Tuesday, August 31, 2010

Midodrine Being Pulled Off the Market!

I am sure a lot of you POTSies have already heard the buzz, but for those of you who haven't, the medicine used to help a lot of people treat POTS and other low-blood pressure illnesses is being pulled off the market. Yep, you read that correctly. No more Pro-Amatine (Midodrine). This comes as a shock to those of us who rely heavily on this drug to get us through the day so we aren't dizzy, tachycardic, or even passing out. Unfortunately, not only did the FDA decide to pull the drug, but I just read that Shire was planning on pulling the drug long before the FDA's announcements went public.



From HealthrelatedInfos.com:

"Philadelphia-based Shire, the pharmaceutical company, has voluntarily removed its orthostatic hypertension drug Midodrine, just after the FDA announced it’s intention to withdraw it’s approval for the drug.

Last November, Shire spoke to the FDA and told them they would be pulling the plug on the drug rather than conduct post-market studies, which were requested by the FDA.
ProAmatine is what the drug is sold to consumers as, will be withdrawn from shelves, effective on the 30th of September, according to a statement released on the company’s website.

The drugs efficacy was never proved to the FDA from post-marketing studies, and there was no evidence available to show that the drug was working. This is the reason why the FDA was withdrawing it’s approval.

This is the first time marketing approval has been reversed since the FDA’s fast track system was put in place.

What happens during the fast track process, is the drug is released on to the market, and studies are done while the drug is being used by patients and suffers, called post-market studies. These are hoped to show the quality and effectiveness of the drug while available to the general population. A decision is then made based on these studies as to whether or not the drug will be allowed to keep it’s approval or will be withdrawn. This fast tracks the process of getting much needed drugs and pharmaceuticals into wide spread use, to ease the pain of suffers."


And, the latest info I read stating Shire planned on pulling the drug, from heartwire:

"Philadelphia, PA - A drugmaker whose hypotension drug was the subject of an FDA drug withdrawal request earlier this week now says it had already intended to voluntarily withdraw the drug, long before the FDA went public with the proposal. In a statement, Shire says that the company notified the FDA and healthcare professionals in November 2009 with the news that the company was opting to withdraw midodrine hydrochloride [ProAmatine], used in the treatment of low blood pressure.

As reported by heartwire, the FDA recommended withdrawal of the drug August 16, noting that the necessary postmarketing studies required to show the drug to be effective have not been done, despite the product being approved in 1996.

But in a statement on its website, Shire states that it acquired the drug "as a part of the acquisition of Roberts Pharma in 1999, and Shire conducted and completed the postmarketing trials that the FDA required. The FDA, however, viewed these trials as inconclusive and required that additional trials be conducted for ProAmatine to maintain its marketing authorization."

Shire says its plan to withdraw midodrine was to go into effect September 30, 2010. The decision is not being driven by any safety concerns, the company added.

As previously reported by heartwire, makers of generic versions of the drug have 30 days (from the date of the FDA's first withdrawal proposal) to submit written comments. A final decision about whether or not to withdraw the drug would be made after any final submissions from drug makers and others are considered."



I have been waiting, trying patiently to make it through until November when I am on Medicare to get back on the Midodrine...and now, that isn't going to happen. Like those of you with POTS who find relief with this drug, I am sure you are feeling the same way I am. I honestly don't know what road I will go down now. It wasn't a cure all, but it certainly helped. I will take any little bit I can get. Now, with the only medicine of its kind on the market being taken away, what are we going to do?

Once the Medicare kicks in, I will be trying saline IVs and going from there. I wish you all the best of luck with a new treatment plan, as well.

xo
dani

7 comments:

Anonymous said...

Ever tried florinef? Also, make sure you are being followed by a cardiologist who does echocardiography or CT angio for your aorta.

Vegan Danielle Davis said...

@Anonymous -

Yes, thanks! The florinef only helped a tiny bit, and only in conjunction with the midodrine. By itself it did nothing. When I last had insurance, I was absolutely followed by a cardio and had my echo done yearly, since I have a slightly dilated aorta. As soon as I get on Medicare, I have a list of docs I will be getting in to see again, getting a wonderful group of people that can help me. Unfortunately, the endocrinologist I was seeing for a few years, she and I went through many rounds of things to try to help the POTS, and this combo (florinef/midodrine) was the only thing that helped. I am sure there are more things I haven't tried, things we didn't think of, and I will now be exploring those, too! :)

Anonymous said...

Some alternatives then:
- pseudophed over the counter - cheap and can help
- beta blockers - usually not tolerated due to side effects of fatigue and depression
- clonidine - no experience with its use except for heroine withdraw
- pyridostigmine - off label but some evidence for its use
- phenylephrine - active ingredient in nasal spray with some evidence and does work orally - this is the ingredient in pseudophed PE

BadGlue said...

some people have been helped by licorice root extract, but it has also hurt other folks. dysautonomia is so weird like that. I haven't tried it.

Anonymous said...

Licorice root actually contains a natural inhibitor of one of the enzymes used to make salt retaining steroids. These steroids are crucial to maintaining blood pressure regulation so I would avoid natural licorice at all costs. What about sea salt? Also, check out this link:

J Am Coll Cardiol. 2010 Jun 22;55(25):2858-68.

Cardiac origins of the postural orthostatic tachycardia syndrome.
Fu Q, Vangundy TB, Galbreath MM, Shibata S, Jain M, Hastings JL, Bhella PS, Levine BD.

Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, Dallas, Texas 75231, USA.

Abstract
OBJECTIVES: The purpose of this study was to test the hypothesis that a small heart coupled with reduced blood volume contributes to the postural orthostatic tachycardia syndrome (POTS) and that exercise training improves this syndrome.

BACKGROUND: Patients with POTS have marked increases in heart rate during orthostasis. However, the underlying mechanisms are unknown and the effective therapy is uncertain.

METHODS: Twenty-seven POTS patients underwent autonomic function tests, cardiac magnetic resonance imaging, and blood volume measurements. Twenty-five of them participated in a 3-month specially designed exercise training program with 19 completing the program; these patients were re-evaluated after training. Results were compared with those of 16 healthy controls.

RESULTS: Upright heart rate and total peripheral resistance were greater, whereas stroke volume and cardiac output were smaller in patients than in controls. Baroreflex function was similar between groups. Left ventricular mass (median [25th, 75th percentiles], 1.26 g/kg [1.12, 1.37 g/kg] vs. 1.45 g/kg [1.34, 1.57 g/kg]; p < 0.01) and blood volume (60 ml/kg [54, 64 ml/kg] vs. 71 ml/kg [65, 78 ml/kg]; p < 0.01) were smaller in patients than in controls. Exercise training increased left ventricular mass and blood volume by approximately 12% and approximately 7% and decreased upright heart rate by 9 beats/min [1, 17 beats/min]. Ten of 19 patients no longer met POTS criteria after training, whereas patient quality of life assessed by the 36-item Short-Form Health Survey was improved in all patients after training.

CONCLUSIONS: Autonomic function was intact in POTS patients. The marked tachycardia during orthostasis was attributable to a small heart coupled with reduced blood volume. Exercise training improved or even cured this syndrome in most patients. It seems reasonable to offer POTS a new name based on its underlying pathophysiology, the "Grinch syndrome," because in this famous children's book by Dr. Seuss, the main character had a heart that was "two sizes too small."

Anonymous said...

Licorice root actually contains a natural inhibitor of one of the enzymes used to make salt retaining steroids. These steroids are crucial to maintaining blood pressure regulation so I would avoid natural licorice at all costs. What about sea salt? Also, check out this link:

J Am Coll Cardiol. 2010 Jun 22;55(25):2858-68.

Cardiac origins of the postural orthostatic tachycardia syndrome.
Fu Q, Vangundy TB, Galbreath MM, Shibata S, Jain M, Hastings JL, Bhella PS, Levine BD.

Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, Dallas, Texas 75231, USA.

Abstract
OBJECTIVES: The purpose of this study was to test the hypothesis that a small heart coupled with reduced blood volume contributes to the postural orthostatic tachycardia syndrome (POTS) and that exercise training improves this syndrome.

BACKGROUND: Patients with POTS have marked increases in heart rate during orthostasis. However, the underlying mechanisms are unknown and the effective therapy is uncertain.

METHODS: Twenty-seven POTS patients underwent autonomic function tests, cardiac magnetic resonance imaging, and blood volume measurements. Twenty-five of them participated in a 3-month specially designed exercise training program with 19 completing the program; these patients were re-evaluated after training. Results were compared with those of 16 healthy controls.

RESULTS: Upright heart rate and total peripheral resistance were greater, whereas stroke volume and cardiac output were smaller in patients than in controls. Baroreflex function was similar between groups. Left ventricular mass (median [25th, 75th percentiles], 1.26 g/kg [1.12, 1.37 g/kg] vs. 1.45 g/kg [1.34, 1.57 g/kg]; p < 0.01) and blood volume (60 ml/kg [54, 64 ml/kg] vs. 71 ml/kg [65, 78 ml/kg]; p < 0.01) were smaller in patients than in controls. Exercise training increased left ventricular mass and blood volume by approximately 12% and approximately 7% and decreased upright heart rate by 9 beats/min [1, 17 beats/min]. Ten of 19 patients no longer met POTS criteria after training, whereas patient quality of life assessed by the 36-item Short-Form Health Survey was improved in all patients after training.

CONCLUSIONS: Autonomic function was intact in POTS patients. The marked tachycardia during orthostasis was attributable to a small heart coupled with reduced blood volume. Exercise training improved or even cured this syndrome in most patients. It seems reasonable to offer POTS a new name based on its underlying pathophysiology, the "Grinch syndrome," because in this famous children's book by Dr. Seuss, the main character had a heart that was "two sizes too small."

Anonymous said...

I read that there isn't enough data to prove that it's effective and that the FDA recommends not using it for lowering blood pressure:

http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm225468.htm

http://www.theheart.org/article/1110411.do