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FDA Safety Labeling Changes: Strattera, Antidepressants [Jul. 15th, 2008|11:53 am]

FDA Safety Labeling Changes: Strattera, Antidepressants

Yael Waknine

May 11, 2005 — The U.S. Food and Drug Administration (FDA) approved in February revisions to safety labeling to advise that use of atomoxetine HCl may be linked rarely to severe liver injury, and that use of drugs approved to treat major depressive disorder is associated with an increased risk of suicidality in children and adolescents.

Atomoxetine HCl (Strattera) Linked Rarely to Severe Liver Injury

On Feb. 14, the FDA approved revisions to the safety labeling for atomoxetine HCl capsules (Strattera, made by Eli Lilly and Co.) to warn of the risk of severe liver injury associated with its use.

The FDA has received two reports of severe liver injury and jaundice in the absence of other explanatory factors in patients receiving atomoxetine. In one patient, elevated levels of hepatic enzymes (up to 40 times the upper limit of normal [ULN]) and bilirubin (up to 12 times the ULN) recurred upon rechallenge. Both patients recovered upon discontinuation of therapy without requiring liver transplantation.

The FDA notes that such reactions may occur several months after therapy initiation, and laboratory abnormalities may continue to worsen for several weeks after discontinuation. Due to probable underreporting, the true incidence of these adverse events remains unknown.

In a small percentage of patients, the FDA warns, severe drug-related liver injury may progress to acute liver failure resulting in death or the need for liver transplantation.

Liver enzyme levels should be immediately evaluated in patients receiving atomoxetine who present with signs or symptoms of liver dysfunction such as pruritus, dark urine, jaundice, right upper quadrant tenderness, or unexplained "flu-like" symptoms. Therapy should be discontinued permanently in patients with jaundice or laboratory evidence of liver injury.

Atomoxetine HCl is indicated for the treatment of attention deficit/hyperactivity disorder.

Antidepressant Use in Children, Adolescents Linked to Increased Risk of Suicidality

On Feb. 18, the FDA approved revisions to the safety labeling for drugs approved to treat major depressive disorder (MDD), warning of the increased risk of suicidal thinking and behavior (suicidality) associated with their use in children and adolescents.

Pediatric patients with MDD may experience worsening of their depression and/or emergence of suicidal ideation and behavior or unusual changes in behavior until significant remission occurs — regardless of whether antidepressants are being taken.

The warning was based on a pooled analysis of data from 24 short-term (up to four months), placebo-controlled trials of nine antidepressant drugs (selective serotonin reuptake inhibitors [SSRIs] and others) in more than 4,400 children and adolescents with MDD, obsessive-compulsive disorder (OCD), or other psychiatric disorders.

The analysis revealed that treatment with antidepressants significantly increased the mean risk of adverse events representing suicidality in this population compared with placebo (4% vs 2%), and that this risk was greater during the first few months of treatment. No suicides occurred in any of the trials.

It is unknown whether the suicidality risk in pediatric patients extends to longer-term use (beyond several months) or to adults.

The FDA advises use of antidepressants in children and adolescents only when the potential benefit outweighs the increased risk of suicidality. Pediatric patients receiving antidepressant therapy should be monitored closely for clinical worsening, suicidality, and unusual changes in behavior — particularly during the initial few months of therapy and when dose changes.

Monitoring should include weekly face-to-face contact with patients or their family members/caregivers during the first month of treatment, then contact every other week for the next month, once at three months, and thereafter as clinically indicated.

Similar monitoring is recommended for adults with MDD or comorbid depression in the setting of another psychiatric illness being treated with antidepressants. The FDA notes that consideration should be given to changing or discontinuing the therapeutic regimen in patients with persistently worsening depression or suicidality that is newly emergent, severe, or abrupt in onset.

The warning applies to safety labeling for citalopram HBr tablets and oral solution (Celexa, made by Forest Laboratories, Inc.); duloxetine HCl delayed-release capsules (Cymbalta, made by Eli Lilly and Co.); venlafaxine HCl tablets and extended-release tablets (Effexor and Effexor XR, made by Wyeth Pharmaceuticals, Inc.); and escitalopram tablets and oral solution (Lexapro, made by Forest Laboratories, Inc.).

The warning also applies to safety labeling for phenelzine sulfate tablets (Nardil, made by Pfizer Pharmaceuticals); fluoxetine HCl tablets, capsules, and oral solution (Prozac, made by Eli Lilly and Co.); fluoxetine HCl capsules (Sarafem, made by Eli Lilly and Co.); doxepin HCl capsules and oral concentrate (Sinequan, made by Pfizer Pharmaceuticals); olanzapine plus fluoxetine HCl capsules (Symbyax, made by Eli Lilly and Co.); and sertraline HCl tablets and oral concentrate (Zoloft, made by Pfizer Pharmaceuticals).

The FDA notes that only fluoxetine is approved for use in treating MDD in pediatric patients. Drugs approved for treating pediatric OCD include fluoxetine, sertraline, fluvoxamine maleate (Luvox, made by Solvay Pharmaceuticals), and clomipramine HCl (Anafranil, made by Mallinckrodt, Inc.). None of the drugs are approved for other pediatric psychiatric indications.

Reviewed by Gary D. Vogin, MD
This is a part of article FDA Safety Labeling Changes: Strattera, Antidepressants Taken from "Discount Prozac Fluoxetine" Information Blog

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Do Randomized Controlled Trials Always Trump Case Reports? [Jul. 10th, 2008|11:51 am]


We identified 260 references. Table 1 lists the search results. Case Reports

Twenty-four case reports or series described an association between a β-blocker and depression.[3-11,19,23-29] Two reports involved two β-blockers.[5,23] For each report, the Naranjo scores never differed by more than 1 point, and discrepancies were easily resolved. Naranjo scores were 0 for one case report, 1–4 for 11 reports, and 5 or higher for 12. Nine of these 12 reports involved propranolol,[5,19,23-25] two were associated with timolol,[7,8] and one was associated with nadolol.[9] In four of the nine cases, the patient had a history of depression.

Three examples illustrate the persuasiveness of some case reports. In these cases, depression began soon after the dosage of a β-blocker was increased, it subsided when the dosage was reduced, and it resumed after the dosage was increased to the level initially associated with symptoms.

In the first case, the patient was a 33-year-old woman who had no history of psychiatric conditions or evidence of depression on psychiatric examination.[24] During 2 months of treatment with propranolol 80 mg/day for ventricular arrhythmia, she developed depressive symptoms. The symptoms increased in severity within 14 days after the dosage was increased to 120 mg/day. When propranolol was switched to placebo, the symptoms improved within 8 days. Four months later, propranolol was restarted at a dosage of 40 mg/day. The patient had depressive symptoms as the dosage increased and asked for the drug to be discontinued. The Naranjo score in this case was 8.

In the second case, the patient was a 42-year-old woman without a history of mental illness who was prescribed propranolol 80 mg/day for hypertension.[25] Depressive symptoms began within 1 month of the start of treatment and worsened for 2 months. The dosage was decreased to 40 mg/day, and within 8 days, the patient's symptoms resolved. The Naranjo score was 7.

In the third case, the patient was a 62-year-old man who had a family history of depression and a depressive episode 36 years before his presentation.[23] He began having low-grade depression when he took propranolol irregularly over 5 years. His symptoms progressed to major depression when he took the drug as prescribed. The symptoms resolved when propranolol was discontinued, and major depression began again 2 weeks after the therapy was restarted months later. Treatment was discontinued, and his symptoms resolved within 1 week. The Naranjo score was 6.Randomized Controlled Trials

Table 2 describes eight randomized controlled trials of β-blockers in which depression was reported as an outcome.[30-39] Three groups evaluated propranolol,[30-32,38] and five evaluated sotalol, atenolol, pindolol, metoprolol, carvedilol, or bucindolol.[33-37,39]

One study showed that propranolol was significantly associated with an increased rate of depression (p < 0.05).[30] In another study, the rate with propranolol increased 24–30% depending on the measure of depression used, but the difference was not statistically significant.[32] Sotalol significantly increased depressive symptoms (p < 0.05),[33] whereas bucindolol significantly decreased symptoms (p < 0.01).[37] Atenolol increased symptoms of depression, but the association was not statistically significant.[34] A striking feature in the comparison of these studies (and the comparison of the three studies that evaluated propranolol) is that the depression rates in the control groups varied substantially—0–40%—and this variation was statistically significant (p < 0.0001). An equally large variation was observed in the treatment groups.

Several factors could have influenced the rate of depression and the association between depression and the β-blocker. An important factor was the method for ascertaining depression. As shown in Table 2 , patients were asked about depression in a number of ways in some studies, whereas in others, they had to report the information without prompting, or an investigator had to suspect the depression. One group used the Center for Epidemiological Studies Depression Scale and the Beck Depression Inventory.[32] Accuracy of the assessment clearly influences researchers' ability to detect an effect of a β-blocker on depression. No evidence suggests that depression rates depended on where the trial was conducted—North America, Britain, or Scandinavia.

Other factors that may have influenced the apparent effect of propranolol or other β-blockers on depression was the timing of the assessment of depression and the patient selection criteria. In general, case reports showed that depression occurred soon after the dosage of propranolol was increased. In four of nine case reports about propranolol with a Naranjo score of 5 or higher, patients had had a previous depressive episode. However, in the study of propranolol in which standardized instruments were used, depression was assessed only at baseline and at 12 months after treatment, and the investigators excluded patients who were likely to be most susceptible to depression (e.g., previous use of an antidepressant).

Although depression might have caused patients to drop out of the studies, none of the researchers noted that they assessed the patients for depression during their early-termination visits.  Printer- Friendly Email This

Pharmacotherapy.  2006;26(2):162-167.  ©2006 Pharmacotherapy Publications
This is a part of article Do Randomized Controlled Trials Always Trump Case Reports? Taken from "Discount Prozac Fluoxetine" Information Blog

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Bipolar Disorder: An Expert Interview With Stephen M. Stahl, MD, PhD [Jul. 3rd, 2008|12:47 pm]

Editor's Note:

The pharmacotherapy of patients with bipolar disorder is sometimes very challenging for the psychiatrist or primary care provider. The number of available medication options continues to expand, but knowing how and when to apply them requires knowledge and skill. On behalf of Medscape, Randall F. White, MD, FRCPC, obtained advice on this matter from expert psychopharmacologist Stephen M. Stahl, MD, PhD, Professor of Psychiatry at the University of California, San Diego.

Dr. White: The first specific treatment for bipolar disorder was lithium, approved by the US Food and Drug Administration (FDA) in 1970. What other medications are now approved by the FDA for the treatment of bipolar disorder?

Dr. Stahl: The answer depends on the phase of the disorder and is in flux, but of course lithium was the first, and the evidence is good that it is effective for the manic and maintenance phases.[1] The evidence for its utility in the depressed phase is perhaps not as robust, but I think that it works in that phase. It's also been used to prevent suicide, for which there is good evidence but no FDA approval.[2]

All of the atypical antipsychotics except clozapine are approved for treatment of the manic phase in bipolar I disorder. Chlorpromazine is approved for the manic phase, but it's not used very much, and I don't advocate using it, given the other options.

In the depressed phase, lamotrigine is thought to work but is only approved for maintenance.[1] In fact, the only currently approved medication for bipolar depression is the combination of olanzapine plus fluoxetine, but we believe that the FDA will rule very shortly on quetiapine, which has 2 positive studies.[3] The other atypical antipsychotics probably work for bipolar depression and are under study, but they are not yet approved.

Divalproex is used for maintenance treatment but not approved for that, and it may work for the depressed phase, but it is approved for the manic phase.[1] Carbamazepine was actually one of the first anticonvulsants widely used for bipolar disorder, but only recently was it approved as a controlled-release formulation for just the manic phase.[4] It may also work in the depressed phase or maintenance. Many other anticonvulsants are used but not approved.

The approvals are for bipolar I disorder. Quetiapine has been studied in bipolar I and II disorders.[5] A lot of clinicians believe that much of bipolar disorder is best diagnosed as not otherwise specified (NOS), and although there are many such patients, no drugs are approved for that indication.

Dr. White: Bipolar disorder has many manifestations and distinct phases of treatment. Which medications have the best evidence as acute antimanic agents, and how does the clinician choose among them?

Dr. Stahl: The best ones are probably divalproex, lithium, and the 5 atypical antipsychotics that the FDA approved for mania.[6] In hospital settings, people tend to prefer olanzapine and risperidone, probably because they came to the market first, often in combination with divalproex. The combination tends to work quickly and provides some sedation.

Dr. White: Does the evidence suggest that patients with nonpsychotic mania should receive both a mood stabilizer and an antipsychotic?

Dr. Stahl: In the past, before atypical antipsychotics were available, we used typical antipsychotics as briefly as possible and only for psychotic mania because of concern about tardive dyskinesia. People with mood disorders may be more vulnerable to tardive dyskinesia than people with schizophrenia when treated with drugs, such as haloperidol. It was a surprise to find that the atypical antipsychotics work not only for psychotic mania but for nonpsychotic mania.[7] They don't treat just the psychosis.

Dr. White: Is a mood stabilizer also necessary then?

Dr. Stahl: Some people quibble about what a mood stabilizer is: If a medication works for mania, is it a mood stabilizer? If so, all 5 atypical antipsychotics are [mood stabilizers]. Does it mean that a medication must work for mania, depression, and maintenance? No drug has all 3 of those claims yet, although some soon may.

The FDA requires evidence and approval for the individual phases of bipolar disorder. Although studies for such purposes have been done with individual medications, most patients are actually on 2 or 3 drugs.[8] One of the atypical antipsychotics is given for mania, and unfortunately, because many patients have difficult-to-treat illness, they will need a second medication. Divalproex is used if the mood is too high, and lamotrigine is often used if the mood is low. Lithium can be added as a third agent if the others are inadequate. Some younger physicians don't know much about lithium because it's been off-patent for a while and isn't actively promoted.

Dr. White: The treatment of bipolar depression is often difficult, yet many bipolar patients spend more time struggling with depression than with mania.[9] What does the existing scientific work suggest is the best approach to treatment of acute bipolar depression?

Dr. Stahl: Lithium or lamotrigine is often used, but neither is approved for acute bipolar depression — only for maintenance. The use of antidepressants is a huge controversy. I think that most experts recommend against antidepressant monotherapy for a patient with bipolar depression, but most would add an antidepressant second or third in line if other agents don't work.[1] Studies have shown that atypical antipsychotics are effective but are not yet approved by the FDA.[3]

The answer to your question is that lithium, lamotrigine, or any atypical antipsychotic is probably adequate first- and second-line treatment for acute bipolar depression. If one or two of those put together is not useful, the next step is adding an antidepressant.

Dr. White: According to one systematic review,[10] tricyclic antidepressants have a high risk of causing a mood switch. Does the evidence say that other antidepressants are in fact less likely to cause mood instability?

Dr. Stahl: Tricyclics are powerful antidepressants. Some evidence suggests that venlafaxine also causes more mood switching,[11] and some suggests that bupropion causes a little less mood switching than others.[12] Even though monoamine oxidase inhibitors are quite powerful, there is little evidence that they cause mood switching, perhaps because they are used infrequently. I think that for someone who is not adequately stabilized, effective antidepressants all have the potential to cause mania. Tricyclics may be worst, but because some evidence exists that bupropion is a little less risky, it may be used preferentially in bipolar depression.

Dr. White: Do existing empirical data provide guidance on the best approach to an acute mixed mood disorder in a bipolar patient?

Dr. Stahl: Unfortunately, very little. Mixed mood states are common, poorly defined, and difficult to manage. According to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), this diagnosis means that the patient simultaneously meets the full criteria for major depression and mania. Many clinical trials of bipolar mania put mixed patients in as well, and therefore some medications have indications for what I call full mixed patients. Quetiapine is the only agent not approved for both mania and mixed states. I believe that's not necessarily because it doesn't work, but because mixed patients were excluded from the trials. Another kind of mixed state is often called dysphoric mania, which is when a patient meets the criteria for mania but has a little depression, too. Some people may meet the criteria for major depression but have a few manic symptoms.

We studied ziprasidone in dysphoric mania, and ratings of both depression and mania went down.[13] You will see in the literature smaller case studies of mixed states, but more common are less-than-full mixed states, which are sometimes called bipolar disorder not otherwise specified. Sometimes these patients are rapid-cycling, going from mania to a mixed state before they crash into full depression.

Dr. White: What about patients with rapid-cycling bipolar disorder?

Dr. Stahl: Four mood switches in a year, as the DSM-IV requires for the diagnosis, are not all that rapid. Some people may change mood 4 times in a day. Mood switches can occur precipitously; people move within hours from one pole to another, and some can have a surge of mania during depression. It's very common for manic patients to crash into depression.

Sometimes drugs will cause rapid cycling, which has been an accusation about too much antidepressant — or any antidepressant at all.[14] You can treat this by removing the antidepressant, but it's not necessarily progress to make a rapid-cycling patient unremittingly depressed. You sometimes need to treat for both mania and depression to avoid causing a switch or increasing the rate of cycling.

Dr. White: Are there data on that?

Dr. Stahl: There are almost no data to support what I just said. Some of the early research on divalproex suggested that it was better than lithium for mixed states and rapid cycling,[15] but more recent studies have indicated that they are equally good.[16] The American Psychiatric Association treatment guidelines[1] suggest using lithium for euphoric mania and divalproex for dysphoric mania and rapid cycling. However, that is irrelevant, because in the real world, someone with rapid cycling is unlikely to get along with 1 drug anyway. The reality is that everybody is treated with 2 or 3 drugs, yet few have done studies on polytherapy.

The only 2-drug studies are with atypical antipsychotics combined with lithium or divalproex for treating mania, not rapid cycling.[6] I'm not aware of any studies suggesting how to mix divalproex with lithium, so we're left with art and anecdote.

Dr. White: According to a recent meta-analysis,[17] lithium is the only true mood stabilizer, meaning that it is effective in mania, depression, and for maintenance. Do you think that other agents may eventually be recognized as true mood stabilizers?

Dr. Stahl: Again, it depends on how one defines a mood stabilizer. I would agree that the level of evidence is best for lithium, and yet it probably is grossly underutilized. You could argue that's because of its adverse effects or lack of promotion. I think that many agents will eventually be found to be mood stabilizers. Some are coming off-patent, such as risperidone and divalproex, so the reality is that those drugs may never get adequate testing. Even lamotrigine is coming off-patent. Could those 3 drugs work for all 3 phases? Maybe we'll never know.

Most likely to be investigated are the atypical antipsychotics with some patent life. I think that the first through the post will be quetiapine. I actually believe that all 5 atypical antipsychotics are true mood stabilizers, just as is lithium; however, none of them are FDA-approved for use in all 3 phases of the disorder. I think that it's very likely that ziprasidone, aripiprazole, and quetiapine will all get there, and maybe olanzapine, but I don't think that the company is trying to get monotherapy approval for bipolar depression.

Dr. White: Many patients are treated for an acute episode with several medications, but do they need to stay on them?

Dr. Stahl: We don't know. The only real evidence that I can cite is current prescribing practice, and it may be ignorance on the part of physicians, but I don't think so. In my practice and that of other psychiatrists who I know, we use more than 1 medication because patients are dissatisfied with outcomes or sometimes with side effects. Studies of monotherapy show that the approved agents are more effective than placebo, but a patient who is only 30% better will ask for more: "I want to be 70% or even 100% better." This leads clinicians to either raise the dose of the drug, which may then become intolerable, or add a second one. The sad thing is that it's difficult for some patients with bipolar disorder to achieve full remission with even 3 or 4 agents.

The effectiveness of polypharmacy has been shown for atypical antipsychotics plus lithium or divalproex in treating mania.[6] I can tell you that most psychiatrists believe that the combination is also effective in the depressed and maintenance phases, but I don't know of any randomized controlled trials to prove it.

Dr. White: When should a psychiatrist turn to clozapine for a patient with difficult-to-treat bipolar mood disorder?

Dr. Stahl: If this is an evidence-based discussion, I'd have to say that we do not have the same level of evidence for bipolar disorder as for schizophrenia. For schizophrenia, clozapine works better than other antipsychotics, as shown by classic studies comparing it with first-generation antipsychotics,[18] and it is probably more effective than other atypical antipsychotics.[19] Despite the lack of evidence, many experts would use clozapine for bipolar disorder somewhat as they would for schizophrenia, namely, after failure of multiple atypical antipsychotics, especially in patients with psychotic mania.[6]

Of course, the medication carries significant risks, including metabolic disorder. The risk vs benefit analysis is not as favorable for bipolar disorder as for schizophrenia because, although the risks are known, the exact benefits are not clearly known. I suspect that most patients who receive clozapine are very treatment-refractory, those for whom it would be worth the risk of developing diabetes.  Printer- Friendly Email This


Medscape Psychiatry & Mental Health.  2006;11(2) ©2006 Medscape
This is a part of article Bipolar Disorder: An Expert Interview With Stephen M. Stahl, MD, PhD Taken from "Discount Prozac Fluoxetine" Information Blog

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Carolina hospitals ready [May. 7th, 2008|10:32 am]

Davys said that given the recent outbreaks of CDAD, related to a more virulent breed of C difficile that is resistant to quinolone therapy, vancomycin may be elite as the preferred federal agent to buy metronidazole online.

Guerrant, MD, professor of internal learned profession at the Schooling
of Medicine/Division of Infectious Disease and film maker of the
Essence for Global Wellness at the Body of VA in Charlottesville, said
the salmagundi of cases for the subject area might not be voice of the
amount signal of cases that were treated, given the learning was
conducted over an extended catamenia of time.
This is a part of article Carolina hospitals ready Taken from "Discount Prozac Fluoxetine" Information Blog

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Prozac Added to Ecstasy Increases Risk of Acute Toxicity [Feb. 1st, 2008|11:55 am]

BOSTON (Reuters Health) Sept 21 - The mathematical operation of fluoxetine (Prozac) and 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy) increases the risk of acute toxic effects of Seventh heaven, and may explain the increasing telephone number of MDMA-related deaths.

Pharmacologists at the Educational institution of MD, Baltimore, presented examination data on the drug-drug action of fluoxetine and MDMA to attendees of the 35th flora confluence of the Indweller Body of Clinical Pharmacology, held here this week.

In presenting the written report findings, Dr.
Vijay V.
Upreti said an increasing performance of MDMA abusers are combine the drug with fluoxetine in an campaign to counteract the imprint that occurs after the drug’s high wears off.

The Baltimore researchers measured noesis and blood plasma levels of MDMA in P-glycoprotein (P-gp)-deficient and normal mice after a 5 mg/kg-dose of MDMA.
Levels were also measured after pretreatment with fluoxetine followed by 10 mg/kg MDMA.

There was no remainder in noesis and blood plasma levels of MDMA between the P-gp-deficient and normal mice.
However, pretreatment with fluoxetine increased intelligence and extracellular fluid MDMA levels by 40% in both groups of animals.

The half-life of MDMA increased from 2 distance to 5 hour with fluoxetine pretreatment.
There was also a 26% reducing in MDMA room when the drugs were combined.

Upreti said the written document suggest that “MDMA is not an efluxed indigenous language of P-gp and hence P-gp will not have a role in determining a drug-drug fundamental interaction.
This is a part of article Prozac Added to Ecstasy Increases Risk of Acute Toxicity Taken from "Discount Prozac Fluoxetine" Information Blog

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Review Article: Intestinal Serotonin Signalling in IBS [Jan. 27th, 2008|10:53 am]

Serotonin is clearly an important signalling material in the start of agent and secretory reflexes and in the activity of sensory signals from the gut to the CNS.
The findings that are described above demonstrate that 5-HT signalling is altered in IBS-D, IBS-C and PI-IBS, but the grounds and consequence human relationship of epigenetic changes in the elements of 5-HT signalling is unclear.
In other Good Book, we do not know whether changes in 5-HT signalling contribute to the alterations in GI single-valued function and sense experience that are the hallmarks of IBS, and/or if elements of 5-HT are altered in reply to disrupted purpose and fervor.

We do not yet know whether 5-HT signalling changes in result to altered gut utility, but several lines of info validation the concept that altered 5-HT signalling can lead to changes in gut mathematical function.
For object lesson, transgenic mice lacking the gene for SERT typically show symptoms similar to those of IBS-D, but some mice are more similar to IBS-C, as they have decreased colonic motion. In vitro studies involving judgement of propulsive mobility in the guinea-pig distal El Salvadoran monetary unit also demonstrate that changes in 5-HT signalling can affect move.
For lesson, body of low concentrations of the SSRI, fluoxetine (Prozac), increases the rate of propulsive move at low concentrations and slows mobility at higher concentrations.[40, 48] Furthermore, term of office of desensitizing concentrations of 5-HT decreases propulsive movement in vivo.
This is a part of article Review Article: Intestinal Serotonin Signalling in IBS Taken from "Discount Prozac Fluoxetine" Information Blog

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Expert Column - Preventing Adverse Drug Reactions [Jan. 22nd, 2008|11:51 am]

Physicians cannot make important dose adjustments if they are not informed of the full scope of possibilities.
Terfenadine (Seldane), the top-selling antihistamine in the human being for over a decennary, was withdrawn because of cardiac toxicities that caused hospitalizations and deaths.
These toxicities occurred in kinsfolk who had deficiencies in their enzymatic metabolic process of terfenadine or who used other medications or food that inhibited terfenadine biological process. Such individuals may have avoided or had less serious ADRs with a lower terfenadine dose.
However, the terfenadine dose was a one-size fits all 60 mg bid, disregard the fact that prerelease studies showed that a 50% lower dose, 20 mg tid, was highly effective. This cognition was not provided in the effect labeling, nor was it mentioned even after terfenadine’s dose-related toxicities became known, so physicians and patients were precluded from considering this lower, possibly safer, effective terfenadine dose.

The cubature unit initial dose of fluoxetine (Prozac) is 20 mg/day for most patients.
Yet, even before receiving FDA support, a discipline showed that just 5 mg was sufficient for treating national leader mental condition in 54% of patients. Quadrupling the dose to 20 mg increased the effectuality by only 11%, to 65% of subjects, while provoking more side effects and dropouts.
Nevertheless, the lower dose was not developed, nor was this substance included in the event labeling.
This is a part of article Expert Column - Preventing Adverse Drug Reactions Taken from "Discount Prozac Fluoxetine" Information Blog

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Consumer-Driven Health Plans [Jan. 17th, 2008|08:49 pm]

Vino Prescriptions Continue to Rise at Public transport Scripts

A evidence 47% of prescriptions processed by Transport Scripts during the beginning unit of time of 2003 were filled generically.
Product drug usage has increased steadily, up from 45.9% in the quartern one-fourth of 2002, 43% in the start soul of 2002, and 41.1% in 2001.

The circle attributed the increment to aggressive content of ware drugs, especially ware versions of popular brand-name drugs, such as Prozac, Glucophage, Zestril/Prinivil, and Zestoretic/Prinzide, that became available during the last 18 months.

Express mail Scripts recommends to its clients that members pay the lowest copayment total for product drugs.
This is a part of article Consumer-Driven Health Plans Taken from "Discount Prozac Fluoxetine" Information Blog

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February 1, 2005 [Jan. 12th, 2008|06:48 pm]

The British Medical Leger has issued a recantation on an earlier structure that accused Prozac concern Eli Lilly of suppressing selective information about the antidepressant’s link to a heightened risk of putting to death.
The drug Lord had launched a body relations accomplishment to punch the charges in that account, arguing that the documents discussed in the BMJ clause had in fact been made people age earlier.

The journal’s therapy said that an freelancer probe had found Eli Lilly’s legal right to be correct.
It did not say anything about broader assertions that the drug business organization was not completely forthcoming about Prozac’s electrical phenomenon risks.
Kaiser Stops Prescribing Bextra

Amid maturation reports of potential difference two-dimensional figure risks associated with the painkiller Bextra , Kaiser Permanente has placed a 6-month suspension on prescriptions, according to the Associated Press/ Wall Environment Piece of writing .
A similar drug, Vioxx , was pulled off the sales outlet by its producer in September.

This is the outset time the nation’s largest nonprofit managed care bourgeois has stopped dispensing a drug approved by the Food and Drug Establishment.
The Oakland-based meshing serves 8.5 zillion patients in 9 states and the District of Columbia.
This is a part of article February 1, 2005 Taken from "Discount Prozac Fluoxetine" Information Blog

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