51 Linfield Street

                                                                        Dundee

                                                                        Angus

                                                                        DD4 8LJ

17th February 2007

 

Dear Stewart,

 

Thank you for your letter of 12th February 2007 detailing that you are setting up a meeting with the ABPI (Association of the British Pharmaceutical Industry) to discuss the strong evidence that Seroxat is a defective medicine and one that must be banned before there is further fatality. I am fully aware based on previous correspondence from your constituency office that Ministers are dragging their heels over the irrefutable evidence that Seroxat causes a range of very serious adverse reactions. Serious adverse reactions that include mood fluctuation, homicide, severe withdrawal reactions and death by suicide in all age groups, not merely those under 18 years or young adults aged between 18 – 29 years. To suggest that such reactions are confined to a specific age group are an utter nonsense. Newspaper reports this week of Pop star Robbie Williams having had to seek expert help from a drug addiction clinic in Arizona to help him withdraw from Seroxat proves without a shadow of a doubt that Seroxat can and does cause severe adverse drug and withdrawal reactions in adults aged over 29 years. Additionally the reports that Robbie Williams was consuming large amounts of caffeine drinks to keep himself awake does not surprise me in the slightest, when prescribed Seroxat over a long period day becomes night and night day and why he needed sleeping tablets. I have the deepest sympathies for Robbie.

 

I have no doubt if Robbie Williams had not checked himself into a clinic that specialises in drug withdrawal he would have committed suicide at some point, I suffered a very similar set of adverse drug and withdrawal reactions to those described in the tabloids. Unlike Robbie however I was prescribed the Benzodiazepine Lorazepam (ending up on the equivalent of 60mg Diazepam!) daily to help me sleep at night and to prevent a serious drug reaction called Akathisia (something the Seroxat patient information leaflet mentions but does not go into detail about), and took various pain killers including Paracetamol for the headaches and other aches and pains caused by Seroxat. I have attached information about Akathisia and its causes (Seroxat is listed as one of the causes) as an addendum to this letter. I personally considered suicide on many occasions due to that antidepressant something I had never contemplated previously and for which GlaxoSmithKline are to blame for, I consider myself lucky to be alive.

 

Please keep me posted of the outcome of the meeting with the ABPI, it is of paramount importance that a moratorium is placed on the prescription of what is a deadly antidepressant medicine.

 

Like you say the reanalysis of SSRI antidepressants by the FDA in 2006 where it was discovered that Seroxat/Paxil causes a 6 fold increase in the risk of suicidal thoughts and acts in children and a 3 fold increase in such serious adverse reactions in adults adds significant weight to our previous calls for a moratorium to new patients.

 

You mention in your letter that you will do everything you can to press the Department of Health in terms of:

 

a)   Taking the issue of Seroxat seriously

b)  Looking at the workings of the MHRA in terms of its closeness to industry as a whole

 

I would like to know just how you aim to achieve this given that GlaxoSmithKline canvassed Members of Parliament with constituency interests in GlaxoSmithKline, circulating a letter telling them not to sign your Parliamentary colleague MP Paul Flynn’s EDM’s (Early Day Motions) critical of the manufacturers conduct in the run up to the airing of the excellent BBC Panorama ‘Secrets of the Drugs Trials’ on January 29th 2007, the fourth in the series of Seroxat documentaries. Clearly the pharmaceutical industry as a whole has significant influence over the UK Government and meddles with the democratic process, something that requires further investigation urgently.

 

I look forward to further correspondence from you in the near future both in terms of the outcome of the meeting between the ABPI, and the other issues I have brought to light in this letter.

 

Yours Sincerely

 

Derek Scott

 

BSc Behavioural Science (Hons)

 

http://www.seroxat.pwp.blueyonder.co.uk

http://en.wikipedia.org/wiki/Akathisia

 

Akathisia

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Akathisia
Classification & external resources

ICD-9

781.0, 333.99

Akathisia (or "acathisia") is an often extremely unpleasant subjective sensation of "inner" restlessness that manifests itself with an inability to sit still or remain motionless, hence the origin of its name: Greek a (without) + kathesis (sitting). Its most common cause is as a side effect of medications, mainly neuroleptics, and rarely, antidepressants.

Akathisia may range in intensity from a mild sense of disquiet or anxiety (which may be easily overlooked) to a total inability to sit still with overwhelming anxiety and severe dysphoria (manifesting as an almost indescribable sense of terror and doom). In the most severe cases, dysphoria can be so severe that the patient is literally compelled to take action, leading, possibly, to suicide attempts.

It is not unknown to have patients (who have been treated most often with neuroleptics for psychotic episodes or prochlorperazine for nausea) to bolt out of hospitals or emergency rooms due to this odd and disconcerting emotion.

Partially because the condition (and its attendant feeling) is difficult for the patient to describe, it is often misdiagnosed.

The presence and severity of akathisia can be measured using the Barnes Akathisia Scale.

Causes

Akathisia is most often the side effect of certain drugs - commonly seen in the antipsychotics, and less so in the others listed below:

*   typical or atypical antipsychotics, such as haloperidol (Haldol®) and droperidol, olanzapine (Zyprexa®), aripiprazole (Abilify®); Pimozide is especially infamous for causing akathisia;

*   SSRIs, such as paroxetine (Paxil/Seroxat®)

*   Other antidepressants, such as the tricyclics and trazodone

*   certain antihistamines, such as promethazine and diphenhydramine (Benadryl®);

*   certain anti-emetic drugs, particularly the dopamine blockers (e.g. metoclopramide (Reglan®) and prochlorperazine (Compazine®)).

*   certain drugs of abuse, such as GHB, methamphetamine and MDMA when administered in excessive doses.

[edit] Treatment

Treatment includes the discontinuation or reduction of dose of the causative agent and the use of typical or atypical antipsychotics (also called major tranquilizers) to reduce the agitation and anxiety. Unfortunately, these neuroleptics are often the cause of the condition and are known to cause irreversible akathisia in some cases. While the administration of these drugs may temporarily ameliorate the symptoms, there is a serious risk of worsening the condition over the longterm.

Therefore, some consider the drug of choice for the treatment of akathisia to be propranolol, along with other beta blockers such as metoprolol. The antihistamine cyproheptadine is also effective, though with shorter effect than beta blockers. Second-line treatments include benztropine and benadryl, though excess use of Benadryl may worsen symptoms. Most of the clinical cases of akathisia can be prevented by not administering the drugs that cause the condition.

Recent studies have shown that Vitamin B6 is effective for the treatment of neuroleptic induced akathisia. [1]

[edit] References

*   T. R. E. Barnes, "A Rating Scale for Drug-Induced Akathisia", British Journal of Psychiatry, vol 154, pp. 672-676, 1989 Abstract

[edit] External links

*   DSM-IV: Neuroleptic Induced Acute Akathisia

*   Information on successfully treating this nemesis

*   Placebo-level incidence of extrapyramidal symptoms (EPS) with quetiapine in controlled studies of patients with bipolar mania, Nasrallah, Henry A1; Brecher, Martin2; Paulsson, Björn3; Bipolar Disorders, Volume 8, Number 5p1, October 2006, pp. 467-474(8)

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