Eosinophilic gastritis, eosinophilic enteritis and eosinophilic colitis are the eosinophilic gastrointestinal disorders that affect the stomach, small bowel and colon. They share the same eosinophil-rich, immune-mediated inflammation as eosinophilic esophagitis (EoE), but they are rarer, more heterogeneous, and until recently far less consistently named.
Naming and depth of disease
An international consensus now names each disorder by the segment it involves: eosinophilic gastritis (EoG) for the stomach, eosinophilic enteritis (EoN) for the small bowel, with the option to specify duodenitis, jejunitis or ileitis, and eosinophilic colitis (EoC) for the colon. When two or more segments are affected, all of them are named; the historical term eosinophilic gastroenteritis is now kept only for disease that involves both the stomach and the small bowel. Multisegment disease occurs in an estimated 41% of patients and is more common in children.
EoG and EoN were originally classified by the layer of the bowel wall that is predominantly involved, the Klein classification:
- mucosal, the most common form at 44% to 57% of cases: the inflammation sits in the innermost layer and produces abdominal pain, nausea, vomiting, bloating, diarrhoea and early satiety; extensive small bowel involvement can cause malabsorption and protein-losing enteropathy.
- muscular, 12% to 30%: the wall thickens and can obstruct, producing the more severe pain, nausea and vomiting of pyloric or duodenal stenosis.
- serosal, 12.5% to 49%: eosinophil-rich ascites produces abdominal bloating, distension and pain.
Clinical features
Symptoms are non-specific, which is why the diagnosis is often delayed. The most common are nausea and vomiting (54%) and abdominal pain (48%), followed by bloating, poor appetite, early satiety, diarrhoea and weight loss. EoC is the rarest form and typically produces abdominal pain (60%), diarrhoea (52%), nausea and vomiting (38%) and bloody stools (24%).
Two laboratory clues raise the chance that a biopsy will be diagnostic: a raised peripheral eosinophil count and a low serum albumin. Atopic disease is common alongside the gut disease. Endoscopic appearance helps as well: in eosinophilic gastritis the common findings are erythema (72%), raised lesions (49%), erosions (46%) and granularity (35%), and these features are graded by the Eosinophilic Gastritis Endoscopic Reference System (EG-REFS).
Diagnosis
The diagnosis is clinicopathological: chronic symptoms together with a tissue eosinophil count above the threshold for the segment involved, after secondary causes have been excluded. As in EoE, a histological finding on its own, without chronic symptoms, is not enough. The thresholds differ from one segment to another:
| Segment | Threshold |
|---|---|
| Stomach (EoG) | ≥30 eos/hpf |
| Duodenum (EoN) | ≥50 eos/hpf |
| Jejunum and ileum (EoN) | ≥60 eos/hpf |
| Caecum and ascending colon (EoC) | ≥100 eos/hpf |
| Transverse and descending colon | ≥80 eos/hpf |
| Rectum and sigmoid colon | ≥60 eos/hpf |
eos/hpf, eosinophils per high-power field.
Because the colon has a wide normal range of eosinophils that falls from the proximal to the distal colon, biopsy specimens must be separated by segment for the pathologist to interpret them. Which layer is involved decides how tissue is obtained: mucosal disease by endoscopic biopsy, muscular disease by cross-sectional imaging and often full-thickness or surgical specimens, and serosal disease by imaging with diagnostic paracentesis. Alternative diagnoses must be excluded, particularly inflammatory bowel disease, autoimmune disease and hypereosinophilic syndrome.
Treatment and course
Management aims at symptom relief and histological remission in the short term, and at preventing long-term complications such as bowel obstruction, upper gastrointestinal bleeding and perforation. The treatments mirror those of EoE: proton pump inhibitors, corticosteroids (systemic to induce remission, followed by topical budesonide directed at the affected segment), and elimination or elemental diets. Mesalamine is used in some cases of EoC, and mast cell stabilisers are occasionally added as steroid-sparing therapy. Several biologics are under study for the non-EoE EGIDs, among them lirentelimab, benralizumab and dupilumab, but none is yet standard.
The course is chronic in more than half of patients: some have a single flare, some a relapsing course, and some continuous disease. Multisegment or progressive disease tends to need longer and more intensive treatment.