Canine Chronic Enteropathy

What you might notice

• Loose or watery stools for three weeks or more, or stools that keep going back and forth between normal and loose
• Throwing up on and off, sometimes only once every few days
• Losing weight even though your dog is still eating
• Needing to go out more often, or more urgently, sometimes with mucus or a streak of fresh blood
• A gurgling, rumbling belly, or a lot of gas
• Picky appetite, or turning away from food she used to love
• Low energy, a dull coat, or looking generally 'off' for weeks
• A swollen belly or puffy legs and face — this can mean protein is leaking out of the gut, but a swollen belly or puffy limbs can also come from the heart, liver or kidneys, so it needs a vet to sort out which. Either way it needs a vet soon, not next month.
• Muscle trembling or twitching, twitching around the face, or rubbing the face — in a dog with low blood protein this can mean the blood calcium has fallen and needs testing
• Faster or heavier breathing than usual, or panting when resting — do not wait on this one, see the red flags below
• If your dog has been unwell like this for three weeks or more, book a vet visit rather than trying another food from the pet shop — the diet that works for this is a specific prescription type and the workup has to come first

Standard of care

1. Confirm the dog is stable, then run a strict elimination or hydrolysed-protein dietary trial FIRST

   Approved / guideline-backed

   Stability gate before the diet clock starts: a collapsing, dehydrated, hypoglycaemic, severely hypoalbuminaemic or rapidly deteriorating dog is stabilised and worked up, not put on a 2–4 week outpatient food trial. In a stable dog, feed a single hydrolysed-protein or novel-protein therapeutic diet exclusively for 2–4 weeks, with absolutely nothing else by mouth — no treats, no chews, no flavoured tablets, no table food. Re-score CIBDAI/CCECAI at the end of the trial. This is the intervention with the best evidence and the best benefit-to-risk ratio in the entire protocol, and nothing injectable should be positioned ahead of it.

   Named products: No drug. Commercial therapeutic hydrolysed-protein and limited-antigen diets. No FDA-approved animal drug carrying a labelled indication for canine chronic inflammatory enteropathy was located in this research. For contrast, maropitant IS approved by FDA's Center for Veterinary Medicine for dogs — for acute vomiting and motion sickness, a different indication — and its label restricts use by age (not for puppies under 8 weeks; the injectable and tablet labels differ on age for motion-sickness use, so read the label in hand). Therapeutic diets are also age- and life-stage-restricted: most hydrolysed and limited-antigen veterinary diets are formulated for adult maintenance and are NOT complete for growth, so a growing puppy, or a pregnant or lactating bitch, needs a diet chosen for that life stage. Check the label of the specific product.

   The 2026 ACVIM-endorsed consensus statement and systematic review evaluates dietary treatment as first-line and assesses all other treatments as additions to first-line dietary management. Direct trial evidence: a randomized, open-label, positively-controlled field trial in 26 dogs with naturally occurring chronic small-bowel enteropathy found that significantly more dogs on a hydrolysed protein diet remained asymptomatic at the second (p=0.0012) and third (p<0.001) re-evaluation than on a highly digestible control diet, with a significantly greater fall in CIBDAI (p=0.010). That trial is not clean and should not be presented as such: it was open-label, the arms were unequal (18 test vs 8 control, allocated 2:1), and despite randomisation baseline CIBDAI was significantly HIGHER in the hydrolysed-diet group (p=0.013); most dogs in both arms had already responded by the first re-evaluation with no difference between groups (p=0.87). The diet-first position rests on the ACVIM systematic review, not on this single trial. A retrospective multicentre cohort of 81 treatment-naive dogs found that where transition to a hydrolysed diet was the ONLY therapeutic change (16/81), 14/16 (88%) had a decreased stool-consistency score (p<0.001). Species: dog.

   Heilmann RM, Jergens AE, Kathrani A, Allenspach K, Salavati Schmitz S, Priestnall SL, Dandrieux JRS, O'Connor AM. ACVIM-endorsed statement: consensus statement and systematic review on guidelines for the diagnosis and treatment of chronic inflammatory enteropathy in dogs. J Vet Intern Med 2026;40(1). PMID 41742497. DOI 10.1093/jvimsj/aalaf017 · Mandigers PJJ, Biourge V, van den Ingh TSGAM, Ankringa N, German AJ. A randomized, open-label, positively-controlled field trial of a hydrolyzed protein diet in dogs with chronic small bowel enteropathy. J Vet Intern Med 2010;24(6):1350-7. PMID 21054541. DOI 10.1111/j.1939-1676.2010.0632.x · Rodrigues SD, et al. Association of diet with treatment response in dogs with chronic enteropathy: a retrospective multicenter study. J Vet Intern Med 2025;39(3):e70071. PMID 40326642. DOI 10.1111/jvim.70071

2. If the first diet fails, try a second, different diet before escalating to drugs

   Controlled trial in this species

   Change protein source and/or formulation class — hydrolysed to novel-protein, or to a restricted-fat or home-cooked restricted-fat formulation where lymphangiectasia is suspected. Give it another 2–4 weeks with the same strictness. A dog labelled 'non-responsive' after one diet has often only had one diet.

   In the same retrospective multicentre cohort, 23 dogs classified as non-responsive enteropathy were transitioned to an alternative diet; this was the sole therapeutic adjustment in 16/23 (70%), and of those 16 dogs, 11 (69%) had a fall in total CIBDAI (p<0.001). Fidelity note for anyone re-checking this: the published abstract prints that denominator inconsistently as '69% (11/23)', which cannot be right either way — 69% of 16 is 11 — so the figure is reported here as 11 of 16; verify against the full text before republishing. Observational, not randomized. Species: dog.

   Rodrigues SD, Mendoza B, Dias MJ, Santos NS, Hebert M, Bettin E, Signorelli F, Procoli F, Hernandez J, Leal RO. Association of diet with treatment response in dogs with chronic enteropathy: a retrospective multicenter study. J Vet Intern Med 2025;39(3):e70071. PMID 40326642. DOI 10.1111/jvim.70071

3. Correct cobalamin (vitamin B12) deficiency in every dog whose level is low

   Approved / guideline-backed

   Supplement cobalamin whenever serum cobalamin is low or low-normal, and recheck. Both daily oral tablets and parenteral injection work; the oral route removes the need for repeated clinic visits, which matters for owner compliance over months. This is cheap, safe, and it is one of the few variables in this disease with a documented link to outcome.

   Named products: Cyanocobalamin (oral tablets) and hydroxocobalamin (parenteral). The doses above are the body-weight-banded doses used in the cited randomized study — 0.25–1.0 mg oral cyanocobalamin daily, 0.4–1.2 mg parenteral hydroxocobalamin — reported as what that trial administered, NOT offered as a prescription; the parenteral dosing interval is specified in the paper's protocol and should be read there rather than assumed. Recheck serum cobalamin at approximately 28 and 90 days, as the trial did. Cobalamin has a wide safety margin and no dose-limiting toxicity was reported, but these are human-labelled vitamin preparations used extra-label in dogs and no veterinary NADA number is claimed here. Dosing in a puppy or a very small dog should be set by the prescribing veterinarian, not scaled by the owner.

   Randomized controlled study in 53 dogs with chronic enteropathies and serum cobalamin <285 ng/L (reference interval 244–959 ng/L). Dogs received either daily oral cyanocobalamin tablets, 0.25–1.0 mg/day banded by body weight (n=27), or parenteral hydroxocobalamin, 0.4–1.2 mg banded by body weight (n=26). ALL dogs in BOTH arms were within or above the reference interval by day 28. The direction of the day-90 result matters and is easy to misread: concentrations changed significantly between day 28 and day 90 in both arms (p<0.001), but they FELL in the parenteral arm (median 2107 → 877 ng/L) while continuing to RISE in the oral arm (median 975 → 1244 ng/L) — i.e. daily oral dosing held concentrations at least as well as injection, which is the better argument for the oral route than any claim of a 'sustained increase' in both arms. Serum was rechecked at 28±5 and 90±15 days. Separately, hypocobalaminaemia <200 ng/L was identified on univariate analysis as a risk factor for negative outcome in 70 dogs with chronic enteropathy. Species: dog.

   Toresson L, Steiner JM, Razdan P, Spodsberg E, Olmedal G, Suchodolski JS, Spillmann T. Comparison of efficacy of oral and parenteral cobalamin supplementation in normalising low cobalamin concentrations in dogs: a randomised controlled study. Vet J 2018;232:27-32. PMID 29428088. DOI 10.1016/j.tvjl.2017.12.010 · Allenspach K, Wieland B, Gröne A, Gaschen F. Chronic enteropathies in dogs: evaluation of risk factors for negative outcome. J Vet Intern Med 2007;21(4):700-8. PMID 17708389

4. In young Boxers and French Bulldogs, exclude granulomatous colitis BEFORE any immunosuppression

   Controlled trial in this species

   This is a hard gate, not a suggestion. A young Boxer or French Bulldog with large-bowel diarrhoea and haematochezia that has not responded to empirical therapy needs colonoscopy with biopsies and FISH for invasive intramucosal E. coli before glucocorticoids are considered. Immunosuppressing an invasive bacterial colitis treats the wrong disease and delays a treatment that produces lasting remission. Fluoroquinolone choice, dose and duration, and culture-guided susceptibility, are the prescribing veterinarian's decision — resistance in this disease is documented and empirical treatment without biopsy confirmation is not the recommendation here.

   Named products: Enrofloxacin, marbofloxacin (fluoroquinolones). Label constraints that must not be omitted: fluoroquinolones are contraindicated in growing dogs because of cartilage damage — the US enrofloxacin label restricts use in small and medium breeds during the rapid growth phase (roughly 2 to 8 months) and warns against use in large and giant breeds during growth, which can extend to 18 months — and this disease presents in dogs under one year old, so the age conflict is real and is the veterinarian's to weigh and document. Enrofloxacin also carries a label contraindication in cats above 5 mg/kg/day because of irreversible retinal degeneration and blindness: never move a dog's fluoroquinolone to a cat. Fluoroquinolones lower the seizure threshold and should be used cautiously in dogs with a seizure history, and their absorption is reduced by aluminium-, calcium-, magnesium- and iron-containing products including antacids and some supplements. Neither drug carries an FDA-approved labelled indication for granulomatous colitis; use here is extra-label.

   Retrospective case series of 6 French Bulldogs with histological granulomatous colitis: ALL were ≤1 year of age with haematochezia refractory to empirical therapy, clinicopathological and faecal analysis were unremarkable, and multifocal PAS-positive macrophages with intramucosal E. coli were present in colonic biopsies of all 6 on 16S rRNA probe evaluation. Enrofloxacin (5/6) or marbofloxacin (1/6) at 4.4–10 mg/kg (median 10 mg/kg) PO q24h for 6–10 weeks was associated with clinical improvement within 5–14 days, and all dogs remained in remission over 3–30 months of follow-up. The disease closely parallels granulomatous colitis of Boxer dogs. A separate case report confirms the FISH-based diagnosis and enrofloxacin response with near-complete remission within 6 weeks. Retrospective, uncontrolled, n=6. Species: dog.

   Manchester AC, Hill S, Sabatino B, Armentano R, Carroll M, Kessler B, Miller M, Dogan B, McDonough SP, Simpson KW. Association between granulomatous colitis in French Bulldogs and invasive Escherichia coli and response to fluoroquinolone antimicrobials. J Vet Intern Med 2013;27(1):56-61. PMID 23206120. DOI 10.1111/jvim.12020 · Sims CS, Nagle J, Tolbert MK, Anderson K, Linder K, Neel J. Correlation of cytology to histology in a case of canine granulomatous colitis in a Boxer dog. Vet Clin Pathol 2021;50 Suppl 1:83-87. PMID 34664295. DOI 10.1111/vcp.13058

5. Add glucocorticoid immunosuppression only for genuinely diet-refractory disease, after biopsies, then taper

   Controlled trial in this species

   Two prerequisites before the first dose: biopsies taken (or a documented decision not to), and hypoadrenocorticism and infectious colitis excluded. Then prednisolone as the usual first immunosuppressant, on top of — not instead of — the diet, with a planned taper driven by serial CCECAI and albumin rather than by the calendar. Ciclosporin or chlorambucil are added in refractory cases and in protein-losing enteropathy. Which combination you choose appears to matter less than the patient's starting severity. Owners must be told explicitly to call before changing, skipping, stopping or doubling any dose, and that abrupt withdrawal of a glucocorticoid after prolonged use risks an iatrogenic adrenal crisis.

   Named products: Prednisolone, cyclosporine (ciclosporin), chlorambucil. None of these was found to carry an FDA-approved labelled indication for canine chronic inflammatory enteropathy; use in this disease is extra-label under AMDUCA and is the prescribing veterinarian's clinical decision. Label constraints and limits that belong on the page: GLUCOCORTICOIDS — contraindicated or used only with explicit justification in animals with systemic fungal infection, in dogs with untreated infection, in diabetes mellitus, in corneal ulceration, and in pregnancy (corticosteroids are associated with fetal loss and abnormalities and with premature parturition); expect polyuria, polydipsia, polyphagia, panting, muscle wasting and behavioural change, with iatrogenic hyperadrenocorticism, GI ulceration, delayed wound healing, opportunistic infection and a diabetogenic effect on longer courses; growth suppression is a real concern in growing dogs. NEVER combine a glucocorticoid with an NSAID. Cats require prednisoLONE rather than prednisone because they convert prednisone poorly — another reason canine prescriptions must never be shared across species. CYCLOSPORINE — vomiting and diarrhoea are common early, plus gingival hyperplasia and papillomatosis; it is an immunosuppressant, so opportunistic and fatal infections including toxoplasmosis and systemic fungal disease are a recognised risk and it should not be given to dogs with a history of neoplasia; it is a CYP3A and P-glycoprotein substrate, so ketoconazole and other azoles, macrolides, and grapefruit-type inhibitors raise blood concentrations substantially, while phenobarbital and rifampin lower them. The FDA-approved canine cyclosporine products are labelled for atopic dermatitis with minimum age and body-weight limits (commonly not for dogs under 6 months or under about 1.8 kg / 4 lb) — read the label of the product in hand. CHLORAMBUCIL — a cytotoxic alkylating agent requiring serial CBCs for myelosuppression; contraindicated in pregnancy; see the safety section for the household handling rules.

   The FRE/IRE classification itself comes from a sequential treatment trial of 70 dogs given an elimination diet followed by steroids only on dietary failure. In a retrospective cohort of 148 dogs with immunosuppressant-responsive enteropathy (113 prednisolone alone, 21 prednisolone + cyclosporine, 14 prednisolone + chlorambucil), 79% were responders at 1 month and 59.5% at 6 months, with 21% and 27% non-responders respectively; therapeutic response was NOT influenced by which immunosuppressive protocol was used, but by hypoalbuminaemia, hypocobalaminaemia and the need for a home-cooked restricted-fat diet. Most deaths and euthanasias occurred within one month of diagnosis. Retrospective, unblinded, no control arm. Species: dog.

   Borella F, Benvenuti E, Pierini A, Borrelli A, Cagnasso F, Zanatta R, Marchetti V, Gianella P. Retrospective evaluation of short- and medium-term therapeutic response to different immunosuppressive and dietary approaches in 148 dogs diagnosed with immunosuppressant-responsive enteropathy. Open Vet J 2025;15(9):4470-4481. PMID 41200357. DOI 10.5455/OVJ.2025.v15.i9.53 · Allenspach K, Wieland B, Gröne A, Gaschen F. J Vet Intern Med 2007;21(4):700-8. PMID 17708389

6. Restrict fat where there is protein-losing enteropathy or intestinal lymphangiectasia

   Early evidence

   A restricted-fat diet, commercial or home-prepared, is the core dietary strategy once lymphangiectasia is on the table. Watch body condition and muscle mass actively in this group — these dogs are frequently underweight at presentation and malnutrition worsens outcome. Because fat restriction also restricts fat-soluble vitamin intake in dogs who already malabsorb them, monitor ionised calcium and vitamin D status in this group rather than assuming the diet alone is sufficient.

   Named products: No drug in this step. Where hypocalcaemia or hypovitaminosis D is confirmed, calcium and vitamin D supplementation is a veterinarian-directed, monitored intervention — vitamin D has a narrow margin and over-supplementation causes hypercalcaemia and renal injury, so it must never be started or adjusted by an owner without repeat bloodwork.

   Review-level, not trial-level. A dedicated review of dietary and nutritional management in canine and feline chronic enteropathy states that fat restriction is the main dietary strategy for intestinal lymphangiectasia, and that approximately two-thirds of dogs with protein-losing enteropathy from chronic enteropathy or lymphangiectasia are underweight. In the 148-dog retrospective above, needing a home-cooked restricted-fat diet was itself a marker of poorer response — i.e. it identifies the severe end of the disease. Ionised hypocalcaemia with hypovitaminosis D is separately documented in canine PLE and lymphangiectasia, including a case presenting with seizures. Species: dog and cat review; the fat-restriction position is applied here to dogs only.

   Kathrani A. Dietary and nutritional approaches to the management of chronic enteropathy in dogs and cats. Vet Clin North Am Small Anim Pract 2021;51(1):123-136. PMID 33131914. DOI 10.1016/j.cvsm.2020.09.005 · Mellanby RJ, Mellor PJ, Roulois A, Baines EA, Mee AP, Berry JL, Herrtage ME. Hypocalcaemia associated with low serum vitamin D metabolite concentrations in two dogs with protein-losing enteropathies. J Small Anim Pract 2005;46(7):345-51. PMID 16035452. DOI 10.1111/j.1748-5827.2005.tb00331.x

7. Do NOT reach for metronidazole reflexively — the evidence argues against it

   Controlled trial in this species

   This is a de-escalation step, and it belongs in a standard-of-care list because reflexive metronidazole is one of the commonest management errors in this disease. Reserve antibiotics for a documented indication.

   Named products: Metronidazole — named here as a therapy to use restrictively, not as a recommendation. If it is used anyway: it is dose- and duration-dependently neurotoxic in dogs, causing vestibular and cerebellar signs (generalised ataxia, vertical positional nystagmus) and encephalopathy, documented at 67.3–129.0 mg/kg/day given for 3–14 days, with 2 of 5 affected dogs euthanised and the survivors taking months to recover (Dow et al. J Am Vet Med Assoc 1989;195(3):365-8, PMID 2768064 — the authors concluded that then-recommended doses may be too high for some dogs). Dose must be reduced in hepatic dysfunction, as metronidazole is hepatically metabolised. It is contraindicated in pregnancy (mutagenic and carcinogenic in rodent studies) and should be avoided in breeding animals. Any ataxia, head tilt, nystagmus or wobbliness in a dog on metronidazole means stop the drug and call the vet the same day.

   A 14-day course of metronidazole in healthy pet dogs significantly decreased faecal microbial richness and key taxa including Fusobacteria (q<0.001), significantly raised the qPCR dysbiosis index (p<0.001), raised faecal lactate and lowered the secondary bile acids deoxycholic and lithocholic acid (p<0.001) — and these changes had NOT fully resolved 4 weeks after the drug was stopped. In a separate prospective, randomized, blinded trial in 27 dogs with acute diarrhoea, metronidazole negatively affected the microbiome while producing no significant difference in the Canine Acute Diarrhea Severity index, faecal consistency or defecation frequency versus a synbiotic — except for the CADS index on one single day. Note the population: that second trial was acute diarrhoea, not chronic enteropathy. Species: dog.

   Pilla R, Gaschen FP, Barr JW, et al. Effects of metronidazole on the fecal microbiome and metabolome in healthy dogs. J Vet Intern Med 2020;34(5):1853-1866. PMID 32856349. DOI 10.1111/jvim.15871 · Stübing H, Suchodolski JS, Reisinger A, Werner M, Hartmann K, Unterer S, Busch K. The effect of metronidazole versus a synbiotic on clinical course and core intestinal microbiota in dogs with acute diarrhea. Vet Sci 2024;11(5):197. PMID 38787169. DOI 10.3390/vetsci11050197

8. Treat faecal microbiota transplantation as unproven, not as standard

   Early evidence

   FMT is safe in the published canine trials and is being actively studied, but in dogs it has not yet beaten a diet change in a controlled comparison. It is reasonable inside a study or as a considered adjunct in refractory disease; it is not a first-line or second-line recommendation, and it should not be sold as one.

   Blinded randomized controlled trial, 42 dogs with chronic enteropathy: FMT by single retention enema plus diet change (n=25) versus diet change alone (n=17). Owner-defined clinical improvement at day 90 was 76% (CI 54–90%) with FMT versus 73% (CI 40–92%) without — no significant difference in owner-reported improvement, CIBDAI or faecal score. The authors note the similar outcome supports high rates of food responsiveness in this population, and that a type II error cannot be excluded. A double-blinded randomized trial of 13 dogs adding FMT to corticosteroid plus hypoallergenic diet found CCECAI fell significantly over time in both arms with no between-group difference (p=0.40). A prospective, randomized, double-blind, placebo-controlled trial of oral FMT in dogs with tylosin-responsive enteropathy (14 entered treatment, 13 analysed: 7 FMT, 6 placebo) found variable microbiome changes and inconsistent clinical response with no clear treatment-specific effect; relapse occurred in 2/7 FMT and 3/6 placebo dogs. Species: dog.

   Allerton F, Whittle MJ, Durkin L, et al. Clinical benefit of faecal microbiota transplantation administered via a single retention enema as an adjunctive treatment in dogs with chronic enteropathy: a randomised controlled trial. J Small Anim Pract 2026;67(9):798-809. PMID 41997887. DOI 10.1111/jsap.70137 · Collier AJ, Gomez DE, Monteith G, et al. Investigating fecal microbial transplant as a novel therapy in dogs with inflammatory bowel disease: a preliminary study. PLoS One 2022;17(10):e0276295. PMID 36256653. DOI 10.1371/journal.pone.0276295 · Hanifeh M, Huhtinen M, Ganz HH, Heilmann RM, Huang W, Spillmann T, Suchodolski JS. Clinical trial reveals limited clinical and microbiome effects following oral fecal microbiota transplantation in dogs with chronic enteropathy responsive to tylosin. J Am Vet Med Assoc 2026:1-11. PMID 42486172. DOI 10.2460/javma.26.03.0178

9. Probiotics and synbiotics: biomarker effects yes, proven clinical benefit no

   Early evidence

   Reasonable, low-risk adjuncts on top of the diet. Do not promise that they change the clinical course, because the controlled trials in dogs do not show that.

   Randomized, double-blind, placebo-controlled trial, 20 completers (11 supplement, 9 placebo), all fed a hydrolysed diet: the synbiotic-IgY supplement lowered faecal calprotectin and CRP and shifted mucosal microbiota, but clinical activity and endoscopic scores decreased in BOTH groups — i.e. the clinical improvement is attributable to the diet. A prospective randomized blinded placebo-controlled trial of Enterococcus faecium added to a hydrolysed elimination diet had 12 completers of 45 recruited (7 synbiotic, 5 placebo) and found no difference in clinical efficacy, histology scores or the expression of any of the 22 intestinal genes measured; the authors state the study was underpowered. A randomized controlled pilot of prebiotics plus glycosaminoglycans versus placebo on a hydrolysed diet found no significant difference in CCECAI, endoscopic or histological score, with a post-hoc calculation that 63 dogs per group would have been required. Species: dog.

   Sahoo DK, Allenspach K, Mochel JP, et al. Synbiotic-IgY therapy modulates the mucosal microbiome and inflammatory indices in dogs with chronic inflammatory enteropathy: a randomized, double-blind, placebo-controlled study. Vet Sci 2022;10(1):25. PMID 36669027. DOI 10.3390/vetsci10010025 · Schmitz S, Glanemann B, Garden OA, Brooks H, Chang YM, Werling D, Allenspach K. A prospective, randomized, blinded, placebo-controlled pilot study on the effect of Enterococcus faecium on clinical activity and intestinal gene expression in canine food-responsive chronic enteropathy. J Vet Intern Med 2015;29(2):533-43. PMID 25776251. DOI 10.1111/jvim.12563 · Glanemann B, Seo YJ, Priestnall SL, et al. Clinical efficacy of prebiotics and glycosaminoglycans versus placebo in dogs with food responsive enteropathy receiving a hydrolyzed diet: a pilot study. PLoS One 2021;16(10):e0250681. PMID 34673776. DOI 10.1371/journal.pone.0250681

10. Score, monitor, and act on the prognostic markers

    Approved / guideline-backed

    Record CCECAI (or CIBDAI) and serum albumin at every recheck, and recheck cobalamin. Dogs with low albumin are the ones who die, and they die early — plan follow-up density accordingly rather than seeing everybody at the same interval. In any dog that stays hypoalbuminaemic, keep the urine protein:creatinine ratio and hepatic assessment in view rather than assuming the gut is the only leak.

    In 70 dogs followed for three years, 13 (18%) were euthanised for intractable disease; a high clinical activity index, a high duodenal endoscopic score, hypocobalaminaemia <200 ng/L and hypoalbuminaemia <20 g/L were risk factors for negative outcome on univariate analysis, and the CCECAI was derived from that same cohort by logistic regression and ROC analysis specifically to predict negative outcome — derivation, not external validation. In 148 dogs, most deaths or euthanasias occurred within one month of diagnosis and non-responders were overwhelmingly the protein-losing phenotype (79.3% of non-responders at 1 month). Species: dog.

    Allenspach K, Wieland B, Gröne A, Gaschen F. Chronic enteropathies in dogs: evaluation of risk factors for negative outcome. J Vet Intern Med 2007;21(4):700-8. PMID 17708389. DOI 10.1892/0891-6640(2007)21[700:ceideo]2.0.co;2 · Borella F, et al. Open Vet J 2025;15(9):4470-4481. PMID 41200357

How it is diagnosed

• Triage for stability FIRST. A dog that is collapsing, dehydrated, hypoglycaemic, hypothermic, dyspnoeic or rapidly deteriorating is stabilised and worked up as an inpatient — sequential outpatient therapeutic trials are for stable dogs only.
• History and diet review: how long, what pattern, what the dog actually eats including treats, chews, flavoured medications and table food. A leaky diet history is the most common reason a dietary trial 'fails'. Ask explicitly about any human medication given at home — NSAIDs and acetaminophen given by owners are a recurring, and reversible, cause of gastrointestinal injury and can confound the entire picture.
• Exclude parasites and infection: faecal examination including Giardia antigen testing, and an appropriate anthelmintic trial before calling anything idiopathic.
• Exclude the systemic mimics and quantify the laboratory picture: CBC, serum biochemistry with albumin and total protein, urinalysis, basal cortisol with ACTH stimulation where indicated (hypoadrenocorticism presents as chronic GI disease and is missed), serum cobalamin and folate, TLI to exclude exocrine pancreatic insufficiency, and cPLI where pancreatitis is a differential.
• In any hypoalbuminaemic dog, do NOT assume the gut. Albumin is lost from three compartments — intestine, kidney and liver — so add a urine protein:creatinine ratio and hepatic assessment (bile acids or ammonia, with imaging) before committing to an enteric diagnosis. Soft-Coated Wheaten Terriers are the classic example of simultaneous familial protein-losing enteropathy and protein-losing nephropathy (Vaden et al. Am J Vet Res 2000;61(5):518-24, PMID 10803646).
• In any hypoalbuminaemic or protein-losing dog, also measure ionised calcium, magnesium and vitamin D status (25-hydroxyvitamin D) with PTH where available. Ionised hypocalcaemia with hypovitaminosis D is documented in canine PLE and lymphangiectasia and can present as tremors, facial rubbing, twitching, tetany or seizures (Mellanby et al. J Small Anim Pract 2005;46(7):345-51, PMID 16035452; Whitehead et al. J Am Anim Hosp Assoc 2015;51(6):380-4, PMID 26535456; de Brito Galvão et al. Vet Clin North Am Small Anim Pract 2017;47(2):249-256, PMID 28012786).
• In a young Boxer or French Bulldog with large-bowel signs and haematochezia, pursue colonoscopy with colonic biopsies and fluorescence in situ hybridisation (FISH) for invasive intramucosal E. coli BEFORE any immunosuppressive trial. Granulomatous colitis is fluoroquinolone-responsive and immunosuppressing it treats the wrong disease (Manchester 2013, PMID 23206120; Sims et al. Vet Clin Pathol 2021;50 Suppl 1:83-87, PMID 34664295).
• Score baseline disease burden with the CIBDAI or CCECAI, and record it — without a baseline score you cannot demonstrate response later.
• Abdominal ultrasound to look for lacteal dilatation, altered wall layering, lymphadenopathy, mass lesions and free fluid; this is where lymphangiectasia and neoplasia start to separate out.
• Sequential therapeutic trials in stable dogs — diet first, per the ACVIM-endorsed guideline — reserving endoscopy for dogs that fail dietary management.
• Endoscopy with multiple mucosal biopsies from several segments, read against WSAVA GI Standardization Group criteria, in dogs that fail a dietary trial and up-front in dogs that are hypoalbuminaemic or systemically unwell. This is the step that separates CIE from alimentary lymphoma, lymphangiectasia and fungal enteritis.
• Sequencing rule: do NOT start glucocorticoids before biopsies are taken. Steroids blur the histological separation of chronic enteropathy from alimentary lymphoma and can partially treat lymphoma, and they must not precede exclusion of hypoadrenocorticism or of infectious colitis. If a dog is sick enough to need immunosuppression now, it is sick enough to be scoped first or to have the decision made explicitly and recorded.