Gastrointestinal Symptoms Rating Scale in Coeliac Disease Patients on Wheat Starch-based Gluten-free Diets

Background: A wheat starch-based gluten-free diet is widely adopted in the treatment of coeliac disease, even though the products contain trace amounts of gluten. The aim here was to establish whether such a diet sustains abdominal symptoms. Methods: The Gastrointestinal Symptom Rating Scale (GSRS) was applied to 58 coeliac disease patients on gluten-free diets and 110 non-coeliac controls. An estimate was made of daily dietary fibre and wheat starch-derived gluten. Psychological well-being was evaluated by a structured interview. Twenty-three coeliac patients consented to small-bowel biopsy. Results: The mean GSRS score in coeliac disease patients did not differ from that in control subjects. Poorer psychological well-being was associated with abdominal symptoms in coeliac patients, whereas the daily amount of wheat starch had no effect on GSRS score. Overall dietary compliance was good, and villous atrophy was found in only 2 out of 23 patients. The average fibre consumption, 13 g per day, was lower than recommended. Conclusions: Wheat starch-based gluten-free products are well-tolerated in coeliac disease patients, provided that their diets are otherwise strict.     

Gastrointestinal symptoms rating scale in coeliac disease patients on wheat starch-based gluten-free diets

BACKGROUND: A wheat starch-based gluten-free diet is widely adopted in the treatment of coeliac disease, even though the products contain trace amounts of gluten. The aim here was to establish whether such a diet sustains abdominal symptoms. METHODS: The Gastrointestinal Symptom Rating Scale (GSRS) was applied to 58 coeliac disease patients on gluten-free diets and 110 non-coeliac controls. An estimate was made of daily dietary fibre and wheat starch-derived gluten. Psychological well-being was evaluated by a structured interview. Twenty-three coeliac patients consented to small-bowel biopsy. RESULTS: The mean GSRS score in coeliac disease patients did not differ from that in control subjects. Poorer psychological well-being was associated with abdominal symptoms in coeliac patients, whereas the daily amount of wheat starch had no effect on GSRS score. Overall dietary compliance was good, and villous atrophy was found in only 2 out of 23 patients. The average fibre consumption, 13 g per day, was lower than recommended. CONCLUSIONS: Wheat starch-based gluten-free products are well-tolerated in coeliac disease patients, provided that their diets are otherwise strict.     

Small-bowel mucosal transglutaminase 2-specific IgA deposits in coeliac disease without villous atrophy: a prospective and randomized clinical study

OBJECTIVE: In coeliac disease, autoantibodies directed against transglutaminase 2 are produced in small-bowel mucosa, and they have been found to be deposited extracellularly. The aim of this study was to investigate whether such mucosal IgA deposits are important in the diagnostic work-up of early-stage coeliac disease without small-bowel mucosal villous atrophy. MATERIAL AND METHODS: Forty-one adults suspected of coeliac disease owing to increased density of mucosal gamma(delta)+ intraepithelial lymphocytes but normal villous morphology were randomized to gluten challenge or a gluten-free diet for 6 months. Clinically and histologically verified gluten dependency was compared with existence of small-bowel mucosal transglutaminase 2-specific extracellular IgA deposits and (coeliac disease-type) HLA DQ2 and DQ8; 34 non-coeliac subjects and 18 patients with classical coeliac disease served as controls. RESULTS: Of the 41 patients, 5 in the challenge group and 6 in the gluten-free diet group were clinically gluten sensitive; all 11 had HLA DQ2 or DQ8. Ten of these 11 patients showed transglutaminase 2-targeted mucosal IgA deposits, which were dependent on gluten consumption. Minimal IgA deposits were seen in only 3 out of 30 patients with suspected coeliac disease without any clinically detected gluten dependency. The deposits were found in all classical coeliac patients and in none of the non-coeliac control subjects. CONCLUSIONS: Clinically pertinent coeliac disease exists despite normal small-bowel mucosal villous architecture. Mucosal transglutaminase 2-specific IgA deposits can be utilized in detecting such patients with genetic gluten intolerance.     

Small-bowel mucosal transglutaminase 2-specific IgA deposits in coeliac disease without villous atrophy: A prospective and randomized clinical study

Objective In coeliac disease, autoantibodies directed against transglutaminase 2 are produced in small-bowel mucosa, and they have been found to be deposited extracellularly. The aim of this study was to investigate whether such mucosal IgA deposits are important in the diagnostic work-up of early-stage coeliac disease without small-bowel mucosal villous atrophy.

Material and methods Forty-one adults suspected of coeliac disease owing to increased density of mucosal γδ+ intraepithelial lymphocytes but normal villous morphology were randomized to gluten challenge or a gluten-free diet for 6 months. Clinically and histologically verified gluten dependency was compared with existence of small-bowel mucosal transglutaminase 2-specific extracellular IgA deposits and (coeliac disease-type) HLA DQ2 and DQ8; 34 non-coeliac subjects and 18 patients with classical coeliac disease served as controls.

Results Of the 41 patients, 5 in the challenge group and 6 in the gluten-free diet group were clinically gluten sensitive; all 11 had HLA DQ2 or DQ8. Ten of these 11 patients showed transglutaminase 2-targeted mucosal IgA deposits, which were dependent on gluten consumption. Minimal IgA deposits were seen in only 3 out of 30 patients with suspected coeliac disease without any clinically detected gluten dependency. The deposits were found in all classical coeliac patients and in none of the non-coeliac control subjects.

Conclusions Clinically pertinent coeliac disease exists despite normal small-bowel mucosal villous architecture. Mucosal transglutaminase 2-specific IgA deposits can be utilized in detecting such patients with genetic gluten intolerance.     

Intolerance to cereals is not specific for coeliac disease

BACKGROUND: Abdominal complaints after ingestion of cereals are not uncommon. We assessed how reliable such a history is as a marker for the presence of overt coeliac disease, and whether we should also take into account latent coeliac disease and cereal allergy. METHODS: The study group comprised 93 consecutive adults from health centres spontaneously reporting abdominal symptoms after consumption of cereals. Small bowel mucosal morphology, CD3+, alphabeta+ and gammadelta+ intraepithelial lymphocytes (IELs), HLA DQ alleles and serum IgA-class endomysial (EmA), tissue transglutaminase (tTg) and gliadin (AGA) antibodies were determined. Skin prick and patch tests and serum radioallergosorbent tests for cereals were carried out. Thirty non-coeliac adults served as biopsy controls. RESULTS: Eight (9%) patients had coeliac disease and one mild partial villous atrophy. Altogether 17 had an increased density of gamma delta+ IELs without atrophy. However, only seven (8%) showed evidence of latent coeliac disease, i.e. both an increase in gammadelta+ IELs and the presence of coeliac disease-type HLA. One or more of the allergy tests for cereals was positive in 19; 9 adopted a gluten-free diet and abdominal symptoms were alleviated in all. In non-coeliac patients, serum EmA and tTg tests were negative in all, whereas AGA was seen in 40%. CONCLUSIONS: Intolerance to cereals is not a specific sign of overt or latent coeliac disease. All experimental dietary interventions before proper diagnosis of coeliac disease are therefore to be discouraged. Allergy to cereals, on the other hand, should be considered even in adults.     

Treatment of dermatitis herpetiformis with corticosteroids and a gluten-free diet: a study of jejunal morphology and function

The jejunal morphological and functional response to either a gluten-free diet or corticosteroid therapy was studied in six patients with dermatitis herpetiformis. In each treatment group there were two patients with subtotal villous atrophy and one with partial villous atrophys. After treatment, in both groups, morphological improvement was seen in villous and surface cell heights, mucosal thickness, and intraepithelial lymphocyte counts. Jejunal function was assessed using the perfusion technique. Absorption of glucose from a 56 mM solution was shown to improve. Water movement from this solution was in a secretory state in four patients (two in each group) before treatment and moved into the normal absorptive range after treatment. These results further outline the similarity between the mucosal lesion of dermatitis herpetiformis and true coeliac disease.     

Villous tip intraepithelial lymphocytes as markers of early-stage coeliac disease

BACKGROUND: An investigation was conducted to determine whether the density of small-intestinal villous tip intraepithelial lymphocytes would be of value in clinical practice in uncovering early-stage coeliac disease. METHODS: Villous tip, CD3+ and gammadelta+ intraepithelial lymphocytes were counted in patients with definite early-stage coeliac disease without villous atrophy, in classic coeliac disease with manifest mucosal lesion and in non-coeliac controls with normal mucosal structure. Villous tip analysis was made of haematoxylin-eosin specimens and CD3+ and gammadelta+ of immunohistochemical stainings from frozen samples. RESULTS: The villous tip intraepithelial lymphocyte count was statistically significantly higher in patients with early-stage coeliac disease than in non-coeliac controls. The sensitivity of this method to detect untreated coeliac disease with normal villous architecture was 0.84; the specificity was 0.88. This method proved superior to CD3+ analysis and was at least as good as gammadelta+ analysis in detecting early-stage coeliac disease. In detecting classic coeliac disease, villous tip analysis also reached a higher sensitivity than CD3+ and gammadelta+ cells. CONCLUSIONS: Villous tip analysis seems to distinguish early coeliac from non-specific changes, thus providing a valuable tool in routine practice, especially when borderline findings are involved. Its value appears to be similar to counting of gammadelta+ cells, which, however, requires frozen biopsy samples.     

The cellular infiltrate of the jejunum in adult coeliac disease and dermatitis herpetiformis following the reintroduction of dietary gluten.

The cellular infiltrate of the jejunal mucosa has been studied in patients with both treated and untreated adult coeliac disease and dermatitis herpetiformis and serially in treated patients before and after the reintroduction of gluten to the diet. In adult coeliac disease and dermatitis herpetiformis the jejunal mucosa showed similar abnormalities of the cellular infiltrate which was characterized by an increase in intraepithelial lymphocytes and lamina propria plasma cells and eosinophils, with the greatest numbers of cells occurring in untreated patients. At 24-48 hours following a single 25-g gluten challenge there was an increase in lamina propria plasma cells, lymphocytes and eosinophils and intraepithelial lymphocytes. This rise was sustained after seven days on a gluten-containing diet for all of these cell groups except lamina propria lymphocytes. These responses were essentially similar in both adult coeliac disease and in those dermatitis herpetiformis patients who had jejunal lesions before treatment. In dermatitis herpetiformis patients with normal jejunal morphology on a normal diet there was an upward trend in lamina propria plasma cells and intraepithelial lymphocytes within one to three weeks of taking extra dietary gluten. These results are compatible with the view that more than one immunological mechanism may be responsible for the pathogenesis of the jejunal lesion of coeliac disease and dermatitis herpetiformis.     

Effect of an oats-containing gluten-free diet on symptoms and quality of life in coeliac disease. A randomized study

BACKGROUND: Evidence suggests the acceptability of oats in a gluten-free diet in coeliac disease. We investigated the impact of an oats-containing diet on quality of life and gastrointestinal symptoms. METHODS: Thirty-nine coeliac disease patients on a gluten-free diet were randomized to take either 50 g of oats-containing gluten-free products daily or to continue without oats for 1 year. Quality of life was assessed using the Psychological General Well-Being questionnaire and gastrointestinal symptoms using the Gastrointestinal Symptom Rating Scale. Small-bowel mucosal villous architecture, CD3+, alphabeta+, gammadelta+ intraepithelial lymphocytes, serum endomysial and tissue transglutaminase antibodies were investigated. RESULTS: Twenty-three subjects were randomized to the oats-containing diet and 16 to the traditional gluten-free diet. All adhered strictly to their respective diet. Quality of life did not differ between the groups. In general, there were more gastrointestinal symptoms in the oats-consuming group. Patients taking oats suffered significantly more often from diarrhoea, but there was a simultaneous trend towards a more severe average constipation symptom score. The villous structure did not differ between the groups, but the density of intraepithelial lymphocytes was slightly but significantly higher in the oats group. The severity of symptoms was not dependent on the degree of inflammation. Antibody levels did not increase during the study period. CONCLUSION: The oats-containing gluten-free diet caused more intestinal symptoms than the traditional diet. Mucosal integrity was not disturbed, but more inflammation was evident in the oats group. Oats provide an alternative in the gluten-free diet, but coeliac patients should be aware of the possible increase in intestinal symptoms.     

Tolerance to oats in dermatitis herpetiformis

Objectives—Recent studies on coeliac diseasehave shown that oats can be included in a gluten-free diet withoutadverse effects on the small bowel. The presence of a rash is also asensitive indicator of gluten ingestion in dermatitis herpetiformis,and this was used to study whether patients with this disease could also tolerate oats.
Patients/Methods—Eleven patients with dermatitisherpetiformis in remission on a gluten-free diet were challenged dailywith 50 g oats for six months. Clinical symptoms were recorded, serum samples taken, and skin and small bowel biopsies performed before andafter the oat challenge. A control group comprised of 11 patients withdermatitis herpetiformis on a conventional gluten-free diet was also studied.
Results—Eight patients challenged with oatsremained asymptomatic, two developed a transient rash, and one withdrewbecause of the appearance of a more persistent but mild rash. Three of the 11 controls also developed a transient rash. IgA endomysial antibodies remained negative in all patients. The small bowel villous architecture, the densities of intraepithelial CD3 and α/βand γ/δ T cell receptor positive lymphocytes and crypt epithelial cell DR expression remained unaltered during the oat challenge.
Conclusions—The results confirm the absenceof oat toxicity on the gluten sensitive small bowel mucosa and suggestthat the rash in patients with dermatitis herpetiformis is notactivated by eating oats.

Keywords:dermatitis herpetiformis; coeliac disease; gluten-free diet; oats

     

Intraepithelial lymphocytes and coeliac disease

The diagnosis of coeliac disease is easy in cases with symptoms and unequivocal small intestinal villous atrophy. However, patients often suffer from only subtle if any symptoms. Borderline villous shortening is common, making the histologic diagnosis difficult. The increase in intraepithelial lymphocytes is typical even in early-stage untreated coeliac disease. Unfortunately, this finding is unspecific. In coeliac disease, the relative density of gammadelta+ intraepithelial lymphocytes is increased. The presence of IgA class anti-endomysium or anti-tissue transglutaminase antibodies clearly increases the likelihood of the disease. Coeliac disease is closely linked to HLA DQ2 and DQ8, and their absence speaks strongly against the condition, whereas a positive finding is virtually of no diagnostic value. In borderline cases, the gluten-dependency of symptoms or mucosal inflammation should be shown by gluten-free diet or gluten challenge. No single test is efficient enough to distinguish unspecific increase in intraepithelial lymphocytes from early coeliac disease; clinical history, histology, serology and gluten-dependency should be taken into account in the diagnostic work-up.     

Dermatitis herpetiformis: diagnosis, diet and demography

We describe a long term study of 76 patients with dermatitis herpetiformis. Unlike patients with coeliac disease, where the peak incidence was during the first and fourth decades, no dermatitis herpetiformis patients presented in the first decade; also, there was a male preponderance in dermatitis herpetiformis which contrasts with the excess of females in coeliac disease. The apparent prevalence of dermatitis herpetiformis was 11 per 100 000 in our population; approximately one fifth of that of coeliac disease. Jejunal villous atrophy was present in 78% of our dermatitis herpetiformis patients, and a single jejunal biopsy was as effective at detecting this as the multiple biopsy technique. A majority of patients were able to stop, or radically reduce their dapsone or sulphapyridine treatment after the institution of a gluten free diet. Spontaneous remission of the skin lesion occurred in only two patients not receiving a gluten free diet. Gastric parietal or thyroid antibodies were detected in 38% of patients, and three cases of thyroid disease and two cases of pernicious anaemia were detected. Lymphoma developed in two patients, one being intestinal in origin. We conclude that a gluten free diet is of therapeutic benefit in dermatitis herpetiformis and that spontaneous remission is uncommon in those not on a diet. Despite patchiness of the enteropathy, a single jejunal biopsy is quite adequate to diagnose the presence of upper intestinal villous atrophy.     

Effects of additional dietary gluten on the small-intestinal mucosa of volunteers and of patients with dermatitis herpetiformis

In an attempt to confirm the existence of latent coeliac disease--dose-related gluten-sensitive enteropathy--we have increased dietary gluten by 20 g daily for 2 weeks, in 6 healthy adults and 11 patients with dermatitis herpetiformis (DH). Six of the DH patients had entirely normal jejunal morphology on a normal diet. Jejunal biopsy specimens were taken before and at the end of the study. Measurements of crypts, villi, and crypt mitoses were made on microdissected specimens; disaccharidases were assayed, and intraepithelial lymphocyte counts performed. In one of the six adult volunteers, gluten loading produced diarrhoea and jejunal biopsy abnormalities. Five DH patients on a gluten-free diet had deterioration of biopsy pathology after the gluten challenge. Features suggestive of a latent gluten-sensitive enteropathy were found in one of the other six DH patients; he developed disaccharidase deficiencies and villus atrophy when 20 g gluten was added to his usual gluten-containing diet. This study supports previous suggestions that a gluten-sensitive enteropathy may be latent and dose-related.     

Celiac disease: clinical and subclinical forms

Coeliac disease is an intolerance to gluten that classically produces a chronic diarrhoea with a picture of malabsorption and a total villous atrophy. These elements regress completely in a sequential way under a prolonged strict gluten-free diet. The progress registered in the understanding of this affection depends on the individualization of the atypical forms (delayed isolated stature, constipation...) of asymptomatic forms thanks to the study of specific antibodies (anti-gliadin, anti-endomysium, and more recently anti-transglutaminase). The auto-immune nature of coeliac disease is well established. The diagnostic criteria are simplified allowing the commencement of a gluten-free diet which must be perfectly detailed. Finally, allergy to wheat flour merits individualization in the framework of coeliac disease (cf. article).     

Comparison of IgA-class reticulin and endomysium antibodies in coeliac disease and dermatitis herpetiformis

The occurrence of IgA class reticulin and endomysium antibodies was examined with the standard immunofluorescence method in coeliac disease and dermatitis herpetiformis. Similar high antibody frequencies were detected in 32 untreated adults (91%) and 18 children (100%) with coeliac disease and in 14 dermatitis herpetiformis patients with subtotal villous atrophy (reticulin antibodies 93% and endomysium antibodies 100%). The specificity of IgA class reticulin antibodies and endomysium antibodies was high because all 45 adult patients with ulcerative colitis or Crohn's disease, 24 non-coeliac children with abdominal symptoms and 99/100 healthy blood donors were negative for these antibodies. The only positive blood donor had both IgA class reticulin antibodies and endomysium antibodies but also she was found to have coeliac disease. IgA class reticulin antibodies and endomysium antibodies declined in parallel during treatment with a gluten free diet and increased on gluten challenge. This suggests that these antibodies can be used to screen for gluten sensitive enteropathy and to monitor dietary treatment. To characterise the tissue specificity of reticulin antibodies and endomysium antibodies four positive sera were absorbed with human and several rodent liver homogenates. Absorption with rat or other rodent livers removed the rodent-specific reticulin antibodies but not the reticulin antibodies detectable with human tissues or the endomysium antibodies detectable with monkey oesophagus. These results show that reticulin antibodies can be divided into the rat and human subtypes. The human subtype could not be separated from endomysium antibodies in the present absorption experiments.     

IgA-class transglutaminase antibodies in evaluating the efficacy of gluten-free diet in coeliac disease

OBJECTIVE : Serum IgA-class tissue transglutaminase antibody has proved effective in screening for coeliac disease. The response to a gluten-free diet has been assessed on the basis of small-intestinal morphology. We investigated whether the tissue transglutaminase antibody test could substitute biopsy in this respect, and whether the test is better than the endomysial antibody test in follow-up. DESIGN : Controlled cross sectional, and follow-up study. METHODS : Serum IgA-class tissue transglutaminase antibodies and endomysial antibodies were determined in 87 coeliac adults on a gluten-free diet. All underwent small bowel biopsy, and the mucosal morphology was interpreted along with Marsh's grading 0-3. In 30 patients histological and serological data could be analysed before and after adopting the diet; Marsh 3 was considered inadequate mucosal recovery during the diet. RESULTS : Of the 87 coeliac patients 27 showed Marsh 3 villous atrophy on gluten-free diet; of these 27, tissue transglutaminase antibody was within normal limits in 16 (59%) and endomysial antibody in 20 (74%). Two (7%) out of 29 with normal mucosa (Marsh 0) had positive tissue transglutaminase antibodies. Six (55%) out of 11 admitting regular dietary lapses remained tissue transglutaminase antibody negative. In the follow-up, serum IgA-class tissue transglutaminase antibody was initially positive in 28 (93%) out of 30 untreated patients; even a significant decrease in tissue transglutaminase antibody did not guarantee mucosal recovery. CONCLUSIONS : A substantial number of coeliac patients with negative tissue transglutaminase or endomysial antibodies may still have manifest mucosal villous atrophy. Small bowel biopsy is therefore still necessary to ensure that the gluten-free diet is adequate.     

Celiac disease, dermatitis herpetiformis and erosive jejunoileitis

A 21-year-old man with coeliac disease and dermatitis herpetiformis presented successively with erosive ileitis (warranting surgical resection) and erosive jejunitis (proven by jejunoscopy). Discontinuous antibiotic therapy was associated with a gluten-free diet and evolution was favorable as judged with five years follow-up. Malabsorption with mucosal ulcerations can be due to: a) chronic ulcerative duodeno-jejuno-ileitis or Jeffries' disease; b) coeliac disease which may be classified as possible, probable, or certain according to the strictness of criteria. Our case is the fourth in which a villous response was proven after gluten-free diet. It is also particular in that the erosions were superficial; c) malignant lymphoma which can reasonably be excluded here. This observation confirms that a gluten-free diet may be effective after surgical resection of the ulcerated segment in complicated coeliac disease and shows that antibiotics may be an useful adjuvant to therapy.     

Transition of care between paediatric and adult gastroenterology. Coeliac disease

Coeliac disease is a condition in which there is an abnormal mucosa in the small intestine. It improves with a gluten free diet, with avoidance of wheat, rye, barley and possibly oats. The history and epidemiology of this condition are discussed. Diagnosis is based on demonstrating that the characteristic histological abnormalities in the small intestine are dependent on gluten ingestion. Diagnostic pitfalls are discussed. The anti-endomysium and anti-tissue transglutaminase antibodies are specific and sensitive diagnostic tools. The wide variety of clinical symptoms and presentations are discussed including the associated condition of dermatitis herpetiformis. Failure to respond to a gluten-free diet can represent simple dietary problems, an alternative diagnosis or, occasionally, the development of a serious complication of coeliac disease such as ulcerative jejunitis or enteropathy-associated T cell lymphoma. Progress towards the characterization of the toxic epitopes within gluten that exacerbate coeliac disease and our current understanding of the genetics of the disorder are presented.     

HLA association with dermatitis herpetiformis is accounted for by a cis or transassociated DQ heterodimer.

HLA-DR, DQ, and DP restriction fragment genotyping was undertaken in 23 dermatitis herpetiformis patients and 53 healthy control subjects. HLA-DQw2 was present in 100% of patients with dermatitis herpetiformis (23 of 23) versus 40% of control subjects (21 of 53). Significant secondary associations occurred with HLA-DR3 (91% of patients versus 28% of control subjects) and DPw1 (39% of patients versus 11% of control subjects). Dermatitis herpetiformis and coeliac disease thus share an identical HLA class II association. It is likely that HLA class II genes directly influence the immune responses leading to mucosal damage in both diseases. The strongest candidate for disease susceptibility to dermatitis herpetiformis is DQw2. The HLA molecule most likely to be involved in coeliac disease is a specific DQ alpha/DQ beta heterodimer, encoded in cis arrangement in DR3 haplotypes or in trans arrangement in a DR5, 7 genotype. Our data on dermatitis herpetiformis patients fits this model perfectly. All these patients are capable of expressing this molecule, which may be responsible for the gluten sensitive enteropathy seen in a subgroup of patients with dermatitis herpetiformis and coeliac disease.     

Resurrection of gliadin antibodies in coeliac disease. Deamidated gliadin peptide antibody test provides additional diagnostic benefit

OBJECTIVE: Circulating antibodies against naive, whole gliadin have been replaced by more accurate endomysial and tissue transglutaminase antibody tests in the diagnosis of coeliac disease. The purpose of this study was to compare these serological tests with a new test recognizing antibodies against deamidated and defined gliadin peptides. MATERIAL AND METHODS: The study population comprised selected coeliac disease patients in a tertiary clinic: newly detected patients before and after a gluten-free diet, patients with persistent small-bowel mucosal villous atrophy despite a strict gluten-free diet and non-coeliac controls reporting abdominal symptoms after ingestion of cereals. Comparisons were made between serum IgA-class gliadin peptide, endomysial, tissue transglutaminase and conventional gliadin antibodies. RESULTS: The deamidated gliadin peptide antibody test showed a sensitivity of 91% and a specificity of 98% in coeliac disease. The tissue transglutaminase antibody test performed equally well. The specificity of endomysial antibody was just as high, but its sensitivity was lower, 80%. The conventional gliadin antibody test showed poor sensitivity and specificity. Combination of the deamidated gliadin peptide and tissue transglutaminase tests offered the best sensitivity without loss of specificity in the diagnosis of coeliac disease. All antibody levels declined in line with mucosal recovery. The deamidated gliadin peptide antibody test showed six of the nine cases with small-bowel mucosal damage persisting on a gluten-free diet, whereas tissue transglutaminase detected only two cases and endomysial antibody none. CONCLUSIONS: The new gliadin peptide antibody test proved highly accurate in the diagnostic work-up and follow-up of coeliac disease and can be endorsed in combination with the tissue transglutaminase test.