Gastroenterology & Immunology & Family Medicine & Nutrition
Celiac disease (gluten intolerance)
Celiac disease is a systemic autoimmune enteropathy triggered by ingestion of gluten - a storage protein found in wheat (gliadins), barley (hordeins) and rye (secalins) - in genetically predisposed individuals carrying HLA-DQ2 (HLA-DQA1*05/DQB1*02 - present in 90-95 % of patients) or HLA-DQ8 (DQA1*03/DQB1*03:02 - present in the remaining 5-10 %). It affects around 1 % of the world's population, with a prevalence of 0.5-1 % in Canada, but remains largely under-diagnosed - an estimated 70-80 % of sufferers remain undiagnosed. The central mechanism involves an adaptive (gliadin-specific CD4+ T lymphocytes in the lamina propria) and innate (activation of IELs - intraepithelial lymphocytes) immune response that leads to progressive destruction of the intestinal villi of the proximal small intestine, resulting in malabsorption. The main autoantigen is tissue transglutaminase (tTG2), an enzyme that deaminates the glutamine residues of gliadins, increasing their immunogenicity to HLA-DQ2/DQ8 molecules. The clinical picture is extremely polymorphic - from the classic form with chronic diarrhea and malabsorption to silent or extra-intestinal forms (iron-deficiency anemia, osteoporosis, neuropathy, infertility, elevated transaminases) - which explains the average diagnostic delay of 6 to 10 years. The only effective treatment is a strict, lifelong gluten-free diet (GFD), which normalizes antibodies, heals the intestinal mucosa and prevents complications (intestinal T-cell lymphoma, other digestive cancers, osteoporosis).
Pathogenesis, genetics, and clinical presentation
- Immunopathogenesis and Molecular Mechanisms of Celiac Disease gluten and immunogenic peptides: gluten is a composite protein → gliادins (alcohol-soluble fraction) + glutenins (insoluble fraction) → gliadins contain peptide sequences rich in glutamine and proline → resistant to complete digestion by gastric + pancreatic + brush border proteases → the peptide 33-mer of α-gliadin is the main immunogenic peptide → survives digestion + crosses intestinal epithelium transcellularly (transcytosis) + paracellularly (tight junctions altered) → role of tissue transglutaminase 2 (tTG2) : ubiquitous enzyme → deaminates glutamine residues to glutamic acid on gliadin peptides → deaminated peptides → stronger binding to HLA-DQ2/DQ8 molecules on APCs (antigen-presenting cells) → presentation to CD4+ helper T lymphocytes → Sollid 2002 - Nature Reviews Immunology: molecular mechanisms of celiac disease + role of tTG2 + adaptive immune response: deaminated peptides presented by APCs to CD4+ LTs → activation of specific CD4+ LTs → production of pro-inflammatory cytokines (IL-21 + IFN-γ + TNF-α) → inflammation of the lamina propria → activation of B lymphocytes → production of anti-tTG2 + anti-deaminated gliadin (anti-DGP) antibodies + innate immune response: activation of IELs (Intraepithelial Lymphocytes - CD8+ + TCR γδ) → expression of cytotoxic molecules (NKG2D + NKp46) → kill enterocytes → villous destruction → the combination of both pathways → villous atrophy + crypt hyperplasia → Marsh-Oberhuber histological classification: Marsh 0: normal mucosa → Marsh 1: increased IEL (>25/100 enterocytes) → Marsh 2: increased IEL + crypt hyperplasia → Marsh 3a: mild villous atrophy → Marsh 3b: moderate atrophy → Marsh 3c: total atrophy (flattened) → Marsh 4: total atrophy + crypt hypoplasia (very rare) → celiac diagnosis requires Marsh ≥2 (usually Marsh 3); genetic: HLA-DQ2 (DQA1*05/DQB1*02): 90-95 % of patients → HLA-DQ2 homozygosite → increased risk + HLA-DQ8 (DQA1*03/DQB1*03:02): 5-10 % of patients → HLA-DQ2 and HLA-DQ8 present in 30-35 % of the general population → but only 1-2 % develop the disease → HLA is necessary but not sufficient → other genes contributing to risk: CTLA4 + PTPN2 + TAGAP + mucosal immunity genes + environmental factors (microbiome + viral infections + mode of introduction of gluten in early childhood) play a role in the onset
- Clinical presentation and associated diseases: classic presentations (malabsorption): chronic diarrhea + steatorrheic stools + abdominal pain + bloating + abdominal distension + weight loss + delayed growth and development (children) + malabsorption syndrome : iron deficiency (iron deficiency anemia) + vitamin D and calcium deficiency (osteopenia + osteoporosis) + vitamin B12 + B9 (folates) + K + zinc + copper + magnesium deficiency + low albumin + hypoprotidemia + steatorrhea → atypical or extra-intestinal presentations (increasingly diagnosed forms): hematological: iron deficiency anemia refractory to oral treatment → always investigate celiac disease in an adult with unexplained iron deficiency anemia (Hershko 2005 - American Journal of Gastroenterology) + cutaneous: dermatitis herpetiformis (DH) - cutaneous form of celiac disease → symmetrical pruritic vesicles on surfaces of extension + buttocks + scalp → IgA in papillary dermis (direct immunofluorescence on perilesional skin) + underlying celiac enteropathy in almost 100 % + osteological: osteopenia + osteoporosis + pathological fractures → even in the absence of digestive symptoms + neurological: peripheral neuropathy + gluten ataxia (anti-ganglioside or anti-tTG6 antibodies) + encephalopathy + epilepsy with occipital calcifications + gynecological: infertility + repeated spontaneous abortions + delayed puberty + menstrual irregularities + hepatological: elevated transaminases (<3× la normale) → hypertransaminasémie cryptogénique → bilan systématique de la cœliaque dans ce contexte (Vajro 2012 — Journal of Pediatric Gastroenterology and Nutrition) + endocriniennes : DT1 + thyroïdite de Hashimoto + maladie de Basedow + prévalence cœliaque 5–8 % dans le DT1 + bucco-dentaires : aphtes récidivants + hypoplasie de l'émail dentaire + troubles psychiatriques : dépression + anxiété + irritabilité + troubles de la concentration + maladie cœliaque silencieuse ou asymptomatique : diagnostic lors d'un dépistage chez les apparentés de 1er degré → prévalence : 10–20 % des proches d'un patient cœliaque → prévalence chez les enfants de parents cœliaques : 10–15 % + groupes à risque de maladie cœliaque (prévalence 3–10 %) : DT1 + thyroïdite auto-immune + syndrome de Down + syndrome de Turner + syndrome de Williams + dermatite herpétiforme + IgA totales basses + deficit en IgA + apparentés 1er degré de patients cœliaques (10–15 %)
Diagnosis, treatment and follow-up
| Domain | Data, criteria and procedures | Key studies and recommendations |
|---|---|---|
| Diagnostic serology and duodenal biopsy Anti-tTG IgA — anti-DGP IgG — anti-EMA — Total IgA — Duodenal biopsy — Marsh — serology — diagnostic criteria — gluten challenge |
Serological tests for the diagnosis of celiac disease: prerequisites ABSOLUTELY REQUIRED before serology and biopsy: the patient must be consuming gluten regularly at the time of testing (gluten-containing diet = minimum 1 to 2 slices of bread/d for at least 6 weeks) → an RSG before testing → normalization of antibodies + partial healing of the mucosa → NEGATIVE FALSE → if the patient is already on RSG without a confirmed diagnosis → a «gluten challenge» (reintroduction of gluten × 6-12 weeks) should be considered before serology and biopsy → anti-tTG IgA (anti-transglutaminase IgA antibodies - ELISA): 1st-line test → sensitivity: 92-98 % + specificity: 94-98 % → Rostom 2005 - Gastroenterology (meta-analysis): anti-tTG IgA = best screening test → very high titre (>10× upper limit of normal) → very high positive predictive value (>99 %) → may dispense with biopsy in children according to ESPGHAN 2020 guidelines (Husby) → but biopsy still recommended in adults according to ACG 2023 + NASPGHAN + total serum IgA : MANDATORY assay at the same time as anti-tTG IgA → selective IgA deficiency (general prevalence 1/300 - 10-15× more frequent in celiac) → false-negative anti-tTG IgA → if low total IgA : resort to IgG anti-tTG or IgG anti-DGP (IgG deaminated anti-gliadin antibodies) → IgG anti-DGP + IgG anti-tTG: useful if IgA deficiency → or if IgA anti-tTG weakly positive or doubtful → IgA anti-endomysium (EMA): indirect immunofluorescence on monkey oesophagus → slightly lower sensitivity than anti-tTG + costly + operator-dependent → reserved for confirmation of doubtful IgA anti-tTG → HLA-DQ2/DQ8: useful: exclude celiac disease if negative (almost no negative predictive value) → indicated if : patient undergoing RSG without confirmed diagnosis (cannot do gluten challenge) + discordant results between serology and histology + assessment of relatives + prophylactic pre-RSG assessment + interpretation of serological results: very high anti-tTG IgA (>10× LSN) + positive anti-EMA : probability of celiac >99 % → biopsy will confirm + anti-tTG IgA low (1-10× LSN): to be confirmed by anti-EMA + biopsy → anti-tTG IgA negative: celiac unlikely → but check total IgA + IgG work-up if IgA deficient + HLA-DQ2/DQ8 if doubt persists; duodenal biopsy - histological gold standard: upper GI endoscopy (FOGD) with biopsies → optimal technique: ≥4-6 biopsies of the second duodenum + ≥2 biopsies of the duodenal bulb (D1) → recommendation of the European Society of Pathology (Bouma 2016 - UEGJ): orientation of biopsies on gelatin - better evaluation of villi → Marsh-Oberhuber histological classification: Marsh 3a (mild atrophy) + 3b (moderate atrophy) + 3c (total atrophy) → confirms diagnosis + grades involvement → Husby 2020 - Journal of Pediatric Gastroenterology and Nutrition (ESPGHAN 2020): criteria for diagnosis without biopsy in children: anti-tTG IgA >10× LSN + positive EMA + positive HLA-DQ2/DQ8 + suggestive symptoms → diagnosis made without biopsy → in adults: biopsy remains recommended (ACG 2023 + BSG 2022 + CAG 2024) | Rostom 2005 - Gastroenterology (meta-analysis): anti-tTG IgA = best screening test → sensitivity 92-98 % + specificity 94-98 % + Husby 2020 - JPGN (ESPGHAN 2020 Guidelines): criteria without biopsy in children → anti-tTG >10× + EMA + HLA → VPP >99 % → dispense with biopsy in this context + Rubio-Tapia 2023 - American Journal of Gastroenterology (ACG 2023 Guidelines): duodenal biopsy still recommended in adults → biopsy protocol (≥4 D2 + ≥2 D1) + diagnosis on gluten diet → HLA-DQ2/DQ8 useful if prior RSG + Ludvigsson 2013 - BMJ: true celiac prevalence 0.5-1 % + diagnostic delay 6-10 years + Bouma 2016 - United European Gastroenterology Journal: duodenal biopsies → orientation on gelatin + ≥4-6 biopsies + Hershko 2005 - American Journal of Gastroenterology: celiac + unexplained iron deficiency anemia → systematic screening recommended + ACG 2023 + BSG 2022 + CAG 2024: biopsy recommended in adults even if serology very positive + Association des patients cœliaques du Canada (ACCA): resources in French |
| Gluten-free diet (GFD) — the sole treatment and cornerstone of management Foods to avoid — foods permitted — cross-contamination — Canadian labeling — dietitian — antibody normalization — scarring — quality of life — incomplete response |
Gluten-free diet (GFD) - the only effective treatment for celiac disease: principle: total and definitive elimination of wheat (all varieties: spelt + kamut + rye + barley + triticale) → rice + corn + buckwheat + quinoa + millet + sorghum + teff + amaranth + potato + legumes are naturally gluten-free → uncontaminated pure oats are generally tolerated (studies show that uncontaminated oats are well tolerated by 90-95 % of adult celiac patients) - but introduce cautiously after mucosal healing + clinical monitoring → Janatuinen 2002 - Gut : uncontaminated pure oats + celiac → well tolerated in the majority + but: frequent cross-contamination of commercial oats → Lundin 2003 - Gut: uncontaminated oats → no activation of celiac CD4+ LTs in the majority + some patients react to avenin (oat protein) → clinical monitoring + antibodies when introducing oats → cross-contamination: even traces of gluten (a few mg) can maintain mucosal inflammation in highly sensitive patients → read labels on all food products → Codex Alimentarius: «gluten-free» foods = gluten content <20 ppm (20 mg/kg) → Canadian labeling (Health Canada): «gluten-free» product = complies with Codex standard → also monitor medicines + cosmetics (lipstick + toothpaste) → avoid gluten in pharmaceutical preparations and medicines; foods to avoid: bread + pasta + pizza + cookies + cakes + cereals (wheat + rye + barley) + beer (made from barley) → and all by-products → sauces (often thickened with wheat flour) + salad dressings + industrial soups → breadcrumbs + breadcrumbs → breaded meats → industrial minced steaks → baking powder (may contain wheat) → imitation seafood (surimi) → some medicines (coating) + some foods labeled naturally gluten-free but potentially contaminated (uncertified oats + some packaged products) → naturally gluten-free foods allowed : rice + corn + potato + legumes + fruits + vegetables + fresh meats + fish + eggs + dairy products + oils + buckwheat + quinoa + millet → consultation with a dietitian/nutritionist specializing in celiac: essential for diagnosis + recommended regularly → Catassi 2014 - American Journal of Gastroenterology : non-compliance with RSG → persistence of mucosal inflammation + long-term risks; follow-up and response to treatment: normalization of IgA anti-tTG: 6-12 months under strict RSG → clinical and biological monitoring at 6 months + 12 months + annually → if anti-tTG does not normalize → probable dietary transgression(s) (often involuntary) → or true refractoriness → histological scarring: 2-5 years under strict RSG for complete healing in most adults → faster in children → Rubio-Tapia 2010 - Gastroenterology: mucosal healing in adults → only 34 % complete healing at 2 years → 66 % at 5 years → better healing in women + young people + patients with strict RSG → quality of life: improves significantly under RSG + notably digestive symptoms + fatigue + mood disorders | Janatuinen 2002 - Gut: uncontaminated oats + celiac → well tolerated in the majority of adults + Lundin 2003 - Gut: oats → no CD4+ LT activation in the majority → some patients react to avenin → monitoring required + Catassi 2014 - American Journal of Gastroenterology: non-compliance RSG → persistent inflammation + long-term risks → strict compliance essential + Rubio-Tapia 2010 - Gastroenterology: mucosal scarring adults on RSG → 34 % at 2 years + 66 % at 5 years → significant healing time → control biopsy at 1-2 years recommended + Health Canada: gluten-free labeling → <20 ppm → Codex Alimentarius standard → ACG 2023 + BSG 2022 + CAG 2024: annual anti-tTG IgA monitoring + nutritionist consultation + follow-up biopsy if symptoms persist or antibodies fail to normalize + Celiac Patient Association of Canada (CPA): list of certified foods + patient resources + Richardson 2020 - World Journal of Gastroenterology: effectiveness of dietary interventions in celiac disease. |
| Complications of untreated celiac disease Intestinal T-cell lymphoma — digestive cancers — refractory disease — osteoporosis — infertility — neuropathy — nutritional deficiencies — collagenous sprue |
Long-term complications of untreated celiac disease or with non-strict GFD: enteropathy-associated intestinal T-cell lymphoma (EATL): most serious malignant complication → risk × 4-10 vs general population → accounts for 50 % of primary intestinal lymphomas → subtype 1 (EATL type I): large cell + often in Caucasian celiac patients + poor prognosis → subtype 2 (EATL type II - or MEITL - Monomorphic Epitheliotropic Intestinal T-cell Lymphoma): less associated with classical celiac → strict GFD significantly reduces this risk → Askling 2002 - Gut: RSG strict → risk of EATL similar to general population after 5 years of RSG + other digestive cancers: adenocarcinoma of small intestine × 2-4 + carcinoma of oropharynx + esophagus + risk of rectal cancers + overall risk of digestive cancers + 40-50 % + Lebwohl 2014 - JAMA: undiagnosed celiac disease + mortality → cardiovascular excess mortality + cancers → early diagnosis + GFD → normalization of mortality; refractory celiac disease (RCD): persistence of malabsorption symptoms + Marsh 3 villous atrophy after 12 months of well-conducted strict GFD → definition: symptoms + Marsh ≥2 despite documented GFD ≥12 months + 2 types: MCR type I: normal IEL profile (TCR αβ + CD3+CD8+) → better prognosis + response to immunosuppressive treatments + MCR type II: aberrant IEL profile (clonal + intracytoplasmic CD3- TCR + CD8 loss) → very high risk of transformation to EATL (50-75 % at 5 years) → poor prognosis → MCR treatment: prior assessment: confirm diagnosis + assess compliance with RSG (dietitian + anti-tTG) + rule out cross-contamination + prednisone + budesonide + immunosuppressants (azathioprine) + anti-IL-15 (AMG714) in clinical trials for MCR type II → cladribine + ASCT (stem cell autotransplant) for high-risk refractory forms; nutritional deficiencies to be monitored and corrected under RSG: iron: CBC + ferritin + serum iron → supplement if deficient → prefer IV route if severe malabsorption + vitamin D + calcium: DXA annually if osteoporosis + calcium supplementation 1,000-1,200 mg/d + vitamin D 800-1,000 IU/d + bisphosphonate if T-score <-2.5 → folates (B9): CBC + serum folates → folic acid 5 mg/d if pregnant + vitamin B12 + zinc + magnesium + copper → complete initial nutritional workup then annual monitoring → annual dietetic consultation → collagen sprue: collagen deposition under the intestinal epithelium → very severe variant of refractory celiac → major malabsorption → poor prognosis → immunosuppressive treatment. | Askling 2002 - Gut: Celiac disease strict → similar risk of EATL in the general population after 5 years → demonstration of the protective effect of celiac disease on lymphomas + Lebwohl 2014 - JAMA: undiagnosed celiac disease + mortality → excess cardiovascular mortality + cancers → diagnostic delay = major risk factor + Rubio-Tapia 2009 - Mayo Clinic Proceedings: refractory celiac disease → definition + treatment + prognosis + Al-Toma 2019 - United European Gastroenterology Journal: refractory celiac disease guidelines → types I and II + treatments + surveillance + ACG 2023 (Rubio-Tapia): surveillance and prevention of complications → DXA annually until normalization + complete nutritional assessment + Lebwohl 2015 - Digestive and Liver Disease: osteoporosis in celiac disease → celiac disease improves BMD + calcium + vitamin D supplementation → recommendations + Celiac Disease Foundation + CCA (Canadian Celiac Association): patient resources |
| Screening, non-celiac gluten sensitivity, and differential diagnosis Risk groups — related screening — gluten sensitivity — NCGS — FODMAP — wheat allergy — IBS — differential diagnosis — non-celiac gluten sensitivity |
Screening for celiac disease - who to screen and when: risk groups to be actively screened (prevalence 3-10 %): 1st degree relatives (parents + children + siblings) of a celiac patient → screening from age 3 (after introduction of gluten) → periodically thereafter if negative + T1DM: screening at diagnosis of T1DM then annually for 5 years + Hashimoto's or Graves' thyroiditis + Down's syndrome + Turner's syndrome + Williams' syndrome + dermatitis herpetiformis → systematic celiac work-up + unexplained iron deficiency anemia → screening + cryptogenic hypertransaminasemia → screening + early osteoporosis without obvious cause → screening + unexplained infertility + repeated miscarriages → screening + selective IgA deficiency → screening with anti-tTG IgG or anti-DGP IgG → general population screening : no recommendation for universal screening at present → Rubio-Tapia 2023 - ACG: targeted screening according to risk groups → USPSTF 2017: insufficient evidence for universal screening; non-celiac gluten sensitivity (NCGS - Non-Celiac Gluten Sensitivity): separate entity from celiac disease and wheat allergy → digestive and extra-digestive symptoms improved by RSG → but : no villous atrophy + no anti-tTG antibodies (or only low titre anti-DGP IgG) + HLA-DQ2/DQ8 often positive → pathophysiology: poorly understood → role of FODMAPs (Fermentable Oligo- Di- Monosaccharides And Polyols) in the majority of symptoms → wheat ATIs (Amylase Trypsin Inhibitors) could activate the innate immune response → Skodje 2018 - Gastroenterology (randomized crossover trial): reintroduction of gluten or fructan (wheat FODMAPs) in SNCG patients → fructan → more symptoms than gluten → role of FODMAPs put forward → Volta 2015 - Clinical Gastroenterology and Hepatology: SNCG → no diagnostic biomarker → diagnosis of exclusion + Biesiekierski 2011 - American Journal of Gastroenterology (seminal study): double-blind crossover → gluten → symptoms even in patients without celiac or wheat allergy → then Biesiekierski 2013 - Gastroenterology: same subjects → reintroduction with FODMAP control → no effect of gluten → questioned role of gluten alone → SNCG exclusion diagnosis: 1/ exclude celiac (serology + biopsy on gluten diet) → 2/ exclude wheat allergy (wheat-specific IgE + prick test) → 3/ if both negative + RSG improves symptoms → SNCG → diagnosis of exclusion → no specific biological test available + wheat allergy: high anti-wheat-specific IgE + positive skin test → immediate allergic symptoms (30-120 min after ingestion) + allergological work-up + no villous atrophy → treatment: avoidance of wheat (not rye or barley as in celiac disease) + differential diagnosis of celiac disease : irritable bowel syndrome (IBS) → no antibodies + no villous atrophy + IBD (Crohn's + UC) → enteroscopy + biopsies + elevated fecal calprotectin + chronic infectious gastroenteritis (Giardia + SIBO - Small Intestinal Bacterial Overgrowth) + exocrine pancreatic insufficiency + Whipple's disease (rare) | Skodje 2018 - Gastroenterology (crossover RCT trial): SNCG → fructan FODMAP → more symptoms than pure gluten → FODMAP = likely cause of symptoms in SNCG + Biesiekierski 2011 - American Journal of Gastroenterology: seminal SNCG study + Biesiekierski 2013 - Gastroenterology: FODMAP + SNCG → gluten not directly responsible → challenges SNCG + Volta 2015 - Clinical Gastroenterology and Hepatology: SNCG → epidemiology + criteria + exclusion diagnosis + Rubio-Tapia 2023 - ACG 2023 Guidelines: targeted screening according to at-risk groups → no universal screening + USPSTF 2017: insufficient evidence for universal screening + Lebwohl 2014 - JAMA: undiagnosed celiac disease → excess mortality → diagnostic delay → importance of screening in at-risk groups + ESPGHAN 2020 (Husby): screening children T1DM + 1st-degree relatives + Down + Turner + Canadian Celiac Association (CCA) + Celiac Disease Foundation: diagnostic resources + screening. |
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Serology and biopsy must ALWAYS be performed under a gluten-containing diet — never after starting a gluten-free diet: A patient who has already adopted a gluten-free diet before receiving a confirmed diagnosis may have false-negative antibodies and partially healed mucosa. In this case, the physician should discuss a gradual reintroduction of gluten (gluten challenge—at least 3 g of gluten per day for 6 to 12 weeks) before performing diagnostic testing, or suggest HLA-DQ2/DQ8 genotyping, which remains valid under a gluten-free diet. Without a confirmed diagnosis, it is impossible to properly educate the patient on the required level of adherence.
Situations requiring urgent or specialized gastroenterological consultation
Known celiac disease with recurrence of severe symptoms (profuse diarrhea + weight loss + abdominal pain) despite strict gluten-free diet for over 12 months, with no apparent dietary transgressions → Refractory celiac disease (RCD) or enteropathy-associated T-cell lymphoma (EATL) → urgent gastroenterology consultation → repeat duodenal biopsies + IEL immunophenotyping + enteroscopy or capsule endoscopy + PET-CT to exclude lymphoma.
Celiac patient with rapid weight loss, persistent abdominal pain, generalized malaise, and palpable abdominal mass → Suspect duodénal or small bowel adenocarcinoma → Urgent gastroenterology consultation → Enteroscopy + videocapsule + biopsies + PET-CT + abdominopelvic CT scan → Maximum délai of 2 weeks.
Severe anemia (Hb <80 g/L) + severe malabsorption + hypoalbuminemia + edema in a patient with undiagnosed celiac disease or non-compliance with a gluten-free diet → severe malabsorption → hospitalization for nutritional assessment + correction of deficiencies + gastroenterology consultation for biopsies and complete workup → parenteral nutrition if necessary.
Child with failure to thrive, chronic diarrhea, distended abdomen, and iron-deficiency anemia for several months → Pediatric celiac disease → Pediatric consultation and pediatric gastroenterology → anti-tTG IgA + total IgA → Biopsies if serology is positive → HLA typing upon confirmed diagnosis.
Consult at Clinique Omicron
Clinique Omicron physicians prescribe and interpret celiac disease serology tests (anti-tTG IgA + total IgA + anti-DGP IgG if necessary), refer to a gastroenterologist for duodenal biopsy, screen at-risk groups, initiate nutritional assessment prescriptions (CBC + ferritin + vitamin D + folate + vitamin B12 + DXA), refer to a dietitian specialized in celiac disease, and provide annual clinical and biological follow-up. Consultations are available at several service points in Quebec and via telemedicine. To make an appointment, visit cliniqueomicron.ca.
The content of this page is for informational purposes only and does not substitute professional medical advice from a doctor or gastroenterologist. Celiac disease requires a diagnosis confirmed by duodenal biopsy before initiating a permanent gluten-free diet.
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