Adverse food reaction – immune (IgE, non IgE)) and non immune
Gluten sensitivity from CD
Non celiac gluten sensitivity (NCGS)
CD is 4 to 4.5 times more common than 50 years ago
World wide 1 in 100 genes
Less than 10% diagnosed from the prevalence in USA
CD epidemic due to increased gluten, environmental factors microbiota
Average age of diagnosis in 5th decade, many are overweight, M=F, recognized in Obstetrics, neuropsychiatric problems, related autoimmune
Gluten free diet is predictive only 36% diagnostic of CD
Increased IBS symptoms in CD patients
Prevalence of CD is 4 x more in IBS pt
FODMAP diet – helps IBS patient.
Now NCGS : Elevated IgA and IgG (antigliadin Ab), no specific HLA association, may have IL-8, IFN-gamma etc activated, increased permiability in SB, might be related to microbiata, wheat amylase trypsin inhibitor protein, immune complex, autoimmune, leaky gut syndrome etc
Wheat ingestion – poorly absorbed carbs, excess fructans, fermentation, now increased gas, SCFA and microbiome changes and now GI symptoms . Or they have CD and gluten mediated symptoms.
Wheat allergy anaphylaxis – This is different from CD. 2-4% adults and 4-8% children. Usually outgrow it.
CD is T cell mediated, NCGS innate immune?, wheat intolerance is non immune and when hypersensitivity is IgE mediated
NCGS prevalence is unknown, cannot differentiate from CD clinically, and role of GS in FGID is unknown.
- Bx second and third part of duodenum.
- There is an ultra short celiac disease which just affects the bulb of duodenum.
- Can have only abnormal changes in proximal jejunum
- It tends to be patchy
- It can mimic acute SBO, perforation, intussuception,
- Skin rashes, dental hyperplasia, short stature, osteopenia, delayed puberty, infertility, mouth ulcers, arthritis, seizures.
- Fertility can recover after treatment of celiac. Warn the patient they can become pregnant.
- Raised alk phos, check sprue.
- Celiac can cause hepatitis with ALT and AST of 300-400
- Hep C treatment can precipitate celiac
- It is world wide. It occurs in Indians too
- Must have bx and serology.
- No role of stool testing for celiac antibodies
- Keep tropical sprue in mind for DD
- You need an expert dietitian
- Family support is crucial
- Increases mortality if patient is non compliant to diet
- No wheat, rye or barley. Also avoid lipstick, balms, mouthwash, toothpaste, play dough, OTC medications, mineral preparations, stamps and envelope glues.
- Refractory sprue – type 1 and type 2 immunity. Type 2 immunity is associated with 40% mortality!!
- Best combo is t Tg Ig A and DGP.
- neg serology in 15% of patients
- Hemolysis reduces anti tTG titer
- Bx is gold standard.
- Marsh Classification
- Patchy disease.
- Need 4-6 biopsies during endoscopy.
- Bulb biopsies increased diagnosis of celiac by 13%
- 4-6 bx from SB and 2 bx from duodenal bulb
- Genetic testing DQ2/DQ8 – 100% of patients with celiac disease have this genotype.
- Thus genetic has 100% negative predictive value.
- Gluten free diet. Support groups CDF, GIG, CSA/USA
- Increased mortality in celiac is from lymphoma (T and B lymphoma and extraintestinal), other cancers are also increased. Increased breast, cervical endometrial cancer also. They should get pneumovaccine also.
- Gluten free diet is protective against malignancy
- Poorly responsive celiac disease – wrong diagnosis, bacterial overgrowth, lactose or fructose intolerance, microscopic colitis, pancreatic insufficiency and refractory celiac disease.
- Refractory celiac disease – type 1 and 2 based on intra epithelial immunohistochemistry. Intra epithelial lymphocytes do not have surface markers then it is type 2 refractory celiac disease. Type 2 is poor prognosis. ALso can do flow cytometry and PCR to differentiate. Type 1 use immonomudolators including steroids, imuran etc. Do not use steroids in type 2 because it increases risk of lymphoma.
- Children should get gluten when being breast fed to reduce their chance of developing celiac disease.