New Information on POTS

March 7, 2005

The abstract is free and I have the full text from the library but this is a "must read"!

When I can find a way to scan it in I will post the text or if anyone has a way to link to the free full text please do!

abstract link: http://hyper.ahajournals.org/cgi/content/abstract/45/3/385

I am so excited about this research...it seems to get closer to what causes the "autonomic storm".

Now we know to ask about having urine methylhistamine levels tested!

tearose

Jersey Girl · March 7, 2005

Thanks for posting this great information. I have yet to have my urine methylhistamine levels tested and think that I should. I definitely reacted very poorly to beta-blockers. Martha

geneva · March 7, 2005

I only read the abstract but found the article interesting. Hope you can post the entire article when you are up to it.

Here's the question....if the urine methlhistamine levels are too high or low, is there somehting they can do to correct the situation? Is this something that is a simple urine test or one of the things you would have tested in the 24 hour test?

thanks Tearose for finding the article.

MomtoGiuliana · March 8, 2005

Thanks so much tearose.

geneva--it looks like the only benefit of this urine test at this time is to predict how you might respond to a beta blocker regime? Certainly very useful information--but still no insight on how to correct or treat the mast cell activation problem? I sent an e-mail to the author asking about this. If I get a response from him, I will post it.

Katherine

geneva · March 8, 2005

Katherine, thanks for the information.

The abstract referenced "treatment directed against mast cell mediators may be required" which is what made me think maybe they had something specific in mind. What a good idea to write the author.

March 8, 2005

I'm trying to find a way to scan the full article into the computer...can I fax it to someone who can scan it in?

The article will answer a lot of your questions! The treatment for Mast Cell Activation to keep from triggering the hyperadrenergic reaction is of all things...something like an antihistamine!!!

Whoever knows where I can fax this to let me know!!!

tearose

MomtoGiuliana · March 8, 2005

I got a very prompt response to my e-mail to Dr. Biaggioni. What a kind soul.

Here is his response. He also sent me the entire article that I will also post next(hopefully that is ok for copyright reasons.)

This is his reply to me:

Many patients do not respond well to a regular dose of beta blockers

and

do better with a low dose.

Lack of response to beta blockers, therefore, is not an indicator of

mast cell activation.

The patients we described had episodes of obvious severe flushing in

the

face and neck. Even in these patients, only half had documented mast

cell activation (with elevated urine methylhistamines immediately after

a spell).

Depending on the patient, we have bee successful in treating

hyperadrenergic POTS with aldomet alone or in combination with

fludrocortisone. Only some patients require more targeted therapy

against mast cell activation, which requires medical supervision.

I hope you understand that these are only general comments. I cannot

make more specific recommendations over the internet.

Hope this helps.

Italo Biaggioni

MomtoGiuliana · March 8, 2005

Here is the text of the article. It is minus the tables of course (except one that I attempted to paste in--but I am afraid it is confusing due to lack of formatting), but perhaps this will be helpful to peruse, regardless!

I didn't include the abstract since that is already available at the link above.

It is six pages, plus a 5-page supplemental and I would be glad to copy and snail mail it to anyone who needs it for $1.75 for the whole thing (enough to cover postage and copying costs! <_< ).

________________________________________________________

Postural tachycardia syndrome (POTS) is a disabling

condition that commonly affects otherwise normal young

females. This disorder is characterized by symptoms of

fatigue, tachycardia, shortness of breath, and even syncope on

standing. The etiology is not clear, but 2 possibilities have

been proposed previously. In the neuropathic variant, the

primary defect is thought to be a partial autonomic denerva-tion

that compromises lower limbs with exaggerated ortho-static

venous pooling,1 and perhaps the kidneys with low

levels of plasma renin activity.2 Patients with the hyperadren-ergic

variant are thought to have centrally driven sympathetic

activation.3

A circulating vasodilator could produce reflex sympathetic

activation, presenting clinically as ?hyperadrenergic? POTS.

In our evaluation of patients with POTS, some described

flushing episodes associated with orthostatic intolerance. On

the basis of this observation, also reported by others, we

hypothesized that activated mast cells may provide a source

of circulating vasodilators in a subset of patients with

hyperadrenergic POTS. If true, histamine and other mast cell

mediators could play an important role in the pathogenesis of

this syndrome.

There is a wide spectrum of disorders associated with mast

cell pathology. Mastocytosis is a common term used to define

abnormal proliferation and accumulation of mast cells in 1 or

more body tissues. The clinical manifestation is produced by

episodic release of mast cell mediators in response to specific

stimuli 8 and can follow either an indolent or aggressive

course ranging from circumscribed cutaneous involvement to

life-threatening mast cell leukemia. In 1991, Roberts and

Oates described the clinical syndrome of idiopathic mast cell

activation (MCA).9 In this condition, there is no evidence of

mast cell proliferation, but patients are disabled by episodic

MCA, documented by accumulation of mediators in plasma

or urine. Patients with this syndrome typically present epi-sodes

or ?attacks? of flushing accompanied by palpitations,

lightheadedness, dizziness, shortness of breath, occasional

nausea and diarrhea, headache, and syncope.

Here we describe patients disabled by persistent orthostatic

intolerance and evidence of MCA. These patients often

present with a typical hyperadrenergic variant of POTS and

biochemical evidence of MCA. _-Blockers should be used

with great caution in these patients, if at all, and treatment

directed against mast cell mediators may be required.

Methods

Subjects

We evaluated 177 subjects referred to the Vanderbilt Autonomic

Dysfunction Clinic for disabling orthostatic intolerance who were

studied as inpatients from January 1995 to January 2004. A patient

was considered to have an MCA disorder and POTS (also known as

orthostatic intolerance) if they met the following criteria. (1) Long-standing

(_6 months) disabling orthostatic intolerance; (2) an

increase in heart rate of _30 bpm within 5 minutes after assuming a

standing position; (3) absence of an underlying cause (debilitating

disease, substantial weight loss, prolonged bed rest, previous history

of any disease producing peripheral neuropathy, or any medication

impairing autonomic reflexes); (4) a history of facial or upper trunk

flushing (defined as objective and intense facial redness witnessed by

a physician or caregiver); and (5) urine methylhistamine _230 _g/g

creatinine associated with a flushing episode.9 Patients were classi-fied

into 3 separate groups. Eight young female subjects met the

criteria of MCA and POTS (MCA_POTS). An additional 5 patients

were identified as having similar characteristics, with the exception

that they presented with orthostatic hypotension (OH; identified by a

decrease in systolic blood pressure of _20 mm Hg or in diastolic

blood pressure of _10 mm Hg; MCA_OH). We thought it impor-tant

to include a group of 16 patients with a history of POTS with

facial flushing but no evidence of MCA (documented by absence of

increased urine methylhistamine, POTS). This provides a compari-son

group to determine whether the presence of MCA modifies the

clinical presentation of POTS. We also include a fourth control

group of 12 normal, healthy, age-matched females.

Procedures

All subjects were admitted to the Vanderbilt General Clinical

Research Center and were fed a low-monoamine, caffeine-free diet

containing 150 mEq sodium and 70 mEq potassium per day for at

least 3 days before evaluation. Medications affecting the autonomic

nervous system were withheld for at least 3 days before admission.

Autonomic function tests were used to evaluate the integrity of the

different reflex arcs. These included Valsalva maneuver, the cold

pressor and handgrip tests to assess cardiovascular autonomic function,

and the sinus arrhythmia ratio (change in heart rate in response to

controlled breathing) to assess cardiac parasympathetic activity.10 All

tests were standardized previously in our laboratory.11 An orthostatic

test was performed to evaluate hemodynamic and hormonal changes on

standing. An indwelling catheter was placed in an antecubital vein to

obtain blood samples while patients remained supine after an overnight

rest. Subjects were encouraged to stand as long as possible or up to 30

minutes. During this period, they were allowed to sit at intervals if

presyncopal symptoms developed. Blood samples were obtained for

catecholamines, aldosterone, and renin measurements. Brachial blood

pressure and heart rate were obtained using an automated sphygmoma-nometer

(Dinamap; GE Medical Systems Information Technologies)

during supine and standing test phases.

Plasma catecholamine levels were determined by high-performance

liquid chromatography with electrochemical detection.12 Plasma renin

enzymatic activity was assessed by the conversion of angiotensinogen to

angiotensin I and expressed as nanograms of angiotensin I produced per

milliliter of plasma per hour. Plasma aldosterone was measured by

radioimmunoassay.13 Urine samples were obtained in patients with a

history of flushing in the face or upper trunk. Patients were asked to

collect urine for 4 hours immediately after a spontaneous severe flushing

episode, defined by a subjective intensity of symptoms of ?7 to 8? on a

scale of ?0? (no symptoms) to ?10? (the worst symptoms ever). This

was done during the inpatient or outpatient evaluation. Samples were

obtained within 4 hours after a spontaneous episode. Methylhistamine

levels were measured by gas chromatography negative ion chemical

ionization mass spectrometry.14 In no case was there any abnormality in

hematologic laboratory results consistent with systemic mastocytosis.

To determine the response to treatment, a research nurse contacted the

patients 3 months after discharge and obtained information about

the medication, the frequency of mast cell episodes with flushing, and

the intensity of orthostatic tachycardia. We were able to obtain infor-

mation on 6 patients with MCA_POTS and in 3 patients with

MCA_OH.

Statistical Analysis

Data were analyzed using SPSS version 11 (SPSS). Frequency tables

were generated for categorical variables. Continuous variables are

expressed as mean_SEM. Group comparisons were made using the

nonparametric Kruskal?Wallis test. Post hoc analysis between 2

groups was made using the nonparametric Mann?Whitney test.

Criterion for significance was P_0.05.

Results

Clinical Characteristics and Autonomic Response

to Posture

Clinical characteristics of patients and controls are presented

in Tables 1 and 2. All patients except 1 were female, and all

were white, non-Hispanic, with an age range between 18 and

50 years. There was no significant difference in age, weight,

and body mass index between groups. Symptoms during

episodes included flushing, palpitations, lightheadedness with

severe orthostatic intolerance, nausea, diarrhea, abdominal

cramping, and polyuria. Blood pressure increased acutely in

some cases. Patients often exhibited hypersomnia, sleeping

for hours after these episodes.

Hemodynamic and humoral responses to posture are shown in

Figures 1 and 2. As expected by the selection of subjects,

standing heart rate was significantly higher in the MCA_POTS,

POTS, and MCA_OH groups compared with normal subjects

(P_0.001). Mean supine diastolic blood pressure was signifi-cantly

different between groups (P_0.005); MCA_OH patients

had higher values compared with MCA_POTS, POTS, and

normal subjects. Upright systolic blood pressure was signifi-cantly

increased in the MCA_POTS group compared with

normal subjects (Table 1; Figure 2; P_0.013). We identified 5

patients who presented with orthostatic hypertension, defined by

an increase in systolic blood pressure on standing of

_20 mm Hg. Furthermore, 4 patients presented with episodes of

sudden onset of hypertension and palpitations. There were no

obvious triggering events, and these episodes resolved sponta-neously.

The supine and upright blood pressure obtained from

these patients as well as the blood pressure values during the

hypertensive crisis are presented in supplemental Table I and

supplemental Figure Ia and Ib (available online at

http://www.hypertensionaha.org).

Mean supine plasma norepinephrine levels were significantly

different between groups: MCA_OH was higher than

MCA_POTS, POTS, and normal subjects (Table 1; Figure 2;

P_0.004). Supine plasma norepinephrine was also significantly

higher in MCA_POTS patients compared with controls

(269_41 and 129_22 pg/mL, respectively; P_0.05; Figure 2)

but not compared with POTS patients. No differences were

observed in supine and upright epinephrine, renin activity, or

aldosterone.

As expected, the methylhistamine levels were different be-tween

patients with MCA_POTS and MCA_OH compared

with POTS controls (P_0.001). Although not statistically sig-nificant,

patients with MCA_OH tended to have higher levels

of urinary methylhistamine compared with MCA_POTS pa-tients

(Table 1).

Characterization of Autonomic Function

Autonomic function tests are presented in Table 3 and Figure

3. No significant differences in systolic blood pressure were

observed between groups at baseline for Valsalva maneuver,

the hyperventilation test, the cold pressor test, and the

handgrip test. There was a difference in systolic blood

pressure during phase IILate of the Valsalva maneuver

(P_0.048; Table 3; Figure 3). The MCA_POTS group had a

significantly higher systolic blood pressure compared with

POTS and normal controls (P_0.023 and P_0.027, respec-tively).

During phase IV of the Valsalva maneuver, we

observed that groups with MCA_POTS and POTS presented

an excessive increase in systolic blood pressure (hypertensive

overshoot) compared with normal controls (Figure 3). The

change in systolic blood pressure between baseline and phase

IV of the Valsalva maneuver was significantly higher in the

MCA_POTS group (50_10 mm Hg) compared with the

POTS group (31_5 mm Hg) and controls (17_3 mm Hg). In

a post hoc analysis, no differences were found between

patients with MCA_POTS and POTS (P_0.168). The sys-

tolic blood pressure and diastolic blood pressure after 1

minute of the cold pressor test and after 3 minutes of the

handgrip test were different between groups. In MCA_POTS

patients, systolic blood pressure increased 35_12 mm Hg

during the cold pressor test, whereas the response in normal

controls averaged 20_5 mm Hg.

Triggering of MCA With Exercise

Because patients often referred to episodes of flushing trig-gered

by exercise, we performed treadmill exercise on 3

subjects. Flushing was triggered in these patients, and this

was associated with an increased in urinary methylhistamine

(supplemental Figure II). In 1 patient, we documented an

increase in plasma histamine, indicative of mast cell degran-ulation

but not of plasma prostaglandin D2 (PGD2), a marker

of newly formed mast cell mediator release (supplemental

Figure II).

Response to Treatment

The response to treatment in patients in whom follow-up was

available is shown in supplemental Table II. Because of the

number of patients, we did not attempt to perform a

controlled study, and these observations remain anecdotal.

However, it is noteworthy that patients improved clinically

when treated with H1 and H2 histamine receptor blockers with

the sympatholytic _-methyldopa, or with a combination of

both. Of note, _-blockers triggered episodes consistent with

acute MCA in 2 patients, and 4 patients had allergic reactions

to aspirin, ranging from bronchoconstriction to anaphylaxis.

Discussion

We describe here a novel syndrome characterized by chronic

disabling orthostatic tachycardia associated with episodes of sys-temic

MCA. It affects otherwise normal young subjects, typically

women, and causes substantial disability. We found no evidence of

a primary diffuse autonomic neuropathy as the cause of this

syndrome; autonomic reflexes appeared to be intact or overactive.

On the contrary, exaggerated sympathetic activation was suggested

by high plasma norepinephrine levels and increased systolic blood

pressure in the upright posture. We and others have described

patients with orthostatic intolerance, in many ways indistinguishable

from patients presented here, who seem to have partial sympathetic

denervation, preferentially involving lower limbs, the ?neuropathic?

POTS.1 The clinical criteria that differentiate between the neuro-pathic

and hyperadrenergic forms of this disease are not defined.

We believe that the patients described in this report correspond to

the hyperadrenergic form of POTS because of the exaggerated

sympathetic pressor response during phase IILate and phase IV of the

Valsalva maneuver and the exaggerated increase in blood pressure

on standing.

Episodes of MCA were documented in these patients by

elevated levels of urinary methylhistamine taken immediately

after a spontaneous event. It should be noted that urinary

methylhistamine is usually normal in between episodes in

patients with MCA disorders,9 and patients should be instructed

to collect urine for a 4-hour period immediately after a severe

spontaneous flushing episode. Urinary histamine is often mea-sured

in the evaluation of flushing, but it is less specific than

methylhistamine and not useful in the diagnosis of MCA. The

symptoms described during these spells are probably induced by

acute release of mast cell mediators such as histamine and

PGD2.15,16 Patients with isolated MCA are symptomatic only

during episodes, whereas our group of patients also experienced

chronic fatigue and orthostatic intolerance in between episodes,

eventually leading to a disabling condition.

Hypertension can be a prominent feature in some patients

with MCA and POTS. We observed 2 different clinical presen-tations

of this association. Patients may present with a consistent

hypertensive response to upright posture or with acute hyperten-sive

crisis. During these hypertensive episodes, blood pressure

can increase to as high as 240/140 mm Hg, and the episodes are

similar to the hypertensive variant of MCA disorders described

previously.9 These events resemble pheochromocytoma inas-much

as they are accompanied by tachycardia, nervousness,

shortness of breath, and hypertension. A similar clinical presen-tation,

known as pseudopheochromocytoma or diencephalic

hypertension, has been described by Page.17 Flushing is promi-nent

in MCA disorders and in pseudopheochromocytoma and is

a useful clinical distinction with pheochromocytoma, which is

accompanied by pallor. Plasma norepinephrine is increased in

both conditions, but levels are much higher in pheochromocy-toma

because catecholamines are released directly into the

circulation, whereas in pseudopheochromocytoma, catechol-amines

are released into the synapse, and only a relatively small

proportion spills over into the circulation.

We also report a group of patients with flushing and orthostatic

intolerance but no evidence of MCA. The cause of flushing in those

patients is not clear. Other entities associated with flushing and

similar clinical characteristics are associated with dopamine release,

as described by Kuchel.18 Panic attacks can also be associated with

flushing and regional sympathetic activation,19 but patients usually

do not experience orthostatic intolerance between attacks.

Mast cells are localized in close proximity to blood vessels and

peripheral nerves and are therefore strategically positioned to

modulate sympathetic activity, vascular tone, and angiogenesis.20

Histamine is a powerful vasodilator that could explain the cutaneous

vasodilatation responsible for flushing. With regard to the patho-physiology

underlying the association between POTS and MCA,

we propose a positive feedback loop by which MCA, with the

subsequent release of vasoactive mediators, may contribute to

vasodilation, reflex sympathetic activation, central volume contrac-tion,

norepinephrine release, and orthostatic intolerance (Figure 4).

Conversely, our results indicate that exercise can lead to MCA,

presumably through sympathetic activation. In this regard, neu-ropeptide

Y (NPY), a 36-aa neuropeptide that is coreleased with

norepinephrine from noradrenergic neurons, has been shown to

induce mast cell degranulation with the release of preformed

mediators in purified rat peritoneal 21,22 and human jejunal mast

cells 23 and to induce hypotension in animals secondary to MCA in

vivo.24 This appears to be a nonreceptor-mediated effect related to

the presence of positively charged amino acid residues of the C

terminus of NPY. Therefore, the physiological significance of

NPY-mediated MCA remains speculative.

Our findings have potential implications for the treatment of

these patients. Because of the prominent orthostatic tachycardia,

_-blockers are commonly used in the treatment of POTS patients.

However, these drugs should be used with great caution in these

patients, if at all, because of possible worsening of MCA. In our

experience, a therapeutic trial with _-methyldopa should be consid-ered,

given the evidence of a hyperadrenergic state. Some patients

may require treatment directed at controlling mast cell mediators,

including H1 and H2 receptor antagonists.

Perspectives

We report a novel syndrome of chronic hyperadrenergic

orthostatic intolerance associated with episodes of MCA.

This syndrome should be considered in POTS patients with a

history of flushing. This symptom is often not volunteered by

patients and may require careful questioning by the physician.

Diagnosis requires biochemical documentation of MCA be-cause

other causes of flushing can be associated with POTS.

A correct diagnosis is important because the presence of

MCA mandates a different approach in the treatment of these

patients. _-Blockers, a commonly used therapeutic option in

POTS patients, should be used with caution, if at all, because

of the risk of triggering MCA. These patients can be treated

with H1/H2 histamine antagonist and central sympatholytics.

Acknowledgments

This research was supported in part by a general clinical research

center grant from National Center for Research Resources and by

grants HL56693 and HL67232 from the National Institutes of

Health. S.R.R. is supported by a K12 grant from the National

Institutes of Health. C.S. is recipient of the international fellowship

in clinical pharmacology supported by Merck Foundation.

References

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Biaggioni I, Ertl A, Black B, Robertson D. The neuropathic postural

tachycardia syndrome. N Engl J Med. 2000;343:1008 ?1014.

2. Jacob G, Robertson D, Mosqueda-Garcia R, Ertl AC, Robertson RM,

Biaggioni I. Hypovolemia in syncope and orthostatic intolerance role of the

renin-angiotensin system. Am J Med. 1997;103:128 ?133.

3. Jordan J, Shannon JR, Diedrich A, Black BK, Robertson D. Increased

sympathetic activation in idiopathic orthostatic intolerance: role of systemic

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5. Biaggioni I. Orthostatic intolerance syndrome, vasoregulatory asthenia and

other hyperadrenergic states. In: Robertson D, Biaggioni I, eds. Disorders of

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6. Streeten DH, Kerr CB, Kerr LP, Prior JC, Dalakos TG. Hyperbradykininism:

a new orthostatic syndrome. Lancet. 1972;2:1048 ?1053.

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Hematol Oncol Clin North Am. 2003;17:1227?1241.

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J Invest Dermatol. 1991;96:19S?24S.

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London, UK: Harwood Academic Publishers; 1995.

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dihydroxyphenylglycol and the intraneuronal disposition of norepinephrine in

humans. J Clin Invest. 1988;81:213?220.

13. Workman RJ, Sussman CR, Burkitt DW, Liddle GW. Circulating levels of

angiotensin I measured by radioimmunoassay in hypertensive subjects. J Lab

Clin Med. 1979;93:847? 856.

14. Roberts LJ, Oates JA. Accurate and efficient method for quantification of

urinary histamine by gas chromatography negative ion chemical ionization

mass spectrometry. Anal Biochem. 1984;136:258 ?263.

15. Morrow JD, Guzzo C, Lazarus G, Oates JA, Roberts LJ. Improved diagnosis

of mastocytosis by measurement of the major urinary metabolite of prosta-glandin

D2. J Invest Dermatol. 1995;104:937?940.

16. Roberts LJ, Sweetman BJ, Lewis RA, Austen KF, Oates JA. Increased

production of prostaglandin D2 in patients with systemic mastocytosis.

N Engl J Med. 1980;303:1400 ?1404.

17. Page IH. A syndrome simulating diencephalic stimulation occurring in

patients with essential hypertension. Am J Med Sci. 1935;190:9 ?14.

18. Kuchel O, Buu NT, Hamet P, Larochelle P, Gutkowska J, Schiffrin EL,

Bourque M, Genest J. Orthostatic hypotension: a posture-induced hyperdo-paminergic

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19. Wilkinson DJ, Thompson JM, Lambert GW, Jennings GL, Schwarz RG,

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20. Feoktistov I, Ryzhov S, Goldstein AE, Biaggioni I. Mast cell-mediated

stimulation of angiogenesis: cooperative interaction between A2B and A3

adenosine receptors. Circ Res. 2003;92:485? 492.

21. Arzubiaga C, Morrow J, Roberts LJ, Biaggioni I. Neuropeptide Y, a putative

cotransmitter in noradrenergic neurons, induces mast cell degranulation but

not prostaglandin D2 release. J Allergy Clin Immunol. 1991;87:88 ?93.

22. Grundemar L, Hakanson R. Neuropeptide Y, peptide YY and C-terminal

fragments release histamine from rat peritoneal mast cells. Br J Pharmacol.

1991;104:776 ?778.

23. Santos J, Saperas E, Nogueiras C, Mourelle M, Antolin M, Cadahia A,

Malagelada JR. Release of mast cell mediators into the jejunum by cold pain

stress in humans. Gastroenterology. 1998;114:640 ?648.

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_______________________________________

If you can interpret this table with its lack of formatting, I thought this might be useful to include. KM

________________________________________

TABLE 2. Clinical Manifestation of Patients With POTS and

MCA Disorder

Orthostatic Symptoms?n (%)

MCA_POTS MCA_OH

n %n%

Flushing 8 100 5 100

Palpitations 8 100 5 100

Lightheadedness 8 100 3 60

Chronic fatigue 7 88 3 60

Headache 5 63 2 40

Dizziness 5 63 4 80

Presyncope/syncope episodes 3 38 1 20

Shortness of breath 3 38 2 40

Confusion 3 38

Increase in blood pressure 3 38

Paresthesias 3 38

Gastrointestinal symptoms (nausea and vomiting) 3 38 4 80

Abdominal cramps and diarrhea 3 38 3 60

Blurred vision 2 25

Anxiety 2 25 1 20

Excessive diuresis 5 100

Orthostatic intolerance exacerbated by?n (%)

After exercise 5 63 5 100

Prolonged standing 3 38 1 20

After meals 3 38 1 20

Premenstrual 2 25 1 20

Heat intolerance 2 25 5 100

Emotional stress 1 13 1 20

Sexual intercourse 1 13

Ernie · March 8, 2005

Thanks Katherine and Tearose for posting this article. I will print it and bring it to my doctors.

Ernie

March 9, 2005

Tearose,

That is a very interesting article. I think I did read the abstract at one time.

It was nice to see to whole thing---thanks MomtoGiuliana

I will copy and paste it to my Microsoft word.

In the beginning of my POTS I was so hyper adrengic and had so many of those attacks I was not able to eat. And I had the attacks on beta-blockers! 60mg of propranolol was not enough----I was truly a mess for about 6 months until Dr. Grubb put me on the Wellbutrin. Then the attacks went away---but I still get milder ones, and unfortunately most of the other potsy symptoms. The the hyper adrengic attacks stopped me in my tracks. Crippling.

I never did have any autonomic testing other then the TT test. All this blood work I read about---I've never had any of it done. I will ask Dr. Grubb why on the 22nd this month---that is my next appointment.

Julie :0)

Ernie · March 9, 2005

I just realised while I was reading this article that I was part of this research! Kind of weird.

Ernie

EarthMother · March 9, 2005

Big thanks to Ernie for being our famous celebrity white rat in the article!

Did anyone else venture to pay for the second article in this month's journal of hypotension. The one that references this study. It looks to be an ed op piece and while it is filled with techno-jargon I can not hope to understand, it may be that the authors disagree with the findings.

Snippit from:

Editorial Commentaries

The Causes of Postural Cardiovascular Disorders

Michael G. Ziegler; Demetri P. Rizos

"Mast cell disorders did not cause OH in most of Shibao?s subjects because reflex sympathetic nervous activation enhanced cardiac output enough to maintain blood pressure.9 However, a patient with a disease that alters cardiovascular physiology will eventually experience other cardiovascular stresses, such as fever, dehydration, or drugs. At that point, the mild cardiovascular disease may manifest itself as OH, often reported to a physician as "feeling too weak to get up." The most important postural cardiovascular tests described by Shibao et al1 are widely available and can often point toward cause and treatment. "

I've printed out both and will review with my doctor at my next appointment. No easy answers. Many thanks to all of you for shedding light on this moving target.

EM

Radha · March 9, 2005

is there any test to confirm you have a mast cell disorder?

radha

March 9, 2005

Radha, I'm still trying to understand the entire article however I do see the way to see if you have this kind of mast cell activation is by urine sample. They look for samples from people who have had an "autonomic storm" a pots diagnosis and then take the sample 4 hours after the storm and check for levels of urine methylhistimine.

this is in the full article:

Urine samples were obtained in patients with a