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Biomedical subjects

K Kaukinen

Publications and source records attributed to K Kaukinen.

At least 19 recordsLinked to original sources
PubMed2006

Immunoglobulin A autoantibodies against transglutaminase 2 in the small intestinal mucosa predict forthcoming coeliac disease.

BACKGROUND: Reliable markers of early developing coeliac diseases are needed. Coeliac autoantibodies in the serum or Marsh I inflammation may be indicators of subsequent coeliac disease. AIM: To investigate whether determination of intestinal transglutaminase 2-targeted autoantibody deposits would detect early developing coeliac disease better than previous methods. METHODS: The study investigated patients previously excluded for coeliac disease: 25 had positive serum coeliac autoantibodies (endomysial), 25 antibody-negative had Marsh I, and 25 antibody-negative had Marsh 0 finding. Seven (median) years after baseline investigation, new coeliac cases were recorded, and small bowel biopsy was offered to the rest of the patients. Serum and intestinal coeliac autoantibodies and intraepithelial lymphocytes were assessed as indicators of developing coeliac disease. RESULTS: Seventeen patients had developed coeliac disease: 13 in the autoantibody-positive group, three in the Marsh I group and one in the Marsh 0 group. At baseline, intestinal coeliac autoantibody deposits had a sensitivity and specificity of 93% and 93% in detecting subsequent coeliac disease, CD3+ 59% and 57%, gammadelta+ 76% and 60%, and villous tip intraepithelial lymphocytes 88% and 71%, respectively. CONCLUSIONS: Endomysial antibodies with normal histology indicates early developing coeliac disease. Transglutaminase 2-targeted intestinal autoantibody deposits proved the best predictor of subsequent coeliac disease.

Adolescent↗
PubMed2006

Self transglutaminase-based rapid coeliac disease antibody detection by a lateral flow method.

BACKGROUND: The conventional coeliac disease antibody tests require patient's sera, and are laborious and time-consuming. AIM: To evaluate a newly developed rapid whole blood test in coeliac disease antibody detection, and its suitability for office use. METHODS: Endogenous tissue transglutaminase found in red blood cells in a whole blood fingertip or venous sample is liberated upon haemolysis and complexes with tissue transglutaminase antibodies, if present. The complexes, captured by a lateral flow system, are visualized within 5 min. Stored samples from 121 untreated, 106 treated coeliac disease patients and 107 controls were evaluated and compared with serum endomysium and tissue transglutaminase antibody tests and histology; 150 patients were prospectively tested on site in the doctor's office. RESULTS: The rapid test showed sensitivity (96.7%) comparable with the serum endomysium and tissue transglutaminase antibody tests from stored samples; specificity was slightly lower (93.5%). When tested on site the results were concordant in 96.7% of cases compared with endomysium and tissue transglutaminase antibody results. The test recognized the disappearance of tissue transglutaminase antibodies on a gluten-free diet. CONCLUSIONS: The self tissue transglutaminase-based rapid test can be easily carried out from a fingertip blood sample on site in the physician's office for both coeliac disease case finding and dietary monitoring purposes.

Adolescent↗
PubMed2006

Oats in the treatment of childhood coeliac disease: a 2-year controlled trial and a long-term clinical follow-up study.

BACKGROUND: The exclusion of oats from the diet in coeliac disease is controversial. AIM: To study the long-term safety of oats in the treatment of children with coeliac disease. METHODS: Altogether 32 children with coeliac disease were enrolled in a 2-year controlled trial. Twenty-three children in remission were randomized either to oats or gluten challenge; when small bowel histological relapse was evident after gluten challenge, a gluten-free diet including oats was started. Furthermore, nine newly detected coeliac patients adopted an oat-containing gluten-free diet. Small bowel mucosal morphology, CD3+, alphabeta+ and gammadelta+ intraepithelial lymphocytes, human leucocyte antigen (HLA) DR expression and coeliac serology were determined. After the trial, the children were allowed to eat oats freely; follow-up was extended up to 7 years. RESULTS: In coeliac children in remission, oats had no detrimental effect on intestinal histology or serology during the 2-year trial. In contrast, the gluten-challenge group relapsed after 3-12 months. Complete recovery from the disease was accomplished in all relapsed and newly detected patients on an oat-containing gluten-free diet. After the trial, 86% of the children preferred to consume oats and they all remained in remission. CONCLUSION: In most children with coeliac disease, long-term consumption of oats is well tolerated, and it does not result in small bowel mucosal deterioration or immune activation.

Adolescent↗
PubMed2006

Malignancies and mortality in patients with coeliac disease and dermatitis herpetiformis: 30-year population-based study.

BACKGROUND AND AIM: To assess the long-term risks of malignant diseases and mortality in patients with coeliac disease and dermatitis herpetiformis in a centre, where the prevalence of these diseases is high. The risks have probably been overestimated, as patients with subtle forms have earlier remained undetected. PATIENTS: The study comprised 17,245 person-years of follow-up in 1147 patients. METHODS: The observed numbers of malignancies and causes of deaths were assessed, and compared to those expected, and standardised incidence ratio and standardised mortality ratio given. RESULTS: The occurrence of all malignant conditions was equal to that in the population both in coeliac disease and dermatitis herpetiformis: standardised incidence ratios of 1.2 (95% confidence intervals 0.9-1.5) and 1.0 (0.6-1.5), respectively. Five patients with coeliac disease and seven with dermatitis herpetiformis had developed non-Hodgkin lymphoma; standardised incidence ratios of 3.2 (1.0-7.5) and 6.0 (2.4-12.4), respectively. Four patients with coeliac disease and one with dermatitis herpetiformis had enteropathy-associated T-cell lymphoma, associated with inadequate dietary compliance. Mortality was increased (standardised mortality ratio 1.26; 1.00-1.55) in coeliac disease, but decreased in dermatitis herpetiformis (standardised mortality ratio 0.52; 0.36-0.72). CONCLUSION: The overall prognosis in our patients was good. Non-Hodgkin lymphoma emerged in patients with undiagnosed or poorly treated coeliac disease. The mortality rate in dermatitis herpetiformis was even lower than in the population. Our data support the early diagnosis and dietary treatment of these conditions.

Adolescent↗
PubMed2006

Endomysial antibody-negative coeliac disease: clinical characteristics and intestinal autoantibody deposits.

BACKGROUND: Some patients with untreated coeliac disease are negative for serum endomysial autoantibodies (EmA) targeted against transglutaminase 2 (TG2). AIMS: To evaluate the clinical and histological features of EmA-negative coeliac disease, and to examine whether EmA-equivalent autoantibodies against TG2 can be seen in the small-bowel mucosa when absent in serum. PATIENTS: Serum EmA was studied in 177 biopsy-proved specimens from adult patients with coeliac disease. 20 patients with intestinal diseases served as non-coeliac controls; three had autoimmune enteropathy with villous atrophy. METHODS: Clinical manifestations, small-bowel mucosal morphology, intraepithelial inflammation and TG2-specific extracellular immunoglobulin A (IgA) deposits were investigated in both serum EmA-negative and EmA-positive patients. RESULTS: 22 patients with IgA-competent coeliac disease were negative for serum EmA. Three of these had small-bowel lymphoma. Patients with EmA-negative coeliac disease were older, had abdominal symptoms more often, and the density of gammadelta+ intraepithelial lymphocytes in their intestinal mucosa was lower than in EmA-positive patients; otherwise the histology was similar. All serum EmA-negative patients with coeliac disease, but none of the disease controls, had gluten-dependent mucosal IgA deposits alongside TG2 in the small-bowel mucosal specimens. In vivo deposited IgA was shown to be TG2-specific by its ability to bind recombinant TG2. CONCLUSIONS: Negative serum EmA might be associated with advanced coeliac disease. TG2-targeted autoantibodies were deposited in the small-bowel mucosa even when absent in serum. This finding can be used in the diagnosis of seronegative coeliac disease when the histology is equivocal. It may also be helpful in the differential diagnosis between autoimmune enteropathy and coeliac disease.

Adolescent↗
PubMed2005

Coeliac disease case finding and diet monitoring by point-of-care testing.

BACKGROUND: Immunoglobulin A class transglutaminase autoantibodies are highly predictive markers of active coeliac disease, a disorder difficult to recognize solely on clinical grounds. AIMS: To develop and evaluate a simple rapid test for point-of-care detection of coeliac autoantibodies. METHODS: The novel whole blood test utilizes the patient's endogenous transglutaminase in red blood cells for detection of transglutaminase-specific immunoglobulin A antibodies present in the blood sample, with normal plasma immunoglobulin A detection as positive test control. We evaluated 284 patients under suspicion of coeliac disease and undergoing jejunal biopsy, and 263 coeliac patients on a gluten-free diet, 383 being tested prospectively in a point-of-care setting. Results were compared with histology, conventional serum autoantibody results and dietary adherence. RESULTS: The rapid test showed 97% sensitivity and 97% specificity for untreated coeliac disease, and identified all immunoglobulin A-deficient samples. Point-of-care testing found new coeliac cases as efficiently as antibody tests in laboratory. Coeliac autoantibodies were detected onsite in 21% of treated patients, while endomysial and transglutaminase antibodies were positive in 20% and 19%, respectively. The positivity rate correlated with dietary lapses and decreased on intensified dietary advice given upon positive point-of-care test results. CONCLUSIONS: Point-of-care testing was accurate in finding new coeliac cases and helped to identify and decrease dietary non-compliance.

Adolescent↗
PubMed2005

Is coeliac disease screening in risk groups justified? A fourteen-year follow-up with special focus on compliance and quality of life.

BACKGROUND: The benefits of serologic screening for coeliac disease in asymptomatic individuals are debatable. AIM: To investigate dietary compliance, quality of life and bone mineral density after long-term treatment in coeliac disease patients found by screening in risk groups. METHODS: The study comprised 53 consecutive screen-detected coeliac patients diagnosed 14 years (median) ago. Dietary compliance was assessed by interview, 4-day food record and serology. Quality of life was evaluated by the Psychological General Well-Being and SF-36 questionnaires, gastrointestinal symptoms by the Gastrointestinal Symptom Rating Scale and bone mineral density by dual-energy x-ray absorptiometry. Comparisons were made to 44 symptom-detected-treated coeliac patients, 110 non-coeliac subjects and the general population. RESULTS: A total of 96% of screen-detected and 93% of symptom-detected coeliac patients adhered to a strict or fairly strict gluten-free diet. In screen-detected patients, quality of life and gastrointestinal symptoms were similar to those in symptom-detected patients or non-coeliac controls and bone mineral density was similar to that in the general population. CONCLUSIONS: Long-term dietary compliance in screen-detected patients was good. Quality of life and bone mineral density were comparable with those in non-coeliac subjects and the general population. Active screening in coeliac disease risk groups seems to be reasonable rather than harmful.

Adult↗
PubMed2004

The safe threshold for gluten contamination in gluten-free products. Can trace amounts be accepted in the treatment of coeliac disease?

BACKGROUND: Gluten contamination in gluten-free products cannot totally be avoided. The safe threshold for gluten remains obscure. AIM: The purpose was to estimate a reasonable limit for residual gluten, based on current literature and measurement of gluten in gluten-free products on the market. METHODS: The gluten content of 59 naturally gluten-free and 24 wheat starch-based gluten-free products were analysed by enzyme-linked immunosorbent assay. The daily intake of flours was calculated in 76 adults on gluten-free diet, and the intake compared with mucosal histology. RESULTS: A number of both naturally gluten-free (13 of 59) and wheat starch-based gluten-free (11 of 24) products contained gluten from 20 to 200 ppm (=mg/kg). The median daily flour consumption was 80 g (range: 10-300). Within these limits, the long-term mucosal recovery was good. CONCLUSIONS: The threshold for gluten-contamination can safely be set at 100 ppm. Provided that the daily flour intake is even 300 g, a level of 100 ppm results in 30 mg of gluten intake. This has been shown to be safe, when correlated to histology, in clinical and challenge studies. The level can be achieved by the industry, and does not make the diet too cumbersome.

Adult↗
PubMed2004

cDNA microarray analysis of gene expression in coeliac disease jejunal biopsy samples.

In coeliac disease in the jejunum of a genetically susceptible person wheat gliadin and related prolamins from rye and barley trigger an immunological reaction, which induces small-bowel mucosal transformations, villous atrophy and crypt hyperplasia. Though CD4+ specific T cells, intraepithelial lymphocytes, infiltrating plasma cells and autoantibodies are known to have an effect on the coeliac disease, the pathogenic mechanisms leading to the tissue injury remain to be elucidated. Our aim was to find novel gene transcripts, which might have a role in coeliac disease pathogenesis. The gene expression in duodenal biopsy samples from untreated coeliac patients (n=4), patients on gluten-free diet (n=4) and healthy controls (n=4) was studied by cDNA microarray analysis. The method allows monitoring of the expression of thousands of genes simultaneously. Compared to healthy controls, the expression of 156 and 60 genes was changed in untreated and treated coeliac disease, respectively. Between treated and untreated coeliac disease, 98 genes had altered expression. Of the 5184 genes or expressed sequence tags, altogether 263 were affected. Many of these genes are directly or indirectly connected to T-cell activation, B-cell maturation or epithelial cell differentiation. By the microarray method, numerous genes were found to evince altered mRNA expression in coeliac disease. The method holds promise in exploring the pathogenetic mechanisms in the small bowel and may reveal new target genes for the therapy of coeliac disease.

Adult↗
PubMed2004

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.

Adult↗
PubMed2004

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.

Adolescent↗
PubMed2003

Wheat-starch-based gluten-free products in the treatment of newly detected coeliac disease: prospective and randomized study.

BACKGROUND: The safety of wheat-starch-based gluten-free products in the treatment of coeliac disease is debatable. Prospective studies are lacking. AIM: : To compare the clinical, histological and serological response to a wheat-starch-based or natural gluten-free diet in patients with newly detected coeliac disease. METHODS: Fifty-seven consecutive adults with untreated coeliac disease were randomized to a wheat-starch-based or natural gluten-free diet. Clinical response, small bowel mucosal morphology, CD3+, alphabeta+ and gammadelta+ intra-epithelial lymphocytes, mucosal human leucocyte antigen-DR expression and serum endomysial, transglutaminase and gliadin antibodies were investigated before and 12 months after the introduction of the gluten-free diet. Quality of life measurements were performed by standardized questionnaires and the bone mineral density was analysed. RESULTS: In both groups, abdominal symptoms were alleviated equally by a strict diet. There were no differences between the groups in mucosal morphology, the density of intra-epithelial lymphocytes, serum antibodies, bone mineral density or quality of life tests at the end of the study. Four patients on a natural gluten-free diet and two on a wheat-starch-based gluten-free diet had dietary lapses; as a result, inadequate mucosal, serological and clinical recovery was observed. CONCLUSIONS: The dietary response to a wheat-starch-based gluten-free diet was as good as that to a natural gluten-free diet in patients with newly detected coeliac disease.

Adult↗
PubMed2002

First-degree relatives are frequently affected in coeliac disease and dermatitis herpetiformis.

BACKGROUND: Coeliac disease and dermatitis herpetiformis are phenotypically distinct gluten-sensitive diseases. Coeliac disease is known to cluster in families, whereas there is little evidence for dermatitis herpetiformis and for the occurrence of both diseases in the same families. METHODS: The study group comprised 380 patients with coeliac disease and 281 patients with dermatitis herpetiformis, with a total of 3158 first-degree relatives, followed up for a mean of 14 years. The patients were questioned about affected first-degree relatives. The prevalence and incidence of biopsy-proven coeliac disease and dermatitis herpetiformis in relatives were determined. RESULTS: Seventy-three (19.2%) patients with coeliac disease and 51 (18.1%) with dermatitis herpetiformis had affected first-degree relatives. The prevalence among relatives was similar for both diseases; 4.7% and 3.9% of the relatives had coeliac disease and 0.8% and 1.5% had dermatitis herpetiformis, respectively. The disease prevalence was 7% among siblings, 4.5% among parents and 3.5% among children. The annual incidence was 3/1,000 relatives, which is 15 times higher than among the general population. Coeliac disease and dermatitis herpetiformis were mixed in several multiple-case families. CONCLUSIONS: The present long-term follow-up study of coeliac disease and dermatitis herpetiformis shows that every fifth patient can have affected first-degree relatives, and that the prevalence among relatives is 5.5%. Dermatitis herpetiformis segregates also in the families of patients with coeliac disease, and vice versa, indicating the same genetic background.

Adolescent↗
PubMed2002

The hunt for coeliac disease in primary care.

BACKGROUND: Serological screening suggests that most coeliac disease goes undetected. AIM: To determine how often coeliac disease is found in patients referred for gastroscopy by general practitioners. DESIGN: Testing of 9971 consecutive patients referred to a single health centre for their first open-access gastroscopy over a 10-year period, without previously-diagnosed coeliac disease or dermatitis herpetiformis. METHODS: Endoscopy and routine duodenal biopsy were in use throughout the study period. The occurrence of coeliac disease was evaluated in patients with dyspepsia, in those with regurgitation, and in those with symptoms suggestive of coeliac disease. RESULTS: Altogether, 147 (1.47%) patients had coeliac disease: 18/2974 (0.61%) with regurgitation, 41/5347 (0.77%) with dyspepsia, and 88/1650 (5.33%) with suspected coeliac disease. Increasing age reduced the risk very slightly (OR 0.98; 95%CI 0.97-0.99). Risk was significantly increased when there was a suspicion of coeliac disease (OR 9.085; 95%CI 5.371-15.369), while no difference was found between patients with dyspepsia and those with reflux disease (OR 1.33; 95%CI 0.75-2.34). The risk in women was not increased (OR 0.97; 95%CI 0.69-1.38). DISCUSSION: In this primary-care setting, <1% of patients with upper abdominal symptoms suffered from coeliac disease; population-based serological screening is expected to yield a corresponding prevalence. When physicians had suspected coeliac disease, the condition was nine times more common.

Adolescent↗
PubMed2002

Blisters in the small intestinal mucosa of coeliac patients contain T cells positive for cyclooxygenase 2.

BACKGROUND AND AIMS: Coeliac disease is characterised by atrophy of the villi and hyperplasia of the crypts in the mucosa of the small intestine. It is caused by an environmental trigger, cereal gluten, which induces infiltration of the mucosa by inflammatory cells. We hypothesised that these inflammatory cells express cyclooxygenase 2 (COX-2), an enzyme that contributes to the synthesis of pro and anti-inflammatory prostaglandins and is known to be expressed at sites of inflammation in the stomach and colon. We have investigated expression of COX-2 in the coeliac disease affected small intestinal mucosa where it may be an indicator of either disease induction or mucosal restoration processes. PATIENTS AND METHODS: Small intestinal biopsy samples from 15 coeliac patients and 15 non-coeliac individuals were stained immunohistochemically for COX-2. Samples from 10 of the patients were also stained after these patients had been on a gluten free diet for 6-24 months. Various cell type marker antigens were used for immunohistochemical identification of the type of cell that expressed COX-2. To further verify colocalisation of the cell type marker and COX-2, double immunoperoxidase and immunofluorescence methods were employed. Immunoelectron microscopy was used to investigate the subcellular location of COX-2. RESULTS: In all samples taken from coeliac patients, clusters of cells with strong immunoreactivity for COX-2 were found in those areas of the lamina propria where the epithelium seemed to blister or was totally detached from the basement membrane. These clusters were reduced in number or totally absent in samples taken after a gluten free diet. No such clusters were seen in any control samples. The density of COX-2 positive cells lining the differentiated epithelium decreased significantly from 13.5 (5.1) cells/10(5) microm(2) (mean (SD)) in the untreated patient samples to 6.5 (2.0) cells/10(5) microm(2) after a gluten free diet (p<0.001), and was 3.3 (1.9) cells/10(5) microm(2) in control samples (p<0.001 compared with untreated or diet treated coeliac samples). Staining for COX-2 was localised to CD3+ T cells and CD68+ macrophages in the mucosal lesions but not all of these cells were positive for COX-2. Immunoelectron microscopy revealed that the ultrastructure of the COX-2 positive cells resembled that of lymphocytes, and the immunoreaction was localised to the rough endoplasmic reticulum and the nuclear envelope. CONCLUSIONS: Our results show that in coeliac disease, blistering of small intestinal epithelial cells is associated with accumulation of COX-2 positive T cells, and the number of these cells decreases after a gluten free diet. These observations suggest that COX-2 mediated prostanoid synthesis contributes to healing of the coeliac mucosa and may be involved in maintenance of intestinal integrity.

Adolescent↗
PubMed2001

Celiac disease without villous atrophy: revision of criteria called for.

Current diagnostic criteria of celiac disease require small bowel villous atrophy, although the damage develops gradually. We therefore searched for evidence of disease in 10 adults suspected to have celiac disease, but evincing only minor mucosal inflammation and increase in gammadelta+ cells without villous atrophy. Twenty untreated celiac and 27 nonceliac patients served as biopsy controls. CD3+, alphabeta+, and gammadelta+ cells were increased in patients with only minor mucosal lesions, but less than in celiac patients. The inflammation resolved on gluten-free diet, and abdominal symptoms were alleviated. Eight of 10 had positive endomysial, seven gliadin, and nine tissue transglutaminase antibodies; all normalized on diet. Eight patients had osteopenia; HLA DQ2 was found in all. Minor mucosal lesions with an increase in gammadelta+ intraepithelial lymphocytes were suggestive of celiac disease. Our patients showed a clinical, histological, and serological recovery on diet; risk of osteopenia speaks in favor of dietary treatment.

Adult↗
PubMed2001

Clinical and subclinical autoimmune thyroid disease in adult celiac disease.

Our aim was to investigate the occurrence of clinical and subclinical autoimmune thyroid disease in 79 patients with celiac disease as reflected in thyroid function, antibodies, and ultrasound. Since subclinical thyroid diseases are common in the population, 184 nonceliac controls were also studied. Normal thyroid function combined with positive antibodies and marked hypoechogenicity was considered subclinical disease. Autoimmune thyroid disease was observed in 13.9% of celiac patients and in 2.1% of controls (P = 0.0005); and subclinical disease in 10.1% and 3.3%, respectively (P = 0.048). The mean thyroid gland volume was 8.3 ml in celiac patients and 10.4 ml in controls (P = 0.007). Hypoechogenicity was found in 73% of celiac patients and in 42% of controls (P < 0.0001). Positive thyroid antibodies were associated with hypoechogenicity in celiac patients but not in controls. In conclusion, the occurrence of both clinical and subclinical autoimmune thyroid disease was increased in celiac disease; subclinical thyroid disease indicates regular surveillance.

Autoimmune Diseases↗