Have any of you heard of mast cell disorders? Mast cells heavily populate the lining of the gut and the skin but are found throughout the body. They are the cells that are "armed" with IgE and degranulate, releasing >60 chemicals including histamine, when triggered by allergens (food, mold, dust, etc.)
I am almost certain I have this. I had a horrible allergic reaction to what I think was a variety of triggers over the last 24 hours. My skins burns, itches, I get dizzy, fatigued, and had multiple bowel movements. I found out about this disorder while researching about my hair loss (which is speeding up now - oh joy!). The treatment includes using anti-histamines and other blockers for the chemicals and treating symptoms according to one journal article I read. I am taking Quercitin, Vitamin C, and Allium Cepa (homeopathic) in addition to my daily Claritin.
I am debating on whether to go to a specialist about this. Thoughts?
The problem is associated to intestinal candida colonization. Epithelial cells are affected by inflammation and candida metabolites (antigens) provoking a histamine reaction.
The result is food allergies and intolerance (food becoming antigens)
Candida sufferers are hypersensitive since the immune system is over-active in a humoral immune response and depressed in a cellular response. Damage to the mast cells as a result of pathogenic colonization causes hyperpermeability of the gut barrier. This is the origin of food reactions. When an undigested protein cross to the blood, the immune system attack it.
Here is an experiment using animal models:
Backgrounds and aims: Controversy still exists as to whether gastrointestinal colonisation byCandida albicans contributes to aggravation of atopic dermatitis. We hypothesised thatCandida colonisation promotes food allergy, which is known to contribute to a pathogenic response in atopic dermatitis. We tested this using a recently established murine Candidacolonisation model.
Methods:Candida colonisation in the gastrointestinal tract was established by intragastric inoculation with C albicans in mice fed a synthetic diet. To investigate sensitisation against food antigen, mice were intragastrically administered with ovalbumin every other day for nine weeks, and antiovalbumin antibody titres were measured weekly. To examine gastrointestinal permeation of food antigen, plasma concentrations of ovalbumin were measured following intragastric administration of ovalbumin.
Results: Ovalbumin specific IgG and IgE titres were higher in BALB/c mice with Candidacolonisation than in normal mice. Gastrointestinal permeation of ovalbumin was enhanced by colonisation in BALB/c mice. Histological examination showed that colonisation promoted infiltration and degranulation of mast cells. Candida colonisation did not enhance ovalbumin permeation in mast cell deficient W/Wv mice but did in congenic littermate control +/+ mice. Reconstitution of mast cells in W/Wv mice by transplantation of bone marrow derived mast cells restored the ability to increase ovalbumin permeation in response to Candidacolonisation.
Conclusions: These results suggest that gastrointestinal Candida colonisation promotes sensitisation against food antigens, at least partly due to mast cell mediated hyperpermeability in the gastrointestinal mucosa of mice.