Skip to content
naulon
Get started

No retraction, correction or concern found when last checked on Oct 24, 2026.

Celiac Disease and Autoimmune-Associated Conditions

Eugenia Lauret, Luis Rodrigo

BioMed Research International · 2013 · Review

doi:10.1155/2013/127589

Abstract

Celiac disease (CD) is frequently accompanied by a variety of extradigestive manifestations, thus making it a systemic disease rather than a disease limited to the gastrointestinal tract. This is primarily explained by the fact that CD belongs to the group of autoimmune diseases. The only one with a known etiology is related to a permanent intolerance to gluten. Remarkable breakthroughs have been achieved in the last decades, due to a greater interest in the diagnosis of atypical and asymptomatic patients, which are more frequent in adults. The known presence of several associated diseases provides guidance in the search of oligosymptomatic cases as well as studies performed in relatives of patients with CD. The causes for the onset and manifestation of associated diseases are diverse; some share a similar genetic base, like type 1 diabetes mellitus (T1D); others share pathogenic mechanisms, and yet, others are of unknown nature. General practitioners and other specialists must remember that CD may debut with extraintestinal manifestations, and associated illnesses may appear both at the time of diagnosis and throughout the evolution of the disease. The implementation of a gluten-free diet (GFD) improves the overall clinical course and influences the evolution of the associated diseases. In some cases, such as iron deficiency anemia, the GFD contributes to its disappearance. In other disorders, like T1D, this allows a better control of the disease. In several other complications and/or associated diseases, an adequate adherence to a GFD may slow down their evolution, especially if implemented during an early stage.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 24, 2026. Paragraph numbers are ours, so an answer can point at one.

1. Introduction

Celiac disease (CD) is a chronic immune-mediated disorder triggered by the ingestion of gluten that appears in genetically predisposed patients The clinical spectrum of CD is wide and includes classic presentation of malabsorption with diarrhea, nonclassical extraintestinal features, subclinical or asymptomatic forms, and potential disease characterized by positive serology with a normal intestinal mucosa on biopsy. Moreover, a significantly increased prevalence of other autoimmune diseases (AD) has been reported in individuals with CD and their first-degree relatives as compared to controls, with an estimated burden of AD in CD cases up to 15%. In celiac patients, an early diagnosis in life and having a family history of autoimmunity are risk factors for developing other AD, while the gluten-free diet (GFD) has a protective effect. By contrast, in relatives of CD cases, the prevalence of AD rises with the age. Conversely, a significantly increased prevalence of CD has been documented in individuals with other AD. It has been suggested that these associations among CD and other AD may be explained by the sharing of a common pathogenic basis involving genetic susceptibility, similar environmental triggers, and the loss of intestinal barrier secondary to dysfunction of intercellular tight junctions with increased intestinal permeability, and possibly by other undiscovered mechanisms. In this review, we present a detailed description of the main AD associated with CD (Table 1).

2. Immunogenetics of Celiac Disease

The name of gluten is applied to a collective set of proteins for the storage that are found in grains of wheat, barley, and rye.

Typically, gluten proteins are rich in glutamine and proline residues. Their high proline content makes them resistant to gastrointestinal digestion. In wheat, gluten proteins are divided into gliadins and glutenins, whereas the gluten proteins of barley and rye are termed hordeins and secalins, respectively. Patients with CD raise CD4+ T cell response against several distinct gluten peptides and these peptides are recognized in the context of CD-associated HLA-DQ molecules. In addition, patients make antibodies specific for gluten proteins.

Autoantibodies in CD were initially detected as reticulin-specific antibodies by staining of rat tissue. Subsequently, IgA endomysium-specific antibodies (EMAs), detected by staining of monkey oesophagus or human umbilical cord, were described. The main antigen recognized by reticulin-specific antibodies and EMAs was identified as the enzyme transglutaminase 2 (TG2) in 1997, by Dieterich et al..

TG2-specific antibodies are found in serum as IgA and IgG isotypes. Assaying for TG2-specific IgA is most commonly used in clinical practice, as this test has the highest disease specificity and sensitivity. In fact, the disease specificity and sensitivity for this test are higher than for any other auto-antigen-disease association. Previously, the detection of histological changes in small intestinal biopsy samples, such as blunting of intestinal villi and infiltration of inflammatory cells, was considered mandatory for the diagnosis of CD.

TG2 antibodies are detected in 0.3–2% of individuals in Europe and in the US, and comparable prevalence rates are observed in a growing number of countries in which gluten is an important component of the diet. Positive serology is more particularly frequent in first-degree relatives, a finding consistent with the importance of genetic predisposing factors, and in patients with AD, notably with type 1 diabetes (T1D) and thyroiditis. In individuals with positive serology, the diagnosis of CD is confirmed by duodenal biopsies that demonstrate typical small intestinal lesions combining villous flattening, crypt hiperplasia and increased numbers of intra-epithelial lymphocytes (IELs).

Several studies highlighting a strong association between CD and the HLA complex and it was established in the late 1980s, with HLA-class II associations for CD and T1D. The majority of CD patients express the HLA-DQ2.5 heterodimer encoded by the HLA-DQA1*05 (alpha-chain) and HLA-DQB1*02 (beta-chain) alleles. Both are carried either “in cis” on the DR3-DQ2 haplotype, or “in trans” in individuals who are DR5-DQ7 and DR7-DQ2 heterozygous. HLA-DQ8 that is encoded by the DR4-DQ8 haplotype, confers a lesser risk of CD. In individuals who are DR3-DQ2 and DR4-DQ8 heterozygous, transdimers DQ8.5 can form and confer a high susceptibility to T1D. Therefore, genetic susceptibility to CD is determined mainly by the HLA-DQ locus. The strongest association is observed with HLA-DQ2.5; thus more than 90% of celiac patients possess one or two copies of HLA-DQ2.5.

Gut lesions of most patients with CD completely normalize when gluten is excluded from the diet, and they reappear when the patients eat gluten again. Both the presence of autoantibodies specific for TG2 and the increased number of intraepithelial cytotoxic T lymphocytes (IE-CTLs) are gluten dependent, as they change after gluten elimination or challenge. Patients with CD, but not healthy controls, have HLA-DQ2 or HLA-DQ8 restricted CD4+ T cells in the gut mucosa that are reactive to gluten. Given the strong HLA association, CD4+ T cells are probably key players in the development of the disease.

Another key aspect of CD is the up-regulation of certain interleukins mainly IL-15 type, and in combination with nonclassical MHC class I molecules in the epithelium. It is probable that the CD4+ T cell response has a role, but it is not sufficient alone to induce these alterations in the intestinal epithelium. Together, these observations are in line with the concept that a strong adaptive immune response is typically paired with an innate component that facilitates the adaptive response.

IE-CTLs can destroy the intestinal epithelial cells in CD on the basis of the presence of stress signals, rather than because they are specific for an epithelial cell antigen. Only cells that up-regulate IL-15 and nonclassical MHC class I molecules will be targeted by IE-CTLs. The receptor-ligand interactions involve noncognate recognition of low affinity self or microbial peptides by the T-cell receptor (TCR) and recognition of inducible nonclassical MHC class I molecules by NK cell receptors. Thus, the presence of CD8+ T cells with lymphokine-activated killer activity and/or a very low activation threshold in the tissue targeted by an autoimmune process could point to an exogenous factor, which probably would be the gluten.

In summary, gluten has a dual effect upon the small bowel mucosa. By one side, small toxic peptides as the 19-mer, induce an innate unspecific immunologic response, characterized by the presence of IL-15 produced by the enterocytes. This interleukin promotes the liberation of the transcription factor NF-κB by the adjacent cells that increase the IL-15 production and the induction of nitric oxide synthase (iNOS), promoting oxidative stress and helping to maintain the innate response. Different molecules such as MICA and/or HLA-E are increased at the enterocytes and induce their apoptosis. Finally, IL-15 opens the tight-junctions between the epithelial cells.

The adaptive response is performed by the increased permeability which permits that immunologic peptides such as 33-mer arrive to the lamina propria where they are deamidated by TG2. IL-15 activates to dendritic cells for presenting the deamidated gluten peptides by the HLA-DQ2/8 molecules to the CD8+ T lymphocytes. These facts start a Th1 response, liberating IFNγ and other metalloproteases. This profile of cytokines is the responsible of the epithelial lesion, characterized by the presence of IELs, crypts hyperplasia, villous atrophy, and chronic inflammatory infiltrate at the lamina propria (Figure 1).

In recent years, the role of prolactin (PRL) as modulator of the immune response has been elucidated. Hyperprolactinemia has been found in the active phase of both nonorgan-specific and organ-specific AD. There is a correlation between PRL level and the number of CD4+ T and B lymphocytes, and this hormone stimulates the release of cytokines and enhances the autoantibody production. The relationship between prolactin and AD could be partially explained because the human prolactin gene is located in short arm of the chromosome 6 close to HLA region. In CD, it was shown that hyperprolactinemia is present in patients in active phase under gluten-containing diet but not in those with nonactive CD following a GFD. Likewise, it was also found a good correlation between serum PRL level with the degree of mucosal atrophy and between the serum concentrations of this hormone and EMAs. For this reason, it has been suggested that PRL level may serve as a potential marker for CD activity.

As mentioned, CD has a strong HLA-DQ association, and this genetic background play a key role in the predisposition to the disease development with an estimated risk effect of 40%. On the other hand, an unknown number of non-HLA genes contribute to the other 60% of genetic susceptibility. Of the later, variants in the genes cytotoxic T lymphocyte antigen 4 (CTLA-4) and myosin 1XB (MYO9B) have been associated with CD, but widespread replication of these findings in large cohorts from different populations remains limited. Additionally, in the past few years, two genome-wide association studies (GWAS) and one fine-mapping project have identified up to 57 non-HLA single-nucleotide polymorphisms (SNPs) that contribute to CD susceptibility. However, taken together these genes still only explain up to 10% of the CD heritability, while many others remain undiscovered.

The relationship between a variant at exon-3 (rs1143679) of Integrin-α-M (ITGAM) and some AD including CD has also been examined. This gene encodes the α-chain of a heterodimeric integral membrane protein, a cell surface receptor that plays an important role in the adherence of neutrophils and monocytes to stimulated endothelium, and also in the phagocytosis of complement coated particles. No association was observed between this genetic variant and CD.

Despite their phenotypic differences, recent genetic studies have shown shared loci between CD and other AD. This common genetic background in conjunction with environmental factors may partly explain the concurrent development of several immune-mediated disorders in celiac patients and their relatives. So, an overlap of HLA haplotypes between CD and other AD has been described. Similarly, it is estimated that of 39 known CD-associated non-HLA loci, approximately 64% are shared with at least one other AD, most of which encodes several genes involved in inflammatory and immune responses. Some of them may act as regulators of proliferation and activity of T lymphocytes (CTLA-4, ICOSLG, and IL18RAP). Other genes have been implicated in nuclear factor-kappa B activity (REL, UBE2LE) and signalling processes (SOCS1, SH2B3) or in more than one function such as T lymphocyte and cytokine activities (IL2, IL21, ILI2A, and IL23R) or T lymphocyte and signalling processes (PTPN2).

3.1. Associated Autoimmune Liver Disease

A variety of hepatobiliary disorders have been described in CD. Liver changes were first recognized by Hagander et al., and later, these findings were confirmed in several studies in which abnormal liver enzyme tests were detected in over 20% of cases. Conversely, in patients with unexplained elevations of liver enzyme levels, it was estimated that up to 10% of cases such abnormalities were due to CD.

Mild liver abnormalities are common in patients with CD and usually resolve with a GFD. In others, clinically significant liver disease is detected, and these cases are not amenable to diet treatment alone. Furthermore, several studies have demonstrated consistent associations between autoimmune liver diseases and CD, such as primary biliary cirrhosis (PBC), autoimmune hepatitis (AIH), and primary sclerosing cholangitis (PSC). The histologic features in these patients with CD-associated autoimmune liver diseases were typical of their respective entities.

3.1.1. Primary Biliary Cirrhosis

In 1978, Logan et al. described the first cases of PBC in celiac patients, and later, this association has been well established in subsequent studies with a prevalence of CD in patients with PBC in around 3–7%. Conversely, the frequency of diagnosed PBC in patients with CD is around 3%, with a 3-fold to 20-fold increased risk of PBC compared to the general population.

Both CD and PBC share several features, including a higher prevalence in females, autoimmune comorbidities, and specific autoantibodies. The breakdown of gut-liver axis equilibrium has been implicated as a mechanism underlying this association. In CD, immunologically active molecules generated from the cross-linking between tissue transglutaminase and food/bacterial antigens reach the liver through the portal circulation owing to the increased intestinal permeability. A molecular mimicry between bacterial antigens and the pyruvate dehydrogenase E2 component, recognized by antimitochondrial autoantibodies, may have a role in PBC pathogenesis. An aberrant intestinal T lymphocyte homing to the liver may contribute to trigger immune hepatic damage.

3.1.2. Autoimmune Hepatitis

A potential association between CD and AIH has also been reported in several publications, with a prevalence of CD in patients with AIH of 3% to 6% and an estimated relative risk in children with AIH of 6.63 (95% CI, 3.86–11.40). However, the reported prevalence of AIH in celiac patients is less than 2%.

CD and AIH share selected combinations of genes coding for class II HLA, which could explain their coexistence. Increased intestinal permeability and circulation of antitissue transglutaminase (tTG) have also been considered as further potential causes of liver damage in CD patients. These antibodies in the liver and in other extraintestinal tissues could modify other external- or self-antigens and generate different neoantigens, which are responsible for liver injury in patients with CD.

Although the treatment of AIH is based in the use of steroids and/or other immunosuppressive drugs, it has been seen that patients with AIH and CD achieve treatment-free sustained remission in a significantly higher proportion than patients with AIH without CD, suggesting a possible adjuvant effect of GFD.

3.1.3. Primary Sclerosing Cholangitis

The association between CD and PSC was initially reported in 1988, and later other publications have described this same relationship, with a prevalence of CD in patients with PSC of up to 3%. However, in several cases, the diagnosis of PSC was made in patients with inflammatory bowel disease, so it is not possible to rule out a confounding factor. Nevertheless, Ludvigsson et al. in a large study utilizing the data of Swedish national register, found a 4-fold increased risk of PSC in celiac patients, and both diseases remained significantly associated after exclusion of individuals with inflammatory bowel disease.

GFD was reported to cause an improvement in hepatic histological characteristics and cholestasis only in a small number of cases, making difficult to confirm whether the diet may slow the progression of this autoimmune liver disorder.

3.1.4. Others

Nonalcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is a very common disorder (up to 25%) in the general population, and its occurrence in patients with CD is likely to be a coincidence rather than a true relationship between both diseases. Some studies have found a prevalence of CD in patients with NAFLD by around 3%, and conversely, CD was associated with 6-fold increased risk of fatty liver. GFD helps normalize the liver blood test abnormalities, but the effect on the reversal of the histological damage is not clear.

Recently, it has been suggested that NAFLD is associated with increased gut permeability caused by disruption of intercellular tight junctions in the intestine, and this fact may play an important role in the pathogenesis of hepatic fat deposition. Similarly, as the loss of intestinal barrier with increased intestinal permeability induced by gliadin has also been described as involved in the pathogenesis of CD, it is possible that both diseases can relate more than mere coincidence since they seem to share a similar pathogenic mechanism.

Wilson's Disease

In a recent study, in which serological markers for CD were tested in patients with various liver diseases with subsequent confirmation of positive cases by intestinal biopsy, it was found a high prevalence of CD in patients with Wilson's disease. Although this association is considered rare and has not been fully analyzed, abnormalities in copper metabolism in CD with impaired copper uptake from the gut and levels in urine higher than in healthy controls have been reported.

Budd Chiari Syndrome

There are also reported cases of hepatic vein obstruction in celiac patients, particularly from North Africa or Southern Europe and isolation in other locations. This disorder has been related to deficiencies in protein C and antithrombin III, malabsorption of vitamin K, decreased synthesis of coagulation factors dependent on this vitamin such as protein C or protein S, and even with dietary or environmental agents. Recently, it has been suggested that the increased incidence of serum antiphosphatidylserine/prothrombin IgG antibodies and higher rates of activity for antiphosphatidylserine/prothrombin IgM and prothrombin IgG autoantibodies observed in celiac patients may be involved in the hypercoagulability predisposition of CD.

3.2.1. Type 1 Diabetes

The association between CD and autoimmune insulin-dependent diabetes mellitus is one of the most intensely studied. The diagnosis of the two diseases is often simultaneous or CD subsequent to diabetes. The prevalence of CD among patients with T1D has been estimated in approximately 4% (range from 2% to 11%), and this risk is highest with diabetes onset in childhood (age < 4 years) but also with the longer diabetes duration. Conversely, it has been described that CD is also associated with an increased risk of subsequent T1D before age 20 years (Hazard ratio (HR) 2.4; 95% CI, 1.9–3.0).

Testing for CD should be offered to children with T1D, due to high prevalence in this at risk group with potential consequences of delayed diagnosis. Similarly, there is disclosed a second peak incidence in adult T1D patients around 45 years of age, which emphasizes that screening for CD is also required in adult diabetic patients.

CD and T1D share HLA risk genotypes. Approximately 90% of individuals with T1D have either DQ2 or DQ8, compared to 40% of the general population. Homozygosity for DR3-DQ2 in the population with T1D carries a 33% risk for the presence of tTG autoantibodies, and conversely, less than 2% of patients lacking DQ2 or DQ8 have CD-related autoantibodies.

In patients with both disorders, GFD prevents a grow failure in children and leads to a better metabolic control of diabetes, although with a slight increase in insulin dose due to correction on the intestinal malabsorption and a higher glycemic index of gluten-free products. Furthermore, GFD has a protective effect on the development of vascular complications in T1D patients. Moreover, T1D and CD have a negative effect on bone metabolism in relation with duration and/or poor control of diabetes, nutritional mechanisms/no compliance to GFD, and immunoregulatory imbalance. In fact, in patients affected by both disorders, osteopenia occurs more frequently in patients with poor compliance to GFD, so that it and the optimization of glycemic control play an important role in preventing the osteopenic status caused by the clustering of these two chronic diseases.

3.2.2. Thyroid Diseases

CD has been found at an increased rate in patients with autoimmune thyroid disease (Grave's disease and Hashimoto's thyroiditis), with a prevalence ranging from 2% to 7%. This same observation has been made in patients with CD, in whom serological signs of autoimmune thyroid disease were found up to 26%, occurrence of thyroid dysfunction was detected in up to 10% of cases, and risk of thyroid disease was estimated 3-fold higher as compared to controls.

It has been described that celiac individuals who are following a GFD may still develop autoimmune thyroid impairment, suggesting that gluten withdrawal does not protect them. By contrast, the decrease of the thyroid antibodies after 2 or 3 years or the normalization of thyroid function after 1 year of GFD has been reported in other studies. These different results may depend on longer duration of GFD in treated patients with CD.

Increased prevalence of CD, autoimmune thyroid disorders, and T1D has been widely reported. Such associations may lead to adverse effects on the growth, metabolism, and fertility, so early detection is necessary to prevent secondary complications to these disorders.

The coexistence of CD and autoimmune thyroid disease has been explained by several mechanisms such as common genetic predisposition and the association of both diseases with the gene encoding cytotoxic T-lymphocyte-associated antigen-4, a gene conferring susceptibility to thyroid autoimmunity. In addition, it has also been demonstrated that tTG-2 IgA antibodies react with thyroid tissue, and this binding could contribute to the development of thyroid disease in CD.

3.2.3. Addison's Disease

Patients with Addison's disease are considered a group at-risk for CD. Several studies had reported a high prevalence of CD among patients with this endocrine disease, ranging from 5% to 12%. Conversely, this association was also confirmed, showing an increased risk of developing Addison's disease among celiac patients (HR 11.4; 95% CI, 4.4–29.6), and it has been described that GFD does not modify the natural history of Addison's disease.

3.3.1. Dermatitis Herpetiformis

Dermatitis herpetiformis (DH) is an inflammatory cutaneous disease, with typical histopathological and immunopathological findings, clinically characterized by intensely pruritic polymorphic lesions with a chronic-relapsing course, first described by Duhring in 1884. In 1966, Marks et al. reported the presence of small bowel changes in DH patients, and later on, these gastrointestinal abnormalities, described in affected patients, were found to be the same as in those with CD. It is now currently considered to be the more common and specific cutaneous manifestation of CD. Its presence is characteristic of this disease, and by consequence, its best treatment is a strict lifelong GFD, for achieving and maintaining a permanent control. It appears in around 25% patients with CD, at any age of life, mainly in adults. It can be considered as the “visiting card” of celiac patients, because its finding appears only in CD individuals.

Primary DH lesions are characterized by the presence of grouped erythematous papules, urticarial plaques, surmounted by vesicles, or also blisters, which may be often replaced by erosions and excoriations, because of the intense itching, characteristically associated with this condition. Chronic pruritus and excoriations might lead to its lichenification (Figures 2 and 3). Furthermore, a postinflammatory hyperpigmentation may occur when the lesion resolves.

The symmetrical distributions of the herpetiform lesions on the extensor surfaces of the elbows (90%), knees (30%), shoulders, middle line of the back, buttocks, and sacral region are the main affected localizations that are the site of constant minor trauma and is also a typical feature of the disease. Anyway, scalp, nuchal area, face, and groins may be also involved. No clinical differences were described between darker and white-skinned individuals, although DH remains primarily predominant in Caucasian population, being rarer in Asian populations, including the Japanese.

Most of the patients suffer not only of itching, but also tickle or burning sensation, even before the onset of the skin lesions. An uncommon skin manifestation of DH is represented by purpuric lesions, occasionally found on palmo-plantar surfaces of children, but rarely reported in adults. Sometimes, petechial lesions on the fingertips may be the only symptom of DH.

However, atypical clinical presentation of DH includes also the presence of palmo-plantar keratosis, wheals of chronic urticarial, and other lesions mimicking prurigo pigmentosa.

The classic histopathological features of DH seen on light microscopy include a subepithelial cleft with neutrophils, that are considered the most likely responsible for the dermoepidermal separation and a few eosinophils at the tips of dermal papillae that are accompanied by a perivascular-mixed inflammatory infiltrate.

The pathophysiology of DH is complex and involves genetic factors such as HLA predisposition (mainly HLA-II, as DQ2, and DQ8), environment trigger (gluten), and dysregulation of the immune system, in predisposed individuals, as occurs in CD patients without skin affectation.

Actually direct immunofluorescence of uninvolved skin biopsies collected in the perilesional site is considered to be the “diagnostic gold standard” for DH. This is because in this location a greater IgA deposition than in nonlesional or lesional skin is found. Two different patterns are found (1) granular deposits in the dermal papillae and (2) Granular deposits along the basement membrane. In both cases, deposits are thought to be polyclonal but are mainly composed of IgA. The two patterns may also be present in combination, resulting in granular IgA deposition along the basement membrane with accentuation at the tips of dermal papillae.

Serologic testing is useful adjunct to tissue-based studies. The patients with DH have positivity for the gluten-induced tTG-2 and tTG-3 autoantibodies, also called tissue-TG (tTG) and epidermal (eTG) respectively, together with the deamidated synthetic gliadin-derived peptides (anti-DGP), more sensitive in children.

A potential explanation of the appearance of DH lesions is related to the presence of an active chronic small bowel mucosal inflammation, as a result of a persistent gluten challenge, with a local immune response and the production of mucosal IgA. A part of the circulating IgA (anti-tTG3) binds to the skin. Consequently, the gastrointestinal immune response results in increased levels of circulating cytokines, which may attract neutrophils, as well as induce an active Th-2 response in the endothelial cells. Ultraviolet beams (UVB) and minor repeated microtrauma to the skin increase the local cytokines production, leading to the egress of neutrophils, deposition of IgA at dermis and thus to the development of the typical skin DH lesions.

Associated AD are more common among DH patients. Family screening for gluten sensitivity is also strongly suggested. Untreated patients should be regularly monitored for malabsorption and lymphomas.

3.3.2. Others

Some cases of alopecia areata associated with CD have been reported. The administration of a GFD to these patients has variable results, and not in all cases, the recovery of hair growth with the diet has been described.

The relationship between vitiligo and CD is controversial. Although some cases of both diseases have been described, this association remains unclear.

Dermatomyositis is a disease characterized by erythematous and edematous changes in the skin and muscle weakness. Some reports have suggested an association between this condition and CD with response to GFD.

3.4. Associated Autoimmune Neurological Diseases

The first study of patients with CD (confirmed by biopsy) and a neurological deficit was published by Cooke and Smith in 1966. Since then, a broad spectrum of neurological manifestations has been related to CD, with a prevalence of approximately 10 to 12%. Gluten ataxia (GA) and peripheral neuropathy are the more common related disorders, and these neurological manifestations can present even in the absence of an enteropathy.

GA can be defined as sporadic ataxia triggered by the ingestion of gluten, with positive serum antigliadin antibodies with or without enteropathy on duodenal biopsy. This disease usually presents with pure cerebellar ataxia or, rarely in combination with myoclonus, palatal tremor or opsoclonus myoclonus. In a study by Hadjivassiliou et al., these authors reported that GA accounted for 36% of cases of idiopathic sporadic ataxia; 72% of these patients had HLA-DQ2, but only 24% of them had gluten-sensitive enteropathy, and only 13% reported gastrointestinal symptoms.

Peripheral neuropathy related to CD is a symmetrical sensorimotor axonal neuropathy and usually presents with burning, tingling, and numbness in hands and feet, with distal sensory loss. It has been described that gluten sensitivity may be the etiology of 34% of cases with idiopathic neuropathy, with a prevalence of biopsy-verified CD at least 9% and presence of HLA types associated with CD in 80% of patients. In a large study with patients from the Swedish national register, the association between CD and later polyneuropathy was confirmed (HR 3.4; 95% CI, 2.3–5.1), and conversely, prior polyneuropathy was a risk factor for subsequent CD (OR 5.4; 95% CI, 3.6–8.2).

One of the mechanisms involved in the GA pathogenesis may be the antibody cross-reactivity between antigenic epitopes on Purkinje cells and gluten proteins. Additionally, while the development of anti-tTG-2 IgA is linked with CD, an anti-tTG-6 IgG and IgA response is prevalent in GA, independent of intestinal involvement. It has been shown that in those patients with ataxia and enteropathy, separate antibody populations react with the two different transglutaminase isozymes. Postmortem analysis of brain tissue showed cerebellar IgA deposits that contained TG-6. So, these antibodies are gluten dependent and appear to be a sensitive and specific marker of GA, and it has been seen that their titers diminish or disappear with GFD.

Antibodies to gangliosides and Purkinje cells have been reported in celiac patients with neuropathy and ataxia, but the pathogenic role of this finding has not been clearly demonstrated.

Early diagnosis and treatment with a GFD can improve both neurological manifestations, although this effect has not been seen in all cases. The response to a diet may depend on the duration of the disorder prior to diagnosis of gluten sensitivity. Loss of Purkinje cells in cerebellum as result of prolonged gluten exposure is irreversible. By contrast, an early treatment is most likely to reverse or stabilize the neurological disease.

Other neurological disorders such as demyelinating diseases have also been described to be associated with CD. The first mention of a possible relationship between CD and multiple sclerosis is recorded in 1965. In a Spanish study, the estimated prevalence of CD in patients with multiple sclerosis was 11%, although this association was not confirmed in other series. Only in a small number of sporadic cases, the combination CD and neuromyelitis optica was found. GFD is recommended for both disorders, although the long-term neurological response with the diet is not clear.

3.5.1. Sjogren's Syndrome

Sjogren's syndrome (SS) is an autoimmune disease characterized by lymphocytic infiltration and malfunction of exocrine glands that presents with sicca symptoms of mucosa surfaces. Systemic manifestations results from cutaneous, respiratory, renal, hepatic, neurologic, and vascular involvement, with a high risk for progression to lymphoma.

Findings of several studies had shown a significant association between SS and CD, confirmed by small bowel disease, with a prevalence rate of CD among patients with SS in the range of 4.5% to 15%. Successful treatment of CD did not relieve sicca symptoms or signs; thus, the two diseases must be treated independently.

3.5.2. Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is a multisystem disorder with manifestations including rash, arthritis, cytopenia, and renal disease.

Some case reports have suggested the association between CD and SLE. In a recent study, the aim was to investigate the risk of this disease in a nationwide cohort of patients with biopsy-verified CD compared to controls matched from the general population. The conclusion was that celiac patients were at 3-fold increased risk of developing SLE, but absolute risk was low. This is striking because both disorders share the human leukocyte HLA-B8 and HLA-DR3 histocompatibility antigens, and a variety of antibodies including the detection of tTG IgA, antinuclear, and antidouble-stranded DNA antibodies. Furthermore, it has been shown that SLE may develop later in the clinical course of de CD, even after a small bowel biopsy response to a GFD.

3.5.3. Juvenile Idiopathic Arthritis and Rheumatoid Arthritis

The term juvenile idiopathic arthritis (JIA) describes a clinically heterogeneous group of autoimmune arthritides characterized by chronic synovitis, which begin before 16 years of age and may be accompanied by other extraarticular manifestations as fever, rash, pericarditis, and uveitis.

Other associated ADs, such as CD, have been previously described in patients with JIA, with a prevalence rate of 2.5% to 7%. Moreover, a significantly increased cases of JIA in first-grade relatives of celiac patients have been found.

Conversely, the relationship between CD and rheumatoid arthritis (RA) has not been demonstrated. In the majority of studies, RA was reported as an associated diagnosis in patients with CD in a lower percentage than controls.

3.6.1. Cardiological Diseases

Dilated cardiomyopathy (DCM) is defined by the presence of left ventricular dilatation and left ventricular systolic dysfunction in the absence of abnormal loading conditions (hypertension, valvular disease) or coronary artery disease sufficient to cause global systolic impairment. Familial and acquired forms have been described, and the latter is related with nutritional deficiencies, endocrine disorders, cardiotoxic drugs, excessive alcohol intake, pregnancy, or infections. Some observations also suggest that immunologic factors might be involved in the pathophysiology of DCM.

An increased prevalence of CD (up to 5.7%) has been recently recognized in patients with idiopathic DCM. Conversely, in a recent nationwide study, it was found that patients with CD had a moderately but not statistically significantly increased risk of idiopathic DCM (HR 1.73; 95% CI, 1.00–3.00). In these patients, a GFD may have a beneficial effect with improvement of echocardiographic parameters as well as in cardiological features and quality of life.

The positive association between CD and DCM may be explained by nutritional deficiencies (iron, carnitine), but also both conditions might be mediated through inflammation and autoimmune mechanisms. CD causes abnormalities of intestinal permeability, leading to an increased systemic absorption of various luminal antigens and infectious agents, which may cause myocardial damage through immune-mediated mechanisms. Myocardial injury can also be attributed to immune response cross-reactivity against antigens present in the small intestine and the myocardium.

A possible association between CD and pericarditis has been described, but only limited to a small number of case-reports with good response with GFD. However, at present, this relationship has not been clearly demonstrated.

3.6.2. Psoriasis

Psoriasis is a chronic and relapsing inflammatory disorder of the skin characterised by scaling, erythema, and less commonly postulation and was reported to be associated with systemic comorbidities.

Patients with psoriasis were found to have significantly higher rates of CD than the general population, with a prevalence reaching up to 4.34% in this group of patients. It has also been reported that in some cases a GFD may improve the skin lesions with no additional pharmacological treatment, particularly in patients with CD-associated antibodies, and these same patients may experience flare-ups with the reintroduction of this protein in the diet.

A recent nationwide cohort study has confirmed CD as a risk factor for developing psoriasis with a HR of 1.72 (95% CI, 1.54–1.92). But in this study, it is noteworthy that this association between CD and psoriasis was found to be independent of a temporal relationship, and this increased risk of developing psoriasis was seen both before and after CD diagnosis.

Several mechanisms might explain the positive association between both diseases, including increased and impaired intestinal permeability, vitamin D deficiency due to malabsorption in CD that predisposes to psoriasis and exposure to gliadin as a trigger factor for CD4 + T-cell response.

3.6.3. Sarcoidosis

Sarcoidosis is a chronic idiopathic granulomatous disease as a consequence of altered immune response to unidentified antigens. Sarcoidosis mainly involves the lungs, even though other organs may be affected.

Sarcoidosis has been associated with different autoimmune disorders and among them with CD, as both diseases seem to share some immunological and genetic disorders. CD has been associated with an increased risk of sarcoidosis (HR 4.03; 95% CI, 2.32–7.00). Similarly, a prior sarcoidosis diagnosis is associated with an increased risk of CD (OR 3.58; 95% CI, 1.98–6.45).

3.6.4. Hematological Disorders

Idiopathic thrombocytopenic purpura (ITP) is an autoantibody-mediated condition characterized by an abnormally low number of platelets in the circulating blood.

The first report of an association between ITP and CD was made in 1982. Since then, other cases have been published linking these two diseases, and it has been suggested that the common mechanism may be genetic through HLA system. A recent cohort study also found that individuals with CD had an increased risk of ITP (HR 1.91; 95% CI, 1.19–3.11).

3.6.5. Thromboembolic Phenomena

CD is associated with hypercoagulability status. Thromboembolism, pregnancy loss, small bowel infarction, atrial fibrillation, Budd-Chiari syndrome, portal and splenic vein thrombosis, and cardiovascular disease have been described in celiac patients. Several mechanisms have been implicated in these thromboembolic disorders such as hyperhomocysteinemia in untreated CD, methylenetetrahydrofolate reductase variants, the high homology between factor XIII and tTG, protein C and S deficiencies due to vitamin K malabsorption, and high levels of thrombin-activatable fibrinolysis inhibitor. Recently, it has been suggested that intestinal injury, endothelial dysfunction, platelet abnormalities, and enhanced apoptosis cause increased exposure of phospholipids or new epitopes, which are the origin of antiphospholipid, antiprothrombin, and antiphosphatidylserine/prothrombin autoantibodies. The levels and activities of these antibodies are increased in celiac patients and might also play a pathogenic role in the thrombophilia associated with this disease.

3.6.6. Pancreatic Disease

It has been described that patients with CD have an increased risk of both acute and chronic pancreatitis, with an HR for gallstone-related acute pancreatitis of 1.59 (95% CI, 1.06–2.40), for nongallstone-related acute pancreatitis of 1.86 (95% CI, 1.52–2.26), for chronic pancreatitis of 3.33 (95% CI, 2.33–4.76), and for supplementation with pancreatic enzymes of 5.34 (95% CI, 2.99–9.53). The risk of any pancreatitis within 5 years of CD diagnosis was estimated in 2.76 (95% CI, 2.36–3.22). It is noteworthy that exocrine pancreatic insufficiency is associated with persisting diarrhea in adult celiac patients.

The mechanisms that may be involved in the relationship between pancreatic disease and CD including impaired secretion of pancreatitis stimulating hormones from the diseased small bowel, alterations in enteric endocrine cells, reduction in precursors for pancreatic enzyme synthesis, structural changes in the pancreas with atrophy of acinar cells and fibrosis of the gland resulting in impaired pancreatic exocrine function, papillary stenosis and shared immunologic traits in both diseases. By contrast, the relationship between autoimmune pancreatitis and CD has not been demonstrated, since there is only so far a case report of this association.

3.6.7. Microscopic Colitis

Some case reports and series have shown an association between CD and microscopic colitis. Up to 15% of patients with collagenous or lymphocytic colitis have CD, and conversely, microscopic colitis was found in 4% of celiac patients representing up to a 70-fold increased risk for individuals with CD compared with the general population. Therefore, CD should be excluded in all patients with microscopic colitis, particularly if diarrhea does not respond to conventional treatment.

4. Enteropathy-Associated T-cell Lymphoma and Celiac Disease

CD is also characterized by an increased mortality. It is well known that this fact is mainly the result of the complications of CD itself, represented by refractory CD (RCD) and enteropathy-associated T-cell lymphoma (EATL). This is a rare complication (<1% of lymphomas) and has a poor prognosis.

RCD is a form of CD that does not respond histologically to at least 12 months of a strict GFD. This can also evolve in patients who initially responded normally to a GFD and who are still maintaining a strict GFD. On the basis of IELs population, RCD is further classified into type 1 and type 2. RCD type 1 (RCD1) is characterized by persisting villous atrophy despite a strict GFD associated with increased but still phenotypically normal IELs. Conversely, a clonal expansion of abnormal IELs lacking surface CD3, CD8, and TCR markers, but expressing intracellular CD3, indicates RCD type 2 (RCD2), a condition that frequently evolves into EATL, the most serious complication of CD. Nevertheless, the RCD prevalence is low, being estimated to appear in around 1% of CD patients.

For RCD prognosis, there are no doubts that it is much worse than that of uncomplicated CD. The 5-year survival rate is reported to be between 80% and 96% in patients with RCD1, but it is only between 40% and 58% in patients with RCD2. Five-year survival dropped to between 8% and 20% in RCD2 patients who developed EATL.

Although the incidence of EATL was reported to be rare in the general population (1 per 106 person-years), it was shown that it occurs in 60% to 80% of patients with RCD2 within 5 years. The description of EATL arising in patients with RCD1 seems to be exceptional. Recent evidence suggests that non-EATLs, including intestinal B-cell and extraintestinal T-cell lymphomas, may rarely occur in celiac patients.

EATL manifests in adult patients with previously diagnosed CD, successfully treated until then with a strict GFD (secondary EATL), as an exacerbation of the classic symptoms of CD, such as abdominal pain, diarrhea, and unexplained weight loss. The concomitant presence of fever and night sweating, together with laboratory parameters indicative for hypoalbuminemia, anemia, and increased lactate dehydrogenase (LDH), should alert physicians to this complication. The median age at diagnosis of EATL is 60 years, with similar frequency between men and women. On the other hand, EATL may also arise in patients without a known history of CD and on a gluten-containing diet (primary EATL), and in these cases, the diagnosis is more difficult and delayed because of the low specificity of symptoms and the very low index of clinical suspicion. In the subjects with EATL identified before CD has been diagnosed, the link between CD and EATL may be suggested by the detection of CD-specific antibodies (either EMAs or anti-tTG), although the latter often disappears once the refractory state is fully developed.

Because EATL may be complicated by gastrointestinal perforation, obstruction, or hemorrhage, many EATLs are diagnosed at laparotomy. At gross examination, EATL appears as a massive tumor infiltration, which may be transparietal with ulcerations and induration of the intestinal wall. Up to 25% of cases have a multifocal presentation, and the proximal small bowel, particularly the jejunum, is a more common localization than the large bowel or rectum. There are reports of an association between EATL and peripheral eosinophilia, mesenteric lymph node cavitation, or splenic atrophy, the latter of which may increase susceptibility to severe infections or sepsis. Malnutrition is a common feature, especially when EATL has an insidious and chronic presentation or manifests after a long-standing RCD. Extraintestinal presentation of EATL is rare, and there is a lack of data on the precise characteristics of its cutaneous, neuromeningeal, or pulmonary manifestations. Systemic or B symptoms, such as fever of no evident cause, night sweats, and weight loss of more than 10% of body weight, should be taken as signs of clinical progression, although they occur in less than 30% of EATLs. A high level of clinical suspicion for an overt lymphoma should lead to an extensive workup, including abdominal imaging, endoscopy, and histologic examination of gut biopsies. Laparotomy with collection of full-thickness biopsy specimens may be necessary in some cases.

Poor adherence to a GFD, HLA-DQ2 homozygosity, and late diagnosis of CD are recognized as risk factors for malignant evolution of CD. The suspicion of EATL should lead to an extensive diagnostic workup in which magnetic resonance enteroclysis, positron emission tomography scan, and histologic identification of lesions represent the best options. Treatment includes high-dose chemotherapy preceded by surgical resection and followed by autologous stem cell transplantation, although biologic therapies seem to be promising. Strict adherence to a GFD remains the only way to prevent EATL.

References 236

  1. 1.
    Spectrum of gluten-related disorders: consensus on new nomenclature and classification · 2012
    No notice
  2. 2.

    Ludvigsson JF, Leffler DA, Bai JC, et al. The Oslo definitions for celiac disease and related terms. Gut. 2013;62(1):43-52.

    Not in our library10.1136/gutjnl-2011-301346

  3. 3.

    Collin P, Reunala T, Pukkala E, Laippala P, Keyriläinen O, Pasternack A. Coeliac disease—associated disorders and survival. Gut. 1994;35(9):1215-1218.

    Not in our library10.1136/gut.35.9.1215

  4. 4.

    Fasano A, Berti I, Gerarduzzi T, et al. Prevalence of Celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study. Archives of Internal Medicine. 2003;163(3):286-292.

    Not in our library10.1001/archinte.163.3.286

  5. 5.

    Cataldo F, Marino V. Increased prevalence of autoimmune diseases in first-degree relatives of patients with celiac disease. Journal of Pediatric Gastroenterology and Nutrition. 2003;36(4):470-473.

    Not in our library10.1097/00005176-200304000-00009

  6. 6.

    Viljamaa M, Kaukinen K, Huhtala H, Kyrönpalo S, Rasmussen M, Collin P. Coeliac disease, autoimmune diseases and gluten exposure. Scandinavian Journal of Gastroenterology. 2005;40(4):437-443.

    Not in our library10.1080/00365520510012181

  7. 7.

    Neuhausen SL, Steele L, Ryan S, et al. Co-occurrence of celiac disease and other autoimmune diseases in celiacs and their first-degree relatives. Journal of Autoimmunity. 2008;31(2):160-165.

    Not in our library10.1016/j.jaut.2008.06.001

  8. 8.

    Cosnes J, Cellier C, Viola S, et al. Incidence of autoimmune diseases in celiac disease: protective effect of the gluten-free diet. Clinical Gastroenterology and Hepatology. 2008;6(7):753-758.

    Not in our library10.1016/j.cgh.2007.12.022

  9. 9.

    Stagi S, Giani T, Simonini G, Falcini F. Thyroid function, autoimmune thyroiditis and coeliac disease in juvenile idiopathic arthritis. Rheumatology. 2005;44(4):517-520.

    Not in our library10.1093/rheumatology/keh531

  10. 10.

    Triolo TM, Armstrong TK, McFann K, et al. Additional autoimmune disease found in 33% of patients at type 1 diabetes onset. Diabetes Care. 2011;34(5):1211-1213.

    Not in our library10.2337/dc10-1756

  11. 11.

    Sumnik Z, Cinek O, Bratanic N, et al. Risk of celiac disease in children with type 1 diabetes is modified by positivity for HLA-DQB1*02-DQA1*05 and TNF-308A. Diabetes Care. 2006;29(4):858-863.

    Not in our library10.2337/diacare.29.04.06.dc05-1923

  12. 12.

    Auricchio R, Paparo F, Maglio M, et al. In vitro-deranged intestinal immune response to gliadin in type 1 diabetes. Diabetes. 2004;53(7):1680-1683.

    Not in our library10.2337/diabetes.53.7.1680

  13. 13.

    Troncone R, Franzese A, Mazzarella G, et al. Gluten sensitivity in a subset of children with insulin dependent diabetes mellitus. American Journal of Gastroenterology. 2003;98(3):590-595.

    Not in our library10.1111/j.1572-0241.2003.07301.x

  14. 14.

    Visser J, Rozing J, Sapone A, Lammers K, Fasano A. Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms. Annals of the New York Academy of Sciences. 2009;1165:195-205.

    Not in our library10.1111/j.1749-6632.2009.04037.x

  15. 15.

    Lammers KM, Lu R, Brownley J, et al. Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3. Gastroenterology. 2008;135(1):194-204.

    Not in our library10.1053/j.gastro.2008.03.023

  16. 16.

    Fasano A. Systemic autoimmune disorders in celiac disease. Current Opinion in Gastroenterology. 2006;22(6):674-679.

    Not in our library10.1097/01.mog.0000245543.72537.9e

  17. 17.

    Shewry RP, Tatham AS, Kasarda DD, Marsh M. Cereal proteins and coeliac disease. Coeliac Disease. 1992.

    Not in our library

  18. 18.
    Nomenclature and listing of celiac disease relevant gluten T-cell epitopes restricted by HLA-DQ molecules · 2012
    No notice
  19. 19.

    Seah PP, Fry L, Rossiter MA, Hoffbrand AV, Holborow EJ. Anti-reticulin antibodies in childhood coeliac disease. The Lancet. 1971;2(7726):681-682.

    Not in our library10.1016/s0140-6736(71)92248-3

  20. 20.

    Ladinser B, Rossipal E, Pittschieler K. Endomysium antibodies in coeliac disease: an improved method. Gut. 1994;35(6):776-778.

    Not in our library10.1136/gut.35.6.776

  21. 21.

    Dieterich W, Ehnis T, Bauer M, et al. Identification of tissue transglutaminase as the autoantigen of celiac disease. Nature Medicine. 1997;3(7):797-801.

    Not in our library10.1038/nm0797-797

  22. 22.

    Aggarwal S, Lebwohl B, Green PHR. Screening for celiac disease in average-risk and high-risk populations. Therapeutic Advances in Gastroenterology. 2012;5(1):37-47.

    Not in our library10.1177/1756283x11417038

  23. 23.

    Lionetti E, Catassi C. New clues in celiac disease epidemiology, pathogenesis, clinical manifestations, and treatment. International Reviews of Immunology. 2011;30(4):219-231.

    Not in our library10.3109/08830185.2011.602443

  24. 24.

    Sollid LM, Markussen G, Ek J, Gjerde H, Vartdal F, Thorsby E. Evidence for a primary association of celiac disease to a particular HLA-DQ α/β heterodimer. Journal of Experimental Medicine. 1989;169(1):345-350.

    Not in our library10.1084/jem.169.1.345

  25. 25.

    Fallang L-E, Bergseng E, Hotta K, Berg-Larsen A, Kim C-Y, Sollid LM. Differences in the risk of celiac disease associated with HLA-DQ2.5 or HLA-DQ2.2 are related to sustained gluten antigen presentation. Nature Immunology. 2009;10(10):1096-1101.

    Not in our library10.1038/ni.1780

  26. 26.

    Sulkanen S, Halttunen T, Laurila K, et al. Tissue transglutaminase autoantibody enzyme-linked immunosorbent assay in detecting celiac disease. Gastroenterology. 1998;115(6):1322-1328.

    Not in our library10.1016/s0016-5085(98)70008-3

  27. 27.

    Molberg O, Kett K, Scott H, Thorsby E, Sollid LM, Lundin KEA. Gliadin specific, HLA DQ2-restricted T cells are commonly found in small intestinal biopsies from coeliac disease patients, but not from controls. Scandinavian Journal of Immunology. 1997;46(1):103-108.

    Not in our library

  28. 28.

    Terrazzano G, Sica M, Gianfrani C, et al. Gliadin regulates the NK-dendritic cell cross-talk by HLA-E surface stabilization. Journal of Immunology. 2007;179(1):372-381.

    Not in our library10.4049/jimmunol.179.1.372

  29. 29.

    de Bellis A, Bizzarro A, Pivonello R, Lombardi G, Bellastella A. Prolactin and autoimmunity. Pituitary. 2005;8(1):25-30.

    Not in our library10.1007/s11102-005-5082-5

  30. 30.

    Shelly S, Boaz M, Orbach H. Prolactin and autoimmunity. Autoimmunity Reviews. 2012;11(6-7):A465-A470.

    Not in our library10.1016/j.autrev.2011.11.009

  31. 31.

    Reifen R, Buskila D, Maislos M, Press J, Lerner A. Serum prolactin in coeliac disease: a marker for disease activity. Archives of Disease in Childhood. 1997;77(2):155-157.

    Not in our library10.1136/adc.77.2.155

  32. 32.

    Kapur G, Patwari AK, Narayan S, Anand VK. Serum prolactin in celiac disease. Journal of Tropical Pediatrics. 2004;50(1):37-40.

    Not in our library10.1093/tropej/50.1.37

  33. 33.

    Hunt KA, van Heel DA. Recent advances in coeliac disease genetics. Gut. 2009;58(4):473-476.

    Not in our library10.1136/gut.2008.155879

  34. 34.

    Trynka G, Hunt KA, Bockett NA, et al. Dense genotyping identifies and localizes multiple common and rare variant association signals in celiac disease. Nature Genetics. 2011;43(12):1193-1201.

    Not in our library10.1038/ng.998

  35. 35.

    Kumar V, Wijmenga G, Withoff S. From genome-wide associations studies to disease mechanisms: celiac disease as a model of autoimmune diseases. Seminars in Immunopathology. 2012;34(4):567-580.

    Not in our library10.1007/s00281-012-0312-1

  36. 36.

    Romanos J, Rosén A, Kumar V, et al. Improving coeliac disease risk prediction by testing non-HLA variants additional to HLA variants. Gut. 2013.

    Not in our library10.1136/gutjnl-2012-304110

  37. 37.

    Anaya J-M, Kim-Howard X, Prahalad S, et al. Evaluation of genetic association between an ITGAM non-synonymous SNP (rs1143679) and multiple autoimmune diseases. Autoimmunity Reviews. 2012;11(4):276-280.

    Not in our library10.1016/j.autrev.2011.07.007

  38. 38.

    Zhernakova A, van Diemen CC, Wijmenga C. Detecting shared pathogenesis from the shared genetics of immune-related diseases. Nature Reviews Genetics. 2009;10(1):43-55.

    Not in our library10.1038/nrg2489

  39. 39.

    Gutierrez-Achury J, Coutinho de Almeida R, Wijmenga C. Shared genetics in coeliac disease and other immune-mediated diseases. Journal of Internal Medicine. 2011;269(6):591-603.

    Not in our library10.1111/j.1365-2796.2011.02375.x

  40. 40.

    Larizza D, Calcaterra V, Klersy C, et al. Common immunogenetic profile in children with multiple autoinmune diseases: the signature of HLA-DQ pleiotropic genes. Autoimmunity. 2012;45(6):470-475.

    Not in our library10.3109/08916934.2012.697594

  41. 41.

    Hagander B, Berg NO, Brandt L, Nordén A, Sjo"lund K, Stenstam M. Hepatic injury in adult coeliac disease. The Lancet. 1977;2(8032):270-272.

    Not in our library10.1016/s0140-6736(77)90954-0

  42. 42.

    Bardella MT, Fraquelli M, Quatrini M, Molteni N, Bianchi P, Conte D. Prevalence of hypertransaminasemia in adult celiac patients and effect of gluten-free diet. Hepatology. 1995;22(3):833-836.

    Not in our library

  43. 43.

    Sainsbury A, Sanders DS, Ford AC. Meta-analysis: coeliac disease and hypertransaminasaemia. Alimentary Pharmacology and Therapeutics. 2011;34(1):33-40.

    Not in our library10.1111/j.1365-2036.2011.04685.x

  44. 44.

    Vajro P, Paolella G, Maggiore G, Giordano G. Meta-analysis: pediatric celiac disease, cryptogenic hypertransaminasemia, and autoimmune hepatitis. Journal of Pediatric Gastroenterology and Nutrition. 2013.

    Not in our library10.1097/mpg.0b013e31828dc5c5

  45. 45.

    Volta U, de Franceschi L, Lari F, Molinaro N, Zoli M, Bianchi FB. Coeliac disease hidden by cryptogenic hypertransaminasaemia. The Lancet. 1998;352(9121):26-29.

    Not in our library10.1016/s0140-6736(97)11222-3

  46. 46.

    Bardella MT, Vecchi M, Conte D, et al. Chronic unexplained hypertransaminasemia may be caused by occult celiac disease. Hepatology. 1999;29(3):654-657.

    Not in our library10.1002/hep.510290318

  47. 47.

    Ludvigsson JF, Elfström P, Broomé U, Ekbom A, Montgomery SM. Celiac disease and risk of liver disease: a general population-based study. Clinical Gastroenterology and Hepatology. 2007;5(1):63-69.

    Not in our library10.1016/j.cgh.2006.09.034

  48. 48.

    Mounajjed T, Oxentenko A, Shmidt E, Smyrk T. The liver in celiac disease: clinical manifestations, histologic features, and response to gluten-free diet in 30 patients. American Journal of Clinical Pathology. 2011;136(1):128-137.

    Not in our library10.1309/ajcpdomy5ri5tpmn

  49. 49.

    Logan RFA, Ferguson A, Finlayson NDC, Weir DG. Primary biliary cirrhosis and coeliac disease. An association? The Lancet. 1978;1(8058):230-233.

    Not in our library10.1016/s0140-6736(78)90480-4

  50. 50.

    Dickey W, McMillan SA, Callender ME. High prevalence of celiac spree among patients with primary biliary cirrhosis. Journal of Clinical Gastroenterology. 1997;25(1):328-329.

    Not in our library10.1097/00004836-199707000-00006

  51. 51.

    Kingham JGC, Parker DR. The association between primary biliary cirrhosis and coeliac disease: a study of relative prevalences. Gut. 1998;42(1):120-122.

    Not in our library10.1136/gut.42.1.120

  52. 52.

    Floreani A, Betterle C, Baragiotta A, et al. Prevalence of coeliac disease in primary biliary cirrhosis and of antimitochondrial antibodies in adult coeliac disease patients in Italy. Digestive and Liver Disease. 2002;34(4):258-261.

    Not in our library10.1016/s1590-8658(02)80145-1

  53. 53.

    Sørensen HT, Thulstrup AM, Blomqvist P, Nørgaard B, Fonager K, Ekbom A. Risk of primary biliary liver cirrhosis in patients with coeliac disease: Danish and Swedish cohort data. Gut. 1999;44(5):736-738.

    Not in our library10.1136/gut.44.5.736

  54. 54.

    Lawson A, West J, Aithal GP, Logan RFA. Autoimmune cholestatic liver disease in people with coeliac disease: a population-based study of their association. Alimentary Pharmacology and Therapeutics. 2005;21(4):401-405.

    Not in our library10.1111/j.1365-2036.2005.02328.x

  55. 55.

    Volta U, Caio G, Tovoli F, de Giorgio R. Gut-liver axis: an immune link between celiac disease and primary biliary cirrhosis. Expert Review in Gastroenterology & Hepatology. 2013;7(3):253-261.

    Not in our library10.1586/egh.13.5

  56. 56.

    Villalta D, Girolami D, Bidoli E, et al. High prevalence of celiac disease in autoimmune hepatitis detected by anti-tissue tranglutaminase autoantibodies. Journal of Clinical Laboratory Analysis. 2005;19(1):6-10.

    Not in our library10.1002/jcla.20047

  57. 57.

    Volta U, de Franceschi L, Molinaro N, et al. Frequency and significance of anti-gliadin and anti-endomysial antibodies in autoimmune hepatitis. Digestive Diseases and Sciences. 1998;43(10):2190-2195.

    Not in our library10.1023/a:1026650118759

  58. 58.

    Panetta F, Nobili V, Sartorelli MR, et al. Celiac disease in pediatric patients with autoimmune hepatitis: etiology, diagnosis, and management. Pediatric Drugs. 2012;14(1):35-41.

    Not in our library10.2165/11593150-000000000-00000

  59. 59.

    di Biase AR, Colecchia A, Scaioli E, et al. Autoimmune liver diseases in a paediatric population with coeliac disease—a 10-year single-centre experience. Alimentary Pharmacology and Therapeutics. 2010;31(2):253-260.

    Not in our library10.1111/j.1365-2036.2009.04186.x

  60. 60.

    Nastasio S, Sciveres M, Riva S, Filippeschi IP, Vajro P, Maggiore G. Celiac disease-associated autoimmune hepatitis in childhood: long-term response to treatment. Journal of Pediatric Gastroenterology and Nutrition. 2013;56(6):671-674.

    Not in our library10.1097/mpg.0b013e31828b1dfa

  61. 61.

    Hay JE, Wiesner RH, Shorter RG, LaRusso NF, Baldus WP. Primary sclerosing cholangitis and celiac disease. A novel association. Annals of Internal Medicine. 1988;109(9):713-717.

    Not in our library10.7326/0003-4819-109-9-713

  62. 62.

    Schrumpf E, Abdelnoor M, Fausa O, Elgjo K, Jenssen E, Kolmannskog F. Risk factors in primary sclerosing cholangitis. Journal of Hepatology. 1994;21(6):1061-1066.

    Not in our library10.1016/s0168-8278(05)80618-x

  63. 63.

    Volta U, Rodrigo L, Granito A, et al. Celiac disease in autoimmune cholestatic liver disorders. American Journal of Gastroenterology. 2002;97(10):2609-2613.

    Not in our library10.1111/j.1572-0241.2002.06031.x

  64. 64.

    Brazier F, Delcenserie R, Sevestre H, Delamarre J, Capron J-P. Primary sclerosing cholangitis and coeliac disease: beneficial effect of gluten-free diet on the liver. European Journal of Gastroenterology and Hepatology. 1994;6(2):183-186.

    Not in our library

  65. 65.

    Cadahía V, Rodrigo L, Fuentes D, Riestra S, de Francisco R, Fernández M. Celiac disease (CD), ulcerative colitis (UC), and primary sclerosing cholangitis (PSC) in one patient: a family study. Revista Espanola de Enfermedades Digestivas. 2005;97(12):907-913.

    Not in our library10.4321/s1130-01082005001200007

  66. 66.

    Bardella MT, Valenti L, Pagliari C, et al. Searching for coeliac disease in patients with non-alcoholic fatty liver disease. Digestive and Liver Disease. 2004;36(5):333-336.

    Not in our library10.1016/j.dld.2004.01.012

  67. 67.

    Iacono OL, Petta S, Venezia G, et al. Anti-tissue transglutaminase antibodies in patients with abnormal liver tests: is it always coeliac disease? American Journal of Gastroenterology. 2005;100(11):2472-2477.

    Not in our library10.1111/j.1572-0241.2005.00244.x

  68. 68.

    Miele L, Valenza V, la Torre G, et al. Increased intestinal permeability and tight junction alterations in nonalcoholic fatty liver disease. Hepatology. 2009;49(6):1877-1887.

    Not in our library10.1002/hep.22848

  69. 69.

    Drastich P, Honsová E, Lodererová A, et al. Celiac disease markers in patients with liver diseases: a single center large scale screening study. World Journal of Gastroenterology. 2012;18(43):6255-6262.

    Not in our library10.3748/wjg.v18.i43.6255

  70. 70.

    Ince AT, Kayadibi H, Soylu A, et al. Serum copper, ceruloplasmin and 24-h urine copper evaluations in celiac patients. Digestive Diseases and Sciences. 2008;53(6):1564-1572.

    Not in our library10.1007/s10620-007-0043-7

  71. 71.

    Marteau P, Cadranel J-F, Messing B, Gargot D, Valla D, Rambaud J-C. Association of hepatic vein obstruction and coeliac disease in North African subjects. Journal of Hepatology. 1994;20(5):650-653.

    Not in our library10.1016/s0168-8278(05)80355-1

  72. 72.

    Afredj N, Metatla S, Faraoun SA, et al. Association of Budd-Chiari syndrome and celiac disease. Gastroenterologie Clinique et Biologique. 2010;34(11):621-624.

    Not in our library10.1016/j.gcb.2010.07.007

  73. 73.

    Kochhar R, Masoodi I, Dutta U, et al. Celiac disease and Budd Chiari syndrome: report of a case with review of literature. European Journal of Gastroenterology and Hepatology. 2009;21(9):1092-1094.

    Not in our library10.1097/meg.0b013e328328f47f

  74. 74.

    Manzano ML, Garfia C, Manzanares J, et al. Celiac disease and Bud-Chiari syndrome: an uncommon association. Gastroenterologia y Hepatologia. 2002;25(3):159-161.

    Not in our library

  75. 75.

    Lerner A, Agmon-Levin N, Shapira Y, et al. The thrombophilic network of autoantibodies in celiac disease. BMC Medicine. 2013;11, article 89.

    Not in our library10.1186/1741-7015-11-89

  76. 76.

    Greco D, Pisciotta M, Gambina F, Maggio F. Celiac disease in subjects with type 1 diabetes mellitus: a prevalence study in western Sicily (Italy). Endocrine. 2013;43(1):108-111.

    Not in our library10.1007/s12020-012-9718-8

  77. 77.

    Cerutti F, Bruno G, Chiarelli F, Lorini R, Meschi F, Sacchetti C. Younger age at onset and sex predict celiac disease in children and adolescents with type 1 diabetes: an Italian multicenter study. Diabetes Care. 2004;27(6):1294-1298.

    Not in our library10.2337/diacare.27.6.1294

  78. 78.

    Mahmud FH, Murray JA, Kudva YC, et al. Celiac disease in type 1 diabetes melittus in a North American community: prevalence, serologic screening, and clinical features. Mayo Clinic Proceedings. 2005;80(11):1429-1434.

    Not in our library10.4065/80.11.1429

  79. 79.

    Salardi S, Volta U, Zucchini S, et al. Prevalence of celiac disease in children with type 1 diabetes mellitus increased in the mid-1990s: an 18-year longitudinal study based on anti-endomysial antibodies. Journal of Pediatric Gastroenterology and Nutrition. 2008;46(5):612-614.

    Not in our library10.1097/mpg.0b013e31815d697e

  80. 80.

    Vicuña Arregui M, Zozaya Urmeneta JM, Martínez de Esteban JP, et al. Study of celiac disease in adults with type 1 diabetes mellitus. Gastroenterologia y Hepatologia. 2010;33(1):6-11.

    Not in our library10.1016/j.gastrohep.2009.07.010

  81. 81.

    Simsek DG, Aycan Z, Ozen S, et al. Diabetes care, glycemic control, complications, and concomitant autoimmune diseases in children with type 1 diabetes in Turkey: a multicenter study. Journal of Clinical Research in Pediatric Endocrinology. 2013;22(5):20-26.

    Not in our library10.4274/jcrpe.893

  82. 82.

    Pham-Short A, Donaghue KC, Ambler G, Chan AK, Craig ME. Coeliac disease in type 1 diabetes from 1990 to 2009: higher incidence in young children after longer diabetes duration. Diabetic Medicine. 29(9);e.286-e.289.

    Not in our library10.1111/j.1464-5491.2012.03720.x

  83. 83.

    Tiberti C, Panimolle F, Bonamico M, et al. IgA anti-transglutaminase autoantibodies at type 1 diabetes onset are less frequent in adult patients and are associated with a general celiac-specific lower immune response in comparison with nondiabetic celiac patients at diagnosis. Diabetes Care. 2012;35(10):2083-2085.

    Not in our library10.2337/dc11-2171

  84. 84.

    Ludvigsson JF, Ludvigsson J, Ekbom A, Montgomery SM. Celiac disease and risk of subsequent type 1 diabetes: a general population cohort study of children and adolescents. Diabetes Care. 2006;29(11):2483-2488.

    Not in our library10.2337/dc06-0794

  85. 85.

    Husby S, Koletzko S, Korponay-Szabó IR. European Society for Pediatric Gastroenterology, Hepatology, and Nutrition guidelines for the diagnosis of coeliac disease. Journal of Pediatric Gastroenterology and Nutrition. 2012;54(4):572-573.

    Not in our library10.1097/mpg.0b013e31821a23d0

  86. 86.

    Bakker SF, Tushuizen ME, Stokvis-Brantsma WH, et al. Frequent delay of coeliac disease diagnosis in symptomatic patients with type 1 diabetes mellitus: clinical and genetic characteristics. European Journal of Internal Medicine. 2013;24(5):456-460.

    Not in our library10.1016/j.ejim.2013.01.016

  87. 87.

    Camarca ME, Mozzillo E, Nugnes R, et al. Celiac disease in type 1 diabetes mellitus. Italian Journal of Pediatrics. 2012;38, article 10.

    Not in our library10.1186/1824-7288-38-10

  88. 88.

    Bao F, Yu L, Babu S, et al. One third of HLA DQ2 homozygous patients with type 1 diabetes express celiac disease-associated transglutaminase autoantibodies. Journal of Autoimmunity. 1999;13(1):143-148.

    Not in our library10.1006/jaut.1999.0303

  89. 89.

    Barker JM, Yu J, Yu L, et al. Autoantibody “subspecificity” in type 1 diabetes: risk for organ-specific autoimmunity clusters in distinct groups. Diabetes Care. 2005;28(4):850-855.

    Not in our library10.2337/diacare.28.4.850

  90. 90.

    Sponzilli I, Chiari G, Iovane B, et al. Celiac disease in children with type 1 diabetes: impact of gluten free diet on diabetes management. Acta Biomedica. 2010;81(3):165-170.

    Not in our library

  91. 91.

    Abid N, Mcglone O, Cardwell C, Mccallion W, Carson D. Clinical and metabolic effects of gluten free diet in children with type 1 diabetes and coeliac disease. Pediatric Diabetes. 2011;12(4, part 1):322-325.

    Not in our library10.1111/j.1399-5448.2010.00700.x

  92. 92.

    Leeds JS, Hopper AD, Hadjivassiliou M, Tesfaye S, Sanders DS. High prevalence of microvascular complications in adults with type 1 diabetes and newly diagnosed celiac disease. Diabetes Care. 2011;34(10):2158-2163.

    Not in our library10.2337/dc11-0149

  93. 93.

    Bakker SF, Tushuizen ME, von Blomberg ME, Mulder CJ, Simsek S. Type 1 diabetes and celiac disease in adults: glycemic control and diabetic complications. Acta Diabetologica. 2013;50(3):319-324.

    Not in our library10.1007/s00592-012-0395-0

  94. 94.

    Valerio G, Spadaro R, Iafusco D, et al. The influence of gluten free diet on quantitative ultrasound of proximal phalanxes in children and adolescents with type 1 diabetes mellitus and celiac disease. Bone. 2008;43(2):322-326.

    Not in our library10.1016/j.bone.2008.04.004

  95. 95.

    Lombardi F, Franzese A, Iafusco D, et al. Bone involvement in clusters of autoimmune diseases: just a complication? Bone. 2010;46(2):551-555.

    Not in our library10.1016/j.bone.2009.09.034

  96. 96.

    Ch’ng CL, Biswas M, Benton A, Jones MK, Kingham JGC. Prospective screening for coeliac disease in patients with Graves’ hyperthyroidism using anti-gliadin and tissue transglutaminase antibodies. Clinical Endocrinology. 2005;62(3):303-306.

    Not in our library10.1111/j.1365-2265.2005.02214.x

  97. 97.

    Hadithi M, de Boer H, Meijer JWR, et al. Coeliac disease in Dutch patients with Hashimoto’s thyroiditis and vice versa. World Journal of Gastroenterology. 2007;13(11):1715-1722.

    Not in our library10.3748/wjg.v13.i11.1715

  98. 98.

    Ch’ng CL, Jones MK, Kingham JGC. Celiac disease and autoimmune thyroid disease. Clinical Medicine and Research. 2007;5(3):184-192.

    Not in our library10.3121/cmr.2007.738

  99. 99.

    Spadaccino AC, Basso D, Chiarelli S, et al. Celiac disease in North Italian patients with autoimmune thyroid diseases. Autoimmunity. 2008;41(1):116-121.

    Not in our library10.1080/08916930701620209

  100. 100.

    Ansaldi N, Palmas T, Corrias A, et al. Autoimmune thyroid disease and celiac disease in children. Journal of Pediatric Gastroenterology and Nutrition. 2003;37(1):63-66.

    Not in our library10.1097/00005176-200307000-00010

  101. 101.

    Elfström P, Montgomery SM, Kämpe O, Ekbom A, Ludvigsson JF. Risk of thyroid disease in individuals with celiac disease. The Journal of Clinical Endocrinology and Metabolism. 2008;93(10):3915-3921.

    Not in our library10.1210/jc.2008-0798

  102. 102.

    Meloni A, Mandas C, Jores RD, Congia M. Prevalence of autoimmune thyroiditis in children with celiac disease and effect of gluten withdrawal. The Journal of Pediatrics. 2009;155(1):51-55.

    Not in our library10.1016/j.jpeds.2009.01.013

  103. 103.

    Mainardi E, Montanelli A, Dotti M, Nano R, Moscato G. Thyroid-related autoantibodies and celiac disease: a role for a gluten-free diet? Journal of Clinical Gastroenterology. 2002;35(3):245-248.

    Not in our library10.1097/00004836-200209000-00009

  104. 104.

    Metso S, Hyytiä-Ilmonen H, Kaukinen K, et al. Gluten-free diet and autoimmune thyroiditis in patients with celiac disease. A prospective controlled study. Scandinavian Journal of Gastroenterology. 2012;47(1):43-48.

    Not in our library10.3109/00365521.2011.639084

  105. 105.

    Ventura A, Neri E, Ughi C, Leopaldi A, Città A, Not T. Gluten-dependent diabetes-related and thyroid-related autoantibodies in patients with celiac disease. The Journal of Pediatrics. 2000;137(2):263-265.

    Not in our library10.1067/mpd.2000.107160

  106. 106.

    Sategna-Guidetti C, Volta U, Ciacci C, et al. Prevalence of thyroid disorders in untreated adult celiac disease patients and effect of gluten withdrawal: an Italian multicenter study. American Journal of Gastroenterology. 2001;96(3):751-757.

    Not in our library10.1111/j.1572-0241.2001.03617.x

  107. 107.

    Diamanti A, Ferretti F, Guglielmi R, et al. Thyroid autoimmunity in children with coeliac disease: a prospective survey. Archives of Disease in Childhood. 2011;96(11):1038-1041.

    Not in our library10.1136/archdischild-2011-300595

  108. 108.

    Naiyer AJ, Shah J, Hernandez L, et al. Tissue transglutaminase antibodies in individuals with celiac disease bind to thyroid follicles and extracellular matrix and may contribute to thyroid dysfunction. Thyroid. 2008;18(11):1171-1178.

    Not in our library10.1089/thy.2008.0110

  109. 109.

    Reunala T, Salmi J, Karvonen J. Dermatitis herpetiformis and celiac disease associated with Addison’s disease. Archives of Dermatology. 1987;123(7):930-932.

    Not in our library

  110. 110.

    Heneghan MA, Mchugh P, Stevens FM, Mccarthy CF. Addison’s disease and selective IgA deficiency in two coeliac patients. Scandinavian Journal of Gastroenterology. 1997;32(5):509-511.

    Not in our library10.3109/00365529709025090

  111. 111.

    O’Leary C, Walsh CH, Wieneke P, et al. Coeliac disease and autoimmune Addison’s disease: a clinical pitfall. Monthly Journal of the Association of Physicians. 2002;95(2):79-82.

    Not in our library10.1093/qjmed/95.2.79

  112. 112.

    Myhre AG, Aarsetøy H, Undlien DE, Hovdenak N, Aksnes L, Husebye ES. High frequency of coeliac disease among patients with autoimmune adrenocortical failure. Scandinavian Journal of Gastroenterology. 2003;38(5):511-515.

    Not in our library10.1080/00365520310002544

  113. 113.

    Biagi F, Campanella J, Soriani A, Vailati A, Corazza GR. Prevalence of coeliac disease in Italian patients affected by Addison’s disease. Scandinavian Journal of Gastroenterology. 2006;41(3):302-305.

    Not in our library10.1080/00365520500206517

  114. 114.

    Betterle C, Lazzaratto F, Spadaccino AC, et al. Celiac disease in North Italian patients with autoimmune Addison’s disease. European Journal of Endocrinology. 2006;154(2):275-279.

    Not in our library10.1530/eje.1.02089

  115. 115.

    Elfström P, Montgomery SM, Kämpe O, Ekbom A, Ludvigsson JF. Risk of primary adrenal insufficiency in patients with celiac disease. The Journal of Clinical Endocrinology and Metabolism. 2007;92(9):3595-3598.

    Not in our library10.1210/jc.2007-0960

  116. 116.

    Duhring LA. Landmark article, Aug 30, 1884: dermatitis herpetiformis. Journal of the American Medical Association. 1983;250(2):212-216.

    Not in our library10.1001/jama.250.2.212

  117. 117.

    Marks J, Shuster S, Watson AJ. Small-bowel changes in dermatitis herpetiformis. The Lancet. 1966;2(7476):1280-1282.

    Not in our library10.1016/s0140-6736(66)91692-8

  118. 118.

    Fry L, Keir P, McMinn RM, Cowan JD, Hoffbrand AV. Small-intestinal structure and function and haematological changes in dermatitis herpetiformis. The Lancet. 1967;2(7519):729-733.

    Not in our library10.1016/s0140-6736(67)91942-3

  119. 119.

    Kárpati S. Dermatitis herpetiformis. Clinics in Dermatology. 2012;30(1):56-59.

    Not in our library10.1016/j.clindermatol.2011.03.010

  120. 120.

    Ingen-Housz-Oro S. Dermatitis herpetiformis: a review. Annales de Dermatologie et de Vénéréologie. 2011;138(3):221-227.

    Not in our library10.1016/j.annder.2011.01.005

  121. 121.

    Cardones ARG, Hall RP. Pathophysiology of dermatitis herpetiformis: a model for cutaneous manifestations of gastrointestinal inflammation. Dermatologic Clinics. 2011;29(3):469-477.

    Not in our library10.1016/j.det.2011.03.005

  122. 122.

    Cottini GB. Symmetrical dermatitis herpetiformis of Duhring localized on the knees and elbows. Annales de Dermatologie et de Syphiligraphie. 1955;82(3):285-286.

    Not in our library

  123. 123.

    Bolotin D, Petronic-Rosic V. Dermatitis herpetiformis: part I. Epidemiology, pathogenesis, and clinical presentation. Journal of the American Academy of Dermatology. 2011;64(6):1017-1024.

    Not in our library10.1016/j.jaad.2010.09.777

  124. 124.

    Moulin G, Barrut D, Franc MP. Pseudopurpuric palmar localizations of herpetiform dermatitis. Annales de dermatologie et de vénéréologie. 1983;110(2):121-126.

    Not in our library

  125. 125.

    Ohshima Y, Tamada Y, Matsumoto Y, Hashimoto T. Dermatitis herpetiformis Duhring with palmoplantar keratosis. The British Journal of Dermatology. 2003;149(6):1300-1302.

    Not in our library10.1111/j.1365-2133.2003.05660.x

  126. 126.

    Powell GR, Bruckner AL, Weston WL. Dermatitis herpetiformis presenting as chronic urticaria. Pediatric Dermatology. 2004;21(5):564-567.

    Not in our library10.1111/j.0736-8046.2004.21509.x

  127. 127.

    Hervonen K, Hakanen M, Kaukinen K, Collin P, Reunala T. First-degree relatives are frequently affected in coeliac disease and dermatitis herpetiformis. Scandinavian Journal of Gastroenterology. 2002;37(1):51-55.

    Not in our library10.1080/003655202753387356

  128. 128.

    Caproni M, Antiga E, Melani L, Fabbri P. Guidelines for the diagnosis and treatment of dermatitis herpetiformis. Journal of the European Academy of Dermatology and Venereology. 2009;23(6):633-638.

    Not in our library10.1111/j.1468-3083.2009.03188.x

  129. 129.

    Nicolas MEO, Krause PK, Gibson LE, Murray JA. Dermatitis herpetiformis. International Journal of Dermatology. 2003;42(8):588-600.

    Not in our library10.1046/j.1365-4362.2003.01804.x

  130. 130.

    Sugai E, Smecuol E, Niveloni S, et al. Celiac disease serology in dermatitis herpetiformis. Which is the best option for detecting gluten sensitivity? Acta Gastroenterologica Latinoamericana. 2006;36(4):197-201.

    Not in our library

  131. 131.

    Alonso-llamazares J, Gibson LE, Rogers RS. Clinical, pathologic, and immunopathologic features of dermatitis herpetiformis: review of the Mayo Clinic experience. International Journal of Dermatology. 2007;46(9):910-919.

    Not in our library10.1111/j.1365-4632.2007.03214.x

  132. 132.

    Corazza GR, Andreani ML, Venturo N, Bernardi M, Tosti A, Gasbarrini G. Celiac disease and alopecia areata: report of a new association. Gastroenterology. 1995;109(4):1333-1337.

    Not in our library10.1016/0016-5085(95)90597-9

  133. 133.

    Bardella MT, Marino R, Barbareschi M, Bianchi F, Faglia G, Bianchi P. Alopecia areata and coeliac disease: no effect of a gluten-free diet on hair growth. Dermatology. 2000;200(2):108-110.

    Not in our library10.1159/000018340

  134. 134.

    Fessatou S, Kostaki M, Karpathios T. Coeliac disease and alopecia areata in childhood. Journal of Paediatrics and Child Health. 2003;39(2):152-154.

    Not in our library10.1046/j.1440-1754.2003.00116.x

  135. 135.

    Abenavoli L, Proietti L, Leggio L, et al. Cutaneous manifestations in celiac disease. World Journal of Gastroenterology. 2006;12(6):843-852.

    Not in our library10.3748/wjg.v12.i6.843

  136. 136.

    Rodríguez-García C, González-Hernández S, Pérez-Robayna N, Guimerá F, Fagundo E, Sánchez R. Repigmentation of vitiligo lesions in a child with celiac disease after a gluten-free diet. Pediatric Dermatology. 2011;28(2):209-210.

    Not in our library10.1111/j.1525-1470.2011.01388.x

  137. 137.

    Marie I, Lecomte F, Hachulla E, et al. An uncommon association: celiac disease and dermatomyositis in adults. Clinical and Experimental Rheumatology. 2001;19(2):201-203.

    Not in our library

  138. 138.

    Song MS, Farber D, Bitton A, Jass J, Singer M, Karpati G. Dermatomyositis associated with celiac disease: response to a gluten-free diet. Canadian Journal of Gastroenterology. 2006;20(6):433-435.

    Not in our library10.1155/2006/574074

  139. 139.

    Cooke WT, Smith WT. Neurological disorders associated with adult coeliac disease. Brain. 1966;89(4):683-722.

    Not in our library10.1093/brain/89.4.683

  140. 140.

    Vaknin A, Eliakim R, Ackerman Z, Steiner I. Neurological abnormalities associated with celiac disease. Journal of Neurology. 2004;251(11):1393-1397.

    Not in our library10.1007/s00415-004-0550-9

  141. 141.

    Hadjivassiliou M, Grünewald R, Sharrack B, et al. Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics. Brain. 2003;126(3):685-691.

    Not in our library10.1093/brain/awg050

  142. 142.

    Chin RL, Sander HW, Brannagan TH, et al. Celiac neuropathy. Neurology. 2003;60(10):1581-1585.

    Not in our library10.1212/01.wnl.0000063307.84039.c7

  143. 143.

    Hadjivassiliou M, Grünewald RA, Kandler RH, et al. Neuropathy associated with gluten sensitivity. Journal of Neurology, Neurosurgery and Psychiatry. 2006;77(11):1262-1266.

    Not in our library10.1136/jnnp.2006.093534

  144. 144.

    Ludvigsson JF, Olsson T, Ekbom A, Montgomery SM. A population-based study of coeliac disease, neurodegenerative and neuroinflammatory diseases. Alimentary Pharmacology and Therapeutics. 2007;25(11):1317-1327.

    Not in our library10.1111/j.1365-2036.2007.03329.x

  145. 145.

    Hadjivassiliou M, Aeschlimann P, Strigun A, Sanders DS, Woodroofe N, Aeschlimann D. Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase. Annals of Neurology. 2008;64(3):332-343.

    Not in our library10.1002/ana.21450

  146. 146.

    Hadjivassiliou M, Mäki M, Sanders DS, et al. Autoantibody targeting of brain and intestinal transglutaminase in gluten ataxia. Neurology. 2006;66(3):373-377.

    Not in our library10.1212/01.wnl.0000196480.55601.3a

  147. 147.

    Hadjivassiliou M, Aeschlimann P, Sanders DS, et al. Transglutaminase 6 antibodies in the diagnosis of gluten ataxia. Neurology. 2013;80(19):1740-1745.

    Not in our library10.1212/wnl.0b013e3182919070

  148. 148.

    Alaedini A, Green PHR, Sander HW, et al. Ganglioside reactive antibodies in the neuropathy associated with celiac disease. Journal of Neuroimmunology. 2002;127(1-2):145-148.

    Not in our library10.1016/s0165-5728(02)00102-9

  149. 149.

    Volta U, de Giorgio R, Granito A, et al. Anti-ganglioside antibodies in coeliac disease with neurological disorders. Digestive and Liver Disease. 2006;38(3):183-187.

    Not in our library10.1016/j.dld.2005.11.013

  150. 150.

    Briani C, Ruggero S, Zara G, et al. Anti-ganglioside antibodies in children with coeliac disease: correlation with gluten-free diet and neurological complications. Alimentary Pharmacology and Therapeutics. 2004;20(2):231-235.

    Not in our library10.1111/j.1365-2036.2004.02016.x

  151. 151.

    Briani C, Zara G, Toffanin E, et al. Neurological complications of celiac disease and autoimmune mechanisms: preliminary data of a prospective study in adult patients. Annals of the New York Academy of Sciences. 2005;1051:148-155.

    Not in our library10.1196/annals.1361.056

  152. 152.

    Hadjivassiliou M, Kandler RH, Chattopadhyay AK, et al. Dietary treatment of gluten neuropathy. Muscle and Nerve. 2006;34(6):762-766.

    Not in our library10.1002/mus.20642

  153. 153.

    Luostarinen L, Himanen S-L, Luostarinen M, Collin P, Pirttilä T. Neuromuscular and sensory disturbances in patients with well treated coeliac disease. Journal of Neurology Neurosurgery and Psychiatry. 2003;74(4):490-494.

    Not in our library10.1136/jnnp.74.4.490

  154. 154.

    Shatin R. Gluten and multiple sclerosis. British Medical Journal. 1965;29(1):1433-1434.

    Not in our library10.1136/bmj.1.5447.1433-d

  155. 155.

    Rodrigo L, Hernández-Lahoz C, Fuentes D, Alvarez N, López-Vázquez A, González S. Prevalence of celiac disease in multiple sclerosis. BMC Neurology. 2011;11, article 31.

    Not in our library10.1186/1471-2377-11-31

  156. 156.

    Nicoletti A, Patti F, lo Fermo S, et al. Frequency of celiac disease is not increased among multiple sclerosis patients. Multiple Sclerosis. 2008;14(5):698-700.

    Not in our library10.1177/1352458507087268

  157. 157.

    Jacob S, Zarei M, Kenton A, Allroggen H. Gluten sensitivity and neuromyelitis optica: two case reports. Journal of Neurology, Neurosurgery and Psychiatry. 2005;76(7):1028-1030.

    Not in our library10.1136/jnnp.2004.055491

  158. 158.

    Bergamaschi R, Jarius S, Robotti M, Pichiecchio A, Wildemann B, Meola G. Two cases of benign neuromyelitis optica in patients with celiac disease. Journal of Neurology. 2009;256(12):2097-2099.

    Not in our library10.1007/s00415-009-5288-y

  159. 159.

    Hernández-Lahoz C, Rodrigo L. Gluten-related disorders and demyelinating diseases. Medicina Clínica. 2013;140(7):314-319.

    Not in our library10.1016/j.medcli.2012.07.009

  160. 160.

    Kassan SS, Moutsopoulos HM. Clinical manifestations and early diagnosis of Sjögren syndrome. Archives of Internal Medicine. 2004;164(12):1275-1284.

    Not in our library10.1001/archinte.164.12.1275

  161. 161.

    Iltanen S, Collin P, Korpela M, et al. Celiac disease and markers of celiac disease latency in patients with primary Sjogren’s syndrome. American Journal of Gastroenterology. 1999;94(4):1042-1046.

    Not in our library10.1111/j.1572-0241.1999.01011.x

  162. 162.

    Szodoray P, Barta Z, Lakos G, Szakáll S, Zeher M. Coeliac disease in Sjögren’s syndrome—a study of 111 Hungarian patients. Rheumatology International. 2004;24(5):278-282.

    Not in our library10.1007/s00296-003-0360-x

  163. 163.

    Alvarez-Celorio MD, Angeles-Angeles A, Kraus A. Primary Sjogren’s syndrome and celiac disease: causal association or serendipity? Journal of Clinical Rheumatology. 2000;6(4):194-197.

    Not in our library10.1097/00124743-200008000-00005

  164. 164.

    Tsokos GC. Mechanisms of disease: systemic lupus erythematosus. The New England Journal of Medicine. 2011;365(22):2110-2121.

    Not in our library10.1056/nejmra1100359

  165. 165.

    Zitouni M, Daoud W, Kallel M, Makni S. Systemic lupus erythematosus with celiac disease: a report of five cases. Joint Bone Spine. 2004;71(4):344-346.

    Not in our library10.1016/s1297-319x(03)00159-3

  166. 166.

    Mirza N, Bonilla E, Phillips PE. Celiac disease in a patient with systemic lupus erythematosus: a case report and review of literature. Clinical Rheumatology. 2007;26(5):827-828.

    Not in our library10.1007/s10067-006-0344-9

  167. 167.

    Hrycek A, Siekiera U. Coeliac disease in systemic lupus erythematosus: a case report. Rheumatology International. 2008;28(5):491-493.

    Not in our library10.1007/s00296-007-0459-6

  168. 168.

    Freeman HJ. Adult celiac disease followed by onset of systemic lupus erythematosus. Journal of Clinical Gastroenterology. 2008;42(3):252-255.

    Not in our library10.1097/mcg.0b013e31802e70a1

  169. 169.

    Ludvigsson JF, Rubio-Tapia A, Chowdhary V, Murray JA, Simard JF. Increased risk of Systemic Lupus Erythematosus in 29,000 patients with biopsy-verified celiac disease. Journal of Rheumatology. 2012;39(10):1964-1970.

    Not in our library10.3899/jrheum.120493

  170. 170.

    Ravelli A, Martini A. Juvenile idiopathic arthritis. The Lancet. 2007;369(9563):767-778.

    Not in our library10.1016/s0140-6736(07)60363-8

  171. 171.

    Alpigiani MG, Haupt R, Parodi S, Calcagno A, Poggi E, Lorini R. Coeliac disease in 108 patients with juvenile idiopathic arthritis: a 13-3ear follow-up study. Clinical and Experimental Rheumatology. 2008;26(1):p. 162.

    Not in our library

  172. 172.

    Lepore L, Martelossi S, Pennesi M, et al. Prevalence of celiac disease in patients with juvenile chronic arthritis. The Journal of Pediatrics. 1996;129(2):311-313.

    Not in our library10.1016/s0022-3476(96)70262-7

  173. 173.

    Francis J, Carty JE, Scott BB. The prevalence of coeliac disease in rheumatoid arthritis. European Journal of Gastroenterology and Hepatology. 2002;14(12):1355-1356.

    Not in our library10.1097/00042737-200212000-00011

  174. 174.

    Iqbal T, Zaidi MA, Wells GA, Karsh J. Celiac disease arthropathy and autoimmunity study. Journal of Gastroenterology and Hepatology. 2013;28(1):99-105.

    Not in our library10.1111/j.1440-1746.2012.07272.x

  175. 175.

    Elliott P, Andersson B, Arbustini E, et al. Classification of the cardiomyopathies: a position statement from the european society of cardiology working group on myocardial and pericardial diseases. European Heart Journal. 2008;29(2):270-276.

    Not in our library10.1093/eurheartj/ehm342

  176. 176.

    Curione M, Barbato M, de Biase L, Viola F, lo Russo L, Cardi E. Prevalence of coeliac disease in idiopathic dilated cardiomyopathy. The Lancet. 1999;354(9174):222-223.

    Not in our library10.1016/s0140-6736(99)01501-9

  177. 177.

    Frustaci A, Cuoco L, Chimenti C, et al. Celiac disease associated with autoimmune myocarditis. Circulation. 2002;105(22):2611-2618.

    Not in our library10.1161/01.cir.0000017880.86166.87

  178. 178.

    Goel NK, McBane RD, Kamath PS. Cardiomyopathy associated with celiac disease. Mayo Clinic Proceedings. 2005;80(5):674-676.

    Not in our library10.4065/80.5.674

  179. 179.

    Chicco D, Taddio A, Sinagra G, et al. Speeding up coeliac disease diagnosis in cardiological settings. Archives of Medical Science. 2010;6(5):728-732.

    Not in our library10.5114/aoms.2010.17088

  180. 180.

    Emilsson L, Andersson B, Elfström P, Green PH, Ludvigsson JF. Risk of idiopathic dilated cardiomyopathy in 29000 patients with celiac disease. Journal of American Heart Association. 2012;1(3).

    Not in our library10.1161/jaha.112.001594

  181. 181.

    Curione M, Barbato M, Viola F, Francia P, de Biase L, Cucchiara S. Idiopathic dilated cardiomyopathy associated with coeliac disease: the effect of a gluten-free diet on cardiac performance. Digestive and Liver Disease. 2002;34(12):866-869.

    Not in our library10.1016/s1590-8658(02)80258-4

  182. 182.

    Curione M, Danese C, Viola F, et al. Carnitine deficiency in patients with coeliac disease and idiopathic dilated cardiomyopathy. Nutrition, Metabolism and Cardiovascular Diseases. 2005;15(4):279-283.

    Not in our library10.1016/j.numecd.2005.01.002

  183. 183.

    Romagnoli E, Boldrini E, Pietrangelo A. Association between celiac disease and idiopathic dilated cardiomyopathy: a case report. Internal and Emergency Medicine. 2011;6(2):125-128.

    Not in our library10.1007/s11739-010-0442-1

  184. 184.

    Dawes PT, Atherton ST. Coeliac disease presenting as recurrent pericarditis. The Lancet. 1981;1(8228):1021-1022.

    Not in our library10.1016/s0140-6736(81)92187-5

  185. 185.

    Faizallah R, Costello FC, Lee FI, Walker R. Adult celiac disease and recurrent pericarditis. Digestive Diseases and Sciences. 1982;27(8):728-730.

    Not in our library10.1007/bf01393769

  186. 186.

    Laine LA, Holt KM. Recurrent pericarditis and celiac disease. Journal of the American Medical Association. 1984;252(22):p. 3168.

    Not in our library

  187. 187.

    Elfström P, Hamsten A, Montgomery SM, Ekbom A, Ludvigsson JF. Cardiomyopathy, pericarditis and myocarditis in a population-based cohort of inpatients with coeliac disease. Journal of Internal Medicine. 2007;262(5):545-554.

    Not in our library10.1111/j.1365-2796.2007.01843.x

  188. 188.

    Ojetti V, Sanchez JA, Guerriero C, et al. High prevalence of celiac disease in psoriasis. American Journal of Gastroenterology. 2003;98(11):2574-2575.

    Not in our library10.1111/j.1572-0241.2003.08684.x

  189. 189.

    Michaëlsson G, Gerdén B, Hagforsen E, et al. Psoriasis patients with antibodies to gliadin can be improved by a gluten-free diet. The British Journal of Dermatology. 2000;142(1):44-51.

    Not in our library10.1046/j.1365-2133.2000.03240.x

  190. 190.

    Addolorato G, Parente A, de Lorenzi G, et al. Rapid regression of psoriasis in a coeliac patient after gluten-free diet: a case report and review of the literature. Digestion. 2003;68(1):9-12.

    Not in our library10.1159/000073220

  191. 191.

    Ludvigsson JF, Lindelöf B, Zingone F, Ciacci C. Psoriasis in a nationwide cohort study of patients with celiac disease. The Journal of Investigative Dermatology. 2011;131(10):2010-2016.

    Not in our library10.1038/jid.2011.162

  192. 192.

    Abenavoli L, Leggio L, Gasbarrini G, Addolorato G. Celiac disease and skin: psoriasis association. World Journal of Gastroenterology. 2007;13(14):2138-2139.

    Not in our library10.3748/wjg.v13.i14.2138

  193. 193.

    James DG. Sarcoidosis. Posgraduate Medical Journal. 2001;77(905):177-180.

    Not in our library10.1136/pmj.77.905.177

  194. 194.

    Bianconcini G, Mazzali F, Candini R, Silingardi M, Iori I. Coeliac disease (familial) and sarcoidosis. Case report and review of literature. Minerva Medica. 1994;85(10):541-553.

    Not in our library

  195. 195.

    Rutherford RM, Brutsche MH, Kearns M, Bourke M, Stevens F, Gilmartin JJ. Prevalence of coeliac disease in patients with sarcoidosis. European Journal of Gastroenterology and Hepatology. 2004;16(9):911-915.

    Not in our library10.1097/00042737-200409000-00016

  196. 196.

    Hwang E, McBride R, Neugut AI, Green PHR. Sarcoidosis in patients with celiac disease. Digestive Diseases and Sciences. 2008;53(4):977-981.

    Not in our library10.1007/s10620-007-9974-2

  197. 197.

    D'Ercole C, Zullo A, Bragazzi MC, Campo SM. Sarcoidosis and coeliac disease: do not forget the association. Internal and Emergency Medicine. 2012;7(supplement 1):p. S25.

    Not in our library10.1007/s11739-011-0561-3

  198. 198.

    Ludvigsson JF, Wahlstrom J, Grunewald J, Ekbom A, Montgomery SM. Coeliac disease and risk of sarcoidosis. Sarcoidosis Vasculitis and Diffuse Lung Diseases. 2007;24(2):121-126.

    Not in our library10.1007/s11083-007-9062-4

  199. 199.

    Cines DB, Bussel JB, Liebman HA, Luning Prak ET. The ITP syndrome: pathogenic and clinical diversity. Blood. 2009;113(26):6511-6521.

    Not in our library10.1182/blood-2009-01-129155

  200. 200.

    Eliakim R, Heyman S, Kornberg A. Celiac disease and keratoconjunctivitis. Occurrence with thrombocytopenic purpura. Archives of Internal Medicine. 1982;142(5):p. 1037.

    Not in our library

  201. 201.

    Stenhammar L, Ljunggren CG. Thrombocytopenic purpura and coeliac disease. Acta Paediatrica Scandinavica. 1988;77(5):764-766.

    Not in our library10.1111/j.1651-2227.1988.tb10749.x

  202. 202.

    Dogan M, Sal E, Akbayram S, Peker E, Cesur Y, Oner AF. Concurrent celiac disease, idiopathic thrombocytopenic purpura and autoimmune thyroiditis: a case report. Clinical and Applied Thrombosis/Hemostasis. 2011;17(6):E13-E16.

    Not in our library10.1177/1076029610378502

  203. 203.

    Olén O, Montgomery SM, Elinder G, Ekbom A, Ludvigsson JF. Increased risk of immune thrombocytopenic purpura among inpatients with coeliac disease. Scandinavian Journal of Gastroenterology. 2008;43(4):416-422.

    Not in our library10.1080/00365520701814028

  204. 204.

    Ludvigsson JF, Welander A, Lassila R, Ekbom A, Montgomery SM. Risk of thromboembolism in 14 000 individuals with coeliac disease. British Journal of Haematology. 2007;139(1):121-127.

    Not in our library10.1111/j.1365-2141.2007.06766.x

  205. 205.

    Ciacci C, Tortora R, Scudiero O, di Fiore R, Salvatore F, Castaldo G. Early pregnancy loss in celiac women: the role of genetic markers of thrombophilia. Digestive and Liver Disease. 2009;41(10):717-720.

    Not in our library10.1016/j.dld.2009.02.050

  206. 206.

    McNeill A, Duthie F, Galloway DJ. Small bowel infarction in a patient with coeliac disease. Journal of Clinical Pathology. 2006;59(2):216-218.

    Not in our library10.1136/jcp.2005.027698

  207. 207.

    Emilsson L, Smith JG, West J, Melander O, Ludvigsson JF. Increased risk of atrial fibrillation in patients with coeliac disease: a nationwide cohort study. European Heart Journal. 2011;32(19):2430-2437.

    Not in our library10.1093/eurheartj/ehr167

  208. 208.

    Haque M, Schumacher PA, Harris A, et al. Late acute celiac and hepatic artery thrombosis with portal vein thrombosis resulting in hepatic infarction 12 years post orthotopic liver transplantation. Annals of Hepatology. 2009;8(4):396-399.

    Not in our library

  209. 209.

    Ludvigsson JF, de Faire U, Ekbom A, Montgomery SM. Vascular disease in a population-based cohort of individuals hospitalised with coeliac disease. Heart. 2007;93(9):1111-1115.

    Not in our library10.1136/hrt.2006.097097

  210. 210.

    Goodwin FC, Beattie RM, Millar J, Kirkham FJ. Celiac disease and childhood stroke. Pediatric Neurology. 2004;31(2):139-142.

    Not in our library10.1016/j.pediatrneurol.2004.02.014

  211. 211.

    Saibeni S, Lecchi A, Meucci G, et al. Prevalence of hyperhomocysteinemia in adult gluten-sensitive enteropathy at diagnosis: role of B12, folate, and genetics. Clinical Gastroenterology and Hepatology. 2005;3(6):574-580.

    Not in our library10.1016/s1542-3565(05)00022-4

  212. 212.

    Wilcox GM, Mattia AR. Celiac sprue, hyperhomocysteinemia, and MTHFR gene variants. Journal of Clinical Gastroenterology. 2006;40(7):596-601.

    Not in our library10.1097/00004836-200608000-00007

  213. 213.

    Sjöberg K, Eriksson S, Tenngart B, Roth EB, Leffler H, Stenberg P. Factor XIII and tissue transglutaminase antibodies in coeliac and inflammatory bowel disease. Autoimmunity. 2002;35(5):357-364.

    Not in our library10.1080/73-0891693021000005402

  214. 214.

    Saibeni S, Bottasso B, Spina L, et al. Assessment of thrombin-activatable fibrinolysis inhibitor (TAFI) plasma levels in inflammatory bowel diseases. American Journal of Gastroenterology. 2004;99(10):1966-1970.

    Not in our library10.1111/j.1572-0241.2004.30203.x

  215. 215.

    Ludvigsson JF, Montgomery SM, Ekbom A. Risk of pancreatitis in 14,000 individuals with celiac disease. Clinical Gastroenterology and Hepatology. 2007;5(11):1347-1353.

    Not in our library10.1016/j.cgh.2007.06.002

  216. 216.

    Rodrigo Sáez L, Álvarez N, Riestra S, et al. Relapsing acute pancreatitis associated with gluten enteropathy: clinical, laboratory, and evolutive characteristics in thirty-four patients. Revista Española de Enfermedades Digestivas. 2008;100(12):746-751.

    Not in our library10.4321/s1130-01082008001200002

  217. 217.

    Sadr-Azodi O, Sanders DS, Murray JA, Ludvigsson JF. Patients with celiac disease have an increased risk for pancreatitis. Clinical Gastroenterology and Hepatology. 2012;10(10):1136-1142.

    Not in our library10.1016/j.cgh.2012.06.023

  218. 218.

    Leeds JS, Hopper AD, Hurlstone DP, et al. Is exocrine pancreatic insufficiency in adult coeliac disease a cause of persisting symptoms? Alimentary Pharmacology and Therapeutics. 2007;25(3):265-271.

    Not in our library10.1111/j.1365-2036.2006.03206.x

  219. 219.

    Freeman HJ. Hepatobiliary and pancreatic disorders in celiac disease. World Journal of Gastroenterology. 2006;12(10):1503-1508.

    Not in our library10.3748/wjg.v12.i10.1503

  220. 220.

    Masoodi I, Wani H, Alsayari K, et al. Celiac disease and autoimmune pancreatitis: an uncommon association. A case report. European Journal of Gastroenterology and Hepatology. 2011;23(12):1270-1272.

    Not in our library10.1097/meg.0b013e32834c7bad

  221. 221.

    Matteoni CA, Goldblum JR, Wang N, Brzezinski A, Achkar E, Soffer EE. Celiac disease is highly prevalent in lymphocytic colitis. Journal of Clinical Gastroenterology. 2001;32(3):225-227.

    Not in our library10.1097/00004836-200103000-00009

  222. 222.

    Green PHR, Yang J, Cheng J, Lee AR, Harper JW, Bhagat G. An association between microscopic colitis and celiac disease. Clinical Gastroenterology and Hepatology. 2009;7(11):1210-1216.

    Not in our library10.1016/j.cgh.2009.07.011

  223. 223.

    Barta Z, Zold E, Nagy A, Zeher M, Csipo I. Celiac disease and microscopic colitis: a report of 4 cases. World Journal of Gastroenterology. 2011;17(16):2150-2154.

    Not in our library10.3748/wjg.v17.i16.2150

  224. 224.

    Stewart M, Andrews CN, Urbanski S, Beck PL, Storr M. The association of coeliac disease and microscopic colitis: a large population-based study. Alimentary Pharmacology and Therapeutics. 2011;33(12):1340-1349.

    Not in our library10.1111/j.1365-2036.2011.04666.x

  225. 225.

    Lebwohl B, Granath F, Ekbom A, et al. Mucosal healing and mortality in coeliac disease. Alimentary Pharmacology & Therapeutics. 2013;37(3):332-339.

    Not in our library10.1111/apt.12164

  226. 226.

    Biagi F, Corazza GR. Mortality in celiac disease. Nature Reviews Gastroenterology and Hepatology. 2010;7(3):158-162.

    Not in our library10.1038/nrgastro.2010.2

  227. 227.

    West J. Celiac disease and its complications: a time traveller’s perspective. Gastroenterology. 2009;136(1):32-34.

    Not in our library10.1053/j.gastro.2008.11.026

  228. 228.

    Roshan B, Leffler DA, Jamma S, et al. The incidence and clinical spectrum of refractory celiac disease in a north american referral center. American Journal of Gastroenterology. 2011;106(5):923-928.

    Not in our library10.1038/ajg.2011.104

  229. 229.

    Malamut G, Murray JA, Cellier C. Refractory celiac disease. Gastrointestinal Endoscopy Clinics of North America. 2012;22(4):759-772.

    Not in our library10.1016/j.giec.2012.07.007

  230. 230.

    Al-toma A, Verbeek WHM, Hadithi M, von Blomberg BME, Mulder CJJ. Survival in refractory coeliac disease and enteropathy-associated T-cell lymphoma: retrospective evaluation of single-centre experience. Gut. 2007;56(10):1373-1378.

    Not in our library10.1136/gut.2006.114512

  231. 231.

    Sieniawski MK, Lennard AL. Enteropathy-associated T-cell lymphoma: epidemiology, clinical features, and current treatment strategies. Current Hematologic Malignancy Reports. 2011;6(4):231-240.

    Not in our library10.1007/s11899-011-0097-7

  232. 232.

    Rubio-Tapia A, Kelly DG, Lahr BD, Dogan A, Wu T-T, Murray JA. Clinical staging and survival in refractory celiac disease: a single center experience. Gastroenterology. 2009;136(1):99-107.

    Not in our library10.1053/j.gastro.2008.10.013

  233. 233.

    Smedby KE, Åkerman M, Hildebrand H, Glimelius B, Ekbom A, Askling J. Malignant lymphomas in coeliac disease: evidance of increased risks for lymphoma types other than enteropathy-type T cell lymphoma. Gut. 2005;54(1):54-59.

    Not in our library10.1136/gut.2003.032094

  234. 234.

    Gale J, Simmonds PD, Mead GM, Sweetenham JW, Wright DH. Enteropathy-type intestinal T-cell lymphoma: clinical features and treatment of 31 patients in a single center. Journal of Clinical Oncology. 2000;18(4):795-803.

    Not in our library10.1200/jco.2000.18.4.795

  235. 235.

    Domizio P, Owen RA, Shepherd NA, Talbot IC, Norton AJ. Primary lymphoma of the small intestine: a clinicopathological study of 119 cases. The American Journal of Surgical Pathology. 1993;17(5):429-442.

    Not in our library10.1097/00000478-199305000-00001

  236. 236.

    di Sabatino A, Carsetti R, Corazza GR. Post-splenectomy and hyposplenic states. The Lancet. 2011;378(9785):86-97.

    Not in our library10.1016/s0140-6736(10)61493-6

Cited by papers we hold 3

Reads

Read by people on this page

None yet.

Checked or read by AI through naulon

None yet.

A person counts once a day per paper. We keep no cookie and no address: a reader is a hash that changes every day. Any month under five reads shows no number.

Are you an author?

Is this your paper?

Claim it to add your note and be paid when agents cite it. Free.