Several autoimmune diseases are associated with CeD. To date, no conclusive evidence is available that proves if the relationship between CeD and autoimmune diseases is mediated by gluten exposure, or if CeD and autoimmune diseases could occur together due to other causes, particularly the injury of the integrity of the intestinal barrier function and the common genetic background (Table 1) [3]. Genetic studies have identified four shared risk chromosomal loci: PTPN2, IL18RAP, TAGAP, and PUS10 in both diseases [4]. This considerable overlap between the associated genetic regions might indicate partial agreement of the pathogenesis both of these diseases. Patients with IBD and CeD have number of common symptoms like diarrhea, malabsorption, weight loss, long-standing history of iron deficiency anaemia, and loss of BMD and this could cause problems in the diagnostics [5–7].

The prevalence of CeD (1:100) multiply exceeds that of IBD (CD 0,1–16:104, UC 0,5–25:104) in general population [8]. Previous studies showed, that the prevalence of IBD is 5–10 times higher in CeD compared with that of the general population [9–12].

In our cohort of patients with CeD the prevalence of IBD was 3,2 %. Other studies carried out among adult coeliac patients also found a similar prevalence of IBD. Yang et al. reported the prevalence of IBD to be 2,20 % in a cohort of 455 CeD patients [13]. Leeds at al. presented an IBD prevalence of 3,30 % among 305 CeD patients, however the prevalence of CeD among IBD patients was comparable with that of the controls [14]. Furthermore, Casella et al. found lower risk of CeD in their cohort of IBD patients than in the general population [15]. Assumed cause of this difference is that the increased intestinal permeability in CeD may lead to increased antigen presentation and therefore generation of autoantibodies or increased bacterial translocation, which has been involved in IBD as a pathogenic mechanism [14, 16].

In our study, CD was more common than UC in a cohort of IBD patients. In contrast to our results, CeD were reported more frequently to be associated with UC than CD [10, 17–19]. Moreover, two further studies reported high prevalence of UC even among the first-degree relatives of patients with CeD [20, 21].

The average time period during the setup of the two diagnosis in our patients’ cohort was 10,7 years, this result correspond well with the results from a previous study [13].

In our setting, in patients with both CeD and IBD, initial CeD serological testing were performed in most of the cases with EMA, which are highly specific for CeD and are not found in IBD [22]. tTG can be false positive in some chronic disorders such as type 1 diabetes mellitus and chronic liver diseases. Di Tola et al. and Farrace et al. both detected increased tTG IgA antibodies levels in patients with CD and UC [23, 24]. These results suggest positive tTG autoantibodies may be a phenomen of autoimmunity and loss of specificity in CeD [25].

At the time of the diagnosis, the majority of our patients the duodenal biopsies presented low stage (M1, M2, M3a) according to Marsh-Oberhuber classification. Histological findings of Marsh 1 were consider not fully sufficient for the diagnosis of CeD, but the one of our patient, how presented M1 stage also had biopsy-proof Dermatitis herpetiformis Duhring, which is the skin manifestation of CeD. Casella and his colleagues observed similar distribution of histological results [15]. However, number of studies has found intraepithelial lymphocytosis and villous atrophy in CD patients without any evidence of CeD [26–28]. This histological status makes it difficult to differentiate CeD from CD.

In our patients’ cohort, the dominant behaviour of IBD was of the inflammatory type, which is in line with data in literature [14, 15, 29].

In our study, the mean body mass index value of 21,53 kg/m2 also falls within the normal range provided by the WHO. Unlike coeliac children, the vast majority of adult coeliacs are not malnourished, even overweight patients are not uncommon [30, 31]. However, malnutrition is a common feature of adult IBD [32]. In contrast to our results, low range of BMI in patients with both CeD and IBD has been reported [33–35].

IBD and CeD are associated with an increased risk of loss on BMD, caused by malabsorption and inflammation. Prevalence of osteoporosis were shown to be 7–35 % in CD patients, 18 % in UC patients, and 36–38 % in untreated in CeD patients, respectively [36–40]. Interestingly, the loss of BMD in our patients with two different disease potentially leading to malabsorption syndrome were not worse than for those suffering in only one of these disorders.