Talk:Angioedema

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House MD Reference[edit]

Refrenced in House MD Season 3 Episode 5 Fools for Love Ashton V. 05:44, Nov 14, 2006 (UTC)

There is not much support for linking every disease to its occurrence in House MD. JFW | T@lk 15:28, 1 November 2007 (UTC)

How "outdated" is angioneurotic edema?[edit]

It is still taught in med schools... —Preceding unsigned comment added by 164.77.106.50 (talk) 01:36, 12 October 2007 (UTC)

It is an incorrect term, and modern publications avoid its use for the obvious reasons that there is not meant to be a neurotic component to it at all. JFW | T@lk 15:28, 1 November 2007 (UTC)

In Europe the term goes either way. It used to be called Quincke's disease. Quincke was the first to coin the phrase. Their may not have been a purpose to mention a neurotic component as we in the 21st century understand neurotic, however the word was a correct term although the above heading says otherwise, probably meaning that in modern times it is useless or wrong. The term angio-neurotic implies a symbiosis of interdependance between the nervous (literally in 19th century English "neurotic"). What our forefathers felt or meant is unknowable and scientificly irrelevant. What they said, literally though, is to see a connection between nervous (system) and blood (angio). I am glad they at one time made a suggestion that speaks from the grave on what they found. I am very happy, also, to not call it HANE, but HAE, because of the abuse the modern term discourages. I think more dignified still is back to "Quincke's Syndrome". Many diseases that are respected are connected to the coin-phrase author. -AH, also re DXM —Preceding unsigned comment added by 67.170.146.158 (talk) 05:55, 27 October 2009 (UTC)

HAE III[edit]

Bork et al present a case series of HAE with normal C1INH: doi:10.1016/j.amjmed.2007.08.021 JFW | T@lk 15:28, 1 November 2007 (UTC)

Whole journal issue[edit]

Annals of Allergy, Asthma and Immunology JFW | T@lk 13:55, 28 July 2008 (UTC)

Better link: http://www.ncbi.nlm.nih.gov/pubmed?term=%22Ann+Allergy+Asthma+Immunol%22[Journal%3A__jrid8743]+AND+100[volume]+AND+1+Suppl+2[issue]+AND+angioedema&TransSchema=title JFW | T@lk 00:19, 9 December 2009 (UTC)

Drugs[edit]

We have no list of drugs reliably linked to angioedema. Only ACE inhibitors are mentioned. PMID 11480492 is from 2001 but discusses this. More recent papers welcome. JFW | T@lk 06:29, 31 July 2008 (UTC)

There is a drug- dextromethorphan. It will induce an HAE edemic attack 100% of the time at a dose of 400mg dextromethorphan in a known 245 lb. man with HAE. The drug is a depressant to the CNS (central nervous system). He took it to aleviate pain, which is a rudimentary way to quell the nervous system and he reported that while it caused CNS depression and then edema, it was preferable to accept having an attack. The attack was small and accompanied by mosquito bite typical edemic attack in fingers, forearms and feet, subsiding after 3-4 hours rather than a full blown (600% heavier) attack. Redness and a heavy level of itching are the worst of it. But in the end, he thought maybe the stress was inevitible and the attack as well. Kind of preferable to control the time of attack rather than have it be random he thought. Not advised. This in 2005. Dextromethorphan. —Preceding unsigned comment added by 67.169.194.113 (talk) 02:43, 23 August 2009 (UTC)

What about adding some more info on ACEi and mechanism involved there, increased bradykinins etc? Also in the drug induced section, is there a reference for that cross reactivity of ACEi and ARBs? Ponsau (talk) 06:58, 26 February 2009 (UTC)

mechanism[edit]

If hereditary angioedema is due to deficiency of C1 esterase inhibitor, shouldn't that decrease the complement pathway? C1 esterase breaks C1 down. So an inhibitor should keep it from bring broken down. And a deficiency of said inhibitor would allow it to be broken down (so many double-negatives). Please explain the mechanism here a little more.

rhetoric (talk) 04:46, 16 September 2008 (UTC)

Okay, nevermind. I found the answer. The C1 esterase allows autoactivation of C1 to follow the classical pathway. Thus, C1 esterase inhibitor keeps it in check, and deficiency of C1-INH allows overactivation (and the overactive bradykinin).

See also: http://www.emedicine.com/med/topic420.htm

Sorry for being confused.  ;)

rhetoric (talk) 04:59, 16 September 2008 (UTC)

If the article is unclear, please change it. JFW | T@lk 06:16, 16 September 2008 (UTC)

I understand erythrocytes swell for HAE patients and as they, en masse, circulate as a liquid organ weighing, say, 8 pints, swell within the veins and arteries and heart...the circulatory system becomes engaged in what could be seen as a traffic problem on a freeway. Wow. What a mess. A physician who had HAE and when he felt he was "making" too much blood, he'd blooddraw himself a few vials. He was even an HAE researcher, the late Dr. Raymond Eugene Giesbrecht of Tigard, Oregon USA, but never shared much. He did share a lot with me. Meditations. Medications. Unusual measures to curb even nuances of symptoms. What I now realise that he did not then was that the erythrocytes were not too many in count...they were many in presence and too swollen individually. He reported the letting helped in some way. I continue to look into these things. -A.H. —Preceding unsigned comment added by 67.170.146.158 (talk) 06:08, 27 October 2009 (UTC)

It is necessary to invent an inexpensive home kit for larygyal swelling to encourage families with members who experience HAE to do first aid. It would involve an attack counter block thru self administration of a non collapsable approved-for-home-use laryngoscopic airway. This kind of kit could be taken anywhere and the mortality rate for HAE laryngyal swelling could very likely be elimated completely. -A.H. son of and keeper of the notes of the late Dr.R.E. Giesbrecht, HAE researcher —Preceding unsigned comment added by 67.170.146.158 (talk) 06:46, 27 October 2009 (UTC)

Researcher's interest[edit]

Any fact, figure or helpful information that is true that you want to share to aide HAE cure research, write here. I believe angioedema can be controlled much better in the future. —Preceding unsigned comment added by 67.170.146.158 (talk) 06:50, 27 October 2009 (UTC)

Aspirin and ibuprofen[edit]

Nadiatalent (talk · contribs) has repeatedly reinserted a case report that discusses aspirin and ibuprofen as precipitants of angioedema. WP:MEDRS is very clear on such studies, and I have asked for a better source. PMID 11480492 does seem to discuss NSAIDs but as I have no fulltext I wonder if aspirin is discussed too. Anyone have access to this paper? JFW | T@lk 00:09, 9 December 2009 (UTC)

This paper discusses angioedema as a whole, not drugs as precipitants of HAE attacks. JFW | T@lk 00:14, 9 December 2009 (UTC)
Not ibuprofen, Rofecoxib, with discussion of Celecoxib (still available). Doctors are still using the out-of-date studies that say aspirin-intolerance (inhibition of the COX-1 enzyme) does not portend a problem with selective COX-2 inhibitors. Most of the survey papers pre-date that indictment of them (the citation that was removed by the above user), which unfortunately looks as if it is "just a case study". This is important information for patients, notably for people afflicted with arthritis-like problems, whose angioedema might not be part of the basic affliction, but caused by the drugs prescribed to them. I found a dozen subsequent papers that discuss COX-2 inhibitors and angioedema, but I don't see any up-to-date complete surveys that would satisfy the above user. The time for survey papers has probably passed. Signing off. Nadiatalent (talk) 14:24, 9 December 2009 (UTC)
It is not Wikipedia's task to be a provider of "important information for patients". As I have tried to explain, WP:MEDRS uses a hierarchy of reference quality, and case reports are at the bottom of the food chain. Again, if you can identify a reliable secondary source that contains a list of medications known to precipitate HAE attacks, please let us know. JFW | T@lk 20:12, 9 December 2009 (UTC)

I'm far too lazy to actually edit the article[edit]

But this source talks about a dutch firms called pharming that is producing C1-INH in rabbits and milking them, then purifying the proteins to inject into patients. " Now if you’re wondering if you are going to see gourmet bunny cheese showing up on your grocery store shelves soon, the answer is “no.” The milk is actually being gathered for a different purpose. The biotech industry is using the rabbits to produce a certain human protein that is then used to produce a—yes, you guessed it—drug.

Pharming, a biotech firm located in the Netherlands, has produced a warren of genetically engineered bunny rabbits that can produce up to 12 grams of a human protein called C1 inhibitor. The protein is then used to make an experimental drug that treats hereditary angioedema. People with this condition don’t produce enough C1 inhibitor, which can lead to painful swelling, cramps, and even possible death through suffocation." --216.67.85.20 (talk) 09:59, 2 February 2011 (UTC)

So where are the clinical data? JFW | T@lk 12:52, 2 February 2011 (UTC)

Overall helpfulness of article[edit]

I think this article would be helpful to more users if there were a succinct summary in everyday terms that non-medical professionals could understand. Absolutely include the stuff about which mutations cause which forms of the hereditary stuff, but put it below a basic encyclopedia entry. — Preceding unsigned comment added by Teodoro123 (talkcontribs) 23:00, 22 March 2013 (UTC)

{{sofixit}} JFW | T@lk 09:47, 24 March 2013 (UTC)