Figures
Abstract
Background
Celiac disease (CD) is an immune-mediated enteropathy triggered by the ingestion of gluten in susceptible individuals, and its prevalence varies depending on the studied population. Given that information on CD in Latin America is scarce, we aimed to investigate the prevalence of CD in this region of the world through a systematic review and meta-analysis.
Methods and Findings
This was a two-phase study. First, a cross-sectional analysis from 981 individuals of the Colombian population was made. Second, a systematic review and meta-regression analysis were performed following the Preferred Reporting Items for Systematic Meta- Analyses (PRISMA) guidelines. Our results disclosed a lack of celiac autoimmunity in the studied Colombian population (i.e., anti-tissue transglutaminase (tTG) and IgA anti-endomysium (EMA)). In the systematic review, 72 studies were considered. The estimated prevalence of CD in Latin Americans ranged between 0.46% and 0.64%. The prevalence of CD in first-degree relatives of CD probands was 5.5%. The coexistence of CD and type 1 diabetes mellitus varied from 4.6% to 8.7%, depending on the diagnosis methods (i.e., autoantibodies and/or biopsies).
Citation: Parra-Medina R, Molano-Gonzalez N, Rojas-Villarraga A, Agmon-Levin N, Arango M-T, Shoenfeld Y, et al. (2015) Prevalence of Celiac Disease in Latin America: A Systematic Review and Meta-Regression. PLoS ONE 10(5): e0124040. https://doi.org/10.1371/journal.pone.0124040
Academic Editor: Domenico Coppola, H. Lee Moffitt Cancer Center & Research Institute, UNITED STATES
Received: November 27, 2014; Accepted: March 10, 2015; Published: May 5, 2015
Copyright: © 2015 Parra-Medina et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
Data Availability: All relevant data are within the paper and its Supporting Information files.
Funding: The authors have no support or funding to report.
Competing interests: The authors have declared that no competing interests exist.
Introduction
Celiac disease (CD) is an autoimmune intestinal disorder. This disease occurs due to an immune-mediated enteropathy triggered by ingested prolamins present in wheat, barley, and rye (generically called gluten). It occurs in susceptible individuals carrying the HLA-DQ2 and HLA-DQ8 haplotype [1].
Recently the American College of Gastroenterology and the British Society of Gastroenterology provided recommendations to perform an initial screen with IgA anti-tissue transglutaminase (tTG) [2,3]. Meanwhile, the ESPGHAN (European Society of Pediatric Gastroenterology and Nutrition) proposed various criteria for diagnosis over time. Initially, the diagnosis required a sequence of three small intestinal biopsies, but recently the guidelines indicated that symptomatic children with high levels of tTG and positive anti-endomysium (EMA) as well as HLA DQ2/8 do not need the biopsy for disease diagnosis [4–6]. IgA tTG and IgA EMA autoantibodies have a sensitivity and specificity of 98–100% [7]. They have been used for the CD diagnosis since the 1990s [8]. Antigliadin (AGA) and anti-reticulin antibodies have also been previously used, but they are currently considered obsolete for diagnosis because of their low sensitivity and specificity [9]. In brief, individuals that have tested positive for celiac autoantibodies are considered as potentially diagnosed patients, regardless of the biopsy results [10].
The distribution of CD has been associated with migratory patterns and changes in feeding habits over time. In the early years, humans were not exposed to gluten contained within cereals. Approximately 10,000 years ago in a small region of the Middle East, farmers successfully cultivated wild wheat and barley grains due to favorable environmental conditions. These people then migrated to the Mediterranean area (Northern Africa and Southern Europe) and Central Europe, searching for new lands to cultivate [11].
CD is a very frequent disorder in highly populated countries where inhabitants have a white ancestry, primarily in Europe and North America. However, CD has also been reported among people with Amerindian and African origins [12,13]. CD affects 0.6 to 1.0% of the population worldwide and exhibits a female-to-male ratio of 2.8:1 [14]. Also the age of onset distribution shows a first peak between nine months to two years and a second peak during the fourth decade [14]. The frequency of CD is likely to increase in many developing countries due to an increased prevalence of a “westernized” diet, involving greater wheat production. For instance, over the past 30 years, the prevalence of CD in the United States has increased five-fold, doubling approximately every 15 years [15].
The presence of CD in the Latin American (LA) population is uncertain. Latin America is the geographical area defined by Mexico, Central America, islands of the Caribbean, and South America. It is a rapidly growing region with almost 600 million inhabitants [16]. The LA population is mixed with ancestries including Africans, Caucasians, and Amerindians [17]. In the present study, we aimed to analyze the prevalence celiac autoimmunity (i.e., tTG and EMA) in a Colombian population as a surrogate of CD [18]. We evaluated the presence of these autoantibodies in healthy individuals and in patients with other autoimmune conditions, given that CD may coexist with and share similar immunopathological mechanisms with other autoimmune diseases (ADs) [19]. In addition, we performed a systematic literature review and meta-regression analysis to determine the estimated prevalence of CD in LA.
Methods
Study population
A total of 981 individuals from two regions in Colombia (Northwest and Central) were assessed for the presence of CD autoantibodies (Table 1). There were 541 affected and 140 unaffected individuals from Northwest Colombia (Group 1), whilst Group 2 (Central Colombia) was comprised of 180 AD patients and 120 non-AD controls, taken from an original cohort of 1667, and sampled according to a stratified sampling design where the strata were different cohorts of patients with ADs.
All of the patients with ADs fulfilled the international classification criteria. These include: the American College of Rheumatology (ACR) criteria for RA and SLE, the McDonald criteria for MS and the American Diabetes Association (ADA) criteria for T1DM [20–23]. Patients with SS met the American-European Consensus Group criteria; including a positive minor salivary gland biopsy (MSGB) [24]. General and clinical characteristics of these patients have been previously described [25–46].
The information regarding patient demographics as well as cumulative clinical and laboratory data was obtained by physical examination, interviewing or chart reviews as described elsewhere [25–46]. All data were collected in an electronic and secure database. The review board and the ethics committee of Universidad del Rosario approved the study according to the ethical guidelines of the Helsinki Declaration and Resolution 008430 of 1993 of the Ministry of Health in Colombia. The study was classified as minimal risk research. All patients completed the written informed consent.
Detection of Autoantibodies
In Group 1, IgA and IgG antibodies against AGA and tTG were assessed by the Bio-Rad BioPlex 2200 system (Bio-Rad Laboratories, Hercules, California, USA) as previously described [25,27,28,36–46].
In Group 2, IgA h-tTG (native human tissue transglutaminase) antibodies were assessed using the ELISA method (INOVA Diagnostic, USA. Cat. 708730) in the DYNEX DS2 ELISA analyzer. According to the manufactured instructions, samples were classified as negative (<20 units), weakly positive (20–30 units) or positive (>30 units). Weakly positive samples were analyzed by indirect immunofluorescence (IFI) assay to evaluate the presence of IgA EMA, using two additional commercial kits (INOVA Diagnostics, USA. Cat. 508154, and AESKU.Diagnostics, Germany. Cat. 512.050).
Search strategy
The search was done using the following databases: PubMed, Cochrane, Scopus, SciELO, and Virtual Health Library, which includes BIREME, LILACS and many other LA sources. The search was related to CD in LA and included articles published up to July 2013. The PRISMA guidelines were followed during data extraction, analysis, and reporting [47].
No limits regarding language, publication type, or publication period were taken into account. The search was done with the following MeSH terms (Medical Subject Headings) and key words in PubMed, Scopus and Chocrane: celiac disease, transglutaminase antibody, antigliadin antibody, gliadin antibody, deamidated gliadin antibody, endomysial antibody, anti endomysium antibody, HLA-DQ2 and HLA-DQ8. Each one was cross-referenced with the following MeSH terms: Latin America, Hispanic Americans, Hispanics, South America, Argentina, Belize, Bolivia, Brazil, Chile, Colombia, Costa Rica, Cuba, Dominican Republic, Ecuador, El Salvador, Guatemala, Haiti, Honduras, French Guiana, Mexico, Nicaragua, Panama, Paraguay, Peru, Puerto Rico, Surinam, Uruguay, and Venezuela.
The same methodology and the term celiac disease (without other cross terms) were used to explore sources of information in Spanish, Portuguese, and English through the SciELO and Virtual Health Library databases. Each MeSH term and keyword was translated into DeCS (Health Sciences Descriptors).
Study selection, data extraction, and quality assessment
Inclusion criteria for the systematic review were the following: (a) studies with screening tests for autoantibodies of CD such as AGA, EMA, tTG, or deamidated gliadin peptide (DGP) in healthy individuals or in patients without CD diagnosis; (b) studies with screening tests for autoantibodies of CD and a positive biopsy in healthy individuals or in patients without CD diagnosis; (c) studies that include the LA population. Studies were excluded if they were reviews or case reports or if they discussed topics not related to CD. Unpublished data were also excluded. A primary reviewer who screened all of the titles and abstracts from the publications performed an eligibility assessment. Retrieved articles were rejected if the eligibility criteria were not met. Also, a secondary reviewer was consulted when eligibility criteria were unclear. References from the articles that seemed to be relevant for our review were hand-searched.
The extracted data from each article were: author name, country where the study took place, year of publication, study design, number of patients, screening protocol and evaluated outcomes. Several studies used different screening protocols to evaluate the presence of autoantibodies. Therefore, we considered the results to be positives based on the cutoff of each protocol. All articles were assessed according to the Oxford Center for Evidence based Medicine: 2011 Levels of Evidence [48].
Meta-regression
A population variable was created which addressed the nature of the cases in each article: Population A: Healthy individuals; Population B: First-degree relatives of CD patients; Population C: T1DM (type 1 diabetes mellitus) patients; Population D: Patients with other ADs; Population E: Patients with other conditions. Studies published previously with the same population were excluded. The data obtained in the present study were involved in the meta-analyses.
During the search, several studies used different screening protocols to estimate the presence of CD. Taking this into account, we performed a meta-regression of the two forms of diagnostic protocols separately; the first set were studies that evaluated the presence of IgA tTG and EMA (sensitivity and specificity of 98–100%), and the second set were the studies that evaluated the positive autoantibodies and positive biopsy, following the statistical model-building approach described below.
The meta-analysis was performed for each diagnostic protocol separately, by fitting a meta-regression model with random effects and testing different combinations of predictor variables available in all articles: a) year of study, b) country and c) population (nature of cases in each study, as described previously) to explain the log-prevalence of the disease. The final predictors included in the two meta-regression models (one for each diagnostic protocol) were selected according to the likelihood ratio test and AIC criteria as described in [49]. Over the selected model, routine diagnostic tests of meta-analysis were performed (test for funnel plot asymmetry, I2, H2, among others). The analysis was performed with the R2.15.2 package METAFOR [49].
Results
Colombian population
In Group 1, IgA tTG was positive only in one relative of a T1DM patient. In Group 2, seven individuals were positive or weakly positive for h-tTG using the reference values from the commercial Kit. In all of these cases, the evaluation of IgA EMA was negative (confirmed by two different kits). These results are shown in Table 1.
Systematic Literature Review
We identified 841 articles in the PubMed database search. Additional records identified through other sources included 823 articles (Scopus, SciELO, Virtual Health Library and Cochrane). Eleven additional records were identified through hand searching. The database searches provided a total of 1,675 publications. Of these, 958 were identified as duplicates. A total of 717 full text articles were assessed for eligibility. Finally, 73 articles that contained interpretable data and fulfilled the eligibility criteria were included [50–122]. In one paper, the data extraction was made from its abstract [50]. Eight articles were from Argentina [51–58], 41 from Brazil [50,59–98], 3 from Chile [99–101], 11 from Cuba [102–112], 5 from Mexico [113–117], 2 from Peru [118,119], 2 from Venezuela [120,121] and one paper was from the Hispanic residents in the United States [122]. The flowchart for systematic literature review and articles included in the analysis is shown in Fig 1. Detailed information is shown in S1 Table.
VHL: virtual health library. CD: Celiac disease. LA: Latin America.
Meta-analysis
Meta-regression for tTG and EMA protocol.
A total of 27 studies comprising 28 articles were included in the model [50,52,54,55,66,69,71–74,78,80,82,83,85–87,89,90,94,97,100,114,116–118,121,122]. The work of Remes-troche, et al. was analyzed as one study because they evaluate the presence of CD in the same population, but in two different time periods [114,117]. In five studies obtained from the systematic review, the population was divided into subpopulations [66,69,78,89,90]. In addition, our two subpopulations from the central area of Colombia were included in the analysis (i.e., healthy individuals and patients with ADs). In summary, 34 populations were analyzed (S1 Fig).
The most parsimonious model (according to the AIC criteria and likelihood ratio tests) was a meta-regression with random effects, which involves the population and country variables as the only moderators. The study from Venezuela was excluded due to low sample size and the high prevalence, and was therefore considered as an outlier [121]. Table 2 shows the estimated parameters of this model.
The parameters associated with countries and populations refer to the log-prevalence between various country and population combinations when compared against Brazil, regarding population A (healthy individuals). The intercept parameter was the log-prevalence for Brazilian individuals regarding controls. Note that this Brazilian population was chosen as a reference level due to its large number of studies. Taking these parameters into account, only Hispanics from the USA had a log-prevalence less than that of the Brazilians, despite the different population groups that were analyzed. However, populations B, C and E had a higher prevalence of the disease than population A. Furthermore, the observed parameters of population D were not significant. This suggests that the prevalence of the disease is higher in individuals with first-degree relatives diagnosed with CD and T1DM (Fig 2 and S1 Fig).
Population: A: Healthy individuals; B: First-degree relatives of CD patients; C: T1DM patients; D: Patients with other ADs; E: Patients with other conditions.
We did not find any evidence of publication bias (test for funnel plot asymmetry: z = -1.8174, p = 0.0692). Additionally, two subpopulations in two different studies presented lack of fit to this model [64, 66] (S2 Table and S3 Fig). This discrepancy could be explained by the characteristic of the studied population (i.e., pediatric inpatients and outpatients).
Meta-regression for autoantibodies positive and biopsy positive protocol.
A total of 49 studies were included in this model [50,52–55,58–73,75,77,79–81,83,85,88,90,94,96,99–102,104,107,109–113,116–121]. Within three studies obtained from the systematic review, the population was divided into subpopulations. As a result, 51 populations were analyzed.
Again, the most parsimonious model (according to the AIC criteria and likelihood ratio tests) was a meta-regression with random effects. As was the case with the previous diagnostic protocol, the only moderators in this model were the population and country variables. Therefore, interpretation of meta-regression parameters was the same as before. Table 3 shows the estimated parameters of the selected model.
Populations from Peru and Argentina have a higher log-prevalence than Brazilian individuals, whilst populations B, C and E had a higher prevalence of the disease than population A. Furthermore, the observed parameters of population D were not significant. As previously found in the tTG and EMA protocol, the prevalence of the disease was higher in individuals with first-degree relatives diagnosed with CD and T1DM (Fig 3 and S2 Fig).
Population: A: Healthy individuals; B: First-degree relatives of CD patients; C: T1DM patients; D: Patients with other ADs; E: Patients with other conditions.
Note that we found evidence of publication bias (test for funnel plot asymmetry: z = -3.4489, p = 0.0006). Additionally, two subpopulations in two different studies exhibited a lack of fit to the model [58,66] (S3 Table and S4 Fig). This discrepancy could once again be explained by the characteristic of the studied population (pediatric inpatients and patients with clinical suspicion), as suggested in the meta-regression analysis for the tTG and EMA protocol.
Discussion
Although CD seems to be a rare condition in Colombians; the general prevalence of the disease in Latin Americans seemingly corresponds to a similar scenario observed in Europeans (0.46% to 0.64%) [123,124]. Our study is the first to summarize and analyze all published studies about CD in the LA population. The presence of the disease was evaluated in a population with different characteristics, and we found 801 patients positive for IgA tTG and IgA EMA and 454 patients positive for autoantibodies and biopsy (S1 Table).
The LA population presents with a notable racial, genetic, and cultural diversity [17]. Therefore in LA, some countries such as Argentina, Brazil, Chile, Cuba, Uruguay and Venezuela, have > 50% of Caucasian component, and certain regions within these nations are more Caucasian than others [111,125]. The highest prevalence of CD has been reported in those countries with a high Caucasian admixture (S1 Table). However, in nations such as Chile, Uruguay and Venezuela, the prevalence of CD is uncertain. Brazil is the only country where the presence of CD has been widely studied. This country is an important migratory destination for European Caucasians. These immigrants are located primarily in the Southern region of Brazil, and most cases of CD have been reported in this region. In contrast, the North and the Northeast region of Brazil have large Amerindian and African ancestral influences respectively. In those regions the presence of the disease is low [126]. In addition, the presence of the disease in native Indian and African-derived communities from the Northeast Brazilian region is null [84,95] (S1 Table).
Our meta-regressions also show that Hispanics in the United States (i.e., a person of Mexican, Puerto Rican, Cuban, South or Central American (except for Brazil), or other Spanish culture or origin, regardless of race) have a different behavior than individuals of other countries. The prevalence of CD in Hispanic was estimated in 2.519 individuals (1.686 Mexican Americans and 833 as other Hispanic groups). Only one patient was positively detected by autoantibodies (IgA tTG and IgA EMA), whilst the other two patients were detected by interview data. However, none of these patients were Mexican-American [122]. Nevertheless, these results are very different from those observed in the Mexican population (Tables 1 and 2, S1 Table, Figs 2 and 3, and S1 and S2 Figs). Thus, this discrepancy in the prevalence on native Mexicans vs. Mexican Americans highlights the major effect of environmental factors over genetic factors in the risk of developing CD.
Polyautoimmunity (i.e., the presence of two or more ADs in a single patient) [19] was observed in our study. The estimated prevalence of CD in the T1DM patients was 4.6 to 8.7%. This number is similar to the prevalence reported in other populations [127]. The association among CD and T1DM can be explained by the presence of common risk alleles including HLA-DQA1*0501 and DQB1*0201 [128]. However, the estimated prevalence of CD in the group of patients with ADs was 0.7% to 1%. This surprisingly low prevalence may be explained by the small number of studies available and the lack of awareness about polyautoimmunity [98]. In fact, most of the studies evaluating this association came from case reports or from studies with a small sample size (S1 Table).
Both familial CD [129] and familial autoimmunity (i.e., the presence of diverse ADs in relatives of CD probands) are frequent conditions [130,131], indicating aggregation of the autoimmune trait. The prevalence of CD in first-degree and second-degree relatives is 10% and 5% respectively [132]. In our results, the estimated prevalence of CD in first-degree relatives was about 5.6%, whereas the estimated prevalence in populations with other conditions, such as at-risk populations, was 0.24% to 0.3% (S1 Table). This result could be explained by the heterogeneity of the study population and the small sample size.
Although the two Colombian population analyzed in this study may disclose a different genetic background [133], no celiac autoimmunity was observed in neither. Colombians in general still eat cultivated food, such as potatoes, tapioca and corn [134]. The seven individuals with positive or weakly positive results from Central Colombia were interpreted as false positives, because the IgA EMA test was negative. In fact, false positive results for the IgA tTG have been also reported in other ADs [6,135].
During the search, we found that some studies have reported the presence of HLA-DQ2 and HLA-DQ8 haplotype in the LA population with high titers of CD autoantibodies and diagnosis of CD (Table 4) [12,85,88,111,136–141]. HLA DQ2.5 is common in the LA population, whilst approximately 90% of studied Amerindian individuals carry the DQ8 haplotype [14,142,143].
Study Limitations
We would like to acknowledge the limitations of our study. First, the diagnostic criteria and the screening to evaluate the presence of CD have changed over time. The autoantibodies previously evaluated are now considered obsolete. For this reason, some older studies were excluded from the statistical model. Second, in some studies, the biopsy was not performed in all antibody-positive individuals. Also, in some studies, the biopsy was not obtained from the duodenum or the interpretation was not performed with the respective histological classification. Thus, in order to obtain accurate results, data from those studies were not included in the statistical model. Third, different ELISA protocols for testing the presence of tTG were used across the studies, so the dilution of positive IgA EMA was different among our analyses. Fourth, most of the data about CD came from populations at high risk. Therefore the prevalence might be overestimated.
Data from Colombia were not considered for estimation of disease prevalence. In addition, the meta-regression has some limitations, because the country effect is a confounding factor in the analysis of populations. All the included studies did not represent the whole country’s population where they were performed.
Conclusions
In general the prevalence of CD in LA is similar to that reported in Europeans. CD in the LA population is frequent and is primarily reported in populations and regions with Caucasian ancestry. Nevertheless, in certain countries with substantial Caucasian ancestry such as Uruguay, the prevalence is unknown.
The low prevalence reported in some regions could be explained mainly by: the lack of knowledge of the disease, low gluten consumption (which does not entail an autoimmune response), changes in quantity and quality of cereal processing, microbiota or early childhood exposure to infectious agents that could impair the natural development of the immune system (i.e., hygiene hypothesis) [144].
Supporting Information
S1 Fig. Forest plot. Prevalence of the disease for each population using the model for tTG and EMA protocol.
Population: A: Healthy individuals; B: First-degree relatives of CD patients; C: T1DM patients; D: Patients with other ADs; E: Patients with other conditions.
https://doi.org/10.1371/journal.pone.0124040.s001
(TIF)
S2 Fig. Forest plot. Prevalence of the disease for each population using the model for autoantibodies positive and biopsy positive.
Population: A: Healthy individuals; B: First-degree relatives of CD patients; C: T1DM patients; D: Patients with other ADs; E: Patients with other conditions.
https://doi.org/10.1371/journal.pone.0124040.s002
(TIF)
S3 Fig. Funnel plot of the model for tTG and EMA protocol.
https://doi.org/10.1371/journal.pone.0124040.s003
(TIF)
S4 Fig. Funnel plot for autoantibodies positive and biopsy positive.
https://doi.org/10.1371/journal.pone.0124040.s004
(TIF)
S1 Table. Presence of autoantibodies positive and biopsy positive in Latin American patients.
Abbreviations: AGA: Antigliadin antibodies; CD: Celiac disease; CMV: Cytomegalovirus; DGP: deamidated gliadin peptide; EBV: Epstein barr virus; EMA: anti-endomysium antibody; GFD: Gluten free diet; HCV: Hepatitis C virus; HEV: Hepatitis E virus; JRA: juvenile rheumatoid arthritis; MS: multiple sclerosis; N/A: Not available; T1DM: Type 1 Diabetes Mellitus; T2DM: Type 2 Diabetes Mellitus; tTG: anti-tissue transglutaminase antibody; RA: Rheumatoid arthritis; SLE: Systemic Lupus Erythematosus; SS: Sjögren syndrome. €: presumptive celiac disease patients.
https://doi.org/10.1371/journal.pone.0124040.s006
(DOC)
S2 Table. Studies with lack of fit to the final model (tTG and EMA protocol).
https://doi.org/10.1371/journal.pone.0124040.s007
(DOC)
S3 Table. Studies with lack of fit to the final model (positive and biopsy positive).
https://doi.org/10.1371/journal.pone.0124040.s008
(DOC)
Acknowledgments
The authors express their gratitude to the patients who participated in the study and to Cilia Rojas and Jenny Amaya-Amaya for their contributions in the study, as well as “Fundación Colombiana de Celiacos” and its president Ximena Guerrero for her continued support and assistance in the searching of patients with possible CD in Colombians.
Author Contributions
Conceived and designed the experiments: JMA. Performed the experiments: RPM JMA NAL MTA ARV NMG YS. Analyzed the data: NMG RPM MTA ARV JMA. Contributed reagents/materials/analysis tools: JMA YS NAL ARV NMG RPM. Wrote the paper: RPM NMG ARV MTA NAL YS JMA.
References
- 1. Schuppan D, Dennis MD, Kelly CP. Celiac disease: epidemiology, pathogenesis, diagnosis, and nutritional management. Nutr Clin care. 2005;8: 54–69. pmid:16013224
- 2. Rubio-Tapia A, Hill ID, Kelly CP, Calderwood AH, Murray JA, American College of Gastroenterology. ACG clinical guidelines: diagnosis and management of celiac disease. Am J Gastroenterol. 2013;108: 656–676. pmid:23609613
- 3. Ludvigsson JF, Bai JC, Biagi F, Card TR, Ciacci C, Ciclitira PJ, et al. Diagnosis and management of adult coeliac disease: guidelines from the British Society of Gastroenterology. Gut. 2014;63: 1210–1228. pmid:24917550
- 4. Meeuwisse GW. Diagnostic criteria in coeliac disease. Acta Paediatr Scand. 1970;59: 461–463.
- 5. McNeish AS Harms HK Rey J Shmerling DH Visakorpi JK Walker-Smith J. The diagnosis of coeliac disease. Arch Dis Child. 1979;54: 783–786. pmid:507902
- 6. Husby S, Koletzko S, Korponay-Szabó IR, Mearin ML, Phillips a, Shamir R, et al. European Society for Pediatric Gastroenterology, Hepatology, and Nutrition guidelines for the diagnosis of coeliac disease. J Pediatr Gastroenterol Nutr. 2012;54: 136–160. pmid:22197856
- 7. Admou B, Essaadouni L, Krati K, Zaher K, Sbihi M, Chabaa L, et al. Atypical Celiac Disease: From Recognizing to Managing. Gastroenterol Res Pract. 2012;2012: 637187. pmid:22811701
- 8. Petaros P, Martelossi S, Tommasini a, Torre G, Caradonna M, Ventura A. Prevalence of autoimmune disorders in relatives of patients with celiac disease. Dig Dis Sci. 2002;47: 1427–1431. pmid:12141796
- 9. Rostom A, Dubé C, Cranney A, Saloojee N, Sy R, Garritty C, et al. The diagnostic accuracy of serologic tests for celiac disease: A systematic review. Gastroenterology. 2005;128: S38–S46. pmid:15825125
- 10. Ludvigsson JF, Leffler DA, Bai JC, Biagi F, Fasano A, Green PHR, et al. The Oslo definitions for coeliac disease and related terms. Gut. 2013;62: 43–52. pmid:22345659
- 11.
Greco L. Epidemiology of coeliac disease. Proceedings of the Seventh International Symposium on Coeliac Disease Tampere: Finland; 1996.
- 12. Parada A, Araya M, Pérez-Bravo F, Méndez M, Mimbacas A, Motta P, et al. Amerindian mtDNA haplogroups and celiac disease risk HLA haplotypes in mixed-blood Latin American patients. J Pediatr Gastroenterol Nutr. 2011;53: 429–434. pmid:21505366
- 13. Brar P, Lee AR, Lewis SK, Bhagat G, Green PHR. Celiac disease in African-Americans. Dig Dis Sci. 2006 May;51: 1012–5. pmid:16642428
- 14. Gujral N, Freeman HJ, Thomson ABR. Celiac disease: prevalence, diagnosis, pathogenesis and treatment. World J Gastroenterol. 2012;18: 6036–6059. pmid:23155333
- 15. Lionetti E, Catassi C. New clues in celiac disease epidemiology, pathogenesis, clinical manifestations, and treatment. Int Rev Immunol. 2011;30: 219–231. pmid:21787227
- 16. González Burchard E, Borrell LN, Choudhry S, Naqvi M, Tsai H-J, Rodriguez-Santana JR, et al. Latino populations: a unique opportunity for the study of race, genetics, and social environment in epidemiological research. Am J Public Health. 2005;95: 2161–2168. pmid:16257940
- 17. Risch N, Choudhry S, Via M, Basu A, Sebro R, Eng C, et al. Ancestry-related assortative mating in Latino populations. Genome Biol. 2009;10: R132. pmid:19930545
- 18. Dahlbom I, Korponay-Szabó IR, Kovács JB, Szalai Z, Mäki M, Hansson T. Prediction of clinical and mucosal severity of coeliac disease and dermatitis herpetiformis by quantification of IgA/IgG serum antibodies to tissue transglutaminase. J Pediatr Gastroenterol Nutr. 2010;50: 140–146. pmid:19841593
- 19. Anaya JM. The diagnosis and clinical significance of polyautoimmunity. Autoimmun Rev. 2014;13:423–426. pmid:24424171
- 20. Arnett FC, Edworthy SM, Bloch DA, McShane DJ, Fries JF, Cooper NS, et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum. 1988;31: 315–324. pmid:3358796
- 21. Tan EM, Cohen AS, Fries JF, Masi AT, McShane DJ, Rothfield NF, et al. The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum. 1982;25: 1271–1277. pmid:7138600
- 22. McDonald WI, Compston A, Edan G, Goodkin D, Hartung HP, Lublin FD, et al. Recommended diagnostic criteria for multiple sclerosis: guidelines from the International Panel on the diagnosis of multiple sclerosis. Ann Neurol. 2001;50: 121–127. pmid:11456302
- 23. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care. 1997;20: 1183–1197. pmid:9203460
- 24. Vitali C, Bombardieri S, Jonsson R, Moutsopoulos HM, Alexander EL, Carsons SE, et al. Classification criteria for Sjögren’s syndrome: a revised version of the European criteria proposed by the American-European Consensus Group. Ann Rheum Dis. 2002;61: 554–558. pmid:12006334
- 25. Anaya J-M, Castiblanco J, Tobón GJ, García J, Abad V, Cuervo H, et al. Familial clustering of autoimmune diseases in patients with type 1 diabetes mellitus. J Autoimmun. 2006;26: 208–214. pmid:16503115
- 26. Tobon GJ, Arango a, Abad V, García J, Cuervo H, Velásquez a, et al. Clinical and immunological characteristics of type 1 diabetes mellitus in a northwestern Colombian population. Diabetes Res Clin Pract. 2006;72: 170–175. pmid:16325957
- 27. Krause I, Anaya JM, Fraser A, Barzilai O, Ram M, Abad V, et al. Anti-infectious antibodies and autoimmune-associated autoantibodies in patients with type I diabetes mellitus and their close family members. Ann N Y Acad Sci. 2009;1173: 633–639. pmid:19758209
- 28. Shor DB-A, Barzilai O, Ram M, Izhaky D, Porat-Katz BS, Chapman J, et al. Gluten sensitivity in multiple sclerosis: experimental myth or clinical truth? Ann N Y Acad Sci. 2009;1173: 343–9. pmid:19758171
- 29. Amaya-Amaya J, Sarmiento-Monroy JC, Caro-Moreno J, Molano-González N, Mantilla RD, Rojas-Villarraga A, et al. Cardiovascular disease in latin american patients with systemic lupus erythematosus: a cross-sectional study and a systematic review. Autoimmune Dis. 2013;2013: 794383. pmid:24294522
- 30. Barragán-Martínez C, Amaya-Amaya J, Pineda-Tamayo R, Mantilla RD, Castellanos-de la Hoz J, Bernal-Macías S, et al. Gender differences in Latin-American patients with rheumatoid arthritis. Gend Med. 2012;9: 490–510. pmid:23217568
- 31. Cárdenas Roldán J, Amaya-Amaya J, Castellanos-de la Hoz J, Giraldo-Villamil J, Montoya-Ortiz G, Cruz-Tapias P, et al. Autoimmune thyroid disease in rheumatoid arthritis: a global perspective. Arthritis. 2012;2012: 864907. pmid:23209899
- 32. Amador-Patarroyo MJ, Arbelaez JG, Mantilla RD, Rodriguez-Rodriguez A, Cárdenas-Roldán J, Pineda-Tamayo R, et al. Sjögren’s syndrome at the crossroad of polyautoimmunity. J Autoimmun. 2012;39: 199–205. pmid:22749530
- 33. Pérez-Fernández OM, Mantilla RD, Cruz-Tapias P, Rodriguez-Rodriguez A, Rojas-Villarraga A, Anaya J-M. Spondyloarthropathies in autoimmune diseases and vice versa. Autoimmune Dis. 2012;2012: 736384. pmid:22400103
- 34. Anaya J-M, Cañas C, Mantilla RD, Pineda-Tamayo R, Tobón GJ, Herrera-Diaz C, et al. Lupus nephritis in Colombians: contrasts and comparisons with other populations. Clin Rev Allergy Immunol. 2011;40: 199–207. pmid:21287296
- 35. Franco J-S, Molano-González N, Rodríguez-Jiménez M, Acosta-Ampudia Y, Mantilla RD, Amaya-Amaya J, et al. The coexistence of antiphospholipid syndrome and systemic lupus erythematosus in colombians. PLoS One. 2014;9: e110242. pmid:25343509
- 36. Shapira Y, Agmon-Levin N, Selmi C, Petríková J, Barzilai O, Ram M, et al. Prevalence of anti-Toxoplasma antibodies in patients with autoimmune diseases. J Autoimmun. 2012;39: 112–116. pmid:22297145
- 37. Shapira Y, Poratkatz B-S, Gilburd B, Barzilai O, Ram M, Blank M, et al. Geographical differences in autoantibodies and anti-infectious agents antibodies among healthy adults. Clin Rev Allergy Immunol. 2012;42: 154–163. pmid:21229335
- 38. Orbach H, Amitai N, Barzilai O, Boaz M, Ram M, Zandman-Goddard G, et al. Autoantibody screen in inflammatory myopathies high prevalence of antibodies to gliadin. Ann N Y Acad Sci. 2009;1173: 174–179. pmid:19758147
- 39. Berkun Y, Zandman-Goddard G, Barzilai O, Boaz M, Sherer Y, Larida B, et al. Infectious antibodies in systemic lupus erythematosus patients. Lupus. 2009;18: 1129–1135. pmid:19880558
- 40. Zandman-Goddard G, Berkun Y, Barzilai O, Boaz M, Ram M, Anaya JM, et al. Neuropsychiatric lupus and infectious triggers. Lupus. 2008;17: 380–384. pmid:18490412
- 41. Pordeus V, Barzilai O, Sherer Y, Luiz RR, Blank M, Bizzaro N, et al. A latitudinal gradient study of common anti-infectious agent antibody prevalence in Italy and Colombia. Isr Med Assoc J. 2008;10: 65–68. pmid:18300578
- 42. Ram M, Anaya J-M, Barzilai O, Izhaky D, Porat Katz B-S, Blank M, et al. The putative protective role of hepatitis B virus (HBV) infection from autoimmune disorders. Autoimmun Rev. 2008;7: 621–625. pmid:18603025
- 43. Barzilai O, Sherer Y, Ram M, Izhaky D, Anaya JM, Shoenfeld Y. Epstein-Barr virus and cytomegalovirus in autoimmune diseases: are they truly notorious? A preliminary report. Ann N Y Acad Sci. 2007;1108: 567–577. pmid:17894021
- 44. Meron MK, Amital H, Shepshelovich D, Barzilai O, Ram M, Anaya J-M, et al. Infectious aspects and the etiopathogenesis of rheumatoid arthritis. Clin Rev Allergy Immunol. 2010;38: 287–291. pmid:19575154
- 45. Altman A, Szyper-Kravitz M, Agmon-Levin N, Gilburd B, Anaja J-M, Barzilai O, et al. Prevalence of rubella serum antibody in autoimmune diseases. Rev Bras Reumatol. 2012;52: 307–318. pmid:22641586
- 46. Zandman-Goddard G, Berkun Y, Barzilai O, Boaz M, Blank M, Ram M, et al. Exposure to Epstein-Barr virus infection is associated with mild systemic lupus erythematosus disease. Ann N Y Acad Sci. 2009;1173: 658–663. pmid:19758212
- 47. Liberati A, Altman DG, Tetzlaff J, Mulrow C, Gøtzsche PC, Ioannidis JPA, et al. The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate health care interventions: explanation and elaboration. J Clin Epidemiol. 2009;62: e1–34. pmid:19631507
- 48. OCEBM Levels of Evidence Working Group. The Oxford 2011 levels of evidence. Oxford Cent Evidence-Based Med. 2011.
- 49. Viechtbauer W. Conducting Meta-Analyses in R with the metafor Package. J Stat Softw. 2010;36:1–48.
- 50. Machado AP de SL, Silva LR, Zausner B, Oliveira J de A, Diniz DR, de Oliveira J. Undiagnosed celiac disease in women with infertility. J Reprod Med. 2013;58: 61–66. pmid:23447921
- 51. Gomez JC, Selvaggio GS, Viola M, Pizarro B, la Motta G, de Barrio S, et al. Prevalence of celiac disease in Argentina: screening of an adult population in the La Plata area. Am J Gastroenterol. 2001;96: 2700–2704. pmid:11569698
- 52. Gomez JC, Selvaggio G, Pizarro B, Viola MJ, La Motta G, Smecuol E, et al. Value of a screening algorithm for celiac disease using tissue transglutaminase antibodies as first level in a population-based study. Am J Gastroenterol. 2002;97: 2785–2790. pmid:12425549
- 53. González D, Sugai E, Gomez JC, Oliveri MB, Gomez Acotto C, Vega E, et al. Is it necessary to screen for celiac disease in postmenopausal osteoporotic women? Calcif Tissue Int. 2002;71: 141–144. pmid:12200648
- 54. Rumbo M, Chirdo FG, Ben R, Saldungaray I, Villalobos R. Evaluation of coeliac disease serological markers in Down syndrome patients. Dig Liver Dis. 2002;34: 116–121. pmid:11926554
- 55. Mora M, Litwin N, Toca M del C, Azcona MI, Solís Neffa R, Ortiz G, et al. Prevalence of celiac disease: multicentric trial among pediatric population in five urban districts of Argentina. 2010;1: 26–31. pmid:23224306
- 56. Bustos D, Moret A, Tambutti M, Gogorza S, Testa R, Ascione A, et al. Autoantibodies in Argentine women with recurrent pregnancy loss. Am J Reprod Immunol. 2006;55: 201–207. pmid:16451354
- 57. Begué C, Beratarrechea AG, Varela E, Piccioni HL, Rodota L, Castro ME, et al. Enfermedad celíaca: prevalencia del diagnóstico en un hospital de comunidad. Acta Gastroenterol Latinoam. 2010;40: 317–322. pmid:21381406
- 58. Sugai E, Moreno ML, Hwang HJ, Cabanne A, Crivelli A, Nachman F, et al. Celiac disease serology in patients with different pretest probabilities: is biopsy avoidable? World J Gastroenterol. 2010;16: 3144–3152. pmid:20593499
- 59. Gandolfi L, Pratesi R, Cordoba JC, Tauil PL, Gasparin M, Catassi C. Prevalence of celiac disease among blood donors in Brazil. Am J Gastroenterol. 2000;95: 689–692. pmid:10710058
- 60. Gandolfi L, Catassi C, Garcia S, Modelli IC, Campos D Jr, Pratesi R. Antiendomysial antibody test reliability in children with frequent diarrhea and malnutrition: is it celiac disease? J Pediatr Gastroenterol Nutr. 2001;33: 483–487. pmid:11698768
- 61. Kotze LM, Utiyama SR, Nisihara RM, Zeni MP, de Sena MG, Amarante HM. Antiendomysium antibodies in Brazilian patients with celiac disease and their first-degree relatives. Arq Gastroenterol. 2001;38: 94–103. pmid:11793949
- 62. Pratesi R, Gandolfi L, Garcia SG, Modelli IC, Lopes de Almeida P, Bocca AL, et al. Prevalence of coeliac disease: unexplained age-related variation in the same population. Scand J Gastroenterol. 2003;38: 747–750. pmid:12889561
- 63. Pratesi R, Gandolfi L, Martins RC, Tauil PL, Nobrega YK, Teixeira WA. Is the prevalence of celiac disease increased among epileptic patients? Arq Neuropsiquiatr. 2003;61: 330–334. pmid:12894262
- 64. Brandt KG, Silva GAP, Antunes MMC. Celiac disease in a group of children and adolescents with type 1 diabetes mellitus. Arq Bras Endocrinol Metab. 2004;48: 823–827. pmid:15761555
- 65. Queiroz MS, Nery M, Cancado EL, Gianella-Neto D, Liberman B. Prevalence of celiac disease in Brazilian children of short stature. Braz J Med Biol Res. 2004;37: 55–60. pmid:14689044
- 66. Trevisiol C, Brandt KG, Silva GA, Crovella S, Ventura A. High prevalence of unrecognized celiac disease in an unselected hospital population in north-eastern Brasil (Recife, Pernambuco). J Pediatr Gastroenterol Nutr. 2004;39: 214–215. pmid:15269636
- 67. Baptista ML, Koda YK, Mitsunori R, Nisihara , Ioshii SO. Prevalence of celiac disease in Brazilian children and adolescents with type 1 diabetes mellitus. J Pediatr Gastroenterol Nutr. 2005;41: 621–624. pmid:16254520
- 68. Lima VM, Gandolfi L, Pires JA, Pratesi R. Prevalence of celiac disease in dyspeptic patients. Arq Gastroenterol. 2005;42: 153–156. pmid:16200250
- 69. Nisihara RM, Kotze LM, Utiyama SR, Oliveira NP, Fiedler PT, Messias-Reason IT. Celiac disease in children and adolescents with Down syndrome. J Pediatr (Rio J). 2005;81: 373–376. pmid:16247538
- 70. Tanure MG, Silva IN, Bahia M, Penna FJ. Prevalence of celiac disease in Brazilian children with type 1 diabetes mellitus. J Pediatr Gastroenterol Nutr. 2006;42: 155–159. pmid:16456407
- 71. Pereira MA, Ortiz-Agostinho CL, Nishitokukado I, Sato MN, Damiao AO, Alencar ML, et al. Prevalence of celiac disease in an urban area of Brazil with predominantly European ancestry. World J Gastroenterol. 2006;12: 6546–6550. pmid:17072989
- 72. Melo SB, Fernandes MI, Peres LC, Troncon LE, Galvao LC. Prevalence and demographic characteristics of celiac disease among blood donors in Ribeirao Preto, State of Sao Paulo, Brazil. Dig Dis Sci. 2006;51: 1020–1025. pmid:16758312
- 73. De Bem RS, Da Ro Sa Utiyama SR, Nisihara RM, Fortunato JA, Tondo JA, Carmes ER, et al. Celiac disease prevalence in Brazilian dilated cardiomyopathy patients. Dig Dis Sci. 2006;51: 1016–1019. pmid:16758314
- 74. Araújo J, Pontes Da Silva GA, De Melo FM. Serum prevalence of celiac disease in children and adolescents with type 1 diabetes mellitus. J Pediatr (Rio J). 2006;82: 210–214. pmid:16729151
- 75. Crovella S, Brandao L, Guimaraes R, Filho JL, Arraes LC, Ventura A, et al. Speeding up coeliac disease diagnosis in the developing countries. Dig Liver Dis. 2007;39:900–902. pmid:17706474
- 76. Nisihara RM, Skare TL, Silva MB. Rheumatoid Arthritis and anti-endomysial antibodies. Acta Reum Port. 2007;32: 163–167.
- 77. Oliveira RP, Sdepanian VL, Barreto J a, Cortez AJP, Carvalho FO, Bordin JO, et al. High prevalence of celiac disease in Brazilian blood donor volunteers based on screening by IgA antitissue transglutaminase antibody. Eur J Gastroenterol Hepatol. 2007;19: 43–49. pmid:17206076
- 78. Utiyama SR da R, Nass FR, Kotze LM da S, Nisihara RM, Ambrosio AR, Messias-Reason IT. [Serological screening of relatives of celiac disease patients: antiendomysium antibodies, anti-tissue transglutaminase or both?]. Arq Gastroenterol. 2007;44: 156–161. pmid:17962863
- 79. Whitacker FCF, Hessel G, Lemos-Marini SH V, Paulino MFVM, Minicucci WJ, Guerra-Júnior G. [Prevalence and clinical aspects when it comes to the association between type 1 diabetes mellitus (DM1) and celiac disease]. Arq Bras Endocrinol Metab. 2008;52: 635–641. pmid:18604376
- 80. Almeida PL, Gandolfi L, Modelli IC, Martins Rde C, Almeida RC, Pratesi R. Prevalence of celiac disease among first degree relatives of Brazilian celiac patients. Arq Gastroenterol. 2008;45: 69–72. pmid:18425232
- 81. Mont-Serrat C, Hoineff C, Meirelles RMR, Kupfer R. [Diabetes and autoimmune diseases: prevalence of celiac disease in children and adolescents with type 1 diabetes] Arq Bras Endocrinol Metabol. 2008;52: 1461–1465. pmid:19197454
- 82. Brandt KG, Silva GAP da. [Soroprevalência da doença celíaca em ambulatório pediátrico, no nordeste do Brasil] Arq Gastroenterol. 2008;45: 239–242. pmid:18852954
- 83. Koehne Vde B, Bahia M, Lanna CC, Pinto MR, Bambirra EA, Cunha AS. Prevalence of serological markers for celiac disease (IgA and IgG class antigliadin antibodies and IgA class antiendomysium antibodies) in patients with autoimmune rheumatologic diseases in Belo Horizonte, MG, Brazil. Arq Gastroenterol. 2010;47: 250–256. pmid:21140085
- 84. Utiyama SR, Ribas JL, Nisihara RM, Kotze LM, de Messias-Reason IJ. Celiac disease in native Indians from Brazil: A clinical and epidemiological survey. N Am J Med Sci. 2010;2: 138–142. pmid:22624128
- 85. Martins Rde C, Gandolfi L, Modelli IC, Almeida RC, Castro LC, Pratesi R. Serologic screening and genetic testing among brazilian patients with celiac disease and their first degree relatives. Arq Gastroenterol. 2010;47: 257–262. pmid:21140086
- 86. Dias Mdo C, De Castro LCG, Gandolfi L, De Almeida RC, Córdoba MS, Pratesi R. Screening for celiac disease among patients with Turner syndrome in Brasília, DF, Midwest region of Brazil. Arq Gastroenterol. 2010;47: 246–249. pmid:21140084
- 87. Modelli IC, Gandolfi L, Almeida RC de, Araújo GMAC, Picanço M de A, Pratesi R. Serological screening for celiac disease in symptomatic 12 to 36 month-old children. Arq Gastroenterol. 2010;47: 61–65. pmid:20520977
- 88. Castro-Antunes MM, Magalhaes R, Nobre JM, Duarte BP, Silva GA. Celiac disease in first-degree relatives of patients. J Pediatr (Rio J). 2010;86: 331–336. pmid:20711550
- 89. Nass FR, Kotze LMDS, Nisihara RM, De Messias-Reason IJ, Ramos Da Rosa Utiyama S. Serological and clinical follow-up of relatives of celiac disease patients from Southern Brazil. Digestion. 2010;83: 89–95. pmid:21042020
- 90. Ribeiro-Cabral VL, da-Silva-Patrício FR, Ambrogini-Junior O, Jankiel-Miszputen S. Anti-tissue transglutaminase antibodies (IgA and IgG) in both Crohn’s disease and autoimmune diabetes. Rev Esp Enferm Dig. 2011;103: 453–457. pmid:21951113
- 91. Goeldner I, Skare TL, de Messias Reason IT, Nisihara RM, Silva MB, da Rosa Utiyama SR. Autoantibodies for gastrointestinal organ-specific autoimmune diseases in rheumatoid arthritis patients and their relatives. Clin Rheumatol. 2011;30: 99–102. pmid:20683740
- 92. Nisihara R, Utiyama SR, Azevedo PM, Skare TL. Celiac disease screening in patients with scleroderma. Arq Gastroenterol. 2011;48: 163–164. pmid:21709960
- 93. Andretta MA, Vieira TD, Nishiara R, Skare TL. Anti-Saccharomyces cerevisiae (ASCA) and anti-endomysial antibodies in spondyloarthritis. Rheumatol Int. 2012;32:551–554. pmid:21305298
- 94. Alencar ML, Ortiz-Agostinho CL, Nishitokukado L, Damião AOMC, Abrantes-Lemos CP, Leite AZ de A, et al. Prevalence of celiac disease among blood donors in São Paulo: the most populated city in Brazil. Clinics (Sao Paulo). 2012;67: 1013–1018. pmid:23018296
- 95. Almeida RC, Gandolfi L, De Nazare Klautau-Guimaraes M, Ferrari I, Sousa SM, Abe-Sandes K, et al. Does celiac disease occur in Afro-derived Brazilian populations? Am J Hum Biol. 2012;24:710–712. pmid:22508149
- 96. Menezes TM, Motta ME. Celiac disease prevalence in children and adolescents with myocarditis and dilated cardiomiopathy. J Pediatr (Rio J). 2012;88: 439–442. pmid:23093320
- 97. Almeida LM, Castro LC, Uenishi RH, de Almeida FC, Fritsch PM, Gandolfi L, et al. Decreased prevalence of celiac disease among Brazilian elderly. World J Gastroenterol. 2013;19: 1930–1935. pmid:23569338
- 98. Skare T, Nisihara RM, Utiyama SRR. Is it worth investigating coeliac disease in patients with rheumatic disorders? Rheumatology (Oxford). 2013;52: 217–218. pmid:22956552
- 99. Araya M, Mondragón a, Pérez-Bravo F, Roessler JL, Alarcón T, Rios G, et al. Celiac disease in a Chilean population carrying Amerindian traits. J Pediatr Gastroenterol Nutr. 2000;31: 381–386. pmid:11045834
- 100. Calderon HP, Valdes AP, Zemelman D V, Poniachik TJ, Hurtado HC, Garmendia MM, et al. [Frequency of celiac disease among patients with psoriasis]. Rev Med Chil. 2007;135: 1296–1303. pmid:18180837
- 101. Madrid SA, Diaz SM, Hurtado HC, Aguilera OL, Mena UB. [Silent celiac disease among 21 patients with cryptogenic epilepsy]. Rev Med Chil. 2011;139: 587–591. pmid:22051708
- 102. Sorell L, Garrote JA, Galvan JA, Velazco C, Edrosa CR, Arranz E. Celiac disease diagnosis in patients with giardiasis: high value of antitransglutaminase antibodies. Am J Gastroenterol. 2004;99: 1330–1332. pmid:15233673
- 103. Castañeda C, Alvarez Fumero R, Sorell L, Galván JA CF. Screening for celiac disease in risk groups in Cuba. J Pediatr Gastroenterol Nutr. 2004;39: S211–S212.
- 104. Sorell L, Galván JA AB. Screening of celiac disease in Cuba. The Global Village of Coeliac Disease Perspectives on Coeliac Disease. 2005. pp. 131–5.
- 105. Galván JA, Castañeda C, Rodríguez EA, Alvarez R, Turcaz N, Novoa LI, et al. Screening for celiac disease in a healthy Cubans children cohort from Pinar del Río province. 2005;II: 5–7.
- 106. Sanchez JC, Cabrera-Rode E, Sorell L, Galvan JA, Hernandez A, Molina G, et al. Celiac disease associated antibodies in persons with latent autoimmune diabetes of adult and type 2 diabetes. Autoimmunity. 2007;40: 103–107. pmid:17364501
- 107. Galván JA, Cabrera-Rode E, Molina G, Díaz-Horta O, Palenzuela DO, Novoa LI, et al. Celiac disease-associated antibodies in type 1 diabetes patients in Cuba. Biotecnol Apl. 2008;25: 47–50.
- 108. Santana-Porbén S, Castellanos-Fernández M. [Malnutrition in adults with gastrointestinal disorders: A new reservoir of celiac disease?] Rev Gastroenterol. 2009;74: 202–211. pmid:19858008
- 109. Galvan JA, Lemos G, Fernandez de Cossio ME, Ruenes C, Martinez Y, Tejeda Y, et al. Silent celiac disease in a cohort of healthy adults. Autoimmunity. 2009;42: 705–708. pmid:19886741
- 110. Guerreiro Hernández AM, Villaescusa Blanco R, Morera Barrios LM, Alonso Valle M, Martínez Cardet L, Junco González Y. Detection of anti-gliadin and anti-transglutaminase antibodies in patients with possible celiac disease. Rev Cubana Hematol Inmunol Hemoter. 2010;26: 28–32.
- 111. Cintado A, Sorell L, Galván JA, Martínez L, Castañeda C, Fragoso T, et al. HLA DQA1*0501 and DQB1*02 in Cuban celiac patients. Hum Immunol. 2006;67: 639–642. pmid:16916661
- 112. Sarmiento L, Galvan JA, Cabrera-Rode E, Aira L, Correa C, Sariego S, et al. Type 1 diabetes associated and tissue transglutaminase autoantibodies in patients without type 1 diabetes and coeliac disease with confirmed viral infections. J Med Virol. 2012;84: 1049–1053. pmid:22585721
- 113. Madrazo de la Garza JA, Santiago-Lomelí M M-AJ et al. Prevalence of serum IgA anti-transglutaminase antibodies(anti-tTG) in an open population in Mexico. Rev Gastroenterol Mex. 2006;71 suppl: 118–9. pmid:17037795
- 114. Remes-Troche JM, Ramírez-Iglesias MT, Rubio-Tapia A, Alonso-Ramos A, Velazquez A, Uscanga LF. Celiac disease could be a frequent disease in Mexico: prevalence of tissue transglutaminase antibody in healthy blood donors. J Clin Gastroenterol. 2006;40: 697–700. pmid:16940881
- 115. Remes-Troche JM, Rios-Vaca A, Ramírez-Iglesias MT, Rubio-Tapia A, Andrade-Zarate V, Rodríguez-Vallejo F, et al. High prevalence of celiac disease in Mexican Mestizo adults with type 1 diabetes mellitus. J Clin Gastroenterol. 2008;42: 460–465. pmid:18344893
- 116. Worona L, Coyote N VP. Prevalencia de la enfermedad celiaca en un grupo de pacientes con diabetes mellitus tipo I del Hospital Infantil de México. Rev Mex Gastroenterol. 2009;74 (Supl 2): 67.
- 117. Remes-Troche JM, Nuñez-Alvares C, Uscanga-Dominguez LF. Celiac disease in Mexican population: An update. Am J Gastroenterol. 2013;108: 283–284. pmid:23381082
- 118. Arevalo F, Roe E, Arias-Stella-Castillo J, Cardenas J, Montes P, Monge E. Low serological positivity in patients with histology compatible with celiac disease in Peru. Rev Esp Enferm Dig. 2010;102: 372–375. pmid:20575597
- 119. Llanos O, Matzumura M, Tagle M, Huerta-Mercado J, Cedron H, Scavino J, et al. [Celiac disease: descriptive study at the Anglo American clinic]. Rev Gastroenterol Peru. 2012;32: 134–140. pmid:23023175
- 120. Landaeta N Fernandez L. Enfermedad Celiaca en pacientes pediátricos con Diábetes Mellitus Tipo 1. Gen. 2008;62: 96–99.
- 121. Landaeta N, Rodríguez M, Fernandez A, Padrón D, Arredondo C. Screening para enfermedad celiaca en familiares de primer grado de niños celiacos. 2009; 108–10.
- 122. Rubio-Tapia C A, Ludvigsson JF, Brantner TL, Murray J a, Everhart JE. The Prevalence of Celiac Disease in the United States. Am J Gastroenterol. 2012;107: 1538–1544. pmid:22850429
- 123. Kang JY, Kang AHY, Green A, Gwee KA, Ho KY. Systematic review: worldwide variation in the frequency of coeliac disease and changes over time. Aliment Pharmacol Ther. 2013;38: 226–245. pmid:23782240
- 124. Kratzer W, Kibele M, Akinli A, Porzner M, Boehm BO, Koenig W, et al. Prevalence of celiac disease in Germany: A prospective follow-up study. World J Gastroenterol. 2013;19:2612–20. pmid:23674868
- 125. Sans M. Admixture studies in Latin America: from the 20th to the 21st century. Hum Biol. 2000;72: 155–177. pmid:10721616
- 126. Pena SDJ, Di Pietro G, Fuchshuber-Moraes M, Genro JP, Hutz MH, Kehdy F de SG, et al. The genomic ancestry of individuals from different geographical regions of Brazil is more uniform than expected. PLoS One. 2011;6: e17063. pmid:21359226
- 127. Bybrant MC, Örtqvist E, Lantz S, Grahnquist L. High prevalence of celiac disease in Swedish children and adolescents with type 1 diabetes and the relation to the Swedish epidemic of celiac disease: a cohort study. Scand J Gastroenterol. 2014;49: 52–8. pmid:24164443
- 128. Concannon P, Rich SS, Nepom GT. Genetics of type 1A diabetes. N Engl J Med. 2009;360: 1646–1654. pmid:19369670
- 129. Greco L, Romino R, Coto I, Di Cosmo N, Percopo S, Maglio M, et al. The first large population based twin study of coeliac disease. Gut. 2002;50: 624–628. pmid:11950806
- 130. Cárdenas-Roldán J, Rojas-Villarraga A, Anaya J-M. How do autoimmune diseases cluster in families? A systematic review and meta-analysis. BMC Med. 2013;18: 11:73.
- 131. Neuhausen SL, Steele L, Ryan S, Mousavi M, Pinto M, Osann KE, et al. Co-occurrence of celiac disease and other autoimmune diseases in celiacs and their first-degree relatives. J Autoimmun. 2008;31: 160–165. pmid:18692362
- 132. Bai JC, Fried M, Corazza GR, Schuppan D, Farthing M, Catassi C, et al. World gastroenterology organisation global guidelines on celiac disease. J Clin Gastroenterol. 2013;47: 121–126. pmid:23314668
- 133. Wang S, Ray N, Rojas W, Parra M V, Bedoya G, Gallo C, et al. Geographic patterns of genome admixture in Latin American Mestizos. PLoS Genet. 2008;4: e1000037. pmid:18369456
- 134. Bourges H, Bengoa J, O′Donnell A. Historias de la Nutrición en América Latina. Soc Latinoam Nutr; 2009.
- 135. Fasano A, Catassi C. Clinical practice. Celiac disease. N Engl J Med. 2012 20;367: 2419–2426. pmid:23252527
- 136. Palavecino EA, Mota AH, Awad J, Derosa S, Herrera M, Chertkoff L, et al. HLA and celiac disease in Argentina: involvement of the DQ subregion. Dis Markers. 1990;8: 5–10. pmid:2311351
- 137. Herrera M, Theiler G, Augustovski F, Chertkoff L, Fainboim L, DeRosa S, et al. Molecular characterization of HLA class II genes in celiac disease patients of Latin American Caucasian origin. Tissue Antigens. 1994;43: 83–87. pmid:8016846
- 138. Silva EM, Fernandes MI, Galvao LC, Sawamura R, Donadi EA. Human leukocyte antigen class II alleles in white Brazilian patients with celiac disease. J Pediatr Gastroenterol Nutr. 2000;31: 391–394. pmid:11045836
- 139. Pérez-Bravo F, Araya M, Mondragón a, Ríos G, Alarcón T, Roessler JL, et al. Genetic differences in HLA-DQA1* and DQB1* allelic distributions between celiac and control children in Santiago, Chile. Hum Immunol. 1999;60: 262–267. pmid:10321965
- 140. Poggio Favotto RC, Mimbacas AB, Crispino B, Jasinski C, Cardoso H. [Association between HLA-DQB1 and HLA-DRB1 alleles and coeliac disease in hospitalized patients] Rev med Urug. 2001;17: 107–113.
- 141. Landaeta N, Fernández-Mestre M, Rodríguez M, Padrón D, Medina M, Layrisse Z. Polimorfismo HLA-DQ en pacientes pediátricos con enfermedad Celíaca. Gen. 2008;62: 92–95.
- 142. Layrisse Z, Guedez Y, Domínguez E, Paz N, Montagnani S, Matos M, et al. Extended HLA haplotypes in a Carib Amerindian population: the Yucpa of the Perija Range. Hum Immunol. 2001;62: 992–1000. pmid:11543901
- 143. Gonzalez-Galarza FF, Christmas S, Middleton D, Jones AR. Allele frequency net: a database and online repository for immune gene frequencies in worldwide populations. Nucleic Acids Res. 2011;39: D913–919. pmid:21062830
- 144. Kondrashova A, Mustalahti K, Kaukinen K, Viskari H, Volodicheva V, Haapala A-M, et al. Lower economic status and inferior hygienic environment may protect against celiac disease. Ann Med. 2008;40: 223–231. pmid:18382888