Talk:Phenytoin/Archive 1

I replaced this link: * Phenytoin American Epilepsy Society. It was dead when I tried to follow it. Replaced with what I think is similar at the Epilepsy Foundation. —Preceding unsigned comment added by Kitetrimmer (talk • contribs) 18:27, 31 July 2008 (UTC)

I'll leave it to someone who cares about this article to fix it, but "chronically high levels" is jibberish.

Dave — Preceding unsigned comment added by 192.150.5.2 (talk • contribs) 18:39, 1 October 2007 (UTC

It says here that Jack Dreyfus prescribed phenytoin to Richard Nixon. This can't be right; first of all, Dreyfus is not a physician, and has never represented himself as one.

I'm going to remove that sentence, reword that paragraph a bit, and replace it with a link at the bottom to a web site about Dreyfus' efforts to expand the indications for phenytoin.

-Ikkyu2 23:56, 28 August 2005 (UTC)

I saw a TV programme about this around 2000, which implied that President Nixon was high (or more likely low) on drugs when he made decisions: it said Dreyfus gave him a bottle of phenytoin. Presumably Nixon's own physician would have prescribed for him when he needed more. That phenytoin could damp down mood swings, and aggressive or other impulses, is not implausible: the bromides were used for this, and currently carbamazepine and valproate, and some newer anticonvulsants, so this may be a class effect of many, if not all, of these drugs. NRPanikker 01:09, 19 October 2006 (UTC)

Someone added the following text to the article to-day:

The primary site of action appears to be the motor cortex where spread of seizure activity is inhibited. Possibly by promoting sodium efflux from neurons, phenytoin tends to stabilize the threshold against hyperexcitability caused by excessive stimulation or enviro'nmental changes capable of reducing membrane sodium gradient. This includes the reduction of posttetanic potentiation at synapses. Loss of posttetanic potentiation prevents cortical seizure foci from detonating adjacent cortical areas. Phenytoin reduces the maximal activity of brain stem centers responsible for the tonic phase of tonic-clonic (grand mal) seizures.

This text is so interesting, pertinent and provocative that I would like to commend the person who placed it for the addition to the article. Also, I believe that it would benefit greatly from sourcing - e.g. from where was this information derived? Once that can be cited, it will certainly be appropriate to put the text back into the article. -ikkyu2 (talk) 22:33, 7 March 2006 (UTC)

Here's one source: http://www.rxlist.com/cgi/generic/phenyt_cp.htm . Don't know where rx-list gets their information from, it looks like a standard blurb of some kind. --Pfh 00:39, 11 July 2006 (UTC)

How about a dedicated section to mechanism of action. It's pretty weak for this drug. Usually you can just look for the section that discusses it thoroughly. 74.190.48.43 (talk) 15:03, 4 February 2009 (UTC)

I agree the article needs more, properly referenced, info about basic mechanism. The statement "Phenytoin (fœnit'oin, IPA) acts to suppress the abnormal brain activity seen in seizure by reducing electrical conductance among brain cells by stabilizing the inactive state of voltage-gated sodium channels" especially needs a reference. However, the paragraph at the start of this Discussion section sounds wrong to me - I doubt very much (almost certain) that phenytoin affects sodium gradients. Paulhummerman (talk) 12:27, 25 October 2011 (UTC)

Comment on Figure: The lipid bilayer, as drawn in the Mechanism of Action figure in the main Article, appears to have a mistake. The polar head groups should be facing the aqueous compartments and the lipid tails should be facing towards each other. In other words: For each of the three states, the top of the page is the extracellular region, the bottom of the page is intracellular and the each view is a side-view "slice" through the membrane and channel protein. In ASCII, the bilayer should be this way (O are the yellow circles in the figure; | | are the green tails):

extracellular
OO
| || |
| || |
OO
intracellular

not as drawn, this way:

extracellular
| || |
OO
OO
| || |
intracellular

(I know it's a lot of work to do the figures but thanks.) AdderUser (talk) 14:17, 6 March 2014 (UTC)

This is in the category Antiarrhythmic agents, but there is no mention of it in the article. --Galaxiaad 08:52, 1 March 2007 (UTC)

Section of this article says Matt Damon's character from Elysium is given a fictional version of this drug, Miporol. But, there's no evidence to suggest he's given phenytoin. He's lethally irradiated and then prescribed Miporol, but there's no mention of what the drug is beyond this, and no other external source I can find seems to suggest there is any real-world analogue for the fictional drug he's given in the movie. Yet, this article mentions that phenytoin, which is prescribed for seizures and not at all for radiation sickness, is the drug he's given. There's no evidence to support this whatsoever, I suggest it be taken out as there is no proof or reason to claim these things as fact. — Preceding unsigned comment added by 24.164.79.12 (talk • contribs) 01:32, 10 February 2014 (UTC)

1. I have SLE in all of my organs, and was put on epilim and toriamate along with anumber of other drugs. However, I was hospitalized and was taken of my current epilepsy medication and put on Phenytoin,well, that was the end....! It slowly changed my mental state, to schizaphrenia,I developed more lung clots(31 in all) and ultimately had my mitral valve replaced.Oh,apart,from losing custody of my son because the judge did not realise any of the side affects of Luus or Phenytion.Jeni Australia

1. Antiarrhythmic : CBZ is not in the Vaughan-Williams Classification of Antiarrhythmics (see any text) although it is sometimes referred to as a "membrane stabilizer".
2. I'm not sure if the toxicities are presented so clearly (in the paragraph "Side Effects"). As I understand, the gum hyperplasia, coarse facial features and hursuitism are common and dose related and the most significant and so they should feature prominently in the article (due to the distress they cause patients).
3. I understand that the teratogenic potential is certain (Holmes LB, Harvey EA, Coull BA, et al. The teratogenecity of anticonvulsant drugs. N Engl J Med 2001;344:1132—8.)
4. Additionally, I thought that the hypersensitivity reactions and skin / liver and bone reactions, whilst rare, are definitely associated with phenytoin. Some texts are vague on this point.
5. I thought this review article regarding the associated Folate-deficiency, Ann Pharmacother. 1995 Jul-Aug;29(7-8):726-35, [[1]] (although also old) is a bit more useful than a 1992 study with rats.
6. I'll aim to chase up a list of solid references when time permits.
7. My personal opinion regarding the use of phenytion and the reluctance of the medical staff to prescribe (it in the Devloped World) is not "... due to mixed results from various studies" but because its common, predictable and significant adverse effects make it a very undesirable drug to use in the majority of the patient population. Note, that it is in guidelines for the Acute Management of Status Epilepticus as the first choice drug for Second line therapy so still has a signicant role (see either APLS, or Status Epilepticus Working Party (United Kingdom 2000)). (Again, IMHO) there seems to be significant bias as the article reads currently. — Preceding unsigned comment added by Jgm74 (talk • contribs) 21:22, 14 August 2007 (UTC)

Does anyone have any information on the sudden and dramatic price increase on Phenytoin Sodium Extended? I work for a pharmacy and have been faced with this question from many customers, and I agree it has jumped significantly recently, but the internet has not provided any information as to why.Sithboy 00:28, 23 August 2007 (UTC)

I have access to Medi-Span's pricing history, and it looks like in November-December of 2006, the AWP (Average Wholesale Price) of Phenytoin EX jumped, on average, 1000%. I checked a half-dozen manufacturers, and they all show the same increases. Either there's a single supplier of a base chemical that increased THEIR prices... or there's a conspiracy among generic drug manufacturers. I'd vote for the second choice - the greed of Big Pharma doesn't seem to have any limits. But, seriously, I think they got together and found a generic drug being sold across the board at fair prices - and they couldn't stand it. —Preceding unsigned comment added by Jcebbing (talk • contribs) 13:28, 11 September 2010 (UTC)

Apparently this is sometimes used as a Nootropic. Can anyone shed any further light on this, e.g. what the benefits are (if any)? --212.159.16.241 (talk) 00:12, 26 January 2008 (UTC)

I've re-added that the FDA found an increased risk of suicide from users of epilepsy drugs. This paragraph was removed by another user as phenytoin was not explicitly named in the article, but I feel it should be included as the FDA explicitly stated that it expects the risk to apply to every epilepsy drug in the article. This was clarified in my submission. Please discuss before removing this addition.

Amcarroll32 (talk) 13:09, 6 February 2008 (UTC)

hi - don't we need something about the pharmokinetics? —Preceding unsigned comment added by 90.218.195.233 (talk) 09:08, 12 February 2009 (UTC)

In studies done by noted Neurologist Dr. Mogens Dam(Epilepsy handbook}, he notes the loss of intellectual capacity and personality change with the continued use of phenytoin. As a 10yr user I can personally confirm this. I used to love to golf and fish, I've done neither in a long time. I've become inverted & depressed. the handbook mentions this also. But I've seen nothing from the American Epilepsy foundations or organizations. WHY! The Dr even mentions the only way to get back a normal life is to switch medications, which I am working on. Someone in the U.S. needs to publish all the facts. Mpr1979 (talk) 16:19, 6 March 2012 (UTC)