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Found this one just now:

Mast cells and the power of local RAS activation


"Stimulation of mast cell degranulation resulted in significant renin-mediated formation of angiotensin I in normal animal hearts. Subsequent local production of angiotensin II elicited norepinephrine release from cardiac sympathetic nerve terminals via the AT1 receptor "

Hyperadrenergic Postural Tachycardia Syndrome in Mast Cell Activation Disorders


MCA+POTS patients were characterized by episodes of flushing, shortness of breath, headache, lightheadedness, excessive diuresis, and gastrointestinal symptoms such as diarrhea, nausea, and vomiting. Triggering events include long-term standing, exercise, premenstrual cycle, meals, and sexual intercourse. In addition, patients were disabled by orthostatic intolerance and a characteristic hyperadrenergic response to posture, with orthostatic tachycardia (from 79?4 to 114?6 bpm), increased systolic blood pressure on standing (from 117?5 to 126?7 mm Hg versus no change in POTS controls), increased systolic blood pressure at the end of phase II of the Valsalva maneuver (157?12 versus 117?9 in normal controls and 119?7 mm Hg in POTS; P=0.048), and an exaggerated phase IV blood pressure overshoot (50?10 versus 17?3 mm Hg in normal controls; P<0.05). In conclusion, MCA should be considered in patients with POTS presenting with flushing. These patients often present with a typical hyperadrenergic response, but ?-blockers should be used with great caution, if at all, and treatment directed against mast cell mediators may be required.

Orthostatic hypertension: when pressor reflexes overcompensate


Interestingly, in this group of patients, the orthostatic hypertension manifested as either a persistent hypertensive response to assumption of an upright posture or as a hypertensive crisis, with BP as high as 240/140, with upright posture. This has not been observed in patients who have POTS but do not have mast-cell activation disorder.

Role of Esophageal Mast Cell Activation in Noncardiac Chest Pain (NCCP)


Chest pain is a common clinical complaint. About 30% patients with chest pain will have a normal coronary angiogram and are described as having noncardiac chest pain (NCCP). It is estimated that 25% of the population complain of chest pain at some time in their lifetime. The pathogenesis of NCCP is unknown. Esophageal hypersensitivity as a result of inflammation is considered to be an important mechanism in the development of this pain sensation. Little is currently known about the interaction between inflammatory mediators and peripheral afferent nerve terminals in the esophagus. The mast cell is one of the most enriched pro-inflammatory cells in the gastrointestinal tract. Activation of the mucosal mast cell releases a variety of mediators into adjacent tissues. We hypothesize that mediators released by mast cells sensitize esophageal nociceptors and induce pain sensation.

results not found yet!

Mast Cells Are Essential for Early Onset and Severe Disease in a Murine Model of Multiple Sclerosis


This one has opened a big can of worms implicating mast cells and autoimmunity (unfortunately none of those articles are free on the web)

In addition to their well characterized role in allergic inflammation, recent data confirm that mast cells play a more extensive role in a variety of immune responses...These data provide a new mechanism for immune destruction in EAE and indicate that mast cells play a broader role in neurologic inflammation.

The earliest article I've found so far on this was from Dr. Robertson (Vandy) from 1988, so I'll look for more...

Edited by flop
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This seems to be from the following reference:

Heuser G, Letter to the editor regarding Mast cell disorder to be ruled out in MCS. Arch Environ Hlth 2000; 55:284-285.


But I couldn't get the Archives on Environmental Health on line. This seems to be the letter of reference though by Heuser.

What interests me is the effect of mast cells on the brain, that this neurologist postulates.


In particular the part about

"Since the limbic system contributes emotional reactions and interpretations to sensory input, and since patients with amygdaloid (the amygdala is part of the limbic system) seizures can develop panic and related attacks during an amygdaloid seizure, our data appear to explain the emotional instability during a reaction to chemicals.

The previously mentioned structures also serve memory and cognitive as well as neuroendocrine and autonomic nervous system functions, all of which can be deranged in a patient with MCS.

In summary, I have shown that patients with MCS can develop hyperactivity in deep structures of the brain and that this may explain their emotional instability which therefore develops on a physiological rather than psychological basis."

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Why SSRI's work for MCAD and POTS?

What is the effect of fluoxetine on mast cell?

Published: Tuesday, December 23, 2008 - 10:01 in Health & Medicine


Mast cells are now recognized as "granular cells of the connective tissue", whose activation exacerbates allergic immune responses and as key players in the establishment of innate immunity as well as modulators of adaptive immune responses. The role of mast cells in the gastrointestinal mucosa is not only to react to antigens, but also to actively regulate the barrier and transport properties of the intestinal epithelium. In clinical studies, it has become clear that psychological factors, especially anxiety and depression, play an important role in gastrointestinal diseases by precipitating exacerbation of symptoms. Fluoxetine hydrochloride (fluoxetine) is a kind of selective serotonin reuptake inhibitors (SSRIs), which belong to a class of antidepressants used in the treatment of depression and anxiety disorders. The research team led by He-Shen Luo, from the Renmin Hospital of Wuhan University of China, investigated the effects of fluoxetine on mast cell morphology and rMCP-1 expression in gastric antrum in a rat model of depression. This will be published on December 7, 2008 in the World Journal of Gastroenterology.

A Sprague-Dawley rat model of chronic stress-induced depression was established. Fifty experimental rats were randomly divided into the five groups: normal control group, fluoxetine + normal control group, depressed model group, saline + depressed model group, and fluoxetine + depressed model group. Laser scanning confocal microscopy (LSCM) immunofluorecence and RT-PCR techniques were used to investigate rMCP-1 expression in gastric antrum. Mast cell morphology was observed under transmission electron microscopy.

They found that depression induced mast cell proliferation, activation, and granule hyperplasia. Compared with the normal control group, the average immunofluorescence intensity of gastric antrum rMCP-1 significantly increased in depressed model group (37.4 ? 7.7 vs 24.5 ? 5.6, P < 0.01) or saline + depressed model group (39.9 ? 5.0 vs 24.5 ? 5.6, P < 0.01), while there was no significant difference between fluoxetine + normal control group (23.1 ? 3.4) or fluoxetine + depressed model group (26.1 ? 3.6) and normal control group. The average level of rMCP-1mRNA of gastric antrum significantly increased in depressed model group (0.759 ? 0.357 vs 0.476 ? 0.029, P < 0.01) or saline + depressed model group (0.781 ? 0.451 vs 0.476 ? 0.029, P < 0.01 ), while no significant difference was found between fluoxetine + normal control group(0.460 ? 0.027) or fluoxetine + depressed model group (0.488 ? 0.030) and normal control group. Fluoxetine showed partial inhibitive effects on mast cell ultrastructural alterations and de-regulated rMCP-1 expression in gastric antrum of the depressed rat model.

These findings will conduce to understand that chronic heterotypic stress may induce the immune responses in gastric mucosa. Treatment with fluoxetine can ameliorate pathological changes in gastric antrum of depressed rat model, suggesting that SSRIs are an effective therapeutic agent for some gastroduodenal diseases caused by psychological factors.

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An article moving in the direction that many of us are going:


Authors: Reinstein, Eyal1; Mekori, Yoseph A; Mor, Adam

Source: Expert Review of Clinical Immunology, Volume 4, Number 2, March 2008 , pp. 267-274(8)

Publisher: Expert Reviews


Allergy and autoimmunity are complex inflammatory processes caused by dysregulation of the immune system. There are select situations in which allergy and autoimmunity coexist pathologically. Traditionally considered unrelated, recent evidence suggests unexpected roles for allergic mediators in several autoimmune diseases. This review presents updated evidence for allergic mediators in several autoimmune diseases, as well as autoimmune phenomena in mast cell-related conditions. We will describe the concomitant manifestation of these conditions in patients and in animal models. The involvement of the main effectors of the immune system mast cells, T lymphocytes, antibodies and cytokines in both conditions is also discussed.

Keywords: allergy; antibody; autoimmunity; inflammation; mast cell; T lymphocyte

Document Type: Research article

DOI: 10.1586/1744666X.4.2.267

Affiliations: 1: Instructor of Medicine, Department of Medicine B, Meir General Hospital, Kfar-Saba, 44281, Israel and, The Sackler School of Medicine, Tel-Aviv University, Israel., Email: eyalre@post.tau.ac.il



Nature 420, 875-878 (19 December 2002) | doi:10.1038/nature01324

Search Pubmed for

o Christophe Benoist

o Diane Mathis

progress Mast cells in autoimmune disease

Christophe Benoist & Diane Mathis


Mast cells are known to be the primary responders in allergic reactions, orchestrating strong responses to minute amounts of allergens. Several recent observations indicate that they may also have a key role in coordinating the early phases of autoimmune diseases, particularly those involving auto-antibodies.

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  • 2 weeks later...
I've done a bit of work on this thread fixing links etc. The only link that I can't get to work is the very first one posted by firewatcher, could you try to please post the full URL and then I can fix the link.



Here is the link to the abstract, you can download the pdf from there.




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Hi, everyone,

The following was sent to me by someone in my Mastocytosis support group. Since many here have wondered about the connection between POTS and mast cells, I thought you might like to read this. I've spoken with the doctor who wrote it, and though I didn't care for his ideas about mast cell diseases; ie, if it isn't in the bone, it doesn't exist, period, I still thought it might be useful to someone here.


Elevated Total Serum Tryptase Levels in Patients with Postural

Orthostatic Tachycardia Syndrome (POTS): A Case Series

Journal of Allergy and Clinical Immunology - February 2005 (Vol. 115, Issue

2 (Supplement), Page S248)

F. H. Hsieh1, M. M. Alam2, A. E. Lichtin3

1Pulmonary, Allergy, and Critical Care Medicine, Cleveland Clinic

Foundation, Cleveland, OH, 2Internal Medicine, Cleveland Clinic Foundation,

Cleveland, OH, 3Hematology and Medical Oncology, Cleveland Clinic

Foundation, Cleveland, OH.

RATIONALE: Serum tryptase is a marker for increased mast cell load or

mast cell activation. Elevated serum tryptase in patients without a

diagnosis of anaphylaxis or mastocytosis may suggest the involvement of mast

cells in other disorders.

METHODS: Serum tryptase values ordered from June 1999 to April 2004

were collected. Elevated serum tryptase was defined by a value > 13.5 ng/ml.

63 out of 265 patients had elevated tryptase. A retrospective review of

these charts was then performed.

RESULTS: 5 patients who did not have a diagnosis of mastocytosis or

anaphylaxis had a diagnosis of POTS. Each patient had 3 or more elevated

tryptase levels performed when the patient was asymptomatic. Mean levels

were 22.6 +/- 3.4 ng/mL. All 5 presented with dizziness and syncope. Every

patient had positive table tilt testing and met clinical criteria for POTS,

which included positional tachycardia and orthostatic intolerance.

Mastocytosis was excluded in 4 patients by bone marrow biopsy, including

negative immunostaining for CD2+/C25+ mast cells and negative c-kit analysis

in selected cases. One patient refused bone marrow analysis. Anaphylaxis


excluded by persistent symptoms and constant elevation of tryptase levels.

CONCLUSIONS: Our study suggests a potential role for mast cells in


pathogenesis of POTS. This may be helpful in exploring diagnostic and

treatment options for POTS.

Elevated Total Serum Tryptase Levels in Patients with PosturalOrthostatic Tachycardia Syndrome (POTS): A Case SeriesJournal of Allergy and Clinical Immunology - February 2005 (Vol. 115, Issue 2 (Supplement), Page S248)F. H. Hsieh1, M. M. Alam2, A. E. Lichtin31Pulmonary, Allergy, and Critical Care Medicine, Cleveland ClinicFoundation, Cleveland, OH, 2Internal Medicine, Cleveland Clinic Foundation,Cleveland, OH, 3Hematology and Medical Oncology, Cleveland ClinicFoundation, Cleveland, OH. RATIONALE: Serum tryptase is a marker for increased mast cell load ormast cell activation. Elevated serum tryptase in patients without adiagnosis of anaphylaxis or mastocytosis may suggest the involvement of mastcells in other disorders. METHODS: Serum tryptase values ordered from June 1999 to April 2004were collected. Elevated serum tryptase was defined by a value > 13.5 ng/ml.63 out of 265 patients had elevated tryptase. A retrospective review ofthese charts was then performed. RESULTS: 5 patients who did not have a diagnosis of mastocytosis oranaphylaxis had a diagnosis of POTS. Each patient had 3 or more elevatedtryptase levels performed when the patient was asymptomatic. Mean levelswere 22.6 +/- 3.4 ng/mL. All 5 presented with dizziness and syncope. Everypatient had positive table tilt testing and met clinical criteria for POTS,which included positional tachycardia and orthostatic intolerance.Mastocytosis was excluded in 4 patients by bone marrow biopsy, includingnegative immunostaining for CD2+/C25+ mast cells and negative c-kit analysisin selected cases. One patient refused bone marrow analysis. Anaphylaxis wasexcluded by persistent symptoms and constant elevation of tryptase levels. CONCLUSIONS: Our study suggests a potential role for mast cells in thepathogenesis of POTS.

Sorry the last part is a bit convoluted.

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Thanks, Linda Joy. More evidence of the relationship between autonomic dysfunctions and mast cell issues! BTW, I'm so sorry for all you are going through. The fact that steroids are helping you is further proof that mast cell issues are contributing to your symptoms. I'm keeping you in my thoughts and prayers.


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New one on MCAD and prevention of symptoms:

Prevention of Mast Cell Activation Disorder-Associated Clinical Sequelae of Excessive Prostaglandin D2 Production

Joseph H. Butterfield, Catherine R. Weiler

Division of Allergic Diseases, Mayo Clinic, Rochester, Minn., USA

Int Arch Allergy Immunol 2008;147:338-343 (DOI: 10.1159/000144042)

* Mast cell activation

* Mastocytosis

* Prostaglandin D2

Background: Patients with systemic mastocytosis have increased numbers of mast cells in the bone marrow and other organs, such as the liver, spleen, gastrointestinal tract and skin. Symptoms result from the local and remote effects of mediator release from mast cells and from the local effects of increased mast cell numbers in various organs. Patients with mast cell activation experience many of the same clinical symptoms as do patients with systemic mastocytosis from chronic or spontaneous release of mast cell mediators. We report 4 patients with mast cell activation symptoms from selective release of prostaglandin (PG) D2, but not histamine, and their improvement with aspirin therapy. Methods: Bone marrow biopsy specimens obtained from 4 patients with symptoms suggestive of mastocytosis were examined by tryptase immunostaining. Baseline levels of serum tryptase and urinary 11beta-PGF2alpha and N-methylhistamine were obtained. In 2 of the 4 patients, urinary 11beta-PGF2alpha and N-methylhistamine samples were also measured during acute symptoms. Results: Baseline increase in urinary excretion of the PGD2 metabolite 11beta-PGF2alpha was found in 2 patients. In the remaining 2 patients, baseline levels of urinary 11beta-PGF2alpha and N-methylhistamine were normal, but during acute symptoms, the excretion of 11beta-PGF2alpha increased markedly. Treatment with aspirin resulted in normalization of 11beta-PGF2alpha excretion in the 2 patients with elevated baseline levels and in prevention of symptoms in all 4 patients. Conclusions: These results suggest that mast cell activation may be manifested by a selective excessive release of PGD2. These patients respond to administration of aspirin but not to antihistamines.

Copyright ? 2008 S. Karger AG, Basel

Correspondence to: Dr. Joseph H. Butterfield

Division of Allergic Diseases, Mayo Clinic

200 First Street SW

Rochester, MN 55905 (USA)

Tel. +1 507 284 8917, Fax +1 507 284 2107, E-Mail butterfield.joseph@mayo.edu

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VERY INTERESTING!!!! Dr. Butterfield is the doctor who my allergist worked under at Mayo. Dr. Butterfield is a masto specialist, but has a strong reputation for not "believing" in MCAD. This is progress, indeed!

BTW, when I had my prostaglandin D-2 measured at B & W, my numbers were high, but not too abnormal. I was already on aspirin therapy for treatment of Reynauds- Unusual treatment. I presented at the ER with a cyanotic finger. I felt nothing and it was BLACK. I was admitted with a supposed blood clot thrown to my finger. Probably not true, but I was on IV coumadin for a few days, then plavix, then aspirin. Voila, with aspirin, MANY of my other symptoms improved.... I've since stuck to 81mg enteric coated every night. Don't know what it treats, but it helps. My fingers are pink and I feel less boin pain and breathe a bit easier.


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  • 3 months later...

One of the interesting theories put forth in this article is the concept of venous vs. arterial dilation and constriction; That the difference in the types should be based on whether the veins or the arteries dilate. Interesting.

The Causes of Postural Cardiovascular Disorders

Ziegler, Michael G.; Rizos, Demetri P.

Shibao et al. describe a series of tests that elucidate mast cell activation as a novel cause of postural orthostatic tachycardia syndrome (POTS) and orthostatic hypotension (OH). Because blood pressure control systems are redundant, patients with OH often have more than a single cause of their postural symptoms, and elucidating these causes can be challenging. The study by Shibao et al illustrates this because all but one of their subjects were premenopausal females. Estrogen and histamine vasodilate, and the patients who developed POTS were predominantly those made more susceptible to excessive vasodilation by age and sex. There are so many syndromes that cause orthostatic symptoms that approaching the problem through differential diagnosis is needlessly difficult. Analysis of the cardiovascular physiology of patients with OH is a better way to elucidate etiology and is also more likely to reveal when there are multiple reasons for impaired blood pressure control.

The cardiovascular systems used to maintain blood pressure during upright posture are most simply pictured as a volume of fluid, a pump, vessels that resist fluid flow, and a system that regulates pump speed and resistance to flow. The corresponding anatomic parts of this system are blood volume, the heart, resistance blood vessels, and the autonomic nervous system. It is possible to test each of these components responsible for maintenance of blood pressure to determine the defect(s) causing POTS or OH. This simple physiological approach is useful in the outpatient setting to diagnose a single patient and in the clinical research laboratory.

Blood volume must be adequate for maintenance of blood pressure. When we stand, 300 to 600 mL of blood pools in our legs. When sympathetic innervation is impaired, an even greater volume of blood pools in the legs. Continued upright posture causes fluid to transude into our legs and feet, causing a 10% hemoconcentration. This rapid loss of blood volume into the legs diminishes cardiac preload and decreases cardiac output by half because the heart can only pump blood delivered by the veins. When blood volume is diminished by anemia, hypoalbuminemia, or dehydration, cardiac preload may fall critically low. Diminished blood volume presents a characteristic clinical picture with increased norepinephrine, renin, and aldosterone levels, a tachycardic response to standing and diminished pulse pressure on standing. All of these characteristics can be seen in the mast cell activation plus OH In contrast to the other groups, that group decreased pulse pressure from 35 to 19 mm Hg on standing. Pulse pressure typically falls in patients with low blood volume because standing causes heart rate to increase while cardiac filling decreases, leading to a much smaller stroke volume. The sympathetic nervous response elicits tachycardia, vasoconstriction, and cool blue fingertips. If a vasodilator such as histamine is present, then reflex vasoconstriction may not be able to compensate for the low cardiac output, leading to OH. Low volume can be treated with salt, water, fludrocortisone, erythropoetin, desmopressin, or, in the case of hypoalbuminemia, with food.

Cardiac output is directly proportional to blood pressure, so it is surprising that congestive heart failure is an uncommon cause of OH. The poor cardiac output in heart failure usually does not cause OH because it is accompanied by increased peripheral vascular resistance, in part driven by increased sympathetic nervous activity. Cardiac preload is increased in congestive heart failure so that preload is adequate even during upright posture. However, when patients with congestive heart failure are treated with diuretics or nitrates, preload falls and they may develop OH. Patients with heart failure have taught us that when OH is caused by diminished cardiac output, the problem usually lies with diminished cardiac preload and not with impaired cardiac contractility.

The autonomic nervous system provides the major reflex mechanism that allows maintenance of blood pressure on standing. Autonomic failure usually divides into central nervous system diseases such as multiple system atrophy (Shy-Drager Syndrome) and peripheral neuropathies. Peripheral neuropathies are often seen with diabetes mellitus or uremia and tend to cause deterioration of the longest autonomic nerves. The vagus and sympathetic nerves to the legs show first damage. The vasovagal reflex can cause a brief withdrawal of sympathetic nervous tone with increased vagal activity. Because central and peripheral causes of autonomic defects generally have diffuse effects, they can be recognized by the many signs and symptoms they cause. Patients with autonomic defects may have defective sweating, poor temperature control, impaired papillary constriction, and poor sphincter tone. They tend to have constipation, difficult urination, impotence, impaired gastric motility, and diminished heart rate variability.

When normal subjects stand, heart rate increases and pulse pressure decreases as a consequence of higher diastolic and lower systolic blood pressure. Blood flow to the hands and feet decreases, and this leads to a change in the color of the palms and fingertips from pink toward blue that becomes visible after [almost equal to]3 minutes of standing. In contrast, when subjects with autonomic insufficiency stand, they decrease diastolic blood pressure without the usual compensatory increase in heart rate. They not only fail to vasoconstrict their hands, they increase blood flow to the feet, with pink or red toes. All of this happens because of impaired norepinephrine release from their sympathetic nerves. This is reflected by a diminished plasma norepinephrine response to standing; norepinephrine should nearly double after 5 minutes of upright posture. The poor norepinephrine release is then reflected by poor renin and aldosterone response to standing. If blood pressure falls low enough, vasopressin levels may rise in response to the stress of hypotension.

Vasodilation from heat, acidosis, infection, bradykinin, or histamine tends to cause POTS rather than OH. A similar response may be seen in patients who have hypertension treated with a single agent such as hydralazine or one of the dihydropyridine calcium channel blockers. The tachycardia without OH that follows arterial vasodilation occurs because arterial dilation increases blood flow, thereby increasing cardiac preload. The heart then has sufficient blood to pump and pumps more forcefully in response to increased sympathetic stimulation. This leads to the common symptom of palpitations among patients who are vasodilated. This type of response to vasodilation is nicely illustrated by the POTS group of Shibao et al,1 who were able to maintain blood pressure because increased cardiac output compensated for decreased peripheral vascular resistance. However, this system fails if blood volume is low. A short time spent in warm sunshine may be pleasant, but if we cannot replace fluids lost through sweating, hypotension and a feeling of weakness and lightheadedness ensue. The cardiovascular consequences are similar to those seen in the OH group of Shibao . Without sufficient blood volume, upright pulse pressure and blood pressure fall in vasodilated persons.

It is important to distinguish between arterial and venous dilation. Arterial dilation increases cardiac output but usually does not cause OH. Venodilation leads to poor cardiac output, which may cause hypotension. Venodilation causes symptoms very similar to volume depletion, because both act to diminish cardiac preload. The difference is dramatically illustrated by arterial and venodilator drugs. Hydralazine causes flushing, palpitations, and tachycardia. The addition of nitrates causes OH.

It is possible to use the classical approach of differential diagnosis for a patient with POTS and OH if the disease is attributable to a single cause. This classical approach fails when there are multiple causes of OH. Let us use the common example of the diabetic with mild autonomic neuropathy. That diabetic?s blood pressure is likely to be elevated in recumbent and standing postures. However, a mild infection can lead to vasodilation from fever and decreased volume from poor intake and glycosuria. The combination of decreased sympathetic nerve function, volume depletion, and vasodilation will cause OH. Without treatment directed toward the OH, the patient will be compromised until the infection has cleared and volume repleted.

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. 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 are widely available and can often point toward cause and treatment.

Hypertension Volume 45(3) March 2005 pp 354-355

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That study is quite interesting. There are lots of bits id never considered.

However it makes a few assumptions; firstly that Mast cell disorders cause POTS through the vasodilating effects of histamine (which is quite possible, but not proven and there are other mechanisms that have been suggested).

Also the bits about the pulse pressure doesnt sound right to me either .

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  • 3 years later...

I'm learning so much on this forum. Thank you for posting all of these articles/links. I have read a lot of them online but there were many that I hadn't seen before. I wish I weren't so tired, I have my second visit with my immunologist to go over blood work and talk about MCAD/MCAS. The geneticist thinks she should have my bone marrow tested. I found out through my GI doctor that I do have mast cells in my colon biopsy from August. I don't know what the immunologist will make of this.

So far her meds regimine hasn't really been helping me so I'm hoping that she will continue to keep trying to find out what it is that I need.

Thanks again for all the great info!

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