Antigliadin Research Articles

S1705 Celiac Disease and Chronic Pancreatitis

Introduction: Celiac disease involves a T-cell-mediated immune response to dietary gluten. Celiac disease has 3-fold increased risk for developing chronic pancreatitis but only has a reported incidence of 0.52%. We present a case of a 61-year-old male with newly diagnosed celiac disease who was incidentally found to have associated chronic pancreatitis. Case Description/Methods: A 61-year-old male with a past medical history of diabetes, hypertension, coronary artery disease, and a remote history of hepatitis presented to our clinic for his first screening colonoscopy and recent anemia. Prior to colonoscopy, the patient noted a 45-pound unintentional weight loss over the past few years, and with recent lab studies revealing a hemoglobin level of 11.7 g/dL. The patient then underwent colonoscopy, esophagogastroduodenoscopy (EGD), and an extensive laboratory work-up that was significant for iron deficiency anemia, anti-gliadin (AGA) IgA >150 U/mL, AGA-IgG 134 U/mL, endomysial (EMA)-IgA positive, tissue transglutaminase (tTG)-IgA >100 U/mL, total IgA 280 mg/dL, fecal elastase 31 mcg/g and was positive for anti-smooth muscle antibodies (1:160). Subsequent results were negative for viral hepatitis panel, antinuclear antibodies, anti-mitochondrial antibodies, alpha-1 antitrypsin levels, and normal ceruloplasmin levels. Colonoscopy was unrevealing except for a diminutive tubular adenoma. EGD later revealed blunted villi with flat mucosa in the first and second portion of the duodenum. Biopsy results later confirmed pathology results compatible with celiac disease. During this course of workup, the patient developed nephrolithiasis and with incidental findings of pancreatic atrophy and pancreatic head calcifications detected on CT urogram. Chronic pancreatitis was later confirmed on endoscopic ultrasound with evidence of multiple intraductal stones. Patient did not have a history of alcohol use or pancreatic problems in the family. After being diagnosed with Celiac disease and secondary chronic pancreatitis with exocrine pancreatic insufficiency, he was started on a gluten-free diet and pancrelipase. Patient was noted to have 9-pound weight gain during a 4 month follow-up appointment. Discussion: Chronic pancreatitis is a rare extraintestinal manifestation of celiac disease, reported to have a threefold increased risk but only with a reported incidence of 0.52% at least 30 days after diagnosis of celiac disease compared to 0.13% in non-celiac disease patients.

Celiac Disease Seropositivity in Dilated Cardiomyopathy Patients and Correlation with Ejection Fraction

Background: Recent evidence suggests a connection between celiac disease and dilated cardiomyopathy. Herein, we serologically screened for celiac in dilated cardiomyopathy patients and investigated its correlation with ejection fraction. Methods: We selected 123 cardiomyopathy patients. Patients were screened for celiac, using anti-tissue transglutaminase (ATA), anti-gliadin (AGA), and anti-endomysial (EMA) immunoglobulin type A (IgA) antibodies. Total IgA levels were also measured. Results: Of 123 patients, 3 were EMA positive (2.4%), 4 were AGA positive (3.3%) and 5 were ATA positive (4.1%). EMA positive patients had significantly lower EF values compared to EMA negative patients (35±5 vs. 46.52±9.21, p-value: 0.034). Similar results were observed for AGA (32.5±14.34 vs. 46.7±8.8, p-value: 0.002), but not for either ATA positivity (40±10 vs. 46.5±9.21, p-value: 0.126) or IgA deficiency (50±5 vs. 46.14±9.37, p-value: 0.480). No significant difference was observed in the age and gender of seropositive patients compared to seronegative. Conclusion: We observed a higher prevalence of celiac seropositivity among dilated cardiomyopathy patients compared to the general population. EMA and AGA positive patients had significantly lower ejection fractions compared to their negative counterparts.

Adrenal Insufficiency Presenting as Hypoglycemia & Hyponatremia in a Patient With Liver Cirrhosis; Hepatoadrenal Syndrome

Hepatoadrenal syndrome is described as a progressive impairment in the adrenocortical reserve in advanced liver disease resulting in relative adrenal insufficiency (AI). This can present as critical hypoglycemia and hyponatremia as in the case described.54 year old male with past medical history of hypothyroidism, pericardial effusion, liver cirrhosis and prior alcohol use disorder presented to the hospital with altered mental status. He felt lethargic and complained of recurrent diarrhea for a month. His blood sugar was 30 mg/dl (n=70–140 mg/dl) for which he received dextrose and his mentation improved. He was hypothermic with stable vitals otherwise. There was no skin hyperpigmentation. Labs demonstrated sodium of 123 mmol/L (n=136–145 mmol/L) and pancytopenia. TSH, ammonia, renal and hepatic functions were within normal limits except mildly elevated AST and total bilirubin. Total protein, albumin, HDL, Insulin and cortisol levels were low. Hepatitis panel was negative. CT Chest, abdomen and pelvis revealed massive abdominopelvic ascites, hepatic cirrhosis and splenomegaly. Adrenal glands appeared normal. Urine studies were consistent with salt-wasting nephropathy. Patient was started on intravenous fluids as well as dexamethasone. Diagnostic and therapeutic paracentesis was performed. Cosyntropin stimulation test revealed a baseline AM cortisol of 2.0 ug/dl (n=4.3–22.4 ug/dl), 30 min value of 4.0 ug/dl and 60 min value of 5.8 ug/dl (n=18-22ug/dl). Delta cortisol level was also low. Treatment with hydrocortisone was initiated until ACTH levels became available. To rule out sarcoidosis, ACE levels were obtained, which were normal. Dihydroxy 1,25 Vitamin D levels were low. ACTH returned as 21.7 pg/ml (n=7.2–63.3 pg/ml). 21 hydroxylase antibody was negative. MRI brain with IV contrast demonstrated no pituitary mass or abnormality. Blood cultures, body fluid cultures, AMA and ASMA were negative. Anti- tTG and Anti Gliadin antibodies were positive confirming celiac disease. Patient was started on gluten free diet which resolved his diarrhea. He responded well to steroids however, he remained intermittently confused which was thought to be related to hypoglycemic brain injury. Patient was converted to hydrocortisone PO 20 mg in AM and 10 mg in PM and advised to follow up outpatient with endocrinologist and gastroenterologist.Hepatoadrenal syndrome is an important differential to consider in patients with liver disease presenting with hypoglycemia and hyponatremia. It is a potentially life-threatening condition requiring immediate treatment and appropriate work up. The condition improves with corticosteroid replacement therapy.Reference: Anastasiadis SN, Giouleme OI, Germanidis GS, Vasiliadis TG. Relative adrenal insufficiency in cirrhotic patients. Clin Med Insights Gastroenterol. 2015;8:13–17. Published 2015 Mar 2. doi:10.4137/CGast.S18127

The Value of Screening for Celiac Disease in Systemic Lupus Erythematosus: A Single Experience of a Tertiary Medical Center.

IntroductionSystemic lupus erythematosus (SLE) is a multi-organ inflammatory disease associated with autoimmune diseases. The aim of the study is to assessed the frequency of celiac disease (CD) in adults and children with SLE (aSLE and cSLE, respectively) and compare them with rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA) patients; the study also explored the clinical impact of CD serologic markers on SLE disease activity and severity.MethodsThis was a cross-sectional study. Patients with SLE who had regular follow-up in rheumatology clinics were evaluated for laboratory and clinical variables using serology and the SLE Disease Activity Index (SLEDAI). To assess the occurrence of CD serology in cSLE and aSLE and the clinical impact of CD serologic markers on SLE, patients were tested for antigliadin (AGA), anti-endomysium (EmA) and anti-tissue transglutaminase (tTG) antibodies. RA and JIA patients were included for comparison. Duodenal biopsy was conducted in patients who exhibited CD markers.ResultsThe CD marker was found in 29 (11.6%) of the 250 patients. AGA was present in seven aSLE patients and tTG in two (11.1%). Among cSLE patients, the autoantibody was present in 17.6% (AGA in four, tTG in two, and EmA in three). For RA patients, five had AGA and tTG and one had EmA, with an overall positivity of 9.7%. Five JIA patients had AGA (four with EmA and five with tTG) with overall positivity of 10.9%; the serum IgA level was normal in all patients except one. Duodenal endoscopic biopsy was performed in patients with positive CD markers (two declined). Histologic confirmation of CD was reported in one RA and one JIA patient but in none of the SLE patients. There was no correlation between the presence of CD markers and autoantibodies in SLE.ConclusionCD antibodies did not influence SLE activity. Thus, SLE patients may not need to be screened for CD antibodies.

3095 Non-Celiac Gluten Sensitivity (NCGS) Presenting as Laryngopharyngeal Reflux (LPR)

INTRODUCTION: Laryngopharyngeal reflux (LPR) is defined as retrograde passage of stomach contents through the esophagus into the larynx and pharynx. Celiac adhering disease is known to cause more severe reflux, often refractory to anti-secretory medications like proton pump inhibitors (PPI). In those cases, the patient will frequently experience symptom relief by adherence to a gluten free diet (GFD). However, little is known about non-celiac gluten sensitivity (NCGS), and the only commercially available test, Antigliadin (AGA) IgG, is positive in about 60% of patients. We present a case of LPR refractory to anti-secretory medication, low acid diet, and reflux surgery that resolved rapidly on a gluten free diet after diagnosing NCGS. CASE DESCRIPTION/METHODS: A 59 years old woman with PMH of gastric bypass surgery (roux-en-Y), GERD, hypothyroidism, MDD, and migraine presented with symptoms of hoarseness, mucous throat clearing, cough, sour taste, and nocturnal choking/laryngospasm events. Flexible fiberoptic laryngoscopy supported the diagnosis of LPR with classic findings of laryngeal edema, erythema, and inflammatory mucus. Treatment with omeprazole 40 mg BID, ranitidine 300 mg QHS, and aluminum hydroxide/magnesium carbonate failed to resolve her symptoms. Persistent severe acid reflux and strong symptom correlation were confirmed with dual sensor pH impedance while esophageal manometry confirmed hypotonic lower esophageal sphincter pressure. She underwent paraesophageal hernia repair and Dor fundoplication resulting in temporary resolution of symptoms that returned one month postoperatively. Although she was unaware of any gluten intolerance, she was tested for gluten sensitivity. Tissue Transglutaminase (TTG) IgA/IgG and Deamidated Gliadin Peptide (DGP) IgA/IgG were normal, but AGA IgG was elevated (111), suggestive of NCGS. She was instructed to follow a GFD, and within one week, all reflux symptoms had resolved, along with headaches, joint pain, and “foggy” mind. DISCUSSION: The patient had classic signs and symptoms of LPR, responsive to GFD, after NCGS was determined by elevated AGA IgG. NCGS remains the least understood form of gluten sensitivity, unlike its counterparts celiac disease and wheat allergy. By exploring the potential connections between LPR and gluten sensitivity, it becomes apparent that some of these patients have gluten sensitivity as the root cause of their reflux symptoms and laryngeal inflammation. More research is needed to better understand the influential diagnosis of NCGS.

Deamidated Gliadin Peptide Antibodies in Celiac Disease: A Diagnostic Driver or just along for the Ride?

Anti deamidated gliadin peptides antibodies are considered as celiac disease associated diagnostic antibodies. They are in clinical use for almost the last two decades. In the first decade they were preferentially used in early childhood, in face of IgA deficiency and occasionally recommended as the prime serological marker, outperforming the anti-tissue transglutaminase autoantibody. Notably, they were recommended in combination with the tissue transglutaminase as enhancer of the diagnostic performances. No more, the circle turned over. In the second decade (2012-2019), most of the studies limited and criticized their past published advantages. They suggested that deamidated gliadin peptides antibodies do not have any advantage over anti-tissue transglutaminase autoantibodies in terms of early childhood, IgA deficiency, diagnostic performances and when both antibodies are combined. It seems that the deamidated gliadin peptide are losing their place in the celiac disease algorithmic diagnostic flow chart.

Celiac-Related Autoantibodies and IL-17A in Bulgarian Patients with Dermatitis Herpetiformis: A Cross-Sectional Study.

Background and objectives: Dermatitis herpetiformis (DH) is a blistering dermatosis, which shares common immunologic features with celiac disease (CD). The aim of the present study was to explore the performance of a panel of CD-related antibodies and IL-17A in Bulgarian patients with DH. Materials and Methods: Serum samples from 26 DH patients at mean age 53 ± 15 years and 20 healthy controls were assessed for anti-tissue transglutaminase (anti-tTG), anti-deamidated gliadin peptides (anti-DGP), anti-actin antibodies (AAA), and IL-17A by enzyme linked immuno-sorbent assay (ELISA), as well as anti-tTG, anti-gliadin (AGA), and anti-Saccharomyces cerevisiae antibodies (ASCA) using immunoblot. Results: The average serum levels of anti-tTG, anti-DGP, AGA, AAA, and the cytokine IL-17A were at significantly higher levels in patients with DH compared to the average levels in healthy persons which stayed below the cut-off value (p < 0.05). Anti-DGP and anti-tTG antibodies showed the highest diagnostic sensitivity and specificity, as well as acceptable positive and negative predictive value. None of the healthy individuals was found positive for the tested antibodies, as well as for ASCA within the DH group. All tests showed good to excellent correlations (r = 0.5 ÷ 0.9, p < 0.01). Conclusions: Although the diagnosis of DH relies on skin biopsy for histology and DIF, serologic testing of a panel of celiac-related antibodies could be employed with advantages in the diagnosing process of DH patients. Furthermore, DH patients who are positive for the investigated serologic parameters could have routine monitoring for gastrointestinal complications typical for the gluten-sensitive enteropathy.

Pentraxin 3 and biopsy status in celiac patients.

In our study we explored a possible relationship between PTX3 and CD. Gluten sensitivity is known as a hallmark of celiac disease (CD). The diagnosis of CD requires demonstration of a typical enteropathy, and positive serology supports the diagnosis. The CD immune response involves the adaptive, as well as the innate immunity and is characterized by the presence of anti-gliadin (AGA) and anti-transglutaminase 2 antibodies (tTGA), lymphocytic infiltration in the intestinal epithelial membrane and expression of multiple cytokines. The long pentraxin 3 (PTX3), an acute-phase inflammatory molecule, plays an important role in innate immunity. 108 CD patients were divided according to Marsh Histological grade following Marsh criteria classification in three groups: Group 1: Marsh 0, patients with a known history of CD under gluten free diet, complete remission; Group 2: Marsh1 and Marsh 2; Group 3: Marsh 3. Healthy age-matched controls without a known history of CD or gastrointestinal symptoms (n=30) served as controls. PTX3 serum levels were measured by sandwich ELISA on an automated platform. PTX3 serum levels were significantly elevated in group 3 and group 2 compared with HC (mean 3.31± 1.27 ng/mL and 3.97 ± 0.54 ng/mL versus 1.06 ± 0.59 ng/mL; P < 0.005), with group 1 (0.76±0.31 ng/mL). No statistically significant differences were found between group 1 and HC group. We found a strong linear correlation between PTX3 serum levels and AGA levels in group 2 (r=0.78, P <0.0001), and group 3 (r =0.63, P < 0.005) but no correlations were detected between PTX3 serum levels and tTGA levels (group 2, r= 0.04; group 3, r=0.24). Serological data revealed that PTX3 correlated with major gastrointestinal damage patients. PTX3 is a component of the humoral arm of the innate immune system. Our data showed that PTX3 serum levels were high in active disease patients with pathological levels of AGA. We also demonstrated that patients with normal AGA IgA levels had PTX3 serum levels compared to healthy control. We hypothesized that PTX3 is able to modulate the innate response to gliadin in CD and it could regulate the adaptive immune response.

Anti gliadin antibodies (AGA IgG) related to peripheral inflammation in schizophrenia

Altered immune function and inflammation are seen in schizophrenia, however, peripheral inflammatory markers are not consistently elevated in all people, suggesting inflammation may be present only in a subgroup. We measured TNF-α and IL-Iβ in 100 people with schizophrenia or schizoaffective disorder and correlated these with antibodies to gliadin, a protein found in wheat, barley and rye that has been found to be elevated in some people with schizophrenia. We hypothesized that higher peripheral antigliadin antibodies (AGA IgG) would be associated with higher peripheral inflammation as measured by TNF-α and IL-1β. Mean log transformed values of TNF-α, (p=.029) and IL-1β (p=.016) were over twofold higher in people with schizophrenia who had high levels of AGA IgG (≥7 U) compared to those who did not have positivity to AGA IgG. We found a significant positive correlation between AGA IgG and the log transformed TNF-α (r=0.42, p<.0001) as well as IL-Iβ (r=0.51, p<.0001). The relationship was independent of cigarette smoking, body mass index and antipsychotic medications. People with schizophrenia having higher levels of AGA IgG show higher levels of peripheral inflammation and may define a subgroup with distinct pathophysiology and potentially novel treatment targets.

Relation of ?-Amylase Activity with Glucose and Anti-Gliadin IgA and IgG in Sera of Patients with Celiac Disease

Celiac disease (CD) is an inflammatory small intestinal disorder that can lead to severe villous atrophy, and malabsorption . Since the measurement of α-amylase activity is the most widely used biochemical test for the diagnosis of pancreatic and non pancreatic disease , therefore serum α-amylase were studied in the present study in an attempt to evaluate the usefulness of this enzyme in the diagnosis of celiac disease and its relationship with anti gliadin IgA and IgG and serum glucose . Thirty one patients with celiac disease were studied and compared with twenty four healthy individuals . Significant elevation of α-amylase activity , glucose and anti gliadin IgA and IgG were observed in the sera of patients with celiac disease compared with the control group . Also a significant positive correlation between α-amylase activity and anti gliadin IgG were found in the present study in the sera of patients with celiac disease while a non significant correlation were found between α-amylase activity and anti gliadin IgA and glucose in the sera of the same patients of celiac disease.&#x0D; Keywords:- α-amylase , anti – gliadin IgA , IgG , glucose , celiac disease .

Mood disorders and non-celiac gluten sensitivity.

The association between gluten related disorders and psychiatric diseases has been firmly demonstrated. Non-celiac gluten sensitivity (NCGS) is a syndrome diagnosed in patients responsive to gluten-free diet after ruling out celiac disease and wheat allergy. The pathogenesis of neuro-psychiatric disorders in NCGS is unclear. An association between gluten and schizophrenia was described for the first time in 1950 by Bender et al. In the 1950's, Dicke noted that gluten-free diet improved mood in celiac patients. In 1970, Goldberg et al., in a study of 80 celiac patients, found that 34% of them showed minor affective disorders. Bipolar disorder patients show an increase of blood anti gliadin deamidated antibodies (IgG). The effect of diet and nutrition on autistic spectrum disorders has been investigated in the last two decades, particularly focusing on the symptoms of hyperactivity and attention. Toxoplasma gondii and other neurotropic pathogens as Influenzavirus and Coronavirus may be associated with mood disorders, probably secondary to an increased intestinal permeability. Abnormalities of host-microbiota interactions or of gut-microbiota composition have been associated with central nervous system disorders, such as autism, anxiety, depression and the integrity of intestinal microbiota may be considered a potential therapeutic goal to treat these conditions.

Are interleukin-15 and -22 a new pathogenic factor in pustular palmoplantar psoriasis?

IntroductionPustular palmoplantar psoriasis (PPP) is a rare type of psoriasis affecting mainly distal parts of the limbs. Despite numerous theories about etiology of PPP, the pathogenesis still remains unclear. Recent data indicate that interleukin (IL)-15, IL-17 and IL-22 enhance a proinflammatory response in certain skin inflammatory diseases such as psoriasis and atopic dermatitis. There is also evidence that anti-endomysial (anti-EMA) and anti-gliadin (AGA) antibodies are engaged in PPP development.AimTo assess IL-15, IL-17, IL-22 serum levels and evaluate the presence of anti-endomysial and anti-gliadin antibodies in patients with PPP.Material and methodsThe study group consisted of 20 females of the mean age of 51.8 suffering from PPP. Additionally 29 healthy individuals, age and sex matched, served as controls. ELISA was performed to evaluate serum IL-15, IL-17, IL-22 concentrations while an indirect immunofluorescence test (IIF) was used to determine anti-EMA and AGA presence.ResultsThe mean value of IL-15 and IL-22 serum concentrations was significantly higher in the study group than in the control group (IL-15: 6.48 vs. 4.88 pg/ml; IL-22: 81.47 vs. 4.90 pg/ml, respectively; p < 0.05 for all comparisons). The IL-17 serum level in the study group was higher when compared to the control group (2.0 vs. 0.75 pg/ml), however the results were not statistically significant (p = 0.26). There were no anti-EMA and AGA antibodies detected, both in the control and study group.ConclusionsThe results obtained may suggest involvement of IL-15 and IL-22 in the pathogenesis of PPP.

Iron Malabsorption Associated with Elevated Serum Gastrin

Iron deficiency anemia (IDA) in the absence of gastrointestinal (GI) bleeding is a common cause for hematologic consultation. During a 24 month period a single hematologist evaluated 36 patients for iron deficiency anemia which was unresponsive to oral iron replacement. Patients who had active GI bleeding, bariatric or extensive gastric surgery, or menorrhagia were excluded from this study. Hematologic testing included a serum gastrin level, Helicobacter pylori antibodies, and anti gliadin antibodies. Serum cobalamin levels were not measured. 28 patients had elevated gastrin levels, 3 patients had positive anti gliadin antibodies, and 2 patients had positive anti Helicobacter antibodies. One patient had both an elevated gastrin level and a positive anti gliadin antibody. One patient had both an elevated gastrin level and an anti helicobacter antibody. One patient had profound hypothyroidism (TSH&gt;100) whose iron deficiency corrected with thyroid replacement. Proton pump inhibitors (PPI) raise the serum gastrin levels. 16 patients with an elevated serum gastrin level were taking PPI when the gastrin measurements were obtained. However, the remaining 14 patients were not taking a PPI when gastrin levels were measured. 23 patients were women and 13 were men. No patient was under 40 years old. 11 were between 45 and 59 years of age. 25 were between 63 and 88 years old. 26 patients were non Hispanic caucasians, 8 were Hispanic caucasians, and 1 patient was African American. In the absence of a gastrin secreting tumor or use of a PPI an elevated gastrin suggests that autoimmune gastric atrophy is present which can cause both iron and vitamin B12 malabsorption. Iron malabsorption does occur in gluten enteropathy which is diagnosed by positive anti gliadin antibodies. Helicobacter infections are also associated with iron malabsorption. Intravenous iron replacement with iron dextran was administered to 35 patients. Two patients had minor reactions to iron dextran. One subsequently received iron sucrose without incident, but the other patient did not tolerate iron sucrose, iron carboxymaltose, and ferric gluconate. The 28 patients with an elevated gastrin has a complete response to intravenous iron replacement except the one patient who was intolerant to all intravenous iron preparations. Those with celiac sprue and helicobacter infections responded incompletely to intravenous iron therapy and required dietary modification and anti helicobacter therapy. An abnormal gastric biopsy was found in 3 of 28 patients with an elevated serum gastrin level. None of the 4 patients with a Helicobacter infection, gluten enteropathy, or severe hypothyroidism had a diagnostic esophagogastroduodenoscopy. In this small study no clear relationship between an elevated gastrin and either gluten enteropathy or a Helicobacter was present. This study has two interesting conclusions. First PPI therapy alone can cause iron deficiency anemia due to iron malabsorption. Also autoimmune gastric atrophy is a probable cause of IDA even when the gastrointestinal evaluation does not demonstrate bleeding or gastric atrophy. Both conditions are associated with an elevated serum gastrin. Serum gastrin measurement should be obtained during an evaluation for iron deficiency of unclear etiology. Disclosures No relevant conflicts of interest to declare.

Evaluation of coeliac disease serological markers

Background: celiac disease, is an autoimmune inflammatory disease of the small intestine that is precipitated by the ingestion of gluten, a component of wheat protein, in genetically susceptible persons. Serologic tests for antibodies against Endomysium, Reticulin, and Gliadin identify most patients with the disease. Early diagnosis and management are important to forestall serious consequences of malabsorption, such as osteoporosis and anemiaAims of the study: This study compared the sensitivity, specificity, and predictive value of, anti-reticulin and anti-gliadin antibodies according to anti endomysium antibodies , in consecutive patients investigated for celiac disease antibodies.Patient&amp; Methods: Total 509 patients (236 males&amp;273 females) celiac disease patients who were referred to the immunology department in Teaching labs from January till December 2012 for serological detection of auto antibodies . Anti- Gliadin (IgG &amp;IgA ) were measured by Enzyme Linked Immunosorbent Assay. whereas Anti-Endomyseal IgA &amp; Anti-Reticulin IgA were detected by Indirect immunofluorescent technique on monkey oesophagus &amp; kidney tissue respectively.Results: Most the cases for celiac disease were reported in the age group (1-10)years as antibodies against Gliadin (IgG,IgA) ,Anti-Endomesial IgA antibodies and anti-Reticulin IgA were detected in 130(66.7%),127(65.8%),39(79.6%) and 49(68.1%) respectively. Both anti-Gliadin IgA and anti Reticulin were detected significantly in females p values( 0.047, 0.008) respectively. The study showed that anti-Gliadin IgA is the most sensitive according to anti Endomyseal IgA and anti Reticulin was the most specific for screening of celiac disease. ; While Receiver Operating Characteristic (ROC) curve showed that anti gliadin IgA had the best sensitivity and specificity according to anti Endomysium test results.Conclusion: Predictive performance of the serological celiac disease tests showed that anti Gliadin IgA had the best sensitivity &amp;specificity according to traditional anti Endomysium antibody test results.

Gastrointestinal involvement in patients affected with 22q11.2 deletion syndrome

Objective. Enteropathy is a very common feature in patients with primary immunodeficiencies. In patients with Del22 gastrointestinal (GI) alterations, including feeding disorders and congenital abnormalities have been often reported, mostly in the first year of life. Material and methods. Aim of this monocentric study is to better define the GI involvement in a cohort of 26 patients affected with Del22 syndrome. Anamnestic information was retrospectively collected for each patient. Weight and height parameters at the time of the screening were recorded. Plasma levels of hemoglobin, iron, ferritin, albumin, total protein, calcium, phosphorus, transaminase levels, antigliadin (AGA) IgA and IgG, and antitissue transglutaminase (anti-TGase) titers were measured. Results. A GI involvement was identified in the 58% of patients. The prominent problems were abdominal pain, vomiting, gastroesophageal reflux and chronic constipation. Weight deficiency, short stature and failure to thrive were reported in 54, 42, and 30% of the patients, respectively. The evidence of sideropenic anemia, in keeping with hypoproteinemia, impaired acid steatocrit or cellobiose/mannitol test suggested an abnormal intestinal permeability. In this cohort, a high prevalence of AGA IgA and IgG positivity was observed. Celiac disease (CD) was suspected in three patients, and in one of them confirmed by histology. In this patient, a long-lasting gluten-free diet failed to restore the intestinal architecture. Conclusions. In conclusion, GI involvement is a very common feature in Del22 patients. A better characterization of GI involvement would be very useful to improve the management of these patients.

Celiac disease in the Red Sea state of Sudan

Celiac disease is characterized by sensitivity to gluten that results in inflammation and atrophy of the small intestine mucosa. The aim of this research was to document the presence of celiac disease and to describe its clinical presentations in the tribes living in the Red Sea state of Sudan. 172 patients suspected to have celiac disease, were examined at the Red Sea Medical Center laboratory, Port Sudan, Sudan, from August 2008 to September 2011. All clinical data was collected using questionnaires. Serum samples were obtained from all patients for serological detection of anti-gliadin (AG) and anti-tissue transglutamase (ATTG) antibodies (IgG and IgA) using the enzyme-linked immuno-sorbent assay (ELISA). 128 patients were found to have celiac disease. The commonest presenting symptom was chronic diarrhea (20.3%) followed by weight loss (14%). Males and females were nearly equally affected. All age groups were affected with a peak incidence between 5 to 10 years. Celiac disease occurs in the Red Sea state and may well be under-diagnosed. The combination of IgA AGA and IgA ATTG tests represent a good diagnostic method to confirm celiac disease in suspected cases. Special attention needs to be given to methods that encourage adherence to gluten-free diet in affected people in this region.

Increased Prevalence of Transglutaminase 6 Antibodies in Sera From Schizophrenia Patients

Gluten can cause extraintestinal manifestations with or without gastrointestinal symptoms and elevated antitissue transglutaminase 2 (tTG2) autoantibodies. Organ-specific gluten reaction involves immune response toward other transglutaminase (TG) isoforms including tTG3 (expressed in the skin, leading to dermatitis herpetiformis) and tTG6 (expressed in the brain, causing gluten ataxia). This analysis focuses on tTG6 antibodies, which have never been studied before in schizophrenia (SZ) and its relationships to tTG2 and to antigliadin antibodies. We previously showed an increased prevalence of tTG2 antibodies in gluten sensitive SZ patients compared with healthy controls (HC) that was not paralleled by an increased prevalence of antiendomysial antibody. To elucidate this discrepancy, we examined those tTG2 positive SZ patients for the presence of tTG6 antibody. We also searched for tTG6 antibodies in our sample of antigliadin (AGA) positive and AGA and tTG2 negative SZ patients. Seventy-four tTG2 positive SZ patients were compared with 148 age and gender-matched HC. Of the 74 tTG2 positive SZ patients, 16 were positive for tTG6 IgA for a prevalence of 22%. Only 4 HC were positive for tTG6 IgA for a prevalence of 2.7%. Among the AGA positive SZ patients, the prevalence of tTG6 IgA was 21.3% while 13.1% of the AGA and tTG2 negative SZ patients were positive for tTG6 IgA. The HC had a prevalence of 6%. Our results indicate a higher prevalence of tTG6 antibodies in SZ that may represent a biomarker useful to identify SZ patients who would benefit from a gluten-free diet.

Accuracy of Diagnostic Antibody Tests for Coeliac Disease in Children

The aim of this study was to summarise the evidence from 2004 to September 2009 on the performance of laboratory-based serological and point of care (POC) tests for diagnosing coeliac disease (CD) in children using histology as reference standard. We searched MEDLINE and EMBASE for studies reporting on children for tests based on IgA and IgG anti-gliadin (AGA), endomysial (EmA), anti-transglutaminase-2 (TG2), and anti-deamidated gliadin peptides (DGP) antibodies or POC tests. For inclusion, histological analysis of duodenal biopsies and sensitivity and specificity for index tests had to be reported. Data were pooled and summary measures calculated for sensitivity, specificity, positive and negative likelihood ratios ("LR+", "LR-"), and diagnostic odds ratios (DOR). In case of elevated statistical heterogeneity, studies reaching 90% sensitivity or specificity were reported. A total of 2510 articles were reviewed; 16 entered meta-analysis, reporting on 3110 patients (1876 with CD, 1234 without CD). For IgA-EmA, sensitivity was ≥90% in 7/11 studies and pooled specificity 98.2%. For IgA-anti-TG2, 11/15 studies yielded sensitivities ≥90% and 13/15 specificities ≥90%. For IgA-DGP, sensitivity ranged between 80.7% and 95.1% (specificity 86.3%-93.1%); for IgG-DGP between 80.1% and 98.6% (specificity 86.0-96.9%). IgA-EmA had the highest pooled DOR (554) and LR+ (31.8) for a laboratory test, followed by IgA-anti-TG2, IgG-DGP, IgA-DGP and IgA-AGA. POC tests showed a pooled sensitivity of 96.4% for IgA-TG2 (specificity 97.7%). IgA-EmA and IgA-anti-TG2 tests appear highly accurate to diagnose CD. IgG-anti-DGP tests may help in excluding CD. IgA-AGA and IgA-DGP tests show inferior accuracy. POC tests may achieve high accuracy in the hands of experienced readers, but IgA-anti-TG2/EmA were superior.

Coeliac disease: changing diagnostic criteria?

Coeliac disease: changing diagnostic criteria?

Prevalence of Autoantibodies Related to Some Autoimmune Disorders in Patients With Chronic Idiopathic Thrombocytopenic Purpura

We investigated the prevalence of antinuclear antibody (ANA), thyroid antimicrosomal (AMA) and antithyroglobulin (ATA), antigliadin (AGA) immunoglobulin G (IgG)-A, anti-endomisium (EMA) IgG-A, and tissue transglutaminase (tTG) IgG-A in 87 patients with chronic idiopathic thrombocytopenic purpura (cITP) and in 95 healthy controls. Antinuclear antibody positivity was found in 13 of 87 patients and 3 of 95 controls (P = .007). Antithyroglobulin positivity was found in 27 of patients and in 7 of the controls (P < .001). AMA positivity was found in 20 of patients and 8 of the controls (P = 0.008). Antigliadin IgG was positive in 17 patients and 1 controls (P < .001) whereas Antigliadin IgA was positive in 9 of patients and in 1 of the controls (P = .007). Anti-endomisium (IgG and IgA were not different between both groups. Tissue transglutaminase IgG was detected in 7 of patients and in 1 of the controls (P = .029). Tissue transglutaminase IgA was detected in 5 of patients and in none of the controls (P = .023). We believe that larger studies are needed to determine the long-term impact and clinical importance of these autoantibodies.