The aetiology and impact of malnutrition in paediatric inflammatory bowel disease

Disease‐associated undernutrition of all types is very common in paediatric inflammatory bowel disease (IBD). Recent weight loss remains one of the triad of clinical manifestations and a cornerstone for the diagnosis of Crohn’s disease (CD), although significantly fewer patients now present as being underweight. Recent evidence suggests that the introduction of medical treatment will quickly restore body weight, although this does not reflect concomitant changes in body composition. CD children present with features of nutritional cachexia with normal fat stores but depleted lean mass. Poor bone health, delayed puberty and growth failure are additional features that further complicate clinical management. Suboptimal nutritional intake is a main determinant of undernutrition, although activation of the immune system and secretion of pro‐inflammatory cytokines exert additional independent effects. Biochemically low concentrations of plasma micronutrients are commonly reported in IBD patients, although their interpretation is difficult in the presence of an acute phase response and other indices of body stores adequacy are needed. Anaemia is a common extraintestinal manifestation of the IBD child. Iron‐deficient anaemia is the predominant type, with anaemia of chronic disease second. Decreased dietary intake, as a result of decreased appetite and food aversion, is the major cause of undernutrition in paediatric IBD. Altered energy and nutrient requirements, malabsorption and increased gastrointestinal losses are additional factors, although their contribution to undernutrition in paediatric CD needs to be studied further.     

Economic impact of work disability due to chronic low back pain from the patient perspective

ObjectivesLow back pain (LBP) is one of the main expenditure items for health systems. Data on the economic impact of LBP are uncommon from the patient perspective. The aim of this study was to estimate the economic impact of work disability related to chronic LBP from the patient perspective.MethodsWe conducted a cross-sectional analysis from patients aged over 17 years suffering from non-specific LBP for at least 3 months. Systematic medical, social and economic assessments were collected: pain duration and intensity; functional disability with the Quebec Back Pain Disability Scale (0–100); quality of life with the Dallas Pain Questionnaire; job category; employment status; duration of work disability due to LBP, and income. Factors associated with loss of income were identified by multivariable logistic regression analysis.ResultsWe included 244 workers (mean age 43 ± 9 years; 36% women); 199 patients had work disability, including 196 who were on sick leave, 106 due to job injury. Three were unemployed due to layoff for incapacity. The mean loss of income for patients with work disability was 14% [SD 24, range −100 to 70] and was significantly less for patients on sick leave due to job injury than on sick leave not related to job injury (p < 0.0001). On multivariable analysis, the probability of loss of income with LBP was about 50% less for overseers and senior managers than workers or employees (odds ratio 0.48 [95% confidence interval 0.23–0.99]).ConclusionWork disability due to LBP resulted in loss of income in our study. The loss of income depended on the type of social protection and job category. It was reduced for patients on sick leave related to work injury and for overseers and senior managers.     

Morbidity leading to grants due to temporary work disability

INTRODUCTION: To identify health conditions leading to benefits due to temporary work disability in a population of insured workers. METHODS: International Classification of Diseases (ICD) codes for conditions resulting in temporary work-disability (E-31) were retrieved from the National Institute of Social Security (INSS) data bank in Porto Alegre, Brazil, in 1998. The ICD codes related to the worker's disability assigned in the early medical expert examination (aX1) were used to describe the main disability causes and groups of conditions. RESULTS: A total of 6,898 disability benefits were allowed to insured workers: 1,486 (22%) were attributed to "external causes"; 1,181 (17%) to "surgery recovery" (subdivided as follows: 34% gastrointestinal; 26% genitourinary; 11% musculoskeletal; and 10% external causes ); and 4,119 (61%) to "medical conditions" (subdivided as follows: 24.8% musculoskeletal diseases; 18.9% mental diseases; and 16.2% cardiovascular diseases). When compared to a similar Brazilian study conducted in 1986, external causes moved up from fourth to the first position as a determinant of temporary work disability. CONCLUSIONS: The main causes of disability identified, accidents and violence, musculoskeletal diseases and mental diseases, are potentially associated to the worsening of the quality of life and work conditions during the study and should be a (preventive and therapeutic) priority in the nation's unified health care (SUS) agenda. The study shows the viability of referring to the INSS data bank in morbidity studies.     

The genetics of inflammatory bowel disease

Over the past 10 years major progress has been made in understanding the genetic contribution to inflammatory bowel disease. NOD2 was recently identified as a major susceptibility gene for Crohn's disease. This and a number of other strong genetic leads are discussed.     

Nutrition in inflammatory bowel disease

Clinical and basic research continues to expand our understanding of the complex pathogenesis of inflammatory bowel diseases. The potential roles played by fatty acid intake, serum leptin, and nitric oxide in the promotion of intestinal inflammation in Crohn's disease and ulcerative colitis will be reviewed. In addition, important advances in the areas of bone disease, vitamin deficiency, growth failure, and home parenteral nutrition will be discussed.     

Nutrition in inflammatory bowel disease

The diet of industrialized nations may contribute to the pathogenesis of both ulcerative colitis (UC) and Crohn disease (CD). Malnutrition is relatively unusual in UC, but in CD, which often affects the small intestine, it is frequent and may be severe. Nutrition support is therefore frequently indicated. First principles of artificial nutrition can be applied effectively using the gut whenever possible. Parenteral nutrition is generally required only in those with short bowel syndrome. An increasing literature (especially in pediatrics) favors the use of defined exclusive enteral nutrition (EN) in the primary treatment of active CD. Controlled trials are, however, lacking, and recommendations are accordingly not of the highest rank. It appears that in this context, simple polymeric regimens are usually sufficient, and there is currently insufficient evidence to make a strong recommendation for disease-specific feeds. In the maintenance of remission in CD, controlled data demonstrate that defined EN reduces the risk of relapse requiring steroid treatment. There are no data in support of primary nutrition therapy in UC either in management of the acute flare or in maintenance. In conclusion, nutrition therapy in adults with inflammatory bowel disease is probably both undervalued and underused, but the evidence base needs to be strengthened to confirm its efficacy, determine better those patients most likely to benefit, and optimize the regimens to be employed.     

Nutrition in inflammatory bowel disease

Recent developments concerning nutritional complications of inflammatory bowel disease include a better understanding of disease-associated anorexia and increasing recognition of the interaction of nutrition and cytokines in the pathogenesis of growth impairment of children. Decreased bone mineral density is a multifactorial complication and an increased focus of research. Enteral nutrition continues to play an important role in the therapy of Crohn's disease. The mechanisms whereby specific nutrients, such as n-3 fatty acids, antioxidants, and butyrate, ameliorate inflammation are being elucidated in in-vitro studies, but beneficial effects have yet to be translated into the clinical sphere.     

Psychological disorder associated to inflammatory bowel disease

The symptomatology of patients with ulcerative colitis or Crohn's disease is not only characterised by bowel related symptoms. There is indeed psychological and psychiatric comorbidity. Depression and anxiety seem to be more common. These disorders could be etiologically related or appear as a consequence of the disease. At present, it seems unlikely that psychogenic disorders or major stressful life events play an important role in the origin of the disesses or in their severity, although there are however neuro-endocrine-immune interactions. Minor daily stressful life events are however important for the quality of life of patients with ulcerative colitis and Crohn's disease.     

The study of infectious intestinal disease in England: socio-economic impact

To assess the socio-economic impact of infectious intestinal disease (IID) on the health care sector, cases and their families, cases of IID ascertained from a population cohort component and those presenting to general practices were sent a socio-economic questionnaire 3 weeks after the acute episode. The impact of the illness was measured and the resources used were identified and costed. The duration, severity and costs of illness linked to viruses were less than those linked to bacteria. The average cost per case of IID presenting to the GP was Pound Sterling253 and the costs of those not seeing a GP were Pound Sterling34. The average cost per case was Pound Sterling606 for a case with salmonella, Pound Sterling315 for campylobacter, Pound Sterling164 for rotavirus and Pound Sterling176 for SRSV. The estimated cost of IID in England was Pound Sterling743m expressed in 1994/5 prices. The costs of IID are considerable and the duration of the illness was found to be longer than previous reports have suggested.     

The attitude of employers to people with inflammatory bowel disease.

Many patients with inflammatory bowel disease are anxious about their future prospects of employment. Personnel managers at 61 major national and 136 principal local employers in Leicester and Cardiff were asked to provide details about their attitude to people with inflammatory bowel disease and the type of health care they offer to employees. Over one million people were employed by these companies. A poor response rate of 27% suggested at best disinterest in the subject on the part of employers. In those who did reply the attitude to people with inflammatory bowel disease was often positive, although up to a quarter (25%) would not continue to employ people if they developed these conditions and many (30%) would not provide time off work to attend hospital clinics. Only 60% of respondents would consider providing lighter duties to affected employees. In general there is a surprisingly negative attitude to promotion of people with chronic diseases such as epilepsy, multiple sclerosis or liver disease. This seems less so in inflammatory bowel disease.     

Pharmacogenetics of inflammatory bowel disease

There are interindividual variations with regard to efficacy and toxicity of many commonly employed drugs. Major causes of interindividual differences of drug effects include genetic variations of drug-metabolizing enzymes, transporters and targets. Pharmacogenetics studies the genetic background of the interindividual variations of drug response. By means of preliminary genetic screening personalized treatment can be achieved, drugs with low efficacy and many side-effects can be avoided. The pharmacogenetically best studied medications of inflammatory bowel disease are azathioprine/6-mercaptopurine. It is obvious that there is a genetic background of the efficacy and toxicity of corticosteroids, 5-ASA drugs, infliximab and other immunosuppressors as well, but further studies now require to confirm the functional significance of it. Therefore, at present, the application and clinical usefulness of pharmacogenetics in the management of inflammatory bowel disease is limited. The aims of future investigations are understanding of the mechanism of drug action, identification of new drug targets and acquainting with genetic factors that determine drug response.     

The malignant side of chronic inflammatory bowel disease

Patients with chronic inflammatory bowel disease (IBD) have a higher risk of colorectal carcinoma, and present with this malignancy at a younger age than non-IBD individuals. In three patients, two men aged 20 and 36 years and one woman aged 34 years, colorectal cancer developed at a young age, following a long history of ulcerative colitis. Surveillance for colorectal cancer in IBD patients needs to be performed by regular colonoscopy with extensive biopsy sampling for the detection of dysplasia, regarded by many as predictive for colon carcinoma. Whenever a dysplasia-associated lesion or mass or a highgrade dysplasia is identified, there is a strong indication for colectomy. When low-grade dysplasia is found, the findings should be discussed with the patient and it should be decided whether the patient should resume surveillance or opt for colectomy.     

Radiology of inflammatory bowel disease

Plain radiographs and barium studies remain the primary imaging procedures in patients with known or suspected Crohn's disease or ulcerative colitis. The newer imaging modalities such as radionuclide studies, ultrasound and angiography have an important role in selected cases.     

Genetics of inflammatory bowel disease

The Inflammatory Bowel Disease (IBD) are multifactorial diseases involving the interaction of genetic and environmental factors. In genetic terms, the IBD are polygenic and multigenic disorders with incomplete penetrance. In the late decade, investigators have applied the complementary techniques of genome-wide scanning and candidate gene analysis to search susceptibility genes. The IBD susceptibility regions, widely replicated, are in chromosomes 16 (IBD1), 12 (IBD2) and 6 (IBD3). Recently, a significant association have been reported with Crohn's disease and NOD2/ CARD15 gene. This gene is an appropriate candidate gene because its localization and function. More studies is necessary to confirm this association, search an other variants of this gene and other candidate gene. This studies provide best comprehension of the disease pathogenesis and deliver clinical application.     

Genotype-phenotype associations in inflammatory bowel disease

Inflammatory bowel disease has traditionally been categorized as either ulcerative colitis or Crohn's disease on the basis of clinical, radiological and histological criteria. Emerging data suggest that inflammatory bowel disease comprises a heterogenous family of inflammatory disorders in which the specific clinical manifestations of disease are determined by the interaction of genetic and environmental factors. Interactions of susceptibility and modifying genes influence the specific features of disease phenotype, penetrance, location, behavior, and complication. CARD15/NOD2 mutations are significantly associated with ileal location, whereas certain HLA haplotypes are associated with colonic disease. The associations with CARD15/ND2 mutations and early age at onset, as well as disease behavior (stricturing, fistulizing type) are less consistent. Distinct HLA alleles contribute to the occurrence of extraintestinal manifestation. With the increasing number of genotype-phenotype relationship, it is hoped that a molecular classification can be created, in which various disease subtypes are categorized according to their specific genotypes. In the future, such sheme may permit early, accurate diagnosis, prediction of disease course, complications, prognosis, as well as treatment response.