MCAD Manifestations of GU and GI disease - Dr. Anne Maitland - 2024 GLC

Dr. Anne Maitland reviews how mast cell activation can drive gastrointestinal and genitourinary symptoms commonly seen in hEDS and dysautonomia/POTS, including reflux, nausea, early satiety, bloating, alternating diarrhea/constipation, abdominal and pelvic pain, dysmotility (gastroparesis-like), SIBO, hernias/prolapse, and bladder issues like frequency, urgency, IC/BPS flares, and UTIs without clear infection. She explains mechanisms—connective tissue fragility, barrier dysfunction, neuro-immune crosstalk, and mast-cell mediators (histamine, prostaglandins, leukotrienes) affecting secretion, permeability, and smooth muscle tone—plus triggers (foods/biogenic amines, infections, hormones, stress, temperature changes, procedures/contrast, medications). Evaluation emphasizes ruling out structural disease, documenting flares and triggers, and considering MCAD workup (baseline/acute tryptase; 24-hr urine or spot metabolites such as N-methylhistamine, PGD2/11β-PGF2α, LTE4) alongside clinical response to therapy. Management is multimodal: trigger mitigation; H1/H2 antihistamines, mast cell stabilizers (e.g., cromolyn, ketotifen), leukotriene antagonists; careful use of PPIs/acid control; topical/vaginal therapies when appropriate; avoiding common MC triggers (opioids, NSAIDs, radiocontrast without premedication). Nonpharmacologic supports include individualized elimination then reintroduction (low-histamine/low-FODMAP when indicated), hydration/salt and compression for POTS, pelvic floor PT, bowel regimen, and coordinated care across allergy/immunology, GI, urogynecology, and pelvic pain specialists. She highlights the frequent overlap of MCAD with hEDS and POTS and the importance of validating symptoms, minimizing iatrogenic harm, and using stepwise, patient-centered plans.