Autoimmune and immune-mediated inflammatory diseases (IMIDs) develop when genetically and environmentally susceptible hosts lose stable immune tolerance. The gut ecosystem is increasingly recognized as a biologically active interface in this process. Its bacterial, fungal, and viral components may shape mucosal and systemic immunity through antigenic stimulation, barrier regulation, and metabolite-dependent signaling, although the strength of evidence is uneven: bacteriome data are currently the most mature, whereas mycobiome, virome, and phageome findings remain more disease-specific and emerging. Dysbiosis may influence autoimmunity through overlapping routes, including epithelial barrier failure, altered short-chain fatty acid, bile acid, and tryptophan metabolism, molecular mimicry, and cross-kingdom microbial interactions. Nutrition is central to this network because dietary substrates determine microbial growth, metabolic output, epithelial integrity, and immune-cell differentiation. In this narrative review, we integrate evidence on disease-associated bacteriome, mycobiome, and virome patterns in systemic autoimmune diseases, with emphasis on rheumatoid arthritis, systemic lupus erythematosus, Sjögren's syndrome, systemic sclerosis, spondyloarthritis, vasculitides, and idiopathic inflammatory myopathies. COVID-19 is considered not as a proven causal driver of autoimmunity, but as an example of an environmental and infectious insult capable of perturbing microbiome-barrier-immune communication. Finally, we discuss diet-based and microbiome-targeted approaches, including probiotics, prebiotics, synbiotics, and postbiotics, as adjunctive strategies that may help restore microbial resilience and immune balance. A better understanding of the diet-microbiome-host immunity axis may support more personalized preventive and therapeutic concepts in autoimmune disease.

Background: Anti-melanoma differentiation-associated gene 5 (anti-MDA5) positive dermatomyositis is a distinct subset of idiopathic inflammatory myopathies (IIMs), often associated with unique cutaneous features and interstitial lung disease (ILD). While East Asian cohorts frequently report high mortality due to rapidly progressive ILD (RP-ILD), data regarding Central and Eastern European populations remain scarce. Methods: We conducted a retrospective multicenter study of anti-MDA5 positive Caucasian patients managed at four Hungarian rheumatology centers between 2020 and 2025. Demographic, clinical, serological, and radiological data were analyzed. Antibody profiling was performed using a standardized 16-antigen immunoblot assay. Results: Anti-MDA5 positivity was confirmed in 24 out of 742 patients (3.23%) treated in the four centers. The median age at diagnosis was 49.5 years (range: 24-81). Classic dermatomyositis was the predominant clinical phenotype (75%), followed by clinically amyopathic dermatomyositis (CADM) (12.5%) and polymyositis (12.5%). ILD was identified in 58.3% of patients, presenting with organizing pneumonia (OP), non-specific interstitial pneumonia (NSIP), and usual interstitial pneumonia (UIP) patterns. At diagnosis, median creatine kinase (CK) (193.5 U/L) and C-reactive protein (CRP) (4.24 mg/L) levels remained low even in the ILD group, whereas lactate dehydrogenase (LDH) was elevated in 91.7% of the cohort. Anti-Ro52 positivity (45.8% overall) emerged as a notable predictor of ILD (odds ratio [OR]: 22.5, 95% confidence interval [CI]: 2.10-240.48; p = 0.0045), being present in 71.4% of affected patients. RP-ILD occurred in two patients (8.3%). Therapeutic management followed an early, aggressive strategy, frequently utilizing cyclophosphamide (45.8%) and methotrexate (37.5%), with Janus kinase (JAK) inhibitors or rituximab employed in refractory cases. Overall disease-specific survival was 100% during the study period (median follow-up: 72.0 months); no mortality was directly attributable to IIM-related complications. Conclusions: Our study demonstrates that anti-MDA5 positive dermatomyositis in a Hungarian cohort is characterized by heterogeneous manifestations and a significant association between anti-Ro52 and ILD. The observed dissociation between low CK/CRP and elevated LDH underscores the necessity for a high index of suspicion, with LDH serving as a superior marker for disease activity. While ILD presents a significant risk, early and intensive multi-modal intervention may yield superior survival outcomes in European patients compared to the historical mortality rates reported in Asian cohorts.

Immune-mediated inflammatory diseases (IMIDs) arise from interactions among genetic susceptibility, epithelial barrier function, microbiota, diet, and other environmental exposures. Modern diets influence mucosal immunity not only through fibre intake, food processing, and microbiota composition, but also through a less explored exposure layer: plant-derived molecules with potential immune activity. Crop breeding, intensive agriculture, global trade, gluten-free substitutes, and plant-based food technologies have changed the spectrum, dose, concentration, and matrix in which plant defence proteins, antinutritional factors, endogenous toxicants, and novel plant antigens reach the intestinal surface. In this structured, hypothesis-generating narrative review, we propose dietary adjuvanticity as a mechanistic framework for considering how selected food-derived molecules may amplify mucosal immune responsiveness, modify antigen presentation, disturb barrier function, or lower tolerance thresholds without necessarily acting as classical autoantigens. The framework differs from general food-derived immunomodulation, nutritional exposomics, and diet-microbiota-host interaction models by focusing specifically on adjuvant-like immune amplification at the intestinal mucosa. The ASIA concept is used only in Shoenfeld's functional sense, as an analogy for exogenous immune amplification through innate activation, danger signalling, bystander activation, epitope spreading, and loss of tolerance in susceptible hosts; it is not applied as a dietary diagnosis. Wheat amylase-trypsin inhibitors, gluten epitopes, lectins, potato glycoalkaloids, saponins, quinoa prolamins, emerging legume proteins, L-canavanine, and tolerance-promoting plant substrates are discussed with explicit separation of established clinical evidence, strong mechanistic evidence, preclinical/ex vivo evidence, and speculative disease-modifier hypotheses. Overall, plant-derived exposures are best interpreted as potential modifiers within the IMID exposome, not as primary causes of autoimmunity. Testing this model will require defined exposures, food-matrix and processing studies, biomarkers of barrier and immune activation, patient stratification, and controlled human studies.

Anti-melanoma differentiation-associated gene 5 (anti-MDA5) antibodies are critical biomarkers in myositis, associated with distinct clinical features and prognosis. This study aimed to evaluate the proportion of anti-MDA5 positivity and compare the diagnostic performance of local immunoblotting (IB) with gold-standard immunoprecipitation (IP). We performed a retrospective analysis of 3272 physician-requested anti-MDA5 IB determinations over a five-year period (2019-2023). A subsequent exploratory pilot study of ten Hungarian patients with myositis was conducted to compare IB results with radiolabeled protein IP. Confirmatory in-house enzyme-linked immunosorbent assay (ELISA) was used to distinguish between 140 kDa bands (anti-MDA5 vs. anti-NXP2). Indirect immunofluorescence (IIF) on HEp-2 cells was also evaluated. In the retrospective cohort, 3.7% (n = 121) of samples were non-negative. Among 64 borderline patients, only one (1.6%) had a definitive diagnosis of dermatomyositis (DM). Conversely, the proportion of confirmed myositis cases was notably higher among patients with strong positive IB results. In our exploratory cross-sectional pilot study, complete concordance between the two assays was observed for negative and strong positive results. Discrepancies were noted in borderline and weak positivity ranges, where anti-MDA5 was not detected by IP; instead, alternative autoantibodies were identified. The three IP-confirmed MDA5 positive samples were all validated by ELISA. The characteristic IIF cytoplasmic staining was identifiable in 2 out of 10 cases (20%). In our cohort, borderline IB cases were frequently potential false positives, highlighting the need for careful clinical evaluation. Borderline and weak results require clinical correlation or confirmatory testing to avoid misdiagnosis.

Background/Objectives: Hodgkin lymphoma (HL) represents a rare but clinically significant complication in patients with Common Variable Immunodeficiency (CVID). Immune dysregulation, impaired viral control, and Epstein–Barr virus (EBV) infection may contribute to pathogenesis and adversely affect treatment tolerance. This case-based review aims to highlight the impact of early CVID recognition and multidisciplinary management on outcomes in CVID-associated HL. Methods: A retrospective screening of 224 patients with HL treated at our institution between 2010 and 2023 identified two individuals with CVID and EBV-positive HL. These cases are presented in detail and contextualized within a structured review of the published literature. Results: The first patient, diagnosed with CVID prior to HL onset, received immunoglobulin replacement and a modified chemotherapy regimen substituting bleomycin with brentuximab vedotin, resulting in sustained complete remission. The second patient, in whom CVID was recognized only after HL relapse, experienced recurrent infections, intolerance to therapy, and fatal disease progression despite treatment with brentuximab vedotin, checkpoint inhibition, and rituximab. The literature review revealed only eight comparable cases, underscoring the rarity and complexity of this association. Conclusions: Early identification of CVID facilitates infection control and enhances tolerance to HL therapy, thereby improving clinical outcomes. Multidisciplinary, individualized management and incorporation of targeted agents are pivotal in optimizing care for this vulnerable population.

Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors that sense lipophilic molecules and act as transcription factors to regulate target genes. PPARs have been implicated in the regulation of innate immunity, glucose and lipid metabolism, cell proliferation, wound healing, and fibrotic processes. Some synthetic PPAR ligands are promising molecules for the treatment of inflammatory and fibrotic processes in immune-mediated intestinal diseases. Some of these are currently undergoing or have previously undergone clinical trials. Dietary PPAR ligands and changes in microbiota composition could modulate PPARs’ activation to reduce inflammatory responses in these immune-mediated diseases, based on animal models and clinical trials. This narrative review aims to summarize the role of PPARs in immune-mediated bowel diseases and their potential therapeutic use.

BACKGROUND:Inflammatory bowel diseases (Crohn's disease and ulcerative colitis) and microscopic colitis (lymphocytic and collagenous colitis) are immune-mediated diseases of the gastrointestinal tract, with distinct pathophysiology.OBJECTIVE:We sought to compare the prevalence of autoimmune diseases between microscopic colitis (MC) and inflammatory bowel diseases (IBDs) in our patient cohorts in their medical history.METHODS:We collected data from 611 patients (508 with IBD, 103 with MC). We recorded cases of other autoimmune diseases. The screened documentation was written in the period between 2008 and 2022. We sought to determine whether colonic involvement had an impact on the prevalence of autoimmune diseases.RESULTS:Ulcerative colitis patients and patients with colonic-predominant Crohn's disease had a greater propensity for autoimmune conditions across the disease course than patients with ileal-predominant Crohn's disease. Gluten-related disorders were more common in Crohn's disease than in ulcerative colitis, and slightly more common than in microscopic colitis. In ulcerative colitis, 10 patients had non-differentiated collagenosis registered, which can later develop into a definite autoimmune disease.CONCLUSIONS:Predominantly colonic involvement can be a predisposing factor for developing additional autoimmune disorders in IBD. Ulcerative colitis patients may have laboratory markers of autoimmunity, without fulfilling the diagnostic criteria for definitive autoimmune disorders (non-differentiated collagenosis).

The consumption of artificial and low-calorie sweeteners (ASs, LCSs) is an important component of the Western diet. ASs play a role in the pathogenesis of metabolic syndrome, dysbiosis, inflammatory bowel diseases (IBDs), and various inflammatory conditions. Intestinal nutrient-sensing receptors act as a crosstalk between dietary components, the gut microbiota, and the regulation of immune, endocrinological, and neurological responses. This narrative review aimed to summarize the possible effects of ASs and LCSs on intestinal nutrient-sensing receptors and their related functions. Based on the findings of various studies, long-term AS consumption has effects on the gut microbiota and intestinal nutrient-sensing receptors in modulating incretin hormones, antimicrobial peptides, and cytokine secretion. These effects contribute to the regulation of glucose metabolism, ion transport, gut permeability, and inflammation and modulate the gut–brain, and gut–kidney axes. Based on the conflicting findings of several in vitro, in vivo, and randomized and controlled studies, artificial sweeteners may have a role in the pathogenesis of IBDs, functional bowel diseases, metabolic syndrome, and cancers via the modulation of nutrient-sensing receptors. Further studies are needed to explore the exact mechanisms underlying their effects to decide the risk/benefit ratio of sugar intake reduction via AS and LCS consumption.

Turner syndrome is one of the most frequently reported sex chromosomal abnormalities, affecting approximately 40 in every 100 000 live female births. The underlying chromosomal alteration is the complete or partial loss of X chromosome or mosaicism. Because of primary ovarian insufficiency, the synthesis of estrogen hormones is compromised, and patients require hormone substitution. Apart from the phenotypical presentation (short stature, primary amenorrhea), the effects of ovarian insufficiency can affect diverse organ systems (such as cardiovascular, endocrine, and lymphatic systems). Hepatobiliary pathology can present on a broad spectrum: from mild asymptomatic hypertransaminasemia to marked architectural changes. Estrogen hormone replacement therapy in these patients can improve the perturbations of laboratory values and can attenuate the progression of hepatic structural changes. Moreover, providing sufficient estrogen replacement has numerous benefits for other conditions of the patients as well. Both the all-cause mortality and deaths from cardiovascular complications are greatly increased in Turner syndrome, and hormone replacement might contribute to the decreased incidence of these events. The diagnostics of Turner syndrome are outside the scope of our paper, and we briefly discuss the cardiovascular complications because many the liver involvement partially involves alterations of vascular origin. Though we sought to highlight the importance of proper hormone replacement therapy, we did not attempt to write a comprehensive recommendation for exact treatment protocols. We provided an overview of preferred therapeutic approaches, as the treatment should be tailored according to the individual patient's needs.

Microscopic colitis (comprising lymphocytic and collagenous colitis, albeit an incomplete variant is gaining recognition as well) is a chronic, immune-mediated inflammatory state of the lower gastrointestinal tract (colon). The diagnosis requires diagnostic colonoscopy with characteristic histopathological findings. They have a propensity to present in senior populations (above 60 years of age), particularly women – who are approximately 2.5–3 times more likely to develop microscopic colitis. Preexisting other immune-inflammatory diseases are also shown to predispose patients for the development of microscopic colitis. The classic presentation is profuse watery diarrhea, often during the night or early morning hours. Fecal incontinence and abdominal pain are frequent as well. Thus, the disease impacts patients’ quality of life and well-being. The first described cases date back to the seventies and eighties of the twentieth century, thereby they can be considered fairly recently discovered disease states. Our understanding of the disease and its pathophysiology is still incomplete. Although there is a lack of unified recommendation for treatment, most clinicians prefer the use of budesonide, and most published guidelines regard this locally acting glucocorticoid as the therapy of choice. In our article, we aimed for a brief, noncomprehensive overview of the clinical significance, diagnosis, and management of microscopic colitis.

Background Microscopic colitides are chronic immune-inflammatory bowel diseases. The typical presentation is chronic, watery diarrhoea. Inflammation mostly cannot be visualized via macroscopic inspection. The diagnosis thus requires histologic sampling. The clinical picture can vary. New investigations can prove valuable in setting up recommendations. Patients A total of 103 patients with microscopic colitis (MC) [28 lymphocytic colitis (LC) 27.2%, 75 collagenous colitis (CC) 72.8%] in the Clinical Centre of the University of Debrecen (tertiary care centre) were included, diagnosed between 1993 and 2020. We aimed for a retrospective analysis characterizing Hungarian MC patients. We sought to compare two subgroups of patients (with either LC or CC). Our investigation focussed on dominant alteration of stool habits, autoimmune and allergic comorbidities. Autoimmune diseases were diagnosed in 39% (40) of the patients, allergic diseases in 26.2% (27) of patients and 22.2% of tested patients had alimentary hypersensitivity to certain foods (18 cases out of 81 tested). Results Age of diagnosis was younger in LC (44.5 years, SD: 5.3 vs. 51.9 years, SD: 12.8, difference= 7.4 years p = .0151). Autoimmune diseases were equally frequent in the two groups (LC: 10 patients 36%, CC: 30 patients, 40%, difference: 4%, p = .7124). Food-linked hypersensitivities were more common in CC (LC: 1 patient, CC: 17 patients). Difference in allergic diseases (asthma, rhinitis, urticaria) did not differ between groups (LC: 6 patients, 21%; CC: 21 patients, 28%, difference: 7% p = .4739). One-third of the patients did not complain about chronic diarrhoea. These patients had chronic constipation as the main symptom (34 patients, 33%). Conclusion Pre-existing autoimmune and allergic diseases were common in patients with MC. Chronic watery diarrhoea is not experienced in many cases. The absence of certain symptoms should not be used to rule out the condition.

OBJECTIVES:Thus far, few attempted to characterize the temporal onset of extraintestinal manifestations (EIM) in inflammatory bowel diseases (IBD). We sought to determine the time of onset of these findings in a patient cohort with IBD.METHODS:We reviewed the electronic health records of 508 IBD patients (303 CD, 205 UC) and summarized general patient characteristics and the temporal relationship and order of presentation of extraintestinal manifestations.RESULTS:CD patients were younger at diagnosis. CD patients with ileocolonic involvement (L3) were younger, and UC patients with pancolitis (E3) were slightly younger at diagnosis. A total of 127 out of 303 (41.91%) CD and 81 out of 205 (39.51%) UC patients had EIMs (p = 0.5898). Some patients presented with EIMs before the diagnosis of IBD (9.45% of Crohn's disease and 17.28% of ulcerative colitis patients with EIMs, respectively). Of these, seven cases (four in CD and three in UC) were visible by inspection of the patients (either dermatologic or ocular findings). The diagnosis of IBD and extraintestinal symptoms often occurred within a year (22.83% of CD and 16.04% of UC patients). Typically, the diagnosis of the first extraintestinal symptoms happened after the onset of bowel disease (+4.3 (±6.3) years, range: 10 years before to 30 years after in Crohn's disease and +3.8 (±10) years, range: 24 years before to 30 years after) in ulcerative colitis. UC patients with pancolitis (E3) usually had EIMs earlier in the disease course and displayed EIMs more frequently before IBD diagnosis. Furthermore, patients with pancolitis developed EIMs more frequently than other sub-groups.CONCLUSION:Extraintestinal manifestations in inflammatory bowel diseases can present at any time, relative to the bowel symptoms. In cases, the presence of a characteristic EIM might be a harbinger of the development of IBD.

OBJECTIVES:Progranulin (PGRN) is a secreted growth factor that helps to regulate neuronal survival by blocking tumor necrosis factor-alpha (TNFα) receptors. The antioxidant alpha-lipoic acid (ALA) is used in diabetic neuropathy to improve nerve conduction and relieve neuropathic pain, but its effects on PGRN levels have not yet been elucidated.METHODS:In this prospective study, 54 patients with type 2 diabetes and peripheral neuropathy received 600 mg of ALA daily for 6 months. Twenty-four patients with diabetes without neuropathy were also included in the study. Serum PGRN and TNFα levels were determined using enzyme-linked immunosorbent assays. In addition, current perception threshold (CPT) testing was used to assess sensory neuropathy.RESULTS:After ALA treatment, serum PGRN levels were significantly increased and CPT values were significantly improved. Furthermore, there were significant positive correlations among TNFα, ICAM-1, and PGRN levels both before and after ALA treatment. A significant negative correlation was observed between the improvements in CPT and the PGRN levels. Furthermore, ICAM-1 levels were an independent predictor of PGRN levels.CONCLUSIONS:Changes in serum PGRN levels indicate that ALA treatment may have beneficial effects on endothelial function and neuronal inflammation.

Aim To evaluate tear film parameters and relationship of objective clinical signs and subjective symptoms of dry eye disease (DED) in inflammatory bowel disease (IBD) subgroups. Methods 39 patients with Crohn's disease (CD), 26 patients with ulcerative colitis (UC), and 39 control persons with no ocular symptoms or surface disorders were included in this prospective, case-control, and cross-sectional study. The ocular surface disease index (OSDI) questionnaire was applied to evaluate dry eye symptoms, and objective tests of DED were performed on both eyes of each subject. Results The average of OSDI scores was 30.59 (±16.68) in CD patients, 24.67 (±23.48) in UC patients, and 11.19 (±5.8) in controls. Except for tear film breakup time (tBUT) and Schirmer-I values other objective parameters were better in UC patients, than in CD patients. CD patients rather than UC patients tend to develop DED. This was associated with immunosuppressant and TNF-α inhibitor use. Conclusions Clinicians must be aware of the spectrum of DED involvement in IBD and suggest using artificial tears in order to decrease severity of ocular complications.

Although celiac disease (gluten-sensitive enteropathy) is a relatively well known malady, yet is surrounded by several misconceptions. It is in fact, a multi-systemic autoimmune disorder with a wide spectrum of possible presentations, though most clinicians regard it as a solely gastrointestinal disease. Another misconception that it is a disease of paediatric age group. Thus, the diagnosis of adult or elderly patients is often delayed. Recognition of the disease in the adults can be challenging, as there are less pronounced gastrointestinal symptoms, and patients present with other manifestations (i.e., neurologic, cardiovascular, hepatobiliary, or hematologic involvement are common). As these extraintestinal manifestations are less well known among practicing physicians, here we propose a brief overview of these. We aimed to summarize the available literature on the extraintestinal manifestations associated with gluten sensitivity. Orv Hetil. 2019; 160(34): 1327-1334.

To the Editor We read the paper by Xiao et al. with keen interest. The authors investigated the clinical relevance of immunoglobulin G (IgG)-mediated “food allergy” in the pathogenesis of inflammatory bowel disease (IBD) and found that certain food antigen-specific IgG class antibodies were highly elevated in the sera of Crohn’s disease (CD) patients (1). Food allergies may be classified as immunoglobulin E (IgE)-mediated (immediate) reactions, non-IgE-mediated (delayed) hypersensitivity and mixed reactions. Beyond the IgE responses, there are other possible adverse reactions to food (i.e. lactase deficiency). These are termed “food intolerances”, although they are not immune reactions by definition. The current gold-standard for diagnosing food allergy is the elimination of the suspicious food antigen followed by its reintroduction (challenge) (2). IgG testing is neither recommended nor has been proven in diagnostic practice. Test results should not be used to advise dietary modification or food elimination. IgG antibodies against food antigens are frequently detected in healthy persons, independently from food-related symptoms. Numerous studies have shown that the production of food-specific IgG is the natural, physiologic response to regularly ingested foods (3). They therefore simply indicate that the person has previously been exposed to that food. This paper raises the question of what came first, the chicken or the egg? Do the mucosal inflammation (IBD) and intestinal barrier dysfunction (“leaky gut”) preceed the elevation of these IgG-type antibodies, or is it the other way around? CD patients have often shown an intense immune response to food antigens, generating both IgEand IgG-type antibodies. The number of IgG-positive food items may serve as a potential diagnostic marker of CD (and related GI-mucosal damage). A diet guided by food antibody tests might aid in disease control and encourage remission (4). Studies on another type of immune-mediated gastrointestinal disease (eosinophilic esophagitis) found that, in the absence of any IgE or IgG antibody testing for food antigens, an empiric elimination diet excluding six food groups (cereals, including wheat, rice, and corn; milk and dairy products; eggs; fish; seafood; and legumes, peanuts, and soy) is an effective and sustainable non-pharmacological dietary treatment option for patients (5). In our opinion, it is unfortunate to use definitions improperly or arbitrarily as synonyms. However, increased levels of IgG-type food-specific antibodies might indicate an increased mucosal permeability to luminal contents (leaky gut). Investigating the introduction of the Six-Food Elimination Diet in CD patients may therefore be suitable, as it might help ameliorate conditions such as eosinophilic esophagitis.

Abstract: Although celiac disease (gluten-sensitive enteropathy) is a relatively well known malady, yet is surrounded by several misconceptions. It is in fact, a multi-systemic autoimmune disorder with a wide spectrum of possible presentations, though most clinicians regard it as a solely gastrointestinal disease. Another misconception that it is a disease of paediatric age group. Thus, the diagnosis of adult or elderly patients is often delayed. Recognition of the disease in the adults can be challenging, as there are less pronounced gastrointestinal symptoms, and patients present with other manifestations (i.e., neurologic, cardiovascular, hepatobiliary, or hematologic involvement are common). As these extraintestinal manifestations are less well known among practicing physicians, here we propose a brief overview of these. We aimed to summarize the available literature on the extraintestinal manifestations associated with gluten sensitivity. Orv Hetil. 2019; 160(34): 1327–1334.

Immunglobulin E (IgE)-based, irregularly recurring, severe anaphylactic reactions occurred in a 50-year-old European white male patient suffering also from Crohn's disease. On the base of immunologic laboratory tests concerning the mechanism of the phenomenon, the idea arose whether molecules derived for certain microbial derivatives could enter the blood circulation via the damaged bowel walls in the patient with Crohn's disease and they might act as allergens. The microbial analysis diagnosed atypical Staphylococcus in the stool. The serum level of IgE was very high. The concomitant use of targeted antibiotics and anti-allergy and immunosuppressive agents resulted in a complete remission during a couple of months. Not only Crohn's disease has improved, but also the total serum IgE level has decreased significantly, and the unpredictable anaphylactic attacks have been completely eliminated. In Crohn's disease, the anaphylactic complications induced by atypical microbial allergens (e.g., derivatives of Staphylococcus) can be effectively treated after the recognition of this pathological mechanism. This is the first description of such a pathologic state. Orv Hetil. 2019; 160(38): 1514-1518.

Abstract: Immunglobulin E (IgE)-based, irregularly recurring, severe anaphylactic reactions occurred in a 50-year-old European white male patient suffering also from Crohn’s disease. On the base of immunologic laboratory tests concerning the mechanism of the phenomenon, the idea arose whether molecules derived for certain microbial derivatives could enter the blood circulation via the damaged bowel walls in the patient with Crohn’s disease and they might act as allergens. The microbial analysis diagnosed atypical Staphylococcus in the stool. The serum level of IgE was very high. The concomitant use of targeted antibiotics and anti-allergy and immunosuppressive agents resulted in a complete remission during a couple of months. Not only Crohn’s disease has improved, but also the total serum IgE level has decreased significantly, and the unpredictable anaphylactic attacks have been completely eliminated. In Crohn’s disease, the anaphylactic complications induced by atypical microbial allergens (e.g., derivatives of Staphylococcus) can be effectively treated after the recognition of this pathological mechanism. This is the first description of such a pathologic state. Orv Hetil. 2019; 160(38): 1514–1518.

Purpose: To evaluate detailed corneal parameters of inflammatory bowel disease (IBD) patients, including Crohn's disease (CD) and ulcerative colitis (UC) patients, and to assess associations between anterior segment values and other clinical variables. Methods: This prospective cross-sectional case-control study at a tertiary referral center included 30 CD patients, 36 UC patients and 80 age- and gender-matched controls with no ocular symptoms or ocular surface disorders. All study participants underwent a comprehensive ophthalmological evaluation with special interest in dry eye disease (DED). Corneal parameters were evaluated by Pentacam. Results: The mean age of CD patients, UC patients, and controls was 45.80 +/- 11.55 years, 52.00 +/- 16.05, and 50.68 +/- 14.62, respectively. The average disease duration was 12.72 +/- 5.83 years for CD patients and 15.94 +/- 10.09 years for UC patients. All pachymetric (center, apex and thinnest) and corneal volume (CV) measurements were significantly decreased, while anterior chamber angle width (ACA) values were significantly increased on both sides in all IBD patients compared to those in controls (p < .05). In addition, several anterior segment parameters were altered unilaterally in CD or UC patients. Negative correlations were found between corneal parameters and Schirmer I test values. Conclusions: Our investigations suggest that IBD patients have thinner corneas compared to that of controls. The coexistence of reduced tear quantity seems to have an additional impact on the thinning of the cornea in IBD patients. Early recognition of corneal impairments, a possible extraintestinal manifestation of IBD, should be included in the disease checkup to reduce vision-threatening developments.