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Background: Histological changes induced by gluten in the duodenal mucosa of patients with non-coeliac gluten sensitivity (NCGS) are poorly defined. Objectives: To evaluate the structural and inflammatory features of NCGS compared to controls and coeliac disease (CeD) with milder enteropathy (Marsh I-II). Methods: Well-oriented biopsies of 262 control cases with normal gastroscopy and histologic findings, 261 CeD, and 175 NCGS biopsies from 9 contributing countries were examined. Villus height (VH, in μm), crypt depth (CrD, in μm), villus-to-crypt ratios (VCR), IELs (intraepithelial lymphocytes/100 enterocytes), and other relevant histological, serologic, and demographic parameters were quantified. Results: The median VH in NCGS was significantly shorter (600, IQR: 400–705) than controls (900, IQR: 667–1112) (p < 0.001). NCGS patients with Marsh I-II had similar VH and VCR to CeD [465 µm (IQR: 390–620) vs. 427 µm (IQR: 348–569, p = 0·176)]. The VCR in NCGS with Marsh 0 was lower than controls (p < 0.001). The median IEL in NCGS with Marsh 0 was higher than controls (23.0 vs. 13.7, p < 0.001). To distinguish Marsh 0 NCGS from controls, an IEL cut-off of 14 showed 79% sensitivity and 55% specificity. IEL densities in Marsh I-II NCGS and CeD groups were similar. Conclusion: NCGS duodenal mucosa exhibits distinctive changes consistent with an intestinal response to luminal antigens, even at the Marsh 0 stage of villus architecture. [ABSTRACT FROM AUTHOR]

Objectives: To study the effects of celiac disease on bone mineral density. Design: Case-control study. Setting: The study was conducted in Department of Anatomy, Sardar Patel Medical College, Bikaner, Rajasthan. Participants: A total of 90 patients, 60 control group healthy normal and 30 celiac disease patients case group were incorporated in study with informed consent. Material and Methods: The bone mineral density was measured in case and control group at calcaneum by peripheral dual X-ray absorptiometry along with body mass index and age. Results: The significant difference was found between the bone mineral density of case and control group (0.87±0.49 & 0.61±0.44: p=0.0001) and 43.33% subjects had osteopenia in case group while only 5% subjects had osteopenia in healthy group. The significant difference of bone mineral density in both groups below the age of 15 years was non existing but between the age group of 16-30 years it was significant (-1.17±0.68 & 0.68±0.21: p=0.001) Conclusion: Celiac disease patients are at higher risk of osteopenia so it is suggested that they should be investigated in early time of diagnosis mainly in the growing years because it affects most at this time. [ABSTRACT FROM AUTHOR]

Celiac disease, an autoimmune disorder triggered by consumption of the gluten protein, is theorized to have originated alongside the domestication of wheat during the European Agricultural Revolution, ca. 8 000 BCE (Freeman 2013). Human conditions that primarily affect soft tissue, like celiac disease, do not leave tangible evidence on the skeleton and therefore it is difficult to prove their presence. However, recent analyses have employed a suite of macroscopic, molecular, and chemical techniques to establish that a Roman Imperial (100-300 CE) individual from Cosa, Italy, likely suffered from celiac disease. This paper analyzes the works of these researchers and argues that this case study exemplifies modern bioarchaeology, which frequently requires an arsenal of methods beyond visual observation. Using similar syntheses of techniques bioarchaeologists can possibly identify celiac disease in individuals predating 100 CE, recreating the origins of celiac disease as well as tackling other previously 'impossible' research questions in this field. [ABSTRACT FROM AUTHOR]

ABSTRACT We have recently identified a significant deterioration of bone microarchitecture in premenopausal women with newly diagnosed celiac disease (CD) using high-resolution peripheral quantitative computed tomography (HRpQCT). The aim of this work was to assess changes in bone microarchitecture after 1 year on a gluten-free diet (GFD) in a cohort of premenopausal women. We prospectively enrolled 31 consecutive females at diagnosis of CD; 26 of them were reassessed 1 year after GFD. They all underwent HRpQCT scans of distal radius and tibia, areal BMD by DXA, and biochemical tests (bone-specific parameters and CD serology) at both time points. Secondary, we compared 1-year results with those of a control group of healthy premenopausal women of similar age and BMI in order to assess whether the microarchitectural parameters of treated CD patients had reached the values expected for their age. Compared with baseline, the trabecular compartment in the distal radius and tibia improved significantly (trabecular density, trabecular/bone volume fraction [BV/TV] [ p < 0.0001], and trabecular thickness [ p = 0.0004]). Trabecular number remained stable in both regions. Cortical density increased only in the tibia ( p = 0.0004). Cortical thickness decreased significantly in both sites (radius: p = 0.03; tibia: p = 0.05). DXA increased in all regions (lumbar spine [LS], p = 0.01; femoral neck [FN], p = 0.009; ultradistal [UD] radius, p = 0.001). Most parameters continued to be significantly lower than those of healthy controls. This prospective HRpQCT study showed that most trabecular parameters altered at CD diagnosis improved significantly by specific treatment (GFD) and calcium and vitamin D supplementation. However, there were still significant differences with a control group of women of similar age and BMI. In the prospective follow-up of this group of patients we expect to be able to assess whether bone microarchitecture attains levels expected for their age. © 2016 American Society for Bone and Mineral Research. [ABSTRACT FROM AUTHOR]

Presents a response by Julio C. Bai and Eduardo Mauriño to a letter to the editor about their article on the characterization of gastric mucosal lesions for patients with celiac disease.

Case finding for celiac disease (CD) is becoming increasingly common practice and is conducted in a wide range of clinical situations ranging from the presence of gastrointestinal symptoms to failure to thrive in children, prolonged fatigue, unexpected weight loss and anemia. Case finding is also performed in associated conditions, such as autoimmune thyroid disease, dermatitis herpetiformis and type 1 diabetes, as well as in patients with irritable bowel syndrome, unexplained neuropsychiatric disorders and first-degree relatives of patients with diagnosed CD. This aggressive active case finding has dramatically changed the clinical characteristics of newly diagnosed patients. For instance, higher numbers of patients who present with extraintestinal symptoms are now being diagnosed with CD. Current recommendations state that due to a high risk for complications if the disease remains undiagnosed, patients with extraintestinal symptoms due to CD require appropriate diagnosis and treatment. Despite criticism regarding the cost-effectiveness of case finding in CD, such an aggressive approach has been considered cost-effective for high-risk patients. The diagnosis of CD among patients with extraintestinal symptoms requires a high degree of awareness of the clinical conditions that carry a high risk for underlying CD. Also, understanding the correct use of specific serology and duodenal histology is key for an appropriate diagnostic approach. Both procedures combined are able to confirm diagnosis in the vast majority of cases. However, in certain circumstances, serology and even duodenal histology cannot confirm or rule out CD. A common cause of negative IgA serology is IgA deficiency. For such eventuality, IgG-based serological tests can help confirm the diagnosis. Importantly, some histologically diagnosed cases still remain seronegative despite exclusion of IgA deficiency. On the other hand, duodenal histology may be normal despite the presence of CD-specific antibodies and active CD. This has been clearly demonstrated in some cases of untreated dermatitis herpetiformis, but may also be due to the patchy condition of CD or lesions that are not adequately recognized by nonexpert endoscopists and/or pathologists. The effectiveness of agluten-free diet depends on the clinical end point addressed. A good example is the outcome of bone loss. While risk for fracture normalizes after the first year of dietary treatment, bone parameters measured by densitometry may not be normalized in the long-term follow-up. Moreover, it is still unclear how far an early gluten-free diet will positively affect associated autoimmune diseases like type 1 diabetes and autoimmune thyroiditis. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

A multidisciplinary panel of 18 physicians and 3 nonphysicians from eight countries (Sweden, UK, Argentina, Australia, Italy, Finland, Norway and the USA) reviewed the literature on diagnosis and management of adult coeliac disease (CD). This paper presents the recommendations of the British Society of Gastroenterology. Areas of controversies were explored through phone meetings and web surveys. Nine working groups examined the following areas of CD diagnosis and management: classification of CD; genetics and immunology; diagnostics; serology and endoscopy; follow-up; gluten-free diet; refractory CD and malignancies; quality of life; novel treatments; patient support; and screening for CD. [ABSTRACT FROM AUTHOR]

OBJECTIVES:Elafin, an endogenous serine protease inhibitor, modulates colonic inflammation. We investigated the role of elafin in celiac disease (CD) using human small intestinal tissues and in vitro assays of gliadin deamidation. We also investigated the potential beneficial effects of elafin in a mouse model of gluten sensitivity.METHODS:Epithelial elafin expression in the small intestine of patients with active CD, treated CD, and controls without CD was determined by immunofluorescence. Interaction of elafin with human tissue transglutaminase-2 (TG-2) was investigated in vitro. The 33-mer peptide, a highly immunogenic gliadin peptide, was incubated with TG-2 and elafin at different concentrations. The degree of deamidation of the 33-mer peptide was analyzed by liquid chromatography-mass spectrometry. Elafin was delivered to the intestine of gluten-sensitive mice using a recombinant Lactococcus lactis vector. Small intestinal barrier function, inflammation, proteolytic activity, and zonula occludens-1 (ZO-1) expression were assessed.RESULTS:Elafin expression in the small intestinal epithelium was lower in patients with active CD compared with control patients. In vitro, elafin significantly slowed the kinetics of the deamidation of the 33-mer peptide to its more immunogenic form. Treatment of gluten-sensitive mice with elafin delivered by the L. lactis vector normalized inflammation, improved permeability, and maintained ZO-1 expression.CONCLUSIONS:The decreased elafin expression in the small intestine of patients with active CD, the reduction of 33-mer peptide deamidation by elafin, coupled to the barrier enhancing and anti-inflammatory effects observed in gluten-sensitive mice, suggest that this molecule may have pathophysiological and therapeutic importance in gluten-related disorders. [ABSTRACT FROM AUTHOR]

Background and Aim Once thought to be uncommon in Asia, coeliac disease ( CD) is now being increasingly recognized in Asia- Pacific region. In many Asian nations, CD is still considered to be either nonexistent or very rare. In recognition of such heterogeneity of knowledge and awareness, the World Gastroenterology Organization and the Asian Pacific Association of Gastroenterology commissioned a working party to address the key issues in emergence of CD in Asia. Methods A working group consisting of members from Asia- Pacific region, Europe, North America, and South America reviewed relevant existing literature with focus on those issues specific to Asia- Pacific region both in terms of what exists and what needs to be done. Results The working group identified the gaps in epidemiology, diagnosis, and management of CD in Asian- Pacific region and recommended the following: to establish prevalence of CD across region, increase in awareness about CD among physicians and patients, and recognition of atypical manifestations of CD. The challenges such as variability in performance of serological tests, lack of population-specific cut-offs values for a positive test, need for expert dietitians for proper counseling and supervision of patients, need for gluten-free infrastructure in food supply and creation of patient advocacy organizations were also emphasized. Conclusions Although absolute number of patients with CD at present is not very large, this number is expected to increase over the next few years or decades. It is thus appropriate that medical community across the Asia- Pacific region define extent of problem and get prepared to handle impending epidemic of CD. [ABSTRACT FROM AUTHOR]

: ObjectiveThe aim of this study was to gain insight into the pathogenesis of bone mass loss and weakening affecting patients with celiac disease, according to the new concepts of bone structure/strength and muscle/bone interrelationships.: MethodsWe studied serum variables and tomographic indicators of bone structure and strength and regional muscle masses in a series of patients at diagnosis and after 1 yr on a gluten-free diet and in gender- and age-matched controls.: ResultsAt diagnosis, serum levels of calcium and vitamin D were low, and indicators of parathyroid hormone activity and bone formation and resorption were increased. All these parameters were normalized by treatment. Peripheral quantitative CT scans of the distal radius revealed that cortical bone was generally more affected than trabecular bone. The cross-sectional area (CSA) and the volumetric mineral content and density of cortical bone (indicators of cortical tissue mass and mechanical quality), and moments of inertia (CSMI, indicator of the bone architectural design) were in the lower end of normal range in men, and below that in 50% of women. In men, the CSMI/CSA ratio (indicator of the architectural efficiency of distribution of the available cortical tissue) was lower than expected and remained unchanged after treatment. In women, the baseline ratio was normal, but both the ratio and the CSMI were low at diagnosis and normalized after treatment. Both baseline values and the treatment-induced changes of cortical and trabecular bone in the radius and the axis (L3) correlated inversely with serum parathyroid hormone levels. Baseline values or changes in the mineral content of the vertebral bone correlated with the CSA of psoas and spine-extensor muscles. Multiple regression analyses showed that metabolic and mechanical parameters were independent determinants of different aspects of the vertebral bone weakening.: ConclusionsOur results show that bone weakening in celiac disease might result from both 1) a metabolic disturbances of bone remodeling affecting trabecular and cortical bone masses and the mechanical quality of the bone material, and 2) a reduction of muscle strength impairing the modeling-dependent optimization of bone architectural design and mass of cortical bone. Dietary treatment seems to correct almost exclusively the metabolically induced disturbances, which were predominant in women. [Copyright &y& Elsevier]

OBJECTIVE:Serological screening for celiac disease (CD) can detect a large number of otherwise undiagnosed patients based on the sequential evaluation of serological tests and intestinal biopsy. The aim of this study was to compare the screening value for CD of two different protocols for the same community-based population.METHODS:We screened 1000 consecutive subjects (497 women, age range 16–71 yr) attending a centralized laboratory for obligatory prenuptial blood tests. Serum samples obtained from all subjects were processed using two different protocols: 1) a three-level classic screening consisting of the parallel use of IgG and IgA antigliadin antibodies as first level, followed by endomysial antibodies and total serum IgA for positive patients, and finally, intestinal biopsy of positive patients; and 2) a study screening protocol consisting of the parallel use of a commercial guinea pig antitissue transglutaminase antibody and total serum IgA as first line, endomysial antibodies (type IgA and/or IgG) for positive patients, and finally, intestinal biopsy.RESULTS:The classic screening protocol identified five subjects who were eligible for intestinal biopsy, which confirmed the presence of CD in all (prevalence 5.0 × 1000, 95% CI = 1.6–11.6). Using the study algorithm, we detected seven new patients including the five patients detected by the first protocol (prevalence 7.0 × 1000, 95% CI = 2.8–14.4). The two additional patients diagnosed using the proposed algorithm had positive IgG antigliadin antibodies and normal total serum IgA and were not detected by the classic protocol. Both patients were endomysial antibodies positive. The comparative analysis showed that the classic approach was more expensive (U.S. $4687 per new patient detected) compared with the proposed study algorithm (U.S. $3006).CONCLUSIONS:Our data showed that a new screening protocol using antitissue transglutaminase as first line followed by endomysial antibodies is a cost-effective screening and yielded more realistic figures of prevalence for CD in a community setting than the classic three-level sequential evaluation using antigliadin antibodies. [Copyright &y& Elsevier]

OBJECTIVE:Refractory sprue is a rare and severe malabsorptive disorder that mimics celiac disease but is refractory to a gluten-free diet and is without initial evidence of overt lymphoma. Treatment is largely empiric and often ineffective, with steroids and immunosuppression being the mainstream therapeutic options. The aim of this study was to evaluate prospectively the effect of azathioprine on a group of patients diagnosed with refractory sprue.METHODS:We studied seven consecutive patients (five women and two men) with a well-defined diagnosis of refractory sprue and a lack of response to oral or parenteral steroids. At diagnosis, five patients had endoscopic evidence of ulcerative jejunitis, and five underwent exploratory laparotomy for exclusion of malignancies. The characteristic monoclonal TCRγ gene rearrangement was shown in five of six patients studied. Patients were treated for a mean of 11 months (range 8–12 months), and clinical, biochemical, molecular, and histological parameters were reassessed at the end of the trial. The study was a prospective, open-label, non-placebo-controlled study using azathioprine (2 mg/kg/day) plus oral prednisone (1 mg/kg/day). A gluten-free diet (n = 7) as well as enteral (n = 6) and parenteral nutrition (n = 5) were administered during the trial.RESULTS:After treatment, five patients had a complete clinical remission, and biochemical and nutritional parameters were significantly improved. Steroids were tapered after the onset of azathioprine, and no patient was on steroids at the end of the trial. Intestinal histology improved significantly in all cases (normal histology in three cases and minor infiltration in the lamina propria in two). Two patients did not respond to treatment at any time and died in months 10 and 9, of an irreversible ventricular fibrillation and sepsis, respectively. No overt lymphoma was demonstrated during the follow-up.CONCLUSIONS:The present study confirms earlier anecdotal reports on the efficacy of azathioprine in refractory sprue, with clear clinical and histological improvement shown in most patients. However, monoclonality persisted after treatment. We consider that a larger number of patients should be evaluated before a definitive recommendation is adopted for use of this drug in refractory sprue. [Copyright &y& Elsevier]

OBJECTIVE: Tissue transglutaminase was identified as the autoantigen eliciting endomysial antibody, A homemade enzyme-linked immunosorbent assay (ELISA)-based test was recently developed to determine quantitative titers of IgA antitissue transglutaminase antibody. Our objective in this study was to assess the suitability of a newly developed commercial kit for quantitative determination of antibody in patients with untreated celiac disease. MATERIALS: We tested serum samples from 79 untreated celiac patients, 42 healthy blood donors, and 18 patients with nonceliac intestinal disorders evaluated in two different centers. Samples were tested for antitissue transglutaminase, and antiendomysial and antigliadin antibodies in the center where diagnosis was performed. To assess interlaboratory variability of methods, 24 samples randomly selected were blindly tested in both centers. Antitissue transglutaminase antibodies were determined using a commercial kit (INOVA Diagnostics, Inc., San Diego, CA). RESULTS: Untreated celiac patients had significantly higher titers of antitissue transglutaminase than healthy and disease controls (p < 0,00001). According to the cut-off provided by the manufacturers (20 AU/mL), overall sensitivity was 92% (85% for one center and 100% for the other) and specificity was 98% (100% and 95%, respectively). Anti-endomysial antibody was 86% sensitive and 100% specific. Discordance between antitissue transglutaminase and anti-endomysial antibodies was detected in 13% of patients. Although two antitissue transglutaminase-negative cases had a positive antiendomysial antibody, the inverse situation was found in eight cases, A blind determination of antitissue transglutaminase on the same samples evidenced a good agreement (κ statistic: 0.66) between both centers when assessment was qualitative (based on the decision of positive or negative). Although correlation of titers for both determinations was highly significant (r: 0.902, p < 0.00001), a very wide interlaboratory variability (median: 50%) was detected when absolute values were considered. CONCLUSIONS: The quantitative determination of antitissue transglutaminase using a commercial kit was highly sensitive and specific for detection of celiac disease. We observed an incomplete overlapping with antiendomysial antibody. The very high variability of values between laboratories still remains to be solved so as to propose the commercial ELIS A assay for the screening of celiac disease. [ABSTRACT FROM AUTHOR]

OBJECTIVES: First-degree relatives of patients with celiac disease are at high risk for developing the disease themselves. Detection of serum antibodies and intestinal permeability tests have been useful to identify candidates for intestinal biopsies. Recently it was demonstrated that abnormal sucrose permeability is a very sensitive marker of active disease. Our objectives in this prospective study were (1) to assess the screening value of permeability tests, and (2) to compare the usefulness of these markers with that of the celiac disease-related serology in screening for celiac disease in a cohort of first-degree relatives of well-known patients. METHODS: We performed sugar tests in 66 first-degree relatives of probands. Subjects ingested 450 ml of a solution containing sucrose (100 g), lactulose (5 g), and mannitol (2 g). Subsequently, a complete overnight urine collection was obtained. Measurement of sugars was performed by high-performance liquid chromatography. All relatives were evaluated for antigliadin (type IgA and IgG) and endomysial antibodies and subjects positive for any test underwent intestinal biopsy. RESULTS: Twelve relatives were diagnosed as having small intestinal mucosal atrophy. Increased sucrose permeability was detected in 9 (75%) of these patients. Four false-positive determinations were found but all had gastric erosions, which is known to increase sucrose permeability independently of duodenal damage. Increased lactulose/mannitol ratios were observed in all new celiac patients. An additional nine relatives had positive results; however, four of them did not accept intestinal biopsy and the remaining five did not seem to have histological evidence of disease. Endomysial antibodies were detected in 11 of 12 patients and no false-positive cases were observed. Antigliadin antibodies were 75% sensitive and 88% specific. CONCLUSIONS: Our study demonstrated that screening using the endomysial antibody test is highly sensitive and specific for detecting celiac disease; however, almost 10% can be missed. The addition of lactulose/mannitol permeability permeability testing to the screening protocol allowed us to detect all relatives who actually presented with evidence of gluten sensitivity. Sucrose permeability exhibited a lower sensitivity; however, it did detect other endoscopically visible lesions. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Several studies have demonstrated that chronic exposure to gluten may damage the structure and function of the gastric mucosa in gluten-sensitive patients. However, until now, these abnormalities have been incompletely studied. Our purpose in the present study was to characterize, in a prospective controlled study, the endoscopic and histological appearance of the gastric mucosa in a large cohort of patients with celiac disease with and without Helicobacter pylori (H. pylori) infection. METHODS: We evaluated biopsy specimens taken from the gastric body and antrum of 218 individuals who underwent upper endoscopy for small bowel biopsy. One hundred-four patients had celiac disease (80 of them at the time of diagnosis-untreated). In 114 subjects celiac disease was excluded. RESULTS: Endoscopic findings did not show a difference between the groups. The prevalence of cases with normal gastric mucosa, chronic superficial gastritis, and atrophic gastritis was similar in patients and controls. Similarly, presence of metaplasia, inflammatory activity, and lymphoid follicles and aggregates did not show differences between the groups. Histological or serological evidence of H. pylori infection was detected in 86% of patients (82% of untreated celiacs and 95% of those on those taking treatment). The infection was highly prevalent in patients (89%) and controls (97%) diagnosed with chronic gastritis. Untreated patients had a significant greater IEL count in the antrum and corpus than controls (p < 0.0001 and p < 0.001, respectively). A global analysis of the data on intraepithelial lymphocyte (IEL) counts in the different populations suggest that the inflammatory state may represent the cumulative effect of H. pylori infection and gluten sensitivity. Only three patients had IEL infiltration compatible with diagnosis of lymphocytic gastritis (count >25%) and three other patients had borderline counts. CONCLUSIO... [ABSTRACT FROM AUTHOR]

Objective: Whereas celiac disease and primary biliary cirrhosis have been reported to coexist in the same patient, the frequency of this relationship has not been clarified. Nowadays, the concept of celiac disease has been extended from that of a severe enteropathy to a broader concept of gluten-driven intestinal immunological response. In this study we assessed features of gluten sensitivity in a cohort of patients with primary biliary cirrhosis. Methods: Ten patients with primary biliary cirrhosis were evaluated a mean of 2 yr after diagnosis. The following features of gluten sensitivity were assessed: serum antigliadin and endomysial antibodies, small bowel histology (degree of atrophy and quantitative histological parameters), the presence of the typical celiac HLA genotype (DQ2), and intraepithelial lymphocyte response in the rectal mucosa after local gluten instillation (rectal gluten challenge). Results: Overall, three patients presented evidence of gluten sensitivity. All three had abnormal titers of antigliadin antibody type IgA and one was positive for endomysial antibody. Two patients had partial villous atrophy. The rectal gluten challenge showed a celiac-like response, evidenced by an increase in intraepithelial lymphocyte in-filtration after gluten exposure, in the three patients. The characteristic celiac HLA genotypes (DQA1 0501 and DQB1 0201) were identified in three patients. One of them also exhibited other features of gluten sensitivity. However, despite evidence of gluten intolerance, patients had minimal or no symptoms characteristic of celiac disease. Conclusion: We detected features of gluten sensitivity in a high proportion of patients with primary biliary cirrhosis. Further studies should be performed to elucidate the clinical significance of this association. [ABSTRACT FROM AUTHOR]

Objective: Decreased bone mineral density is a common finding in untreated celiac disease patients. However, the precise pathophysiology of osteopenia remains incompletely understood. Pathological features of gluten sensitivity are associated with local release of proinflammatory and antiinflammatory cytokines. We investigated the serum levels of IL-1β IL-6, and IL-1 receptor antagonist in celiac patients and correlated them with bone density measurements. Methods: We assessed serum samples of 16 female patients at the time of diagnosis (on an unrestricted diet) and after a mean time of 37 months on a gluten-free diet. At the same time, bone mineral density in the lumbar spine and total skeleton was determined by DEXA. Results: Untreated patients had high serum levels of IL-1β and IL-6 and normal IL-I-RA. Treatment produced a decrease in median IL-1β levels (p = NS) and a significant diminution of IL-6 (p < 0.05). On the contrary, IL-I-RA increased significantly after treatment (p < 0.05). Baseline lumbar spine Z-score and IL-6 levels exhibited a significant inverse correlation (r = -0.61; p < 0.01). Patients with more severe baseline osteopenia (< -2 Z-scores) had a significantly lower IL-1-RA than those with less bone compromise (>-2 Z-scores). Conclusions: Our data demonstrate that the inflammatory process observed in active celiac disease is associated with high serum levels of IL-1β and IL-6 and normal levels of IL-1-RA. Treatment significantly reduces both proinflammatory cytokines and significantly increases the antiinflammatory one. We also suggest that these cytokines might have a role in the osteopenia associated with celiac disease. [ABSTRACT FROM AUTHOR]

Background/Aims: Rectal gluten challenge is a simple, sensitive, and specific test of mucosal gluten sensitivity. Our aims in this study were to evaluate gluten sensitivity in a group of relatives of celiac patients and to compare these findings with those obtained on small bowel histology, celiac disease-related serology, and HLA typing. Methods: A 4-h rectal gluten challenge was performed with 6 g of crude gluten in saline solution in 29 first-degree relatives, 20 well-diagnosed celiac patients, and 10 subjects in whom celiac disease had been excluded. The number of intraepithelial lymphocytes in pre- and postchallenge frozen rectal biopsies (pan T-cell immunocytochemistry) was quantified by computerized image analysis. Results: The intraepithelial lymphocyte response after gluten instillation was significantly higher in celiac disease patients (median, 126% increase above the baseline count; 95% confidence interval: 61-213%) compared with control subjects (median, -5%; 95% confidence interval: -29-5%). Using a cut-off of 20% change in intraepithelial lymphocyte count, 14 relatives (48%) showed a celiac-like response. Two of these subjects had partial villous atrophy and increased lymphocyte counts in the small bowel mucosa. One of them also exhibited a positive celiac disease-related serology and the typical celiac human lymphocyte antibody (HLA) DQ2. The remaining 12, and all those relatives with a negative challenge, had normal small bowel mucosa and were negative for antigliadin and endomysial antibodies. The characteristic celiac HLA (DQA1 0501 DQB1 0201 heterodimer) was identified in five relatives with positive challenge (including the patient with more severe mucosal atrophy) but was also present in eight relatives with no evidence of gluten sensitivity in the rectal mucosa. Conclusions: Our study characterizes a subgroup of relatives of celiac patients who show mucosal evidence of sensitization after local instillation of gluten in the rectum but who... [ABSTRACT FROM AUTHOR]

Objectives: This prospective study was designed to assess the nutritional changes associated with the long-term treatment of celiac disease. In addition, we analyzed whether these changes were related to the degree of compliance with a gluten-free diet. Methods: We studied nutritional parameters and body composition in 25 newly diagnosed celiac patients after a mean period of 37 months (range 25-49 months) on a gluten-free diet. Body composition parameters (fat, lean tissue, and bone masses) were measured by dual energy x-ray absorptiometry. Anthropometry was measured according to conventional formulas. Results: At diagnosis, fat (-49%), lean tissue (-12%), and bone (-24%) compartments were reduced, compared with that of sex- and age-matched controls. After treatment, we noted a significant increase in body weight (p < 0.0001), fat mass (p < 0.0005), bone mass (p < 0.002), and body mass index (p < 0.005). In contrast, we did not observe a significant increase in lean-tissue mass or muscle mass. Patients who adhered strictly to a gluten-free diet experienced a greater, though nonsignificant improvement in fat mass, body weight, and body mass index than patients whose compliance had been partial. Mean caloric intake at the end of the study was significantly lower among those patients who had adhered strictly to a gluten-free diet, compared with those who had complied only partially with the diet (p < 0.05). Conclusions: This study shows that the institution of a gluten-free diet in celiac disease patients results in a significant improvement in nutritional parameters, as measured by anthropometry and/or body composition. This effect was more pronounced in patients who followed strict gluten restriction and was related mainly to changes in fat and bone compartments. [ABSTRACT FROM AUTHOR]

Background/Aims: Osteopenia is a common complication of celiac disease. The aims of this study were to evaluate whether treatment produces hone remineralization and whether calcium and vitamin D supplementation are necessary to reduce osteopeinia. Methods: Bone mineral density and biochemical parameters of bone and mineral metabolism were measured in 14 newly diagnosed adult celiac disease patients. All patients were treated with a gluten-free diet and were randomized to receive diet only (n = 7) or diet plus calcium (1.0 g/day) and vitamin D (32.000 lU/wk) supplementation (n = 7). Bone density was measured at baseline and at 6 and 12 months of follow-up. Tests for biochemical determinations were repeated every 3 months. Results: At diagnosis. 11 patients had evidence of osteopenia (>1 SD below normality) in the spine and total skeleton. After 12 months of gluten restriction, overall hone mass had increased 5.0% (p < 0.01) in the lumbar spine and 5.0% (p < 0.002) in the total skeleton. When one only considers those 11 patients who strictly followed gluten restriction, bone density increased 8.4% in the lumbar spine and 7.7% in the total skeleton. Kemineralization occurred throughout the skeleton but was more pronounced in the axial than in the peripheral skeleton. The increase in hone mass was independent of age or menopause. Remineralization in patients treated with diet only was similar to that of patients treated with diet and supplements. Basal biochemical parameters showed a high bone turnover with secondary hyperparathyroidism. Treatment induced a decrease in hone turnover activity. However, a complete restoration of biochemical parameters was not achieved. Conclusions: Strict gluten avoidance promoted a significant increase in hone mineral density. However, values still remain markedly low after 1 yr in several patients. Although calcium and vitamin D supplementation did not provide additional benefit to that obtained by diet... [ABSTRACT FROM AUTHOR]

Background/Aim: This is a study of patients with asymptomatic celiac disease. The aims of this study were: 1) To evaluate the nutritional status of asymptomatic patients with newly diagnosed celiac disease, and 2) to compare these findings with those of untreated/symptomatic and treated patients. Material: We examined 41 patients with celiac disease divided into three groups: a) 8 asymptomatic (diagnosed in a study of first-degree relatives of probands), b) 20 untreated/symptomatic patients, and c) 13 treated patients. Nutrition of patients from groups A and B was assessed at the time of diagnosis. Methods: Nutritional status was evaluated by: 1) body composition (fat and lean mass) by dual energy x-ray absorptiometry (DEXA), and 2) anthropometric measurements. Results: Compared with sex and age matched controls (n = 153), asymptomatic patients presented a moderate but significant reduction of the fat compartment (-29%; p < 0.001), but not of the lean-tissue mass (p = NS). Untreated/symptomatic patients showed a more severe depletion of fat (-46%; p < 0.001) and lean mass (-9.0%; p < 0.05) compared with healthy controls. Although fat mass of treated patients was significantly reduced with respect to controls (-24%; p < 0.003), lean mass was not affected. The anthropometric measurements of fat showed a significant correlation with the evaluation by DEXA (multiple regression analysis r = 0.918). Conclusion: Asymptomatic patients in our study with an unequivocal diagnosis of celiac disease established by mucosal biopsy exhibited a modified body composition. [ABSTRACT FROM AUTHOR]

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 absorptiometry 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 eeliacs, 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 eeliacs. 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. [ABSTRACT FROM AUTHOR]

One hundred and thirty-two different intestinal α1-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 α1-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 < 0.05) between the α1-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 α1-antitrypsin clearance may he a reliable method to evaluate the activity of the disease and useful in following the efficacy of treatment. [ABSTRACT FROM AUTHOR]

Our aim in this study was to monitor changes of the intestinal structure by α1-antitrypsin clearance (α1-ATCL) in order to offer an alternative to the gluten challenge biopsy. In addition, we evaluated the possibility of reducing the time of gluten challenge. Twelve patients had a presumptive diagnosis of celiac disease based on clinical and histological grounds. They were studied when the jejunal histology was normal after gluten-free diet and an α1-ATCL was normal. The gluten was introduced by returning to a normal diet. The challenge lasted 4 wk. We measured α1-ATCL at the end of the 1st and 4th wk, and a new jejunal biopsy was obtained at the end of the 4th wk. By wk 1, α1-ATCL was abnormal in 11 patients but normal in one. By wk 4, α1-ATCL was abnormal in 10 patients and still normal in one. The post-challenge biopsies showed atrophy in 11 and was normal only in the patient with normal α1-ATCL at wk 1 and 4. One patient with abnormal α1-ATCL had to stop the challenge at the first week. The patient with normal clearance at wk 1 and 4 and normal biopsy at wk 4 bad abnormal results at 6 months. These data support our hypothesis that α1-ATCL can be used as evidence of gluten toxicity after gluten challenge, and that this test can be abnormal as early as 1 wk after gluten is reintroduced. [ABSTRACT FROM AUTHOR]

Many approaches have been proposed to differentiate between steatorrhea due to pancreatic insufficiency and intestinal disease. Bo-Linn and Fordtran recently suggested that fecal fat concentration (FFC) is a useful screening test for this distinction. Our aim was to validate their result in a large group of patients. Fecal fat concentrations were calculated for 613 fecal fat tests in 538 patients. Included were 88 patients with pancreatic steatorrhea (13 pancreatic carcinoma, 6 cystic fibrosis, and 69 chronic pancreatitis) and 525 with nonpancreatic steatorrhea. The mean FFC of patients with pancreatic disease (15.0 ±1.9 g%, mean ± SEM) was significantly higher than that of patients with other diseases causing malabsorption (8.9 ± 0.3g%, p < 0.001). Forty-two percent of patients with pancreatic steatorrhea had an FFC below 10g%. The overlapping of the FFC of steatorrhea due to pancreatic disease and that produced by celiac disease, gastric resection, and other conditions suggests that this approach does not differentiate between pancreatic and intestinal steatorrhea. [ABSTRACT FROM AUTHOR]

Background/Aims: Malabsorption syndromes commonly result from a pathological interference of the normal digestive process. There have been major advances in the last 4 years. The purpose of this review is to highlight in the form of a brief summary the most outstanding information available. Methods: The review was performed based on a medical literature search using MEDLINE (1993–1997), bibliographic reviews of book chapters and review articles. As a consequence of the extensive information incorporated in the period and the limited scope of this review, the review will focus in three aspects: (1) an overview on some clinical aspects of malabsorption; (2) diseases in which predominates the disturbed mucosal phase of the digestive process, and (3) providing information on diagnostic testing regarding malabsorption. Results: Major advances on celiac disease, Whipple’s disease, giardiasis, tropical sprue, malabsorption of oligo- and disaccharides, vitamin B[sub 12] and bile salts are discussed. New aspects on diagnostic procedures for malabsorption are also presented. Conclusion: Although major advances have given a great support to the investigation of malabsorption, yet the syndrome remains a major diagnostic dilemma. Based on the limited availability of most diagnostic tests, a simple and practical diagnostic algorithm is presented. [ABSTRACT FROM AUTHOR]

The prevalence of class I and class II HLA antigen was analyzed in 14 patients (12 males, two females) with Whipple's disease, diagnosed an average of 9.7 yr (range 6 months to 25 yr) before the typing. They were compared with 174 healthy control subjects of the same geographic area in Argentina. Class I antigens (locus A, B, C) were studied by lymphocytotoxic test, and class II antigens (locus DR, DQ) were detected by the double immunofluorescence technique. HLA-B27 was positive in one patient (7.7%) and in 4% of the control population. No significant association was found with the antigens tested. We observed no difference in the clinical picture or in the frequency of arthralgias, compared with those reported in the literature. Our data suggest that there is no conclusive proof of an association between HLA-B27 and Whipple's disease. [ABSTRACT FROM AUTHOR]

A case study of 72-year-old woman presented with chronic dyspepsia and iron deficiency anemia. It informs the patients undergone gastrointestinal endoscopy, which revealed esophageal candidiasis and pangastritis with appearance of gastric intestinal metaplasia. It also informs that atrophic gastritis can be a risk factor for squamous metaplasia of gastric mucosa.

The article offers information on the guidelines for serologic diagnosis of Celiac Disease, a autoimmune disorder, in adults. Topics discussed include following of European Society of Pediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) guidlines, analyzing the performance of serologic tests, and administering of Immunoglobulin A endomysial antibodies.

A letter to the editor is presented in response to the article "Double-Blind, Randomised, Placebo-Controlled Intervention Trial to Evaluate the Effects of B. longum CECT 7347 in Children With Newly Diagnosed Coeliac Disease" by M. Olivares et al.

A 55-yr-old man with ileocolic Crohn's disease developed granulomatous dermatitis in the malar region. He was treated with metronidazole 1.5 g/day for 1 month, with remission of the skin lesion after 10 days. [ABSTRACT FROM AUTHOR]