Celiac disease ‘CD’(Gluten enteropathy)‫الداء البطنى‬

Abdominal distention & prominent abdomen, muscle wasting, and severe malnutrition. Loss of SC fat. Muscle wasting, affecting
mostly the buttocks, thighs, and shoulder, contrasts markedly with prominent abdominal distension
Definition:
 Autoimmune mediated systemic disorders triggered by wheat gluten & related prolamins in a genetically susceptible
individual.
Incidence : 1/80 to 1/300 in children in general populations ‫ عالميا‬, in adult 1/100 to 1/500
Age of onset : 6mo to 90 years , can appear at any time , classic type appears : 6mo-24mo.
Pathophysiology :
 Gluten  gliaden (Lumen)  penetrate junctional intestinal mucosa( with the help of zonulin protein)
 deamidated gliaden (by tTG enzyme )
swallowed by APC  processed  exposed it on its surface with DQ2/DQ8 recognized by T
helper As a foreign antigen release cytokines which damage the tissues & activate B cells 
plasma cells release antibodies

@Environmental triggers (cereals containg toxic proteins Gliadin , Secalin, hordein)

@Genetic predisposition‫ تأهب جينى‬: HLA-DQ2/8 genes(+ve in 90%), the receptors (DQ2/8)formed by these genes
( at surface of antigen presenting cells)
@APC swallow gliaden antigen  processing it presenting it associated with the these receptors to
T helper cells  release mediators & stimulate other immune cells .
@Autoimmune due to loss mucosal barriers ( T cell mediated autoantibodies TTG,EMA,DPG)
Notes; Celiac disease is a disease of genes and grains
Environmental factors: adenovirus serotype 12 , late introduction of cereals ‫على عكس المتوقع‬
Pathology :
 Affect the mucosa of small intestine mainly proximal small bowels
 it starts gradually from mucosal inflammation, crypt hyperplasia & villous atrophy

Clinical features :
Symptoms occurs after starting cereals from the age of 6 -24mo, recent studies--> tends to present later (6-14 y)
90% of toddlers present with classic symptoms, 50% of teenagers present with atypical symptoms.
Typical presentations: (Intestinal manifestations) ( infants )
 Anorexia, irritability, recurrent nausea & vomiting (‫) حالة جاءت` بأعراض قىء دورى وطلعت سلياك‬
 Chronic/intermittent diarrhea 65%: loose , bulky ,pale , greasy &offensive motions (‫) اسهال دهنى‬
 Loss of wt, wasted buttocks (‫هزال االرداف‬-‫ الضمور العضلى وغياب النسيج الشحمى لالليتين‬- ‫) االليه الحزينة‬, distended abdomen
 Occasional constipations 8%( ‫ )عكس المتوقع‬, recurrent aphthus stomatitis
 Rarely Celiac crises5%: severe watery intractable diarrhea, dehydration, marked distension, hypotension, lethargy,
hypokalemia, hypoproteinemia, death (refractory sprue) IV fluids , steroids (or immuran )
 Notes : ‫أى حالة امساك مزمن أعمل تحليل الغدة الدرقية وسيلياك‬
Atypical presentations ,extraintestinal ( older children-adolesents–adult )‫هى األكثر شيوعا اآلن‬
o Iron resistant anemia 60%, short stature 10%, delayed puberty and rickets in long standing cases
o Dermatitis herpitiforms 2%(itchy, vesiculopapular, symmetrical, on extensor surfaces),alopecia
o Dental enamel hypoplasia, osteopenia/osteoporosis, delayed puberty, amenorrhea
o Celiac hepatitis (high transaminase)
o Arthritis /arthralgia, neuropathy, gluten cerebellar ataxia , headache , psychiatric disorders
o Autoimmune disorders eg T1DM, autoimmune thyroiditis, autoimmune hepatitis.
o Notes :
 Extraintestinal manifestations can result in delay in diagnosis.
 Intestinal symptoms subsides as the child grows older
 The most frequent extraintestinal manifestation in children is Iron def anemia(IDA)
 IDA  malabsorption of nutrients , occult blood , chronic inflammation
 Short stature  may present alone , caused by malnutrition & ↓GH , Tx(GFD)
 Dermatitis herpitiforms  Pathognomonic extra intestinal manifestation of CD
 Celiac Previously called tropical sprue
 Celiac disease can present at any age
Asymptomatic:GI symptoms are lacking or not prominent ,although extra-GI may be present( silent , latent )
Items Extra intestinal alone Intestinal & extraintestinal
Children 18% 60%
Adult 9% 62%
 2.5years – 5.5 kg – before Rx 6.8 kg after 2wks of Rx
System Manifestations Possible causes
GIT Diarrhea , distension , anorexia , failure to thrive , apthtus Villous atrophy , malabsorption
Hematologic Anemia ( Iron, folate ,B12) Iron malabsorption
Skeletal Rickets, osteoporosis, permanent teeth enamel hypoplasia 30% Ca & ViTD malabsorption
Muscular Muscle wasting Malnutrition
Neurologic Peripheral neuropathy , gluten ataxia , (epilepsy with occipital Thiamin /B12 deficiency
calcifications in adult) autoimmunity (for cerebellar
ataxia)
Psychiatric Autism , ADHD, intellectual disability, mood changes Unclear, micronutrient def.,
autoimmune
Endocrine Short stature, delayed puberty, amenorrhea , Malnutrition, malabsorption
Dermatologi Dermatitis herpitiforms (adult) ‫التهاب الجلد شبيه الهربس‬ Autoimmunity
c
Liver Aminotransferase elevations ( celiac hepatitis) Reactive hepatitis
Other lab Vitamin ADEK deficiency Malabsorption
Clinical spectrum : ( celiac iceberg)‫ الطيف االكلينيكى حسب االعراض والموجودات النسيجية والمخبرية‬-‫جبل جليد السيلياك‬
Items DQ2/ Serology Histology Symptoms
8
Active CD + + + +
‫المصاب‬- ‫النشط‬
Silent CD + + + -
‫الصامت‬

Latent CD + -/+ - -
‫الكامن‬

Potential CD + + - -/+
‫المحتمل‬

Symptomatic(active): symptomatic ( Typical /atypical )- antibodies – mucosal changes

Silent ‫الصامت‬ Asymptomatic & Abs & mucosal changes ( detected by screening at high risk groups )
Latent ‫الكامن‬ Asymptomatic & Abs & no mucosal changes
Potential ‫المحتمل‬ ± symptomatic & Abs & no mucosal changes ‫ ممكن يتطور الى النشط‬، ‫يحتاج متابعة‬
‫ الكالسيكى‬، ‫ العرضى‬، ‫النشط‬ ‫ موجودات نسيجية‬+ ‫ موجودات مخبرية‬+‫أعراض سريرية هضمية و خارج هضمية‬
Silent ‫الصامت‬ ‫ يكشف عند المجموعات عالية الخطورة‬، ‫ موجودات نسيجية‬+ ‫ موجودات مخبرية‬+ ‫ال أعراض‬
Latent ‫الكامن‬ ‫ ال موجودات نسيجية‬+ ‫ موجودات مخبرية‬+ ‫ال أعراض‬
Potential ‫المحتمل‬ ‫ ال موجودات نسيجية‬+ ‫ موجودات مخبرية‬+ ‫من الممكن تطور أعراض‬
‫ملحوظة ‪ :‬أى نوع قد يتطور الى النوع اآلخر ألسباب غير معروفه‬
Risk modifiers:
 Infection with Rota virus & adenovirus (↑risk )
 Gluten introduction early before 3 months (↑risk )
 Longer duration of Breast Feeding is protective
 Smoking is protective against adulthood celiac ‫ هللا أعلم‬.
Investigations :
 Barium meals: clumping of barium ( Normal : featherapy appearance )
 Antitissue transglutaminase( anti-TTG/ Ig A)(95%) + Quantitative (IgA) test why?
 )‫ فى االضداد= التحسن‬v‫ الغذائي ( اانخفاض‬v‫ يجرى أيضا لمتابعة حالة المريض ومدى التزامه بالرجيم‬v‫هذا االختبار‬
 If Quantitative (IgA) is low(10%of cases)  false – ve result for ( anti-TTG) Ig A
 Alternative test in this case : (TTG/IgG), deamidated gliadin pepide/IgG (DPG/IgG)
 Antigliadin antibodies ( 80%) has frequent false +ve  no longer recommended
 Anti endomysial antibodies ( 100%), done by indirect immunofluorescence ( 600 pounds)
 Tests depends on IgA are less accurate in children under 2 years of age
 Intestinal biopsy  lymphocytes infiltrations , deep crypts, flat mucosa (definite diagnosis )
 IgA deficient and who are positive at any level for an IgG based serological test should be biopsied
No biopsy approach (ESPGHAN 2019)
 Symptomatic cases
 If High TTG/IgA ≥ 10 x upper limit of normal & +ve EMA/IgA‫ = من عينة أخرى‬confirmed CD (no biopsy)
 Genetic testing for HLA DQ2/8 ( not recommended in new guidelines )
o ‫لو سلبى تعنى اليوجد داء زالقى لو أيجابى عديمة الفائدة‬
o Used to exclude CD but not to diagnose it
Testing for clinical suspicion of celiac disease &screening for risk groups (symp/asymptomatic)
Test Result Explanation
TTG/IgA -ve Not celiac or
False –ve& needs further testing (IgA def, < 2y , low gluten diet , high clinical suspicion)
TTG/IgA +ve & + ve EMA ( in second sample )  confirmed celiac ( no biopsy approach ) ‫التحتاج منظار‬
≥ 10xULN -ve EMA--- consider biopsy
TTG/IgA +ve & -ve EMA  consider re-testing on sufficient gluten containg diet ( & consider biopsy)
< 10xULN
Duodenal distal & March 0 (normal mucosa) M1(lymphocytes infiltrations) M2( crypts proliferations) ,
biopsy bulb M3 (villous atrophy, partial/complete) , M4 (Total mucosal atrophy )
Multiple biopsies (multiple tissue samples )  because mucosal involvement may be patchy
Notes Initial test : TTG/IgA( N < 10 u/ml) & total IgA( N 20-100 mg/ml)
≥ 10xULN = ≥ 10 upper limit of normal  predict enteropathy ( marsh 2-3)
5 biopsies 5 1 ( ‫ عينات‬at least from the bulb & 4 at least from distal deudenum ( patchy ‫ بقعى‬disease )
EMA : in separate 2nd blood sample , it may be +ve or – ve (no titer )
Further testing using: combined TTG/DPG IgA &IgG (in < 2y , IgA def, high clinical suspicion )
TTG/DPG IgA &IgG is more sensitive than TTG/IgA alone and detects 100% of celiac patients
Alternatives to Small Bowel biopsy for Celiac Disease
 IgA TTG levels ≥10x normal confirmed by +ve EMA OR
 Skin biopsy consistent with Dermatitis Herpetiformis ‫التهاب الجلد شبيه الهربس‬
Serology Form Sensitivity Specificity Notes
Gliaden AGA IgA/IgG 75% 80% False –ve with mucosal injury

T.transglutaminas TTG IgA 95% 95% Initial test ( standared test)

e IgG 99% 100% In IgA defiency

Endomythial EMA IgA 97% 100 Expensive , operator
dependent
Deamidated DGP IgA 85% 90% Better than AGA , but not
better than TTG ,
gliadin peptide IgG 90% 90% used with IgA deficiency
Notes TTG & DGP/IgA best combination for sensitivity & specificity
In Ig A deficiency  TTG Ig G ± DPG IgG- consider biopsy if in doubt
< 2 years  DGP/ IgA - IgG ( is better than other tests).
If TTG Ig A - ve & Total Ig A normal , isolated elevation of TTG Ig G is insignificant
EMA IgA excellent specificity & analytical challenges
HLA DQ2/8 to exclude CD ‫مفيد فقط لو كان سلبى يقولك مافيش داء زالقى – لو كان ايجابى اليفيد واليضر‬
‫مفيد أيضا لو كانت األضداد والعينة النسيجية محيرة يعنى موش قادر تقول ايجابى" وموش قادر تقول سلبى‬
Causes of false – ve < 2yrs –Lab error – Gluten free diet - selective Ig A defiency – immunosuppressive drugs
‫يجب أن يستمر الطفل على الطعام العادى المحتوى على الجلوتين" على األقل لمدة شهرين قبل اجراء التحاليل والمنظار‬
 tests

Other lab tests at time of initial diagnosis:

o Complete Blood Count with platelets
o Iron studies (Serum Iron, TIBC, Ferritin)
o Serum Vitamin B12, Serum Folate
o Calcium , Phosphate
o Renal Function tests (Blood Urea Nitrogen, Creatinine)
o Liver Function Tests (AST, ALT, Albumin, Alk Phos) ↑transaminase in 20% of cases
Differential diagnosis:
 Amebaiasis ( stool analysis),
 Cystic fibrosis :early onset, good appetite ,sweat Cl test
 Bacterial overgrowth, CMPA, Crohns disease
 Eosinophilic gastroenteritis
 In adult : IBS , 10% of adult with Iron deficiency anemia has undiagnosed CD
Treatment :
 Gluten free diet (GFD)long life) Barley ,‫ الشعير‬Rye‫الجاودار‬, Oat ‫ الشوفان‬,Wheat ‫) القمح‬BROWfood
 Prolamins : Gliaden (wheat) , Hordein (barley ) , Secalin (Rye) , Avenin (Oat )
 Pure oats ‫الشوفان‬may be safe, but avoid in 1st year.( eat gluten free oat bec of cross contamination)
 Lactose free diet in the first few wks of treatment ( bec . of atrophy of villi )
 Multivitamin, folic acid, iron, VitD, Ca , trace elements
 Pancreatic enzymes Rx : may improve failure to thrive
 Dapsone(0.5mg/kg/day)&GFD for dermatitis herpitiforms
 Refractory disease common in adult ( steroid – immunosuppressive )
 Methylcellulose for constipation
 Vaccinate for encapsulated bacteria , may be functionally asplenic
 Notes : Not all “wheat-free” items are “gluten-free” however, all “gluten-free foods “are “wheat-free”
Monitoring :
 Consider monitoring with serologic markers (TTG/IgA)
 Should return to normal within 3-12 months of starting Gluten-Free Diet
 Persistent positive markers suggest continued gluten exposure
High risk groups, Associations , Needs screening, half of cases are asymptomatic
o 1st degree relatives with celiac disease 12%,2nd degree relatives 5%
o Autoimmune disorders:
o Type 1 diabetes 12%, autoimmune thyroiditis 7% , autoimmune hepatitis 12%, Addison disease ,
o IgA nephropathy 5% , Idiopathic dilated cardiomyopathy 5% , sjogrens 7% , juvenile arthritis
o Down 12% , turner5% , Williams syndromes 9%
o Selective Ig A deficiency 10%
Complications:
o T cell lymphoma, NHK lymphoma & adenocarcinoma of small bowel 10%
o Ulcerative jujenitis & strictures
o Nutritional deficiency: osteopenia, osteoporosis, anemia
o Neurological: cerebral occipital calcifications, ataxia, peripheral neuropathy , epilepsy
Prognosis :
 GFD usually results in clinical, serologic, and histologic remission
 GFD protect against malignancy & other autoimmune diseases
 Symptoms improve in 2-4wks on GFD
 Some may persist for 3-6mo
 CD not responding to Gluten free diet (GFD)has poor prognosis
Celiac pattern :
Extensive enteropathy (22%) Limited duodenal Enteropathy12% Patchy jejunum enteropathy 1%
whole duodenum &Patchy Jejunum

CD is a patchy disease like Crhons so multiple biopsies is needed , ‫يعنى بتأخذ" عينات من أكثر من مكان من األمعاء الدقيقة‬
At least 6 biopsy samples from 1st part of deudenum , 2nd part of deudenum , stomach , esophagus
There is a concomitant association between celiac , esinophilic esophagitis & IBD
Notes :
 HLA typing not required to confirm the diagnosis (HLA DQ2 90% & HLA DQ8 10% of celiac pt. )
o Anti-TTG/ Ig A = normal range < 10 U/ml ,
o Ig A = normal range 20-100 mg/dl
o At least 4 biopsies(fragments) from from distal duodenum & 1 at least from the bulb ( patchy disease)
o EMA : in separate 2nd blood sample , it may be +ve or – ve ( no titer )
o ‫أى حالة داء سكرى تحرى عن السلياك وأى حالة سيلياك تحرى عن الداء السكرى‬
o The patient should be on gluten containing diet at least 6wks before testing bec sensitivity of serology ↓ with GFD
o Wheat ( Gliadin ) , Rye (Secalin), barley (Hordein), oat (avenin)
o Wheat Gluten Gliadin + Glutenins
o Prolamins:
o Gluten prolamins :Wheat (Gliadin) , Rye (Secalin), barley (Hordein), oat (avenin)
o Non gluten prolamins : Maise , Rice
o Tissue transaminase enzyme  change gliadin to deamidated gliadin
o Pt. with Dermatitis herpitiforms confirmed by skin biopsy = confirm celiac disease without investigations
o In dermatitis herpitiforms : Skin biopsy  Typical IgA deposits
o In dermatitis herpitiforms 80% has no GI symptoms. 70% has villous atrophy
o All dermatitis herpitiformis has celiac disease but not the opposite
o In dermatitis herpitiformis  symmetric distribuation , severe itching , elbows 90%, knees 30%
o 2ndry hyperparathyroidism due to malabsorption of ca & VitD - osteopenia & osteoporosis
o Common nutrient malabsorption: FIC (folic – Iron – Ca )
o The incisors are most commonly affected in enamel hypoplasia of permanent teeth
o Monitor the patient by serological markers, repeated biopsy is not necessary
o Belly abdomen: due to weak muscles & gases
o Celiac & heart: 7% of cardiomyopathy , 4% autoimmune myocarditis has celiac .
o Celiac & liver : 30% of celiac has ↑ liver enzymes , 7% of autoimmune hepatitis has celiac
o Celiac & CNS: ataxia , dementia , leukoencephalopathy , cerebral calcifications , occipital epilepsy
o Celiac & autism : ‫بعض االطفال تحسنوا على االطعمة الخالية من الجلوتين‬
o Syndrome associated with celiac: Down , turner , William
o Other causes of villous atrophy:
o Giardiasis, lymphoma, whipple disease, PEM, CMPA, bacterial overgrowth
o Primary immune deficiency, chemotherapy, eosinophilic gastroenteritis
 Celiac hepatitis : Mild elevation of SGPT&SGOT , Common , Reversed
Occurs in patient with confirmed celiac disease, 60% in children, 40% in adult
Resolved after Rx with gluten free diet (GFD )
Pathogenesis:
o Intestinal inflammation
o Impaired intestinal barrier
o ↑intestinal permeability
o Passage of mediators to the liver ( toxins , antigens , cytokines) Liver injury
Clinical features:
o Occurs in symptomatic & asymptomatic CD
o Asymptomatic with mild elevation of hepatic transaminase
Investigations:
o mild elevations of hepatic transaminase< 5 times normal ie < 200 , ratio SGOT/SGPT< 1
o Sonar : normal liver
Rx : Gluten free diet (GFD)improves liver enzymes within 6-12 mo
Indications of liver biopsy:
o Suspicion of lymphoma (elevated GGT& ALP)
o Persistent of elevations of hepatic enzymes > 12mo with GFD
Liver disorders associated with celiac disease :
o Auto immune liver disease: Autoimmune hepatitis , primary biliary cirrhosis ( no improvement with GFD)
o Viral hepatitis (less responsive to hepatitis B vaccine)
o Fatty liver - Cryptogenic cirrhosis
 Celiac disease(CD) &Type1 diabetes mellitus ( T1DM)
Incidence of celiac disease alone (1%) in general population ↑up to (6-10%) in T1DM (10 times )
There is a genetic link between Type 1 diabetes and celiac disease.
Developing one of the diseases increases the risk of developing the other.
Celiac disease can develop at any time in T1DM during the 1st 10 yrs of diabetes
Asymptomatic children > 9years at T1DM onset had the lowest risk to develop CD.
Most children with T1DM & celiac disease are asymptomatic (70%) ” silent CD” ( unlike celiac alone)
New onset T1DM may have low titer of TTG/IgA (in absence of celiac) that improve without Rx within 6-18mo
TTG/IgA↓ spontaneously in 40% of children with T1DM and became – ve in 20%, despite gluten consumption .
Pathophysiology:
 Both are autoimmune condition & shared a common genetic location (HLA
DQ2/8)
 Genetics, environment and immune dysregulation are shared etiological
factors .
 In T1DM & celiac there is destruction of ) β cells of islets & enterocytes (
 T1DM manifests first followed by celiac
 When celiac manifests before diabetes, symptoms of diabetes are severe
&associated with other autoimmune disease
Clinical features:

 Clinical features of celiac in T1DM patients may be subtle, atypical, or asymptomatic

 Celiac suggestive:
o Abd discomfort , wt loss , growth delay , recurrent aphthous stomatitis , osteopenia
o compensatory hyperthyroidism, iron Resistant anemia , herpetiform dermatitis , lymphoma
 T1DM with celiac : recurrent hypoglycemia ,↑ risk of retinopathy &nephropathy
Screening tests: for symptomatic or asymptomatic
Done for new onset T1DM & within 5 yrs of the onset of diabetes
TTG/IgA & total IgA (symptomatic/asymptomatic)
o TTG/IgA – ve  not celiac disease
 ≥ 10 x upper limit of normal‫( أكثر من عشر أضعاف الحد االعلى للطبيعى‬ULN) ( > 100 u/ml) 
o + ve ( EMA/IgA & and HLA-DQ2/DQ8 ) confirmed celiac disease ‫النحتاج الى منظار‬
o – ve EMA/IgA  consider biopsy
 < 10 x ULN  -ve EMA  consider re- testing on sufficient gluten containing diet
If TGA-IgA is only borderline positive confirm sufficient gluten intake and considerer re-testing of TGA-IgA and EMA.
TTG/IgA are used for screening& follow up & EMA (Endomysial IgA) are used as confirmatory test
EMA (Endomysial IgA) : should be used in a separate sample from the intial test ( 2 nd serum sample)
ScreenT1DM for CD at diagnosis then annually for the first 4 yrs and once every 2 yrs for the following 6yrs
Small intestinal biopsy remains the gold standard for the diagnosis of celiac disease (CD)
All patients who are IgA deficient and who are positive for an IgG based serological test should be biopsied
‫ بسبب‬، ‫ في حاالت السيلياك مع السكرى ولكن يجب االعتماد على المنظار والعينات‬serology tests ‫هناك بعض اآلراء بعدم االعتماد على‬
False positive serology tests
Treatment :
 Rx are the same as for all patients with CD.
 A strict gluten free diet (GFD)
o for those of serological & histological evidence of CD
o symptomatic CD + High anti TTG titer
 Multivitamin , minerals , Ca & vitamin D
Prognosis :
 Symptoms improve in 2-4wks on GFD
 Some may persist for 3-6mo ( non-responsive)
 Quality of life may be lower in patients with both diagnoses
 ↑ed risk of diabetic retinopathy and nephropathy
TTG/IgA & total IgA in symptomatic
o TTG/IgA – ve not celiac disease (further testing in IgA def, < 2y , low gluten diet , severe symptoms )
 ≥ 10 x upper limit of normal‫( أكثر من عشر أضعاف الحد االعلى للطبيعى‬ULN)( > 100 u/ml)  coinside with M3
o + ve ( EMA/IgA)  confirmed celiac disease (no biopsy approach) ‫النحتاج الى منظار‬
o – ve EMA/IgA  consider biopsy
 < 10 x ULN  -ve EMA  consider re- testing on sufficient gluten containing diet
Testing for clinical suspicion of celiac disease &screening for risk groups (symp/asymptomatic)
Test Result Explanation
TTG/IgA -ve Not celiac – further testing in cases of IgA def, < 2y , low gluten diet , severe symptoms
TTG/IgA +ve & + ve EMA ( separate sample )  confirmed celiac ( no biopsy approach ) ‫التحتاج منظار‬
≥ 10xULN -ve EMA--- consider biopsy
TTG/IgA +ve & -ve EMA  consider re-testing on suffient gluten containg diet ( & consider biopsy)
< 10xULN
Duodenal distal & March 0 ( normal mucosa ) M1(lymphocytes infiltrations) M2( crypts proliferations) ,
biopsy bulb M3 ( villous atrophy partial/complete) , M4 (hypoplasia os small bowel architectures)

Notes ≥ 10xULN = ≥ 10 upper limit of normal ‫أكثر من عشر أضعاف الطبيعى‬

Elevated TTG/IgA = coinside with ↑ villous atropy
Do TTG/IgA( N < 10 u/ml) & total Ig A ( N 20-100 mg/ml)
At least 4 biopsies from from distal duodenum & 1 at least from the bulb ( patchy disease)
EMA : in separate 2nd blood sample , it may be +ve or – ve (no titer )
Further testing using : combined TTG/DPG IgA&IgG (in < 2y , IgA def, High clinical suspicion )
TTG/DPG IgA&IgG is more sensitive than TTG/IgA alone and detects 100% of celiac patients