Immunogenetic, Molecular and Microbiotic Determinants of Eosinophilic Esophagitis and Clinical Practice-A New Perspective of an Old Disease.

Eosinophilic oesophagitis (EoE) is a chronic, allergic disease associated with a T-lymphocyte response inducing esophageal eosinophilic infiltration in the esophagus. Inflammation and tissue fibrosis are responsible for the main clinical symptoms such as food impaction and dysphagia. The etiopathogenesis is multifactorial in which genetic and environmental factors coexist. The most common trigger is a non-IgE-mediated food allergy to milk, wheat, egg, soybean, nuts, fish, and seafood. The second factor we focus on is the contribution of genetic variation to the risk of EoE, describing the expression profile of selected genes associated with eosinophilic oesophagitis. We raise the topic of treatment, aiming to eliminate inflammation through an elimination diet and/or use of pharmacologic therapy with the use of proton pump inhibitors or steroids and endoscopic procedures to dilate the esophagus. We demonstrate that early diagnosis and effective treatment prevent the development of food impaction and decreased quality of life. The increasing presence of EoE requires bigger awareness among medical specialists concerning clinical features, the course of EoE, diagnostic tools, and management strategies.

The impact of genetic factors on response to glucocorticoids therapy in IBD.

Glucocorticosteroids (GCs) are used for many years as first-line drugs for the achievement of remission in exacerbations of inflammatory bowel disease (IBD). However, close to 20% of patients are resistant to GCs, and 40% of patients become dependent on GCs. The challenge of today's personalized medicine is the anticipation of the steroid therapy effects even before the initiation of treatment. As several studies show, individually variable response to GCs in population has a genetic background and may depend on gene variability encoding proteins involved in the function and metabolism of GCs. To those genes belong: NR3C1--responsible for the synthesis of GC receptor (GR); Hsp90, HSP70, STIP1, FKB5--genes of GR protein complex; ABCB1 and IPO13 coding glycoprotein p170; and importin 13--involved in GCs transport; IL1A, IL1B, IL2, IL4, IL8, IL10, TNF, and MIF--genes of the epithelial pro-inflammatory factors synthesis, which excessive activation causes steroid resistance as well as CYP3A4 and CYP3A5--encoding GCs biotransformation enzymes. This work systematizes and sums up the state of current knowledge in the field of pharmacogenetics as well as expectations for the future in the realm of individualized medicine in IBD patients treated with GC drugs.

Parenteral and Enteral Nutrition: A Bridge to Healing and Biological Therapy in a Patient With Enterocutaneous Fistula and Sepsis Complicated Crohn's Disease.

Inflammatory bowel disease (IBD) patients with severe infections, abscess, or sepsis are ineligible for standard treatment using biological and immunosuppressive drug regimens. We report a case of complicated Crohn's disease with ruptured abdominal abscess, presence of enterocutaneous fistula, and sepsis. We also report and discuss patient management with parenteral nutrition (PN) and enteral nutrition (EN) and treatment outcomes. We report a case of a 31-year-old female with a 10-year history of IBD in clinical remission, who, after previous total proctocolectomy with J-pouch, presented to the clinic with severe abdominal pain of 2 days, unintentional weight loss, fatigue, fever, and abdominal abscess, which ruptured, and her clinical state became complicated by sepsis. PN was initiated using individually prepared admixture according to patient requirements, because of inability to tolerate any oral intake. Following the remittance of ileus symptoms, EN was added using a semielemental formula via a nasojejunal tube. Upon completion of the treatment, the fistula resolved, the wound had healed, and Crohn's Disease Activity Index score showed remission. This qualified the patient for initiation of biological therapy with infliximab. Patients with severe infections, abscesses, or sepsis are ineligible for standard IBD treatment using biological and immunosuppressive drug regimens. Furthermore, usually patients' nutrition condition prevents them from combating infection and initiating proper healing process. This case demonstrates the importance of considering nutrition therapy-PN and EN-in unstable patients who cannot be treated with standard pharmacological therapy. Nutrition therapy offers a bridge that allows patients to stabilize and heal before starting standard pharmacological treatment with immunosuppressive agents or biological therapy.

Home parenteral nutrition a life-saving therapy in a primary intestinal lymphangiectasia patient affecting the entire GI tract - 3 year follow-up case report.

INTRODUCTION AND IMPORTANCE: Primary intestinal lymphangiectasia (PIL) is a rare protein-losing gastroenteropathy of unknown etiology, characterized by impaired lymphatic vessels drainage. The pathological changes in PIL result in usually localized or diffuse dilatation of intestinal lacteals, leading to leakage of lymphatic fluid rich of proteins, lymphocytes, and immunoglobulins into the intestinal lumen. PIL may be asymptomatic or mildly symptomatic in moderate forms of the disease. In some patients, though, the outcome may be poor or even life-threatening. This case report demonstrates the severity of protein malnutrition, in some cases, and the extent of GI tract affected, requiring to start PN early and the need for its continuation as home parenteral nutrition (HPN). CASE PRESENTATION: We present a case of 39-year-old male with Factor V Leiden deficiency, who presented initially with symptoms of malnutrition and anasarca. The diagnosis was confirmed by histopathological findings pathognomonic for PIL from biopsies of the stomach, small intestine and colon. CLINICAL DISCUSSION: The patient was started on low fat, high protein parenteral nutrition from the beginning of the treatment and required a long-term HPN for 3 years, because trials of tapering off and discontinuation of PN led to worsening of the biochemical results and recurrence of symptoms. Patient gradually improved and stabilized with persistent nutritional support. CONCLUSIONS: The presented case report shows the magnitude of nutritional support (HPN) needed for severe PIL patients. HPN offers PIL patients with poor outcome and life-threatening complications a chance to improve and lead a normal life.

Is there a relation between vitamin D, interleukin-17, and bone mineral density in patients with inflammatory bowel disease?

INTRODUCTION: In inflammatory bowel diseases (IBD), osteopenia and osteoporosis constitute a significant medical problem. Cytokines, especially IL-17, play an important role in the pathogenesis of IBD and osteoporosis. Vitamin D is a regulator of bone metabolism, and helps maintain immune system homeostasis. MATERIAL AND METHODS: The research sample consisted of 208 persons: 83 patients (age 35 ±11.99 years) with Crohn's disease (CD); 86 patients (age 39.58 ±14.74 years) with ulcerative colitis (UC); and 39 persons (age 30.74 ±8.63 years) in the control group (CG). Clinical data on bone mineral density of the lumbar spine (L2-L4), bone mineral density of the femoral neck (FN), and body mass index (BMI) were collected. 25OHD and IL-17 serum concentrations were also measured. RESULTS: Body mass index (kg/m2) results: in CD, 21.51 ±3.68; in UC, 23.31 ±4.38; and in CG, 24.57 ±3.45 (p < 0.01). Densitometry results for L2-L4 T-score SD: in CD -0.83 ±1.45; in UC -0.47 ±1.15; in CG 0.09 ±0.70. Densitometry results for FN T-score SD: in CD -0.62 ±1.26; in UC -0.29±1.17; in CG 0.41 ±1.03 25OHD (ng/ml) serum concentrations: in CD, 21.33±12.50; in UC, 22.04±9.56; in CG, 21.56±9.11 (ns). IL-17 (pg/ml) serum concentrations: in CD, 8.55±10.99; in UC, 11.67±12.97; in CG, 5.16±9.11 (ns). CONCLUSIONS: Inflammatory bowel diseases patients and persons from the CG did not differ in vitamin D or IL-17 levels. Patients with a mild course of the disease had a higher vitamin D concentration and bone mineral density. In UC, higher vitamin D concentrations were associated with lower IL-17 concentrations. The IBD patients with a severe course of the disease had a lower body mass than those in the CG and the patients with a mild course of the disease.

Influence of chlorinated water on the development of allergic diseases - An overview.

Indoor swimming pools can be used all year round and serve for one of the most popular sport pursued for recreation. The positive effect of swimming arises in particular from the involvement of all the muscles of the body, decreasing the burden on the joints, as well as functional improvement of both the lungs and heart. Chlorine is typically used to disinfect swimming pool water and as a result the changes that take place lead to the formation of by-products, such as monochloramines (NH2Cl), dichloramines (NH2Cl2) i trichloramines (NH2Cl3), trihalogenometans (THM) or haloacetic acid (HAA). The highest concentration of these substances is just above the water surface and they may cause irritation of skin, eyes and mucosa of the respiratory tract. The toxic effect of high chlorine concentration and its side-products on the respiratory system is known, but the effect of low concentrations of these compounds is still not fully determined. Recent studies suggest that development of allergic diseases among swimmers may be increased by epithelial disorders driven by airway barrier dysfunction caused by chlorine irritation. Swimming in chlorinated water may be linked to symptoms of bronchial hyperreactivity, asthma and rhinitis especially in children, elite swimmers and employees of indoor swimming pools. Hypersensivity pneumonitis related to the use of swimming pools may manifest as a swimming pool or sauna user lung, most commonly caused by water polluting pathogens. The article summarizes recent data concerning the influence of chlorinated water on the development of allergic diseases.

Prevalence of osteoporosis and osteopenia in a population of patients with inflammatory bowel diseases from the Wielkopolska Region.

Introduction The incidence of osteoporosis in patients with inflammatory bowel disease (IBD) varies across different populations. Objectives The aim of this study was to evaluate the prevalence of osteoporosis in Polish patients with IBD, as well as the effect of the body mass index (BMI), disease duration, the number of hospital stays, and the use of glucocorticoids on bone mineral density (BMD). Patients and methods BMD of 208 patients with IBD (103 with Crohn disease [CD] and 105 with ulcerative colitis [UC]) and 41 healthy controls was measured using dual­energy X­ray absorptiometry. The association of BMD with the other parameters was analyzed using statistical methods. Results Osteoporosis of the lumbar (L2-L4) spine (T­score) was observed in 11.7% of patients with CD and in 3.8% of those with UC, whereas that of the femoral neck (FN), in 5.8% and 2.9% of the patients with CD and UC, respectively. Osteopenia occurred in 35.9% (FN) and 36.9% (L2-L4) of CD patients, and in 25.7% (FN) and 29.5% (L2-L4) of UC patients. In CD patients, BMI was associated with lumbar and femoral BMD and with L2-L4 T­score, whereas FN T­score correlated with BMI. In UC patients, the cumulative glucocorticoid dose correlated with L2-L4 T­score, FN BMD, FN T­score, and FN Z­score; the disease duration correlated with FN BMD, while the FN T­score, with the number of hospital stays and FN BMD. Conclusions Osteoporosis and osteopenia are frequent in Polish patients with IBD. BMD correlated with BMI in all patients. In UC patients, BMD was associated with the cumulative glucocorticoid dose, disease duration, and number of hospital stays.