Perhaps because it can be a multisystem disorder, I'm struggling to find something that tells me what symptoms or constellation of symptoms (or perhaps number of symptoms) should send me to a doctor to ask for test for MCAS.
The problem is, because mast cells selectively release up to hundreds of mediators, everyone will have a different cluster of symptoms. I invite you to have a look at this long presentation by Dr. Afrin, a mast cell activation syndrome expert:
Systemic Mast Cell Disease: An Update (PowerPoint). In this presentation, you'll be able to find a bunch of case studies that, at first blush, don't have anything to do with MCAS.
I'm wondering if I've missed something somewhere where there's a decision algorithm for people to look at their symptoms and know whether that's likely to mean MCAS is possible/likely.
This is the way that I see it: the symptoms you describe as having are
all explainable by MCAS (or sistemic mastocytosis, for that matter.) Of course, this doesn't mean that MCAS is the right explanation. However, in my opinion, it is an explanation worth exploring. Why? Because, unlike ME/CFS, it is both
testable and
treatable!
I just wanted you to know that I took what you said seriously as a possibility and I wanted to explain my reasoning for not immediately seeing it as a strong possibility.
Fair enough. I see it then as a failure on my part to properly communicate what I was trying to say!
Oh, by the way, orthostatic intolerance may indeed be associated with mast cell issues:
Hypertension. 2005 Mar;45(3):385-90. Epub 2005 Feb 14.
Hyperadrenergic postural tachycardia syndrome in mast cell activation disorders.
Shibao C,
Arzubiaga C,
Roberts LJ 2nd,
Raj S,
Black B,
Harris P,
Biaggioni I.
Source
Division of Clinical Pharmacology, Department of Medicine and Pharmacology, and the Autonomic Dysfunction Center, Vanderbilt University School of Medicine, Nashville, Tenn 37212, USA.
Abstract
Postural tachycardia syndrome (POTS) is a disabling condition that commonly affects otherwise normal young females. Because these patients can present with a flushing disorder, we hypothesized that mast cell activation (MCA) can contribute to its pathogenesis. Here we describe POTS patients with MCA (MCA+POTS), diagnosed by episodes of flushing and abnormal increases in urine methylhistamine, and compared them to POTS patients with episodic flushing but normal urine methylhistamine and to normal healthy age-matched female controls. 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 beta-blockers should be used with great caution, if at all, and treatment directed against mast cell mediators may be required.
Comment in
PMID:
15710782
