Onset Inflammatory Bowel Disease Research Articles

Pediatric inflammatory bowel diseases, features of the disease course: a clinical case of complicated course of ulcerative colitis

The article is devoted to one of the urgent problems of pediatric gastroenterology – inflammatory bowel diseases (IBD), which currently include ulcerative colitis (UC) and Crohn’s disease (CD). The prevalence of IBD is inferior to other gastroenterological diseases, but according to the severity of the course, the frequency of complications and the level of mortality, IBD occupy one of the leading places in the structure of diseases of the gastrointestinal tract. The problem of IBD constantly attracts the attention of doctors of various specialties – pediatricians, gastroenterologists, surgeons and others. This is due to an increase in the incidence of this pathology, a variety of clinical manifestations, including extra-intestinal manifestations, faced by doctors of various specialties. In childhood, there is more often a greater prevalence of the lesion, a less specific and erased picture, there is an impact on the physical development of the child. The article provides information on the prevalence, significant factors in the development of the disease; research data revealing the relationship between taking med ications and the risk of IBD onset. The problems of the pathogenesis of the disease, the significance of the genetic status in the development of CD and UC are described. The article presents data on the features of the clinical picture of UC in childhood, recommendations for the primary diagnosis of IBD, including modern laboratory and instrumental research methods. The article also describes the recommended international criteria for assessing the severity of IBD and the problems of differential diagnosis. As a demonstration, the authors’ own observations are presented. The clinical example describes an atypical case of UC in a teenager, occurring with the involvement of the cardiovascular, bronchopulmonary and urinary systems with the development of polyserositis. Early diagnosis of IBD is necessary to prevent disability of patients, ensure further development of the child, improve the quality of life.

Inflammatory Bowel Disease in Adults and Elderly: The Use of Selected Non-IBD Medication Examined in a Nationwide Cohort Study.

Real-world data on medications used for conditions other than inflammatory bowel disease (IBD) are sparse. We examined how the onset of IBD affects the prescription pattern of selected non-IBD medication and the risk of becoming an incident user. This nationwide cohort study utilized data from Danish health registers. We included incident patients with young adult-onset IBD (18-39 years of age), adult-onset IBD (40-59 years of age), and elderly-onset IBD (60+ years of age), from 1998 to 2018 and followed all for 3 years. We examined redeemed prescriptions before and after the onset of IBD and estimated the risk of becoming a user of non-IBD medications using logistic regression models. We identified 36165 patients, 16 771 (46%) with young adult onset, 10615 (29%) with adult onset, and 8779 (24%) with elderly onset. The onset of IBD increased the use of antidepressants, antipsychotics, sedatives/hypnotics, opioids, nonopioid analgesics, antidiabetics, and proton pump inhibitors, even in patients with no other underlying comorbid diseases. The adjusted odds ratio for using antidepressants 1 year after the onset of IBD in elderly was 1.50 (95% confidence interval [CI], 1.14-1.82), in opioids 1.69 (95% CI, 1.45-1.95), in nonopioid analgesics 2.10 (95% CI, 1.77-2.48), in cardiovascular medication 2.20 (95% CI, 1.86-2.61), and in proton pump inhibitors 1.51 (95% CI, 1.31-1.74) compared with adults. In all 3 age groups, the proportions of patients with redeemed prescriptions for several groups of non-IBD medication were significantly increased after the IBD diagnosis compared with before. The risk of becoming an incident user for several groups of non-IBD medication was increased in elderly patients.

Efficacy and Safety of Anti-Tumor Necrosis Factor Alpha in Very Early Onset Inflammatory Bowel Disease.

Very early onset inflammatory bowel disease (VEOIBD) is defined as disease onset in patients younger than 6 years. Challenges in treatment of VEOIBD include lack of approved therapies and increased incidence of monogenic immunodeficiencies. We report on patterns of anti-TNF use, efficacy, and safety in a large cohort of patients with VEOIBD. Very early onset inflammatory bowel disease patients receiving care at a single center were prospectively enrolled in a data registry and biorepository starting in 2012. Whole exome sequencing was available to all patients. Clinical data including IBD medication use and response were extracted from the medical record. We examined antitumor necrosis factor (anti-TNF) cumulative exposure and time to failure and evaluated the effect of covariates on anti-TNF failure using Cox proportional hazard regression. In this cohort of 216 VEOIBD patients with median 5.8-year follow-up, 116 (53.7%) were TNF-exposed. Sixty-two TNF-exposed patients (53.4%) received their first dose at younger than 6 years. Cumulative exposure to anti-TNF was 23.6% at 1 year, 38.4% at 3 years, and 43.4% at 5 years after diagnosis. Cumulative exposure was greater in patients with Crohn's disease (P = .0004) and in those diagnosed in 2012 or later (P < .0001). Tumor necrosis factor failure occurred in 50.9% of those exposed. Features predictive of anti-TNF failure included ulcerative colitis/IBD-unclassified (hazard ratio, 1.94; P = .03), stricturing (hazard ratio, 2.20; P = .04), and younger age at diagnosis (hazard ratio, 1.25; P = .01). Adverse events occurred in 22.6% of infliximab-exposed and 14.3% of adalimumab-exposed. Efficacy and safety of anti-TNFs in VEOIBD is comparable to what has previously been reported in older patients.

Older Adult-Onset of Inflammatory Bowel Diseases Is Associated With Higher Utilization of Analgesics: A Nationwide Cohort Study.

Patients with inflammatory bowel diseases (IBD) commonly require analgesic medications to treat pain, which may be associated with complications. We examined trends of analgesic use according to age at IBD onset. This nationwide cohort study included adults diagnosed with IBD between 1996 and 2021 in Denmark. Patients were stratified according to their age at IBD onset: 18-39 years (young adult), 40-59 years (adult), and older than 60 years (older adult). We examined the proportion of patients who received prescriptions for analgesic medications within 1 year after IBD diagnosis: strong opioids, tramadol, codeine, nonsteroidal anti-inflammatory drugs, and paracetamol. Multivariable logistic regression analysis was performed to examine the association between age at IBD onset and strong opioid prescriptions and the composite of strong opioid/tramadol/codeine prescriptions. We identified 54,216 adults with IBD. Among them, 25,184 (46.5%) were young adults, 16,106 (29.7%) were adults, and 12,926 (23.8%) were older adults at IBD onset. Older adults most commonly received analgesic prescriptions of every class. Between 1996 and 2021, strong opioid, tramadol, and codeine prescriptions were stable, while paracetamol prescriptions increased and nonsteroidal anti-inflammatory drug prescriptions decreased. After multivariable logistic regression analysis, older adults had higher adjusted odds of receiving strong opioid prescriptions (adjusted odds ratio 1.95, 95% confidence interval 1.77-2.15) and the composite of strong opioid/tramadol/codeine prescriptions (adjusted odds ratio 1.93, 95% confidence interval 1.81-2.06) within 1 year after IBD diagnosis compared with adults. In this nationwide cohort, older adults most commonly received analgesic prescriptions within 1 year after IBD diagnosis. Additional research is needed to examine the etiology and sequelae of increased analgesic prescribing to this demographic.

Is Occupation a Risk Factor for Developing Inflammatory Bowel Disease? A Case–Control Study

Abstract Background and aims The role of occupation is uncertain in the onset of inflammatory bowel diseases. The aim of this study is to identify if there is a role of occupation in these diseases. Materials and methods A case–control study with incident cases with inflammatory bowel diseases was designed. Cases and controls were recruited simultaneously and controls followed a sex and age frequency matching with cases. A detailed questionnaire was completed by all the participants. To analyze the results, a logistic regression was used. A subgroup analysis was performed for each inflammatory bowel disease. Results A total of 141 patients with incident inflammatory bowel disease (80 ulcerative colitis, 55 Crohn’s disease, and 6 unclassified colitis) and 114 controls were included. There were no statistically significant differences in type of work, working hours, contact with animals, or physical activity at work between inflammatory bowel disease patients and controls. After stratifying results according to type of IBD, there were no statistically significant differences either. Conclusions There seems to be no risk for inflammatory bowel disease onset regarding the type of work, working hours, contact with animals, or sedentariness.

S1175 Examination of Dysplasia and Cancer Surveillance Compliance With Guidelines Among Pediatric Onset Inflammatory Bowel Disease at a Tertiary Referral Center

S1175 Examination of Dysplasia and Cancer Surveillance Compliance With Guidelines Among Pediatric Onset Inflammatory Bowel Disease at a Tertiary Referral Center

S923 Distinct Phenotypic and Treatment Differences in Late Onset Inflammatory Bowel Disease: A Large Population-Based Study

S923 Distinct Phenotypic and Treatment Differences in Late Onset Inflammatory Bowel Disease: A Large Population-Based Study

Outcome of Very Early Onset Inflammatory Bowel Disease Associated With Primary Sclerosing Cholangitis: A Multicenter Study From the Pediatric IBD Porto Group of ESPGHAN.

Whether primary sclerosing cholangitis related to inflammatory bowel disease (PSC-IBD) diagnosed before 6 years (ie, VEO-IBD) has a distinct phenotype and disease course is uninvestigated. We aimed to analyze the characteristics and natural history of VEO-PSC-IBD, compared with early and adolescent-onset PSC-IBD. This is a multicenter, retrospective, case-control study from 15 centers affiliated with the Porto and Interest IBD group of ESPGHAN. Demographic, clinical, laboratory, endoscopic, and imaging data were collected at baseline and every 6 months. Inflammatory bowel disease-related (clinical remission, need for systemic steroids and biologics, and surgery) and PSC-related (biliary and portal hypertensive complications, need for treatment escalation and liver transplantation, cholangiocarcinoma, or death) outcomes were compared between the 2 groups. Sixty-nine children were included, with a median follow-up of 3.63 years (interquartile range, 1-11): 28 with VEO-PSC-IBD (23 UC [82%], 2 IBD-U [7%] and 3 [11%] CD), and 41 with PSC-IBD (37 UC [90%], 3 IBDU [7.5%] and 1 [2.5%] CD). Most patients with UC presented with pancolitis (92% in VEO-PSC-UC vs 85% in PSC-UC, P = .2). A higher number of patients with VEO-PSC-IBD were diagnosed with PSC/autoimmune hepatitis overlap syndrome than older children (24 [92%] vs 27 [67.5%] PSC-IBD, P = .03), whereas no other differences were found for PSC-related variables. Time to biliary strictures and infective cholangitis was lower in the VEO-PSC-IBD group (P = .01 and P = .04, respectively), while no difference was found for other outcomes. No cases of cholangiocarcinoma were reported. Primary sclerosing cholangitis related to inflammatory bowel disease has similar baseline characteristics whether diagnosed as VEO-IBD or thereafter. A milder disease course in terms of biliary complications characterizes VEO-PSC-IBD.

VEO-IBD NOX1 variant highlights a structural region essential for NOX/DUOX catalytic activity

Inflammatory bowel diseases (IBD) are chronic intestinal disorders that result from an inappropriate inflammatory response to the microbiota in genetically susceptible individuals, often triggered by environmental stressors. Part of this response is the persistent inflammation and tissue injury associated with deficiency or excess of reactive oxygen species (ROS). The NADPH oxidase NOX1 is highly expressed in the intestinal epithelium, and inactivating NOX1 missense mutations are considered a risk factor for developing very early onset IBD. Albeit NOX1 has been linked to wound healing and host defence, many questions remain about its role in intestinal homeostasis and acute inflammatory conditions. Here, we used in vivo imaging in combination with inhibitor studies and germ-free conditions to conclusively identify NOX1 as essential superoxide generator for microbiota-dependent peroxynitrite production in homeostasis and during early endotoxemia. NOX1 loss-of-function variants cannot support peroxynitrite production, suggesting that the gut barrier is persistently weakened in these patients. One of the loss-of-function NOX1 variants, NOX1 p. Asn122His, features replacement of an asparagine residue located in a highly conserved HxxxHxxN motif. Modelling the NOX1-p22phox complex revealed near the distal heme an internal pocket restricted by His119 and Asn122 that is part of the oxygen reduction site. Functional studies in several human NADPH oxidases show that substitution of asparagine with amino acids with larger side chains is not tolerated, while smaller side chains can support catalytic activity. Thus, we identified a previously unrecognized structural feature required for the electron transfer mechanism in human NADPH oxidases.

A case of neonatal sweet syndrome associated with mevalonate kinase deficiency

BackgroundSweet syndrome (SS), also known as acute febrile neutrophilic dermatosis, is an immunologic syndrome characterized by widespread neutrophilic infiltration. Histiocytoid Sweet syndrome (H-SS) is a histopathologic variant of SS. While SS most commonly occurs in adults, this case report discusses an infant patient who presented with H-SS.Case presentationThrough a multidisciplinary approach, this patient was also found to have very early onset inflammatory bowel disease (VEO-IBD) and Mevalonate kinase-associated disease (MKAD). While prior case studies have characterized an association between VEO-IBD and MKAD, there is no literature describing the association of all three diagnoses this case: H-SS, VEO-IBD and MKAD. Initiation of canakinumab in this patient resulted in successful control of the disease.ConclusionsThis case highlights the importance of a multidisciplinary approach to rare diagnoses, and collaboration during cases with significant diagnostic uncertainty.

Cerebral venous sinus thrombosis in young children with inflammatory bowel disease: A report of two cases

We describe two young children aged 2 and 5-year-old with very early onset inflammatory bowel disease (IBD), who developed focal seizures during an acute flare of disease. Cerebral venous sinus thrombosis (CVST) was confirmed with magnetic resonance imaging and magnetic resonance venography of the brain. CVST is a rare complication of paediatric IBD that can cause significant morbidity and mortality. The important risk factor for CVST in our children was active disease, which exposed them to an increased prothrombic state. Aggressive treatment of IBD resulted in full neurological recovery of our patients and resolution of the CVST. Our case report is the youngest reported age of CVST associated with IBD to date and highlights the need for clinicians to be vigilant for this rare complication, even in young children with IBD.

A Deep View of the Biological Property of Interleukin-33 and Its Dysfunction in the Gut.

Intestinal diseases have always posed a serious threat to human health, with inflammatory bowel disease (IBD) being one of them. IBD is an autoimmune disease characterized by chronic inflammation, including ulcerative colitis (UC) and Crohn's disease (CD). The "alarm" cytokine IL-33, which is intimately associated with Th2 immunity, is a highly potent inflammatory factor that is considered to have dual functions-operating as both a pro-inflammatory cytokine and a transcriptional regulator. IL-33 has been shown to play a crucial role in both the onset and development of IBD. Therefore, this review focuses on the pathogenesis of IBD, the major receptor cell types, and the activities of IL-33 in innate and adaptive immunity, as well as its underlying mechanisms and conflicting conclusions in IBD. We have also summarized different medicines targeted to IL-33-associated diseases. Furthermore, we have emphasized the role of IL-33 in gastrointestinal cancer and parasitic infections, giving novel prospective therapeutic utility in the future application of IL-33.

Fractal Parameters as Independent Biomarkers in the Early Diagnosis of Pediatric Onset Inflammatory Bowel Disease

Inflammatory bowel disease (IBD), which encompasses two different phenotypes—Crohn’s disease (CD) and ulcerative colitis (UC)—consists of chronic, relapsing disorders of the gastrointestinal tract. In 20–30% of cases, the disease begins in the pediatric age. There have been just a few studies that used fractals for IBD investigation, but none of them analyzed intestinal cell chromatin. The main aim of this study was to assess whether it is possible to differentiate between the two phenotypes in pediatric patients, or either of the phenotypes versus control, using the fractal dimension and lacunarity of intestinal cell chromatin. We analyzed nuclei from at least seven different intestinal segments from each group. In the majority of colon segments, both the fractal dimension (FD) and the lacunarity significantly differed between the UC group and CD group, and the UC group and control group. In addition, the ileocecal valve and rectum were the only segments in which CD could be differentiated from the controls based on the FD. The potential of the fractal analysis of intestinal cell nuclei to serve as an observer-independent histological tool for ulcerative colitis diagnosis was identified for the first time in this study. Our results pave the way for the development of computer-aided diagnosis systems that will assist the physicians in their clinical practice.

Serum and Urine Metabolomic Profiling of Newly Diagnosed Treatment-Naïve Inflammatory Bowel Disease Patients.

Inflammatory bowel disease (IBD) is a prevalent chronic noncurable disease associated with profound metabolic changes. The discovery of novel molecular indicators for unraveling IBD etiopathogenesis and the diagnosis and prognosis of IBD is therefore pivotal. We sought to determine the distinctive metabolic signatures from the different IBD subgroups before treatment initiation. Serum and urine samples from newly diagnosed treatment-naïve IBD patients and age and sex-matched healthy control (HC) individuals were investigated using proton nuclear magnetic resonance spectroscopy. Metabolic differences were identified based on univariate and multivariate statistical analyses. A total of 137 Crohn's disease patients, 202 ulcerative colitis patients, and 338 HC individuals were included. In the IBD cohort, several distinguishable metabolites were detected within each subgroup comparison. Most of the differences revealed alterations in energy and amino acid metabolism in IBD patients, with an increased demand of the body for energy mainly through the ketone bodies. As compared with HC individuals, differences in metabolites were more marked and numerous in Crohn's disease than in ulcerative colitis patients, and in serum than in urine. In addition, clustering analysis revealed 3 distinct patient profiles with notable differences among them based on the analysis of their clinical, anthropometric, and metabolomic variables. However, relevant phenotypical differences were not found among these 3 clusters. This study highlights the molecular alterations present within the different subgroups of newly diagnosed treatment-naïve IBD patients. The metabolomic profile of these patients may provide further understanding of pathogenic mechanisms of IBD subgroups. Serum metabotype seemed to be especially sensitive to the onset of IBD.

Spontaneous episodic inflammation in the intestines of mice lacking HNF4A is driven by microbiota and associated with early life microbiota alterations.

The inflammatory bowel diseases (IBD) occur in genetically susceptible individuals who mount inappropriate immune responses to their microbiota leading to chronic intestinal inflammation. Whereas IBD clinical presentation is well described, how interactions between microbiota and host genotype impact early subclinical stages of the disease remains unclear. The transcription factor hepatocyte nuclear factor 4 alpha (HNF4A) has been associated with human IBD, and deletion of Hnf4a in intestinal epithelial cells (IECs) in mice (Hnf4aΔIEC) leads to spontaneous colonic inflammation by 6-12 mo of age. Here, we tested if pathology in Hnf4aΔIEC mice begins earlier in life and if microbiota contribute to that process. Longitudinal analysis revealed that Hnf4aΔIEC mice reared in specific pathogen-free (SPF) conditions develop episodic elevated fecal lipocalin 2 (Lcn2) and loose stools beginning by 4-5 wk of age. Lifetime cumulative Lcn2 levels correlated with histopathological features of colitis at 12 mo. Antibiotic and gnotobiotic tests showed that these phenotypes in Hnf4aΔIEC mice were dependent on microbiota. Fecal 16S rRNA gene sequencing in SPF Hnf4aΔIEC and control mice disclosed that genotype significantly contributed to differences in microbiota composition by 12 mo, and longitudinal analysis of the Hnf4aΔIEC mice with the highest lifetime cumulative Lcn2 revealed that microbial community differences emerged early in life when elevated fecal Lcn2 was first detected. These microbiota differences included enrichment of a novel phylogroup of Akkermansia muciniphila in Hnf4aΔIEC mice. We conclude that HNF4A functions in IEC to shape composition of the gut microbiota and protect against episodic inflammation induced by microbiota throughout the lifespan. IMPORTANCE The inflammatory bowel diseases (IBD), characterized by chronic inflammation of the intestine, affect millions of people around the world. Although significant advances have been made in the clinical management of IBD, the early subclinical stages of IBD are not well defined and are difficult to study in humans. This work explores the subclinical stages of disease in mice lacking the IBD-associated transcription factor HNF4A in the intestinal epithelium. Whereas these mice do not develop overt disease until late in adulthood, we find that they display episodic intestinal inflammation, loose stools, and microbiota changes beginning in very early life stages. Using germ-free and antibiotic-treatment experiments, we reveal that intestinal inflammation in these mice was dependent on the presence of microbiota. These results suggest that interactions between host genotype and microbiota can drive early subclinical pathologies that precede the overt onset of IBD and describe a mouse model to explore those important processes.

Intestinal Immune Imbalance is an Alarm in the Development of IBD.

Immune regulation plays a crucial role in human health and disease. Inflammatory bowel disease (IBD) is a chronic relapse bowel disease with an increasing incidence worldwide. Clinical treatments for IBD are limited and inefficient. However, the pathogenesis of immune-mediated IBD remains unclear. This review describes the activation of innate and adaptive immune functions by intestinal immune cells to regulate intestinal immune balance and maintain intestinal mucosal integrity. Changes in susceptible genes, autophagy, energy metabolism, and other factors interact in a complex manner with the immune system, eventually leading to intestinal immune imbalance and the onset of IBD. These events indicate that intestinal immune imbalance is an alarm for IBD development, further opening new possibilities for the unprecedented development of immunotherapy for IBD.

Clinical and cellular phenotypes resulting from a founder mutation in IL10RB.

Inborn errors of immunity are a group of rare genetically determined diseases that impair immune system development or function. Many of these diseases include immune dysregulation, autoimmunity, or autoinflammation as prominent clinical features. In some children diagnosed with very early onset inflammatory bowel disease (VEOIBD), monogenic inborn errors of immune dysregulation underlie disease. We report a case of VEOIBD caused by a novel homozygous loss of function mutation in IL10RB. We use cytometry by time-of-flight with a broad panel of antibodies to interrogate the immunophenotype of this patient and detect reduced frequencies of CD4 and CD8 T cells with additional defects in some populations of T helper cells, innate-like T cells, and memory B cells. Finally, we identify the patient's mutation as a founder allele in an isolated indigenous population and estimate the age of this variant by studying the shared ancestral haplotype.

Hematopoietic stem cell transplantation for CYBB heterozygous mutation resulting in very early onset inflammatory bowel disease in children: a case report

BackgroundInflammatory bowel disease (IBD) is a heterogeneous group of disorders associated with environmental triggers and dysregulated immune responses resulting in chronic, recurrent intestinal inflammation. Very early-onset IBD (VEO-IBD) refers to patients with symptoms or diagnosis before the age of 6 years and is widely thought to be associated with monogenic mutations. Traditional drug therapy is often ineffective in this patient population, while hematopoietic stem cell transplantation (HSCT) represents the definitive cure for patients with gene mutations.Case presentationWe report a case of VEO-IBD associated with a monogenic mutation in a 2-year-old girl presenting mainly with gastrointestinal symptoms, including recurrent hematochezia and abdominal pain for more than 3 months. A gastroscopy revealed erosive gastritis and bulbar duodenitis, while a colonoscopy indicated erosive colitis. Abnormal results were obtained from the dihydrohodamine (DHR) assay and immunoglobulin testing. Whole-exome sequencing identified a heterozygous and de novo nonsense mutation (c.388 C > T; p.R130X) in the CYBB gene leading to deficiency of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) (encoded by CYBB), a critical component of phagocytes. HSCT was performed successfully, and the DHR assay showed that normal neutrophil function was restored. Six months after HSCT, clinical remission was observed, and a repeat colonoscopy revealed intestinal mucosal healing was attained.ConclusionsPatients with CYBB mutations often develop recurrent or severe bacterial or fungal infections, mostly in the lungs, skin, lymph nodes, and liver. Here, we report on a young female child with CYBB mutations presenting predominantly with gastrointestinal symptoms. This study explores the mechanisms of inflammatory bowel disease caused by a monogenic mutation in CYBB to improve early diagnosis and effective treatment rates of this patient population.

Diagnostic markers of yersiniosis in patients with inflammatory bowel diseases

Relevance. This study is related to the study of the etiology, pathogenesis and clinic of inflammatory bowel diseases (IBD). In a number of patients with IBD who are refractory to anti-inflammatory/immunosuppressive therapy, there are signs of current or transferred yersiniosis infection, not diagnosed by routine methods.Aim. According to the scientific literature and the results of our own research, to identify the presence and assess the nature of the influence of yersinia on the occurrence and development of IBD.Materials Methods. In our study, we conducted a bacteriological examination of feces by polymerase chain reaction (PCR) in patients with a diagnosis of IBD (UC and CD) in the acute phase (MMDAI ≥ 4 points for UC and Best index ≥ 150 points for CD), as well as immunological diagnostics using enzyme immunoassay (IFA) in the version of line-blotting (IB). Using the results obtained, clinical and instrumental semiotics were evaluated in subgroups of individuals suffering from IBD with confirmed yersiniosis ("IBD+ IER+") and without it ("IBC+ IER–"). We also assessed the role of intestinal infection by determining the effectiveness of initial antibacterial therapy in the treatment of exacerbation of IBD.Results. A significant part (in the case of our sample – 45%) of patients with IBD, when examined by high-tech methods, demonstrate the presence of markers of a transferred or current yersiniosis infection. Its role in the initiation and development of autoimmune intestinal inflammatory process requires further clarification.Conclusions. In 45% of patients with IBD, high-precision examination reveals markers of transferred or current yersiniosis infection. Routine clinical methods for the diagnosis of yersiniosis have low sensitivity and do not allow us to convincingly assess the role of this bacterial agent as a trigger factor for the onset or recurrence of IBD. There is a tendency for greater manifestation in the debut of IBD in patients with markers of systemic yersiniosis. The fact of improvement against the background of empirical antibacterial therapy in 24% of patients with IBD, achievement of early clinical remission in 57% of patients receiving antibiotic therapy, indicates a significant role of bacterial enterocolopathogens in the genesis of chronic intestinal inflammation in a number of patients.

Final adult height in childhood-onset inflammatory bowel disease.

Long-term growth may be compromised in patients with inflammatory bowel disease (IBD). The aims of the study were to evaluate the final height in a cohort of patients with pediatric-onset IBD with respect to genetic target and to determine factors influencing long-term growth. This is a monocentric retrospective cohort study. All patients with diagnosed prepubertal onset IBD were enrolled. Patients were classified into two groups on the basis of the achievement of target height at time of the last follow-up. Clinical parameters were also recorded. Eighty-tow patients were identified: 42 with Crohn's disease (CD) and 40 with ulcerative colitis (UC). The mean age at diagnosis was 11.0 (SD 4.0) years. Eighty-nine percent of patients achieved final target height. Mean difference between final and target height was -1.2 cm (SD: 5,4). No statistical significance was detected between CD and UC patients final height (P=0.16). Growth failure at the diagnosis and disease severity were the only factors associated with final height achievement failure (P=0.001 and P=0.01 respectively). Most part of CD and UC patients achieve the target final height. Disease severity and low height at diagnosis seem to be the two best predictive factors for low final height.