB, Tamura R, Tepner R, Tollefson G (1999) Continuing treatment of panic disorder after acute response randomised, placebo-controlled trial with fiuoxetine. The Fluoxetine Panic Disorder Study Group. Br J Psychiatry 174 213-218... 

A 17-year-old with major depressive disorder is treated with fluoxetine at 40 mg/d. She has a ligament injury while playing soccer. Fluoxetine is discontinued 5 days before surgery. After surgery, she is given oxycodone and continues to complain of pain. 

Loof et al. (1995) reported the use of carbamazepine (300-1200 mg/day, serum levels 10-11.5 pg/mL) in 28 children and adolescents with sexual abuse histories. By treatment end, 22 of 28 patients were asymptomatic of PTSD. The remaining six were significantly improved in all PTSD symptoms except for continued abuse-related nightmares. Half of this cohort had com-orbid ADHD, depression, ODD or polysubstance abuse and were treated with concomitant medications, e.g., methylphenidate, clonidine, sertraline, fluoxetine, or imipramine. 

Relapse prevention with medication has been studied in BN as well as AN. In 1991 Walsh et al. placed bulimics who had a 50% or more reduction in binge eating on desipramine in maintenance treatment. About half of the patients relapsed below the 50% reduction within 4 months, despite continued use of the medication. In a second multicenter collaborative study examining the efficacy of fluoxetine maintenance in bulimic patients who had responded to the drug with a 50% reduction of symptoms, the patients who were maintained on the active drug were significantly less likely to relapse than those who were switched to placebo at the end of the acute treatment phase (Romano, 1999). 

In more recent years the tricyclic anhdepressants have lost their position as the mainstay of therapy for depression and have been gradually supplanted by the selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine. The tricyclics, however, do continue to be valuable in the management of chronic pain states such as headache or neuropathy. 

Several trials have been performed with antidepressants in the prevention of recurrence of major depression. In an exemplary trial of this kind, Reimherr et al. (1998) explored the optimal length of therapy in a long-term, placebo-controlled continuation study of patients who had responded to 12 14 weeks of open-label fluoxetine treatment (20mg/day) for major depression. Different maintenance schedules were represented by four treatment arms ... 

A larger set of placebo-controlled studies show conclusively that imipramine is also effective for the treatment of panic disorders. Other agents shown to be effective in panic disorders include the SSRIs paroxetine, sertraline, fluvoxamine, fluoxetine and citalopram. Generally, initial treatment of moderate to severe panic disorders may require the initiation of a short course of benzodiazepines e.g. clonazepam (0.5 1 mg twice daily), and an SSRI. The patient will obtain immediate relief from panic attacks with the benzodiazepine whereas the SSRI may take 1 6 weeks to become effective. Once a patient is relieved of initial panic attacks, clonazepam should be tapered and discontinued over several weeks and SSRI therapy continued thereafter. There are no pharmacological treatments available for specific phobias, however controlled trials have shown efficacy for several agents, e.g. phenelzine, moclobemide. clonazepam, alprazolam, fluvoxamine. sertraline and paroxetine in the treatment of social phobia (Roy-Byrne and Cowlev, 2002). 

Reimherr, F.W., Amsterdam, J.D., Quitkin, F.M., et al. Optimal length of continuation therapy in depression a prospective assessment during long-term fluoxetine treatment. Am. J. Psychiatry 155, 1247-1253, 1998. 

The majority of positive studies have found that later generation antidepressants, especially those with strong serotonergic effects, are effective and may have a more rapid onset of action when used for PMDD (27). Thus, studies with SSRIs (e.g., fluoxetine, sertraline), nefazodone, venlafaxine, and clomipramine have all shown promise. In several studies, luteal phase dosing has been as effective or more effective than continuous dosing in women with PMDD. 

Approximately 5% of women in the child-bearing years will have prominent mood and physical symptoms during the late luteal phase of almost every cycle these may include anxiety, depressed mood, irritability, insomnia, fatigue, and a variety of other physical symptoms. These symptoms are more severe than those typically seen in premenstrual syndrome (PMS) and can be quite disruptive to vocational and interpersonal activities. The SSRIs are known to be beneficial to many women with PMDD, and fluoxetine and sertraline have been approved for this indication. Treating for 2 weeks out of the month in the luteal phase may be as effective as continuous treatment. The rapid effects of SSRIs in PMDD may be associated with rapid increases in pregnenolone levels. 

Over the past decade there has been a substantial improvement in the ability to predict metabolism-based in vivo drug interactions from kinetic data obtained in vitro. This advance has been most evident for interactions that occur at the level of cytochrome P450 (CYP)-catalyzed oxidation and reflects the availability of human tissue samples, cDNA-expressed CYPs, and well-defined substrates and inhibitors of individual enzymes. The most common paradigm in the prediction of in vivo drug interactions has been first to determine the enzyme selectivity of a suspected inhibitor and subsequently to estimate the constant that quantifies the potency of reversible inhibition in vitro. This approach has been successful in identifying clinically important potent competitive inhibitors, such as quinidine, fluoxetine, and itraconazole. However, there is a continuing concern that a number of well-established and clinically important CYP-mediated drug interactions are not predictable from the classical approach that assumes reversible mechanisms of inhibition are ubiquitous. 

Slater et al., from the Eli Lilly Research Labs, published an article in 1978 concerning the inhibition of REM sleep in cats. Disruption of REM sleep can cause emotional disturbances. The Eli Lilly researchers reported that they were at a loss to explain why cats receiving fluoxetine for several days began to hiss and growl or why this behavior decreased with continued treatment. ... 

A 44-year-old man with depression was given hydroxyzine hydrochloride 100 mg/day, clonazepam 2 mg/ day, and citalopram 20 mg/day. Two years before he had tolerated fluoxetine for 6 months for an episode of depression, with good effect. After 7 weeks he developed weakness and weight loss. Physical examination was normal but the serum aspartate transaminase (AsT) was raised at 277 IU/L (reference range < 36 IU/1). His bilirubin was normal. Citalopram was withdrawn and the other drugs were continued intermittently 5 days later the serum aspartate transaminase had fallen by a half, and within 2 months it had returned to normal. 

Clozapine and SSRIs are often used together, because depressive syndromes are common in patients with schizophrenia. Clozapine carries a relatively high risk of agranulocytosis, but this adverse effect is very rarely seen with SSRIs, although a case of possible fluoxetine-induced neutropenia has been described (SEDA-22, 15). Two cases in which the addition of paroxetine to clozapine was associated with neutropenia have been reported (11). The patients had been taking stable doses of clozapine for 6-12 months and had previously tolerated other SSRIs without adverse hematological consequences. In both cases the white cell count recovered when clozapine was withdrawn, although paroxetine was continued. 

A 48-year-old woman developed anxiety, tremor, depression, dry mouth, nausea, and marked weight loss (503). Physical examination, electrocardiography, chest X-ray, CT scan, and laboratory investigations were unremarkable. The Hamilton D score was 44 for 17 items. She had taken mefloquine 250 mg/week for 8 weeks for malaria prophylaxis, and after 2 weeks had started to feel unwell, with dysphoria, depression, and weakness. She was given fluoxetine 20 mg/day and alprazolam 1.5 mg/day. Her condition continued to deteriorate. The dose of fluoxetine was increased to 40 mg/day and flunitrazepam was added. She was later instead given milnacipran, a serotonin and noradrenaline reuptake... 

---