Fasting breath hydrogen in celiac disease

We studied the possible clinical significance of high basal levels of H2 by analyzing the breath excreted by the following fasting subjects: 50 healthy volunteers, 149 subjects with functional bowel disorders, 16 patients with small bowel bacterial overgrowth proven by bacteriology, 34 patients with untreated celiac disease, 40 patients with celiac disease on a gluten-free diet, and 40 patients with disorders of the small intestine other than celiac disease (disease controls). The fasting levels of H2 in untreated celiac patients (mean 22.5 +/- 19.3 ppm) were significantly higher than those in healthy volunteers (5.8 +/- 3.1 ppm), patients with functional bowel disorders (6.6 +/- 4.4 ppm), treated celiac patients (9.9 +/- 8.1 ppm), and disease controls (7.0 +/- 6.7 ppm). No significant difference was found between patients with untreated celiac disease and bacterial overgrowth (mean 14.7 +/- 14.0 ppm). The percentage of patients with elevated H2 fasting levels in untreated celiac disease (58.8%) was significantly higher than that in the other groups, except for the patients with bacterial overgrowth (43.7%). In 14 celiac patients, studied before and after a gluten-free diet, fasting H2 levels decreased from 26.6 +/- 18 to 11.6 +/- 10 ppm, becoming normal only in those patients with healing of intestinal lesions. Our results show that high fasting H2 levels are a frequent feature of untreated celiac disease and that the return to normal of these levels is predictive of villous regrowth.     

Antroduodenojejunal motor activity in untreated and treated celiac disease patients

Background and Aim:  Patients with celiac disease may present with abnormal upper gut motor activity. However, it is not known if these abnormalities persist after the introduction of a gluten-free diet. The present study aimed to compare antroduodenojejunal motor variables recorded in untreated celiac patients with those of celiac patients given a gluten-free diet and healthy volunteers.
Methods:  Eleven untreated celiac disease patients, 12 age- and sex-matched celiac patients on a gluten-free diet (at least 12 months), and 33 controls entered the study. Antroduodenojejunal motility was recorded for 6 h during fasting and for 3 h after a standard meal by means of a perfused, multiple lumen catheter.
Results:  More than 80% of untreated celiac patients had discrete motor abnormalities of the upper gut, in both fasting and fed recordings, compared to the other subjects. Patients on a gluten-free diet also showed motor abnormalities, albeit to a lesser extent. In these patients histological evaluation showed the persistence of mild mucosal abnormalities.
Conclusions:  Upper gut motor abnormalities are frequent in patients with celiac disease, even in those on a gluten-free diet. In the latter group, these abnormalities may suggest an incomplete adherence to the dietary regimen.     

Calcaneal ultrasound attenuation and vitamin-D-receptor genotypes in celiac disease

BACKGROUND: Osteopenia is common in patients with celiac disease and is believed to result from malnutrition. Osteoporosis in otherwise healthy individuals is related to genetically determined polymorphisms within the vitamin-D-receptor (VDR) gene. We hypothesized that in celiac patients particular genes of the VDR enhance the susceptibility for malnutrition-associated low-bone density. METHODS: We determined allelic frequencies within the VDR gene by restriction fragment length polymorphism analysis in 92 patients with celiac disease (age, 15-83 years). Thirty-eight patients were on a gluten-free diet; 54 patients did not adhere to a diet. The determined VDR polymorphisms in 111 unrelated newborns served as controls. Osteopenia was determined by means of ultrasound measurements of the calcaneus (n = 78). Bone turnover was estimated by osteocalcin determination (n = 60). RESULTS: There was no difference in the frequency of the VDR gene polymorphisms in patients with celiac disease compared with controls. Adjusted ultrasound measures of the calcaneus were low in 47% of patients, but there was no difference of the VDR gene frequencies in these patients compared with those with normal ultrasound results or controls. Bone turnover was higher in patients without a gluten-free diet (P = 0.02). Again, there was no association with any particular VDR gene. CONCLUSIONS: Patients with celiac disease frequently have osteopenia, which is not related to any of the determined genes within the VDR.     

Calcaneal Ultrasound Attenuation and Vitamin-D-Receptor Genotypes in Celiac Disease

Background: Osteopenia is common in patients with celiac disease and is believed to result from malnutrition. Osteoporosis in otherwise healthy individuals is related to genetically determined polymorphisms within the vitamin-D-receptor (VDR) gene. We hypothesized that in celiac patients particular genes of the VDR enhance the susceptibility for malnutrition-associated low-bone density. Methods: We determined allelic frequencies within the VDR gene by restriction fragment length polymorphism analysis in 92 patients with celiac disease (age, 15-83 years). Thirty-eight patients were on a gluten-free diet; 54 patients did not adhere to a diet. The determined VDR polymorphisms in 111 unrelated newborns served as controls. Osteopenia was determined by means of ultrasound measurements of the calcaneus (n = 78). Bone turnover was estimated by osteocalcin determination (n = 60). Results: There was no difference in the frequency of the VDR gene polymorphisms in patients with celiac disease compared with controls. Adjusted ultrasound measures of the calcaneus were low in 47% of patients, but there was no difference of the VDR gene frequencies in these patients compared with those with normal ultrasound results or controls. Bone turnover was higher in patients without a gluten-free diet (P = 0.02). Again, there was no association with any particular VDR gene. Conclusions: Patients with celiac disease frequently have osteopenia, which is not related to any of the determined genes within the VDR.     

Immunohistochemical analysis of ZO-1 in the duodenal mucosa of patients with untreated and treated celiac disease

BACKGROUND/AIM: ZO-1 is a good marker for tight junction integrity which may be damaged in many intestinal diseases. ZO-1 can also accumulate in the cellular nucleus in addition to sites of cell-cell contact, suggesting a potential role in cellular proliferation and differentiation. We evaluated the expression and distribution of ZO-1 in patients with celiac disease before and after a gluten-free diet. METHODS: The ZO-1 expression was evaluated semiquantitatively by means of immunohistochemical analysis in duodenal bioptic specimens of 10 consecutive patients with celiac disease before and after a gluten-free diet and in 10 controls. Furthermore, the nuclear staining was analyzed quantitatively, evaluating 3,000 cells for each count, and it was expressed as a percentage of labeled nuclei over the total of analyzed cells. RESULTS: The intestinal mucosa of untreated celiac disease patients shows a globally lower ZO-1 labeling than that of controls. The expression of ZO-1 in the treated celiac mucosa did not differ significantly from normal intestinal mucosa of healthy subjects. At the crypt level of untreated celiac mucosa, a low intensity of nuclear labeling (1.75 +/- 0.32%) was found, while in both treated celiac disease patients and in normal subjects we observed a statistically significant higher percentage of strongly labeled nuclei (53.72 +/- 6.30% and 56.79 +/- 5.45%, respectively; p = 0.0002). CONCLUSIONS: Our data show a global underexpression of ZO-1 in the duodenal mucosa of active celiac disease patients. Gluten withdrawal allows a normalization of the ZO-1 expression in treated celiac disease patients. Furthermore, the particular pattern of ZO-1 resembles the cellular distribution in undifferentiated cells and may be the result of immaturity of the enterocytes in untreated celiac sprue.     

α1-Antitrypsin Clearance as an Aid in the Management of Patients with Celiac Disease

One hundred and thirty-two different intestinal alpha 1-antitrypsin clearance tests were performed in 48 untreated adult celiac patients, 64 patients taking a gluten-free diet, and 20 adult healthy controls. In the untreated group, 95% of patients had enteric protein loss with values higher than the upper limit of normality (mean +/- 2 SD). In the treated group of patients, only 22% had abnormal levels of alpha 1-antitrypsin clearance. Sixteen patients who had elevated clearance before treatment had decreased clearance after an average of 7.4 months on a gluten-free diet. There was a significant relation (p less than 0.05) between the alpha 1-antitrypsin clearance and the degree of alteration of the jejunal histological structure. We conclude that enteric protein loss is a very frequent finding in celiac patients and the measurement of alpha 1-antitrypsin clearance may be a reliable method to evaluate the activity of the disease and useful in following the efficacy of treatment.     

Gluten-free diet induces regression of T-Cell activation in the rectal mucosa of patients with celiac disease

Objective: An increase in the number of intraepithelial lymphocytes (IEL) in the rectal epithelium of patients with active celiac disease has been described. No data are available about how they vary during a gluten-free diet. The aim of the study was to assess the effect of a gluten-free diet on T-cell activation in the rectal mucosa of adult patients with celiac disease.
Methods: Frozen duodenal and rectal biopsies were available in four celiac patients (one male, three female, mean age 39 yr) both before and after 7 to 24 months on a gluten-free diet. Biopsy samples were stained using monoclonal antibodies directed against CD3, βF1, TcRδ1, CD25, and HLADR. Numbers of IEL were estimated by counting the peroxidase-stained cells per 100 epithelial cells. Four patients without histological abnormalities were used as control subjects.
Results: In the four patients with active celiac disease but in none of the controls, CD25 was expressed by both duodenal and rectal lamina propria cells and HLADR was expressed by duodenal (4/4) and rectal (2/4) epithelial cells. In addition, two patients with active celiac disease had features of lymphocytic colitis, i.e. , >20 IEL per 100 epithelial cells. After a gluten-free diet, the mean number of rectal CD3⁺βF1⁺ IEL decreased (9% vs 21%) and the expression of CD25 and HLADR was no longer present. These changes mirrored those found in the small intestinal biopsies.
Conclusion: These results suggest that in celiac disease, gluten-driven T-cell activation is not restricted to the proximal part of the intestine but is present on the whole intestinal length. Assessment of the effectiveness of a gluten-free diet through rectal biopsies warrants investigation, as it could lessen discomfort for patients and prove more cost-effective.     

Assessment of body composition by bioelectrical impedance in adolescent patients with celiac disease

OBJECTIVE: Assessment of body composition is of primary importance in the management of celiac adolescents. We aimed to evaluate body composition by dual-energy x-ray absorptiometry and bioelectrical impedance in celiac adolescents on a gluten-free diet to investigate whether impedance may provide an alternative method to assess nutritional status in these patients. METHODS: We studied body composition in 43 adolescents affected by celiac disease on a gluten-free diet for > or = 1 yr and 30 healthy subjects. Fat, fat-free, and bone masses were assessed by dual-energy x-ray absorptiometry. Fat and fat-free masses were also assessed by bioelectrical impedance. All anthropometric measurements were performed according to standard procedures. RESULTS: All patients had a significantly lower body weight, height, fat-free mass, bone mineral density (p < 0.001), and body mass index (p < 0.01) compared with controls. In contrast, parameters predicting fat compartment (sum of skinfolds and fat mass) did not differ from those of controls. No significant difference was found between patients strictly adherent to a gluten-free diet and patients partially compliant. Compared with dual-energy x-ray absorptiometry measurements, bioelectrical impedance showed a high accuracy to estimate fat-free mass (R2 = 0.97) and limited accuracy for fat mass (R2 = 0.75). Furthermore, impedance was more reliable for estimating hydration of soft tissue underlying the fat-free mass changes. CONCLUSIONS: In adolescents with celiac disease, after a mean of 1 yr of gluten-free diet all the parameters assessing body compartments, except fat mass, were affected, compared with healthy controls. Bioelectrical impedance holds promise for routine assessment of body composition changes in celiac adolescents on a gluten-free diet.     

Esophageal Impairment in Adult Celiac Disease With Steatorrhea

Objective: A high prevalence of reflux esophagitis in celiac children and gut motor disorders in adult patients have been described. The aim of this study is to investigate the prevalence of esophageal symptoms and the esophageal motility pattern in adult celiac patients before and after gluten-free diet.
Methods: In 22 consecutive adult celiac patients, before and after gluten-free diet, and in controls we calculated an esophageal symptom score regarding heartburn, regurgitation, dysphagia, and chest pain, and performed esophageal manometry using a constantly perfused multilumen catheter.
Results: Patients were divided into two groups: with and without steatorrhea. Before gluten-free diet, the prevalence of esophageal symptoms was 45.5% in all patients, but was significantly higher in patients with steatorrhea than in those without and in 44 control subjects (80% vs 16.7% and 27%,   p < 0.05  ). Lower esophageal sphincter pressure was 17.5 ± 5.3 in all patients, but was significantly lower in patients with steatorrhea than in patients without steatorrhea and 11 controls subjects (13.1 ± 4.1 vs 21.0 ± 2.9 and 20.7 ± 3.7 mm Hg (mean ± SD,   p < 0.05  ). After the diet, the prevalence of esophageal symptoms diminished in all patients (9% vs 45.4%,   p < 0.05  ) and lower esophageal sphincter pressure, measured in 13 patients, increased (19.0 ± 3.7 vs 15.7 ± 5.3 mm Hg,   p < 0.05  ).
Conclusion: Adult celiac patients with steatorrhea present a higher prevalence of esophageal symptoms and a lowered lower esophageal sphincter pressure compared with celiac patients without steatorrhea and control subjects, but these phenomena can be reverted to control levels by gluten-free diet.     

Reduced chemokine receptor 9 on intraepithelial lymphocytes in celiac disease suggests persistent epithelial activation

BACKGROUND & AIMS: Celiac disease is caused by an inappropriate immune response to dietary gluten, with increased epithelial lymphocyte infiltration in the duodenum/jejunum as a hallmark. The chemokine receptor 9 (CCR9) is a small intestinal homing receptor normally found on most mucosal T cells in this organ. Because CCR9 expression appears to be activation dependent, we examined CCR9 on duodenal T cells from untreated and treated (gluten-free diet) patients with celiac disease and healthy controls. METHODS: Duodenal biopsy specimens and blood samples were obtained for histologic analysis and flow-cytometric CCR9 analysis of isolated lymphocytes. CCR9 expression after activation was studied in peripheral blood T cells from healthy volunteers. RESULTS: The median number of CCR9(+) cells among CD3(+) T cells in epithelium and lamina propria, respectively, was 56% and 48% in controls, 11% and 40% in treated patients, and 1% and 8% in untreated patients. Significant differences occurred between controls and treated or untreated patients in the epithelium but only between controls and untreated patients in the lamina propria (P=.008, all comparisons). No such differences were seen in peripheral blood, but stimulation with phorbol myristate acetate and ionomycin and, to a lesser extent, stimulation via NKG2D reduced the CCR9 expression on blood T cells. CONCLUSIONS: CCR9 expression is reduced on epithelial and lamina propria T cells in untreated celiac disease. Down-regulation of CCR9 persists in intraepithelial T cells from well-treated patients. This suggests ongoing immune activation preferentially within the epithelium.     

Anti-ganglioside antibodies in coeliac disease with neurological disorders

BACKGROUND: Anti-ganglioside antibodies have been described in sera of coeliac patients with peripheral neuropathy and cerebellar ataxia. AIMS: To investigate the correlation between anti-ganglioside antibodies and neurological involvement in coeliac disease before and after gluten-free diet. PATIENTS AND METHODS: Twenty-two untreated coeliac patients with neurological dysfunction and 30 untreated coeliacs without neurological dysfunction, 20 patients with neurological disorders, 50 autoimmune disease and 20 blood donors were tested for anti-GM1, anti-GD1b and anti-GQ1b IgG and IgM antibodies by enzyme-linked immunosorbent assay. RESULTS: IgG antibodies to at least one of the three antigens tested were positive in 64% of coeliac patients with neurological symptoms compared to 30% of coeliacs without neurological dysfunction (P=0.02), 50% of patients with neurological disorders (P=ns), 20% with autoimmune diseases (P=0.003) and none of blood donors (P=0.0001). A strict gluten-free diet determined anti-ganglioside antibody disappearance in about half of coeliacs. CONCLUSIONS: A significant correlation between anti-ganglioside antibodies and neurological disorders in patients with an underlying coeliac disease has been found. Anti-ganglioside antibodies may represent a new immunological marker to identify neurological impairment in patients with coeliac disease.     

Small intestinal permeability as an indicator of jejunal mucosal recovery in patients with celiac sprue on a gluten-free diet

Lactulose/mannitol excretion ratios were measured in 13 patients with celiac disease at diagnosis and after 5-8 months on a gluten-free diet. Jejunal biopsies were assessed histologically at diagnosis and during treatment. The excretion ratios in untreated patients were significantly higher than in 25 normal controls (P less than 0.01). On the diet, the excretion ratios fell in every patient, but in only eight did the ratio return to normal. There was a good correlation between the ratio and jejunal histological grading. During treatment, the ratios significantly inversely correlated with jejunal villous height/mucosal thickness ratios (P less than 0.001). Therefore, excretion ratios provide a well-tolerated noninvasive means of assessing the jejunal mucosa in patients with celiac disease on a gluten-free diet.     

Celiac disease and insulin-dependent diabetes mellitus

We screened for celiac disease, by means of IgA class anti-endomysium antibodies (EmA), 383 consecutive adults with insulin-dependent diabetes mellitus (IDDM). Two control populations entered the study as well: 151 adults with biopsy proven celiac disease, as true positives; and 520 controls (healthy and diseased) as true negatives. IgA-EmA positivity was found in 145 of 151 (96%) celiac disease patients but in none of the controls (100% specificity). EmA were positive in 12 of 383 (3.13%) IDDM patients: 10 of these positives underwent intestinal biopsy, which showed either partial or total villous atrophy. Only one patient presented with gastrointestinal complaints, but severe iron deficiency was found in all. The IDDM celiac patients were started on a gluten-free diet: four refused both the diet and the follow-up protocol. Approximately one year after gluten withdrawal no significant change in the degree of diabetes control was observed, while an increased requirement for insulin was observed in three of four patients who strictly complied with the diet. The prevalence of biopsy-proven celiac disease among adult IDDM patients (1:38), eight times higher than that recently estimated for the general Italian population and the absence, except in one case, of gastrointestinal symptoms emphasizes the benefit of screening programs on populations at risk.     

Bone Mineral Affection in Asymptomatic Adult Patients with Celiac Disease

Objectives: Osteopenia is a well-known complication of overt celiac disease, but whether such defective bone mineralization is present among asymptomatic or silent patients is not known. Our objectives were: 1 ) to examine bone mineralization of a group of asymptomatic celiac patients; 2 ) to compare these results with those of symptomatic patients. Methods: Bone mineral density of the spine and total skeleton by dual energy x-ray ab-sorptiometry and serum parameters of mineral metabolism of eight recently diagnosed asymptomatic patients with celiac disease were studied. Results were compared with those obtained in 20 untreated symptomatic celiacs, 14 patients treated with gluten-free diet for a mean time of 15 yr, and 153 healthy adult subjects, matched by sex and age. Results: Four and five out of eight asymptomatic patients presented with reduced mineralization of the spine and the total skeleton, respectively (>1 SD below normal values for sex and age). Two patients presented with severe osteopenia of the spine, and the other three presented with severe osteopenia of the whole skeleton (>2 SD below mean normal values). Osteopenia at plane bone level (total skeleton) was significantly lower when compared to healthy controls ( P < 0.02). Symptomatic untreated patients had significantly more severe deterioration of bone mineralization than did asymptomatics ( P < 0.05) and treated patients ( P < 0.05). No difference in bone mineral density was observed between treated patients and asymptomatic celiacs. Serum levels of calcium, alkaline phosphatase, 25-OH vitamin D, and parathormone did not show conclusive abnormalities. Conclusions: Our findings provide direct evidence that reduced bone mineralization occurs in asymptomatic celiac patients before any other symptom becomes evident. Only early diagnosis and treatment of celiac disease can avoid the deterioration of the bone structure observed in all clinical status of celiac disease.     

Gluten-Free Diet Normalizes Mouth-to-Cecum Transit of a Caloric Meal in Adult Patients with Celiac Disease

The mechanisms responsible for boweldisturbances in celiac disease are still relativelyunknown. Recent reports suggested that small bowel motorabnormalities may be involved in this pathologicalcondition; however, there are no studies addressing smallbowel transit in celiac disease before and after agluten-free diet. We studied the mouth-to-cecum transittime of a caloric liquid meal in a homogeneous group of celiac patients presenting with clinical andbiochemical evidence of malabsorption and complaining ofdiarrhea. Sixteen patients were recruited andinvestigated by means of hydrogen breath test through ingestion of 20 g lactulose together with anenteral gluten-free diet formula. A urinary D-xylosetest was also done in each patient. Both breath testsand D-xylose tests were carried out basally and after a period of gluten-free diet. Twenty healthyvolunteers were recruited as a control group andunderwent the same breath testing. At the time of thediagnosis, mouth-to-cecum transit time was significantly prolonged in celiacs with respect to controls(243 ± 10 vs 117 ± 6 min, P = 0.0001). TheD-xylose test was also abnormal (average urinaryconcentration 2.8 ± 0.25 g, normal values>4.5). No correlation was found in patients between mouth-to-cecum transit timeand urinary D-xylose output (r = 0.22). After thegluten-free diet period, mouth-tocecum transit time inceliacs was significantly reduced compared to prediet transit (134 ± 8 vs 243 ± 10 min,P = 0.0001) and did not show statistical difference whencompared to that found in controls (P = 0.1). TheD-xylose test reverted to normal in all but twosubjects, who were found to be noncompliant with the diet.Mouth-to-cecum transit time is significantly prolongedin patients affected by untreated celiac disease whencompared to healthy controls. This alteration might notbe correlated to intestinal malabsorption, and theprolonged orocecal transit could be due to impairedsmall bowel function (deranged motility?). Sinceintestinal transit returned to normal values after an adequate gluten-free period, a link with severeactive mucosal lesions is suggestive.     

Superior mesenteric artery blood flow in celiac disease

Measurements of the hemodynamic parameters of the superior mesenteric artery were performed in 18 patients with celiac disease. Ten were studied at the time of diagnosis, when a small bowel biopsy showed a flat mucosa. The remaining eight patients were studied after complete clinical and histological recovery induced by a gluten-free diet. Doppler ultrasound flowmetry was used to measure blood flow in physiological and fasting conditions and after a mixed liquid test meal (Ensure-Plus). The results were compared with those of healthy subjects (N=7). Mean basal flow was 50% higher in untreated celiac disease patients than in healthy controls and patients with chronic pancreatitis (P=NS). Postprandial mesenteric blood flow was significantly increased (P<0.002) and delayed in time (P<0.005) in celiac disease as compared to controls. Successful treatment reduced the mesenteric blood flow in celiac disease to normal values. Our study demonstrates that pathophysiological changes in the small bowel mucosa during the active clinical phase of celiac disease induce an abnormal splanchnic circulation.     

Gynecologic and obstetric findings related to nutritional status and adherence to a gluten-free diet in Brazilian patients with celiac disease

This study shows a broad analysis of gynaecological and obstetrical disturbances in patients with celiac disease in relation to their nutritional status and adherence to a gluten-free diet. Seventy-six adult celiac patients were analyzed according to nutritional status and 18 children/adolescents to gluten-free diet adherence. As controls, 84 adults and 22 adolescents with irritable bowel syndrome were used The significant findings were observed as follow: adult celiac patients, irrespective of the nutritional status, were younger than controls, presented delayed menarche, secondary amenorrhea, a higher percentage of spontaneous abortions, anemia and hypoalbuminemia. No differences were observed regarding the number of pregnancies, age at menopause and duration of the reproductive period. After treatment, patients presented with normal pregnancies and one patient presented spontaneous abortion. The adolescents who were not adherent to gluten-free diet presented delayed menarche and secondary amenorrhea. In conclusion, gluten per se could explain the disturbances and malnutrition would worsen the disease in a consequent vicious cycle. Therefore, celiac disease should be included in the screening of reproductive disorders.     

Frontal cortical perfusion abnormalities related to gluten intake and associated autoimmune disease in adult coeliac disease: Tc-ECD brain SPECT study

OBJECTIVE: Since brain perfusion abnormalities have been described by single-photon emission computed tomography in some autoimmune diseases, the aim of the present study was to evaluate the incidence of perfusion abnormalities by brain single-photon emission computed tomography in a group of coeliac disease patients, and to investigate whether gluten intake and associated autoimmune diseases may be considered risk factors in causing cerebral impairment. METHODS: Thirty-four adult coeliac patients (16 on a gluten-free diet and 18 on a gluten-containing diet, 18 (53%) with autoimmune diseases) underwent 99mTc-ethyl cysteinate dimer brain single-photon emission computed tomography and qualitative evaluation of brain perfusion was performed together with a semiquantitative estimation using the asymmetry index. Ten subjects on our database, matched for sex, age and ethnic group, who were proved normal by histology ofjejunal mucosa (four males and six females; median age 39 years, range 27-55 years), were included as control group. RESULTS: Twenty-four out of 34 patients (71%) showed brain single-photon emission computed tomography abnormalities confirmed by abnormal regional asymmetry index (>5%; range 5.8-18.5%). Topographic comparison of the brain areas showed that the more significant abnormalities were localised in frontal regions, and were significantly different from controls only in coeliac disease patients on unrestricted diet. The prevalence of single-photon emission computed tomography abnormalities was similar in coeliac disease patients with (74%) and without (69%) associated autoimmune disease. CONCLUSIONS: Abnormalities of brain perfusion seem common in coeliac disease. This phenomenon is similar to that previously described in other autoimmune diseases, but does not appear to be related to associated autoimmunity and, at least in the frontal region, may be improved by a gluten-free diet.     

Serum nitric oxide levels in children with celiac disease

OBJECTIVES: To determine serum nitric oxide levels in pediatric patients with celiac disease and to compare them with the results obtained after 1 year of gluten-free diet. METHODS: We studied serum nitric oxide levels in 41 newly diagnosed patients with celiac disease. Serum levels of nitric oxide were reevaluated after 1 year of gluten-free diet in 23 of them. Mean age was 10.4 +/- 3.4 years (range 2-17 years). RESULTS: The levels of nitric oxide in pretreatment 41 patients with celiac disease and healthy children were detected as 198.33 +/- 20.22 micromol/L and 135.63 +/- 21.17 micromol/L, respectively (P = 0.0001). Serum nitric oxide level, measured in the blood samples 1 year after gluten-free diet, was 148.27 +/- 27.25 micromol/L (P = 0.001). Serum nitric oxide levels were statistically correlated with the degree of histologic changes in celiac disease. In the patients with celiac disease, pretreatment level of nitric oxide was not correlated with the levels of triglyceride, cholesterol, albumin, aspartate aminotransferase, alanine aminotransferase, or creatine kinase. We found correlations with the level of nitric oxide and Hb, mean corpuscular volume, and ferritin. CONCLUSION: Higher serum nitric oxide levels found in children who had not compliance with gluten-free diet suggested the role of serum nitric oxide as an indicator of diet compliance. Because determination of serum nitric oxide is a simple, rapid, cheap, noninvasive, and highly sensitive method for celiac disease, we think that this parameter can be used in the evaluation of diet compliance in children with celiac disease or even instead of gluten challenge, due to more noninvasive property.     

Influence of Previously Ingested Wheat on Fasting Breath Hydrogen in Celiac Patients

The excretion of hydrogen in breath commonly persists, despite an overnight fast. Although the elevation of hydrogen concentration above the fasting value after the administration of a test sugar is evidence of malabsorption, the level of the fasting value itself in untreated celiac patients is unknown. Therefore, we studied the fasting breath hydrogen (FBH₂) concentration in 40 healthy controls, 35 subjects with functional bowel disorders, and 30 patients of untreated celiac disease with and without bread or wheat diet one day before the test. The fasting level of hydrogen concentration in untreated celiac patients (28.7 ± 19.5 ppm) was significantly higher than those in healthy volunteers (9.5 ± 3.4 ppm) and subjects with functional bowel disorders (10.6 ± 4.5 ppm). The percentage of patients with elevated H₂ fasting levels in untreated celiac disease (82.5%) was significantly higher than that in healthy controls (10%) and subjects with functional bowel disorders (17.1%). In 30 celiac patients, studied with and without wheat-free diet one day before the test, the fasting hydrogen levels decreased from 28.7 ± 19.5 ppm to 10.6 ± 3.5 ppm, and becoming normal in all patients of celiac disease. Our results show that the patients of untreated celiac disease should be instructed not to eat things made up of wheat one day before hydrogen breath testing so that the normal fasting hydrogen concentration can be obtained and false-negative hydrogen breath test results can be avoided.