Food allergy.

Food allergies manifest in a variety of clinical conditions within the gastrointestinal tract, skin and lungs, with the most dramatic and sometimes fatal manifestation being anaphylactic shock. Major progress has been made in basic, translational and clinical research, leading to a better understanding of the underlying immunological mechanisms that lead to the breakdown of clinical and immunological tolerance against food antigens, which can result in either immunoglobulin E (IgE)-mediated reactions or non-IgE-mediated reactions. Lifestyle factors, dietary habits and maternal-neonatal interactions play a pivotal part in triggering the onset of food allergies, including qualitative and quantitative composition of the microbiota. These factors seem to have the greatest influence early in life, an observation that has led to the generation of hypotheses to explain the food allergy epidemic, including the dual-allergen exposure hypothesis. These hypotheses have fuelled research in preventive strategies that seek to establish desensitization to allergens and/or tolerance to allergens in affected individuals. Allergen-nonspecific therapeutic strategies have also been investigated in a number of clinical trials, which will eventually improve the treatment options for patients with food allergy.

Improvement of Refractory Ulcerative Proctitis With Sacral Nerve Stimulation.

BACKGROUND AND AIMS: Sacral nerve stimulation (SNS) is recognized for its efficiency and safety for anal incontinence, preventing high morbidity. Evidence from the literature suggests extending SNS to diseases associated with problems of intestinal barrier permeability. The aim of this study was to highlight clinical evidence of the beneficial impact of SNS in a refractory proctitis case report. MATERIALS AND METHODS: A permanent SNS was performed successfully in a patient with proctitis after implantation of the neuromodulator. Despite immunosuppressive drugs, the patient was experiencing mucus and blood discharge, pain, and fecal incontinence. To relieve fecal incontinence, SNS was tested without modification of medications. Disease activity, endoscopic and histologic score, ex vivo barrier permeability, expression of inflammatory cytokines (transforming growth factor-ß, tumor necrosis factor α, Interleukin-6, Interleukin-8), and junctional proteins (ZO-1, claudin-1, occludin) were assessed before and after SNS to observe the impact of SNS other than for incontinence. RESULTS: After a 3-week period of temporary stimulation, the patient experienced significant improvement with a decrease in fecal incontinence and disease activity scores. Both endoscopic and histologic scores showed improvement. The rectal barrier permeability decreased with SNS, whereas junctional protein mRNA expression transiently increased. Clinical and histologic improvement was sustained over time. After 18 months of permanent stimulation, the patient remained improved by SNS. CONCLUSION: This work demonstrates the relevance to explore further indications of SNS beyond fecal incontinence.

[The ethiology, pathogenesis, diagnostics and clinical features of the complicated posttraumatic rectal fistulae].

The ethiology, pathogenesis, diagnostics, clinical features and the capabilities of modern instrumental methods in the diagnosis of 134 patients with posttraumatic rectal fistulaes. The main causes of the rectal fistulae formation was the mechanism of the forecoming trauma, late hospital admission and postoperative complications. The use of modern diagnostic facilities allows to know the anatomic features of the fistulae, the presence of the septic cavities of the pararectal tissue, the involvement of sphincter muscles to the inflammatory process and their functional state. All the listed above facilitate the efficacy of the surgical treatment.

Proctocolitis alérgica, enterocolitis inducida por alimento: mecanismos inmunes, diagnóstico y tratamiento / No disponible

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Pathophysiology, diagnosis and treatment of food protein-induced gastrointestinal diseases.

PURPOSE OF REVIEW: Although our general understanding of food hypersensitivity has improved in recent years, gastrointestinal food protein-induced diseases still pose diagnostic and therapeutic dilemmas. RECENT FINDINGS: Food allergy in children and adults may involve any part of the gastrointestinal tract. Clinical presentations include protein-induced enterocolitis syndrome, enteropathy and proctocolitis, as well as eosinophilic gastroenteritis and related disorders. For many of these conditions, our understanding of the pathophysiology is incomplete. Manifestations are mostly non-IgE mediated, and skin prick testing and measurement of food-specific IgE antibody levels are of limited diagnostic value. Atopy patch testing may be of benefit in identifying food items associated with late-onset gastrointestinal reactions. A definitive diagnosis of gastrointestinal food allergy, however, still relies on formal food challenges. Depending on the clinical presentation, gastrointestinal biopsies may be required. In infancy, hypoallergenic formula or maternal elimination diets have been shown to effectively control the gastrointestinal manifestations of food allergies. Growth parameters and micronutrient levels need to be carefully monitored while on elimination diets for prolonged periods. In older children and adults with eosinophilic gastrointestinal disorders, the response to dietary restriction is variable. Corticosteroids may be required to control symptoms in those who failed to respond to hypoallergenic diets. In eosinophilic esophagitis, steroids can be administered topically in the form of swallowed aerosols. Leukotriene receptor antagonists and other novel therapies may be useful as steroid-sparing agents. SUMMARY: Early diagnosis and treatment of food protein-induced gastrointestinal diseases may prevent significant nutritional complications. Further research is needed to develop diagnostic tools for these mainly cell-mediated disorders.

Natural history of late radiation proctosigmoiditis treated with topical sucralfate suspension.

Rectal bleeding due to radiation proctosigmoiditis is often difficult to manage. We had earlier shown the efficacy of short-term therapy with topical sucralfate in controlling bleeding in the radiation proctosigmoiditis. We now report our long-term results with this form of therapy. The study comprised 26 patients with radiation proctosigmoiditis. Sigmoidoscopically, 9 (34.6%) patients had severe changes, 15 (57.69%) had moderate, and 2 (7.69%) had mild changes. Severity of bleeding was graded as severe (> 15 episodes per week), moderate (8-14 episodes per week), mild (2-7 episodes per week), negligible (< or = 1 episode per week), or nil (no bleeding). Ten patients had moderate rectal bleeding, while 16 had severe bleeding. All patients were treated with 20 ml of 10% rectal sucralfate suspension enemas twice a day until bleeding per rectum ceased or failure of therapy was acknowledged. Response to therapy was considered good whenever the severity of bleeding showed improvement by a change of two grades. Rectally administered sucralfate achieved good response in 20 (76.9%) patients at 4 weeks, 22 (84.6%) patients at 8 weeks, and 24 (92.3%) patients at 16 weeks. This change was significant by Wilcoxon matched-pairs signed-ranks test. Two patients required surgery due to poor response. Over a median follow-up of 45.5 months (range 5-73 months) after cessation of bleeding, 17 (70.8%) patients had no further bleeding while 7 (22.2%) had recurrence of bleeding. All recurrences responded to short-term reinstitution of therapy. No treatment-related complications were observed. Ten patients had other associated late toxicity due to pelvic irradiation in the form of asymptomatic rectal stricture (N = 3), rectovaginal fistula (N = 1), intestinal stricture (N = 1), vaginal stenosis (N = 1), and hematuria (N = 6). Three patients had progression of the primary disease in the form of pelvic recurrence (N = 2) and hepatic metastases (N = 1). We conclude that topical sucralfate induces a lasting remission in a majority of patients with moderate to severe rectal bleeding due to radiation proctosigmoiditis.

Progression of ulcerative proctosigmoiditis: incidence and factors influencing progression.

OBJECTIVE: To assess the changing distribution of disease within the large bowel in patients presenting with ulcerative proctitis or proctosigmoiditis. To evaluate the influence of clinical exacerbations, smoking, parity and family history in disease extension. DESIGN: Retrospective single-centre study in a university hospital. METHODS: Case records of patients presenting over a 40-year period were examined to evaluate the clinical course and disease distribution from initial presentation to final follow-up. For each patient whose disease extended to the more proximal colon, an age- and sex-matched control patient was identified whose disease remained confined to the original site. Patients completed a questionnaire to provide information on family history, smoking and parity. The differences in clinical exacerbations, family history, smoking and parity were then compared between the two groups. RESULTS: Among 145 patients presenting with proctitis or proctosigmoiditis followed prospectively for a median period of 10.9 years, the disease extended in 53 patients. Using actuarial methods the disease progressed beyond the rectosigmoid area in 16% of patients at 5 years and 31% at 10 years. Among the patients whose disease progressed, progression was preceded in 68% of cases by a clinical exacerbation of the colitis. When patients whose disease progressed were compared with those whose disease remained confined to the original site, no differences were detected in the number of clinical exacerbations, smoking habit, family history or parity. CONCLUSIONS: The factors that are associated with the extension of colitis are probably different from those that predisposed an individual to develop inflammatory bowel disease initially.

Butyrate absorption and lactate secretion in ulcerative colitis.

PURPOSE: Fecal electrolytes and organic anion concentrations are altered in ulcerative colitis, presumably reflecting changes in colon epithelial transport. Information of mucosal absorption of butyrate in active ulcerative proctosigmoiditis is not available. METHODS: Dialysis bags containing 70 mmol/liter of butyrate in an isotonic electrolyte solution were placed in the rectum for 30 minutes. Net absorption or secretion rates of butyrate, lactate, and electrolytes were determined in the rectum of 12 patients with active ulcerative colitis (UC) and in 10 patients with quiescent UC and then compared with 10 healthy controls. RESULTS: Net flux rates demonstrated a considerable absorption of butyrate in patients with active inflammation of 7.5 +/- 0.4 mumol/cm2/h and quiescent colitis of 6.6 +/- 0.4 mumol/cm2/h, equal to absorption in healthy controls of 6.3 +/- 0.5 mumol/cm2/h, P = 0.12. Despite normal butyrate absorption, sodium absorption was compromised in active ulcerative colitis (11.5 +/- 1.4 mumol/cm2/h) compared with quiescent (15.4 +/- 1.0 mumol/cm2/h) and controls (18.7 +/- 0.8 mumol/cm2/h) (P = 0.0006). Mucosal secretion of L-lactate was minimal in both healthy controls and quiescent UC but significantly increased in patients with proctosigmoiditis (0.2 +/- 0.1 mumol/cm2/h, 0.2 +/- 0.1 mumol/cm2/h vs. 0.9 +/- 0.2 mumol/cm2/h; P = 0.0001). Appearance of D-lactate was negligible in all three groups. CONCLUSIONS: This study demonstrates that rectal butyrate absorption is normal in UC, and it follows that butyrate supplied in enemas can be expected to be absorbed. The inflamed colonic mucosa secretes L-lactate, and the increased fecal lactate concentrations can be explained by mucosal origin of lactate.

Experimental colitis alters visceromotor response to colorectal distension in awake rats.

The influence of intermittent colorectal distension (CRD) on proximal colonic motility and abdominal pain perception was investigated in awake rats equipped with intraparietal electrodes on the cecum, proximal colon, and abdomen, before and three days after rectocolitis induction by trinitrobenzene sulfonic acid (TNB)/ethanol. The normal myoelectrical activities of cecum and proximal colon [5.2 +/- 0.5 and 9.7 +/- 0.7 long spike bursts (LSB) per 5 min, respectively] were significantly (P < 0.05) and gradually decreased by control CRD, at diameters above 9 mm. At the maximum CRD diameter (13.7 mm), 1.6 +/- 0.6 cecal and 3.9 +/- 0.8 colonic spike bursts occurred per 5 min (respectively, 69 and 60% decreases). This upstream inhibition was accompanied by a significant (P < 0.05) and gradual increase in abdominal contractions (0.4 +/- 0.4 per 5 min in control vs 23.4 +/- 1.9 in response to 13.7 mm in diameter). Three days after TNB/ethanol, visceromotor and abdominal responses were significantly (P < 0.05) enhanced at the least CRD diameter of 9 mm (cecum: 3.1 +/- 0.4 after TNB vs 5.0 +/- 0.7 in control; proximal colon: 5.1 +/- 0.9 vs 9.3 +/- 2.2; abdomen: 7.7 +/- 1.5 vs 0.5 +/- 0.4). We conclude that in awake rats, CRD evokes both abdominal contractions in response to pain and inhibition of cecal and proximal colonic motility, which thresholds are both lowered by TNB-induced rectocolitis.

[The blood circulation of the rectal mucosa and the functional status of the rectal sphincter in acute infectious enterocolitis]. / Krovobih slyzovoï obolonky priamoï kyshky i funktsional'nyi stan rektal'noho sfinktera pry hostrykh infektsiinykh enterokolitakh.

Significant decrease in the tone of the rectal mucosa venules was to be seen at the climax of acute Proteus and Klebsiella enterocolitis, as evidenced by examinations with the aid of rheorectograph and an analyzer of intracavitary motor activity, general blood supply to the intestinal segment under study being not compromised. The tone of the rectal mucous membrane arterioles is raised at the climax of acute dysentery caused by a Flexner type of organism in erosive and haemorrhagic proctosigmoiditis. With the clinical recovery being set in, the blood supply to this area fails to return to normal. The excitability of the inner anal sphincter was noted to be on the increase at the climax of acute S. flexneri dysentery, this showing up predominantly in erosive and haemorrhagic proctosigmoiditis, ceasing to reveal itself in the period of reconvalescentia.

Inflammatory bowel disease and irritable bowel syndrome.

The irritable bowel syndrome accounts for 30 to 50 per cent of patients cared for by gastroenterology practices. Irritable bowel syndrome is more common than inflammatory bowel disease. Therefore, it should not be surprising that some patients with inflammatory bowel disease are initially told that they have irritable bowel syndrome before a diagnosis of inflammatory bowel disease is firmly established. This article contends that many people have both irritable bowel syndrome and inflammatory bowel disease.

Is the rectum usually empty?--A quantitative study in subjects with and without diarrhea.

The authors have investigated the frequency with which the rectum contains feces by recording the presence or absence of fecal contamination of the membrane or of discoloration by feces of the contents of dialysis bags placed in the unprepared rectum for one hour. Feces were present in the rectum in 31 per cent of 32 studies in normal control subjects, in 49 per cent of 80 studies in obese subjects (P less than 0.05 from controls), in 36 per cent of 28 studies in patients with the irritable bowel syndrome, and in 31 per cent of 103 studies in patients with ulcerative proctocolitis, whether or not they had diarrhea. Fecal staining of the bag and its contents occurred much more frequently in 27 studies in subjects with various other diarrheal diseases (67 per cent, P less than 0.02 from controls), including eight with steatorrhea (87 per cent, P less than 0.02 from controls). The frequency with which feces were present was unaffected by age, sex, or time of day of the study. These results provide quantitative support for the assertion that in subjects without diarrhea the rectum is usually empty. In patients with diarrhea or steatorrhea and no distal large intestinal inflammation, however, the rectum usually does contain fecal material.