These are great in shedding some light into who should be screened for POTS and MCAS
The connection between DGBI (Disorders of Gut-Brain Interaction, formerly known as functional GI disorders) and MCAS (Mast Cell Activation Syndrome) lies in overlapping symptoms and possible shared mechanisms involving immune dysregulation, nervous system hypersensitivity, and inflammation.
Both DGBI and MCAS commonly present with:
These similarities can make diagnosis tricky, especially in children or adolescents.
This can amplify the sensation of GI symptoms, even in the absence of structural disease.
Mast cells are heavily present in the gut lining. When they release mediators (histamine, prostaglandins, tryptase), they can cause:
In people with DGBI, some researchers suspect mast cells may be dysregulated even without full-blown MCAS.
Both conditions are frequently associated with:
This suggests a broader dysautonomic or connective tissue basis that may link MCAS and DGBI in some patients.
In some cases, patients initially labeled with DGBI may later be found to have MCAS, especially if symptoms are multi-systemic.
New medical position supports overlap or co-exist, especially in complex, multi-system presentations. Some patients diagnosed with DGBI may actually have subtle mast cell dysregulation contributing to symptoms.
The connection between DGBI (Disorders of Gut-Brain Interaction, formerly known as functional GI disorders) and MCAS (Mast Cell Activation Syndrome) lies in overlapping symptoms and possible shared mechanisms involving immune dysregulation, nervous system hypersensitivity, and inflammation.
Overlapping Symptoms
Both DGBI and MCAS commonly present with:
- Abdominal pain
- Bloating and gas
- Diarrhea and/or constipation
- Nausea
- Food sensitivities
- Fatigue, brain fog, anxiety
These similarities can make diagnosis tricky, especially in children or adolescents.
Nervous System Hypersensitivity
- DGBI is marked by visceral hypersensitivity and altered gut-brain signaling (e.g., IBS, functional dyspepsia).
- MCAS can provoke nerve endings and lead to neuroinflammation, heightening pain perception and GI motility changes.
This can amplify the sensation of GI symptoms, even in the absence of structural disease.
Mast Cells in the Gut
Mast cells are heavily present in the gut lining. When they release mediators (histamine, prostaglandins, tryptase), they can cause:
- Smooth muscle contractions → motility symptoms
- Increased gut permeability → leaky gut
- Stimulation of nerves → pain, urgency
In people with DGBI, some researchers suspect mast cells may be dysregulated even without full-blown MCAS.
Shared Comorbidities
Both conditions are frequently associated with:
- Ehlers-Danlos syndrome (hEDS)
- POTS (Postural Orthostatic Tachycardia Syndrome)
- Autoimmune conditions
- Allergies or atopy
This suggests a broader dysautonomic or connective tissue basis that may link MCAS and DGBI in some patients.
Diagnostic Complexity
- DGBI is a diagnosis of exclusion (based on Rome IV criteria).
- MCAS is harder to pin down; requires lab confirmation (e.g., elevated tryptase, histamine, or prostaglandin metabolites) and symptom criteria.
In some cases, patients initially labeled with DGBI may later be found to have MCAS, especially if symptoms are multi-systemic.
Treatment Overlap
- H1/H2 antihistamines
- Mast cell stabilizers (e.g., cromolyn)
- Low histamine diets
- Stress modulation (CBT, gut-directed hypnotherapy)
New medical position supports overlap or co-exist, especially in complex, multi-system presentations. Some patients diagnosed with DGBI may actually have subtle mast cell dysregulation contributing to symptoms.
