Although different diagnostic criteria are published, a commonly used strategy to diagnose patients is to use all three of the following:

Symptoms consistent with chronic/recurrent mast cell release:  Recurrent abdominal pain, diarrhea, flushing, itching, nasal congestion, coughing, chest tightness, wheezing, lightheadedness (usually a combination of some of these symptoms is present)
Laboratory evidence of mast cell mediator (elevated serum tryptase, N-methyl histamine, prostaglandin D2 or 11-beta- prostaglandin F2 alpha, leukotriene E4 and others)
Improvement in symptoms with the use of medications that block or treat elevations in these mediators"The World Health Organization has not published diagnostic criteria. Treatment
Common pharmacological treatments include:

Mast cell stabilizers, including cromolyn sodium and natural stabilizers such as quercetin
H1-antihistamines, such as cetirizine or ketotifen or fexofenadine or loratadine
H2-antihistamines, such as ranitidine or famotidine
Antileukotrienes, such as montelukast or zileuton as well as natural products (e.g., curcumin or St. Johns wort extracts)
Nonsteroidal anti-inflammatory drugs, including aspirin can be very helpful in reducing inflammation in some patients, while others can have dangerous reactions

Prognosis
The prognosis of MCAS is uncertain because of lack of studies. History
The condition was hypothesized by the pharmacologists John Oates and Jack Roberts of Vanderbilt University in 1991, and following a build-up of evidence featured in papers by Sonneck et al. and Akin et al., named in 2007.Diagnostic criteria were proposed in 2010 and revised in 2019. See also
FcεRI
Histamine intolerance
Immunoglobulin E

References


== External links ==
However, the evidence in favour of selective tryptophan restriction remains insufficient and the consensus is evolving towards the restriction of lysine only. In the Amish community, where GA1 is overrepresented, patients with GA1 typically do not receive tryptophan-free formulas, either as the sole source of amino acids or as a supplement to protein restriction. Enhancement of precursor anabolic pathways
Lysine and hydroxylysine anabolic pathway enhancement
A possible way to prevent the build-up of metabolites is to limit lysine and hydroxylysine degradation, as lysine is one of the most abundant amino acids and tryptophan is one of the least abundant amino acids. Interaction of GCDH deficiency with vitamin C levels
Humans lack the enzyme L-gulonolactone oxidase, which is necessary for the synthesis of ascorbic acid (vitamin C), leaving them dependent on dietary sources of this vitamin. Vitamin C is a necessary cofactor for the utilization of lysine in collagen synthesis. Collagen, the most abundant protein in the human body, requires great amounts of lysine, the most abundant amino acid in proteins. Ascorbic acid, the main hydroxyl radical quencher, works as the cofactor providing the hydroxyl radical required for collagen cross-linking; lysine thus becomes hydroxylysine. GA1 worsens during stresses and catabolic episodes, such as fasts and infections. Endogenous catabolism of proteins could be an important route for glutaric acid production. It follows that collagen breakdown (and protein breakdown in general) should be prevented by all possible means. Ascorbic acid is used to prevent multiple organ failure and to lessen mortality and morbidity in intensive care units.