Crohn disease
Chronic Colitis

DIET AND CROHN’S DESEASE

Diet sometimes is not consider important in this disorder but it cuold be consider as effective as drugs in acute fase of disease.
Nutritional treatment was initially included in the management of Crohn’s disease because patients are often poorly nourished as a result of reduced intake and hypercatabolism. Total parenteral nutrition has been used to induce remission in this disease on the basis that it “rest the bowel”. We belive that Crohn’s disease consist of two main components: an underlying predisposition to ulceration of the gut, and a secondary immunological reaction to the passage of large amounts of foreign protein through the damage gut wall. In an attempt to treat this secondary aspect C. O. Morain, A. W. Segal and A. J. Levi gave patients an elemental diet which contains all essential nutrients but is free of all protein, nitrogen being supplied in the form of amino acids. The result were encouraging enough to warrant a prospective controlled trial of the efficacy of the treatment. They report the results of that trial, in which the therapeutic effect of an elemental diet as sole treatment of acute Crohn’s disease was compared with the response to prednisolone, the most effective conventional treatment. Crohn’s disease was diagnosed on the basis of the typical clinical and radiological features and diagnostic or compatible histological findings. The disease was cosidered to be in an active phase if the patient had a least of one either weight loss of more than 2 kg in the previous month, diarrhoea (three or more loose stools a day) abdominal pain resulting in severe limitation of activiy, abdominal wall or perianal fistulas, or a temperature exceeding 38°C for one week or if at least two of the following laboratory measurements were abnormal: haemoglobin concentration (<12.5 g/dl in men, <10.5 g/dl in women) erythrocyte sedimentation rate (> 20 mm in first hour), and serum albumin concentration (<35 g/l). Patients must not have received specific treatment in the past and were excluded if they had contraindications to the use of prednisolone. Any patient whose condition deteriorated to an extent that necessitated a change of treatment, as judged by two physicians, was withdrawn. Twenty one patients (14 men, 7 women) were admitted to the trial. All were ill enough to require hospital admission. Rectal biospsy specimens were characteristic in four and compatible with the diagnosis of Crohn’s disease in another four, in whom there were also relevant clinical and radiological features. Thirteen had the characteristic radiological apparances and clinical pictures of Crohn’s disease. All the patients had abdominal pain and diarrhoea, accompained by weight loss in 17. Eight patients had had a fever of 38°C for one week. All had a sedimentation rate greater than 20 mm in the first hour, 12 had a haemoglobin concentration of less than 12.5 g/dl (men) or 10.5 (women), and 13 had a serum albumin concentration of less than 35 g/l. After initial inpatient assessment the patients were allocated at random to one of two treatment groups. Ten were trated with prednisolone 0.75 mg/kg body weight daily for two weeks and then with reduced dosages as clinically appropriate. Eleven were treated with an elemental diet whereby all food except tea and coffe (without milk) was withdrawn and repleced with Vivonex, supplying 150-250 hJ (40-60 kcal)/kg body weight and 8-12 g of nitrogen daily. The concentration of the elemental diet was gradually increased from one third to the full recommended strength over three days to reduce side effects such as diarrhoea and abdominal colic, which occurs beacause the preparation is hyperosmolar (600 mmol). After four weeks normal food was gradually reintroduced, its consistency being increased from fluid to solid over three days. Treatment was institued in hospital but all the patients were allowed home once they had improved clinically.
Clinical symptoms and laboratory values were assessed before treatment and at weekly intervals for four weeks and then at three months. Clinical severity was quantified using prearrange scoring system based on the five items of the “simple activity index.” General wellbeing was noted as excellent, fair with no limitation of activity, poor with some limitation of activity, or very poor with considerable limitation of activity and assigned corresponding scores of zero to three. Numbers of liquid stool were recorded as fewer than three, three to five, and more than five a day and assigned corresponding scores of zero to two. Abdominal mass was noted as absent, dubious of definite and scored zero to two. Abdominal tenderness was also looked for and scored as mild (one), moderate (two), or severe (three). Complication affecting eyes, joints, skin, or fistuals were scored as one per item. The sum of these scores was called the clinical score. The higher the score the more active was the disease, and negative changes meant clinical improvement. Subsequent values were compared with baseline using Student’s t test for each group. The changes in values obtained for both groups were compared with one another by one way analysis of variance. Of the 21 patients, seven were women, of whom five were randomised to receive steroid treatment. Two patients in each treatment group were withdrawn from the study. One of these developed a steroid psychosis, and another failed to improve clinically and developed toxic megacolon. In another two cases the patients could not tolerate the elemental diet by mouth. All four patients were withdrawn in the first 10 days of treatment. Eight of the 10 steroid treated and nine of the 11 dietetically treated patients were considered to be in remission at four weeks. At three months one patient in each group was considered to be a treatment failure. Of these, the patient in the steroid treated group relapsed with symptoms as severe as on first entry to the trial and was successfully treated with an elemental diet. The other patient presented with symptoms of a free perforation two days after returning to whole food. Both groups showed similar highly significant reductions in their average clinical scores within a week, and this improvement continued throughout. There were no significant differences in the rate or degree of improvement between the two groups. Body weight also showed a consistent upward trend for the steroid treated group, but the dietetically treated group diverged significantly (p<0.05) from this pattern by the end of treatment and after three months. At that time, however, patients in the drug treatment group were still taking 10-20 mg prednisolone daily, whereas those in the other group were receiving no specific treatment. Haemoglobin concentration showed a small but significant rise by the fourth week of treatment, but at three months this was maintained only in patients given the elemental diet. Both groups showed a significant rise in serum albumin concentrations, but rises were greater in the dietetically treated group. There was a significant and comparable fall in the sedimentation rate in the two groups. This paper reports on the first controlled trial of an elemental diet in the treatment of acute Crohn’s disease, and the results show that the diet was as effective as steroids in inducing a remission: 80% of the patients in both groups were in remission by four weeks. They think it unlikely that the changes in these patients resulted from a placebo effect or simply admission to hospital. It was thought to be inappropriate to withhold treatment from these acutely ill patients, and therefore a placebo group was not included. In the national cooperative Crohn’s disease trial only 30% of patients given placebo went into remission. In another controlled trial the placebo treated group showed the same degree of disease activity after 16 weeks as they did at the outset. It is most unlikely that the therapeutic effect observed in this series was due to bed rest alone, as the median stay in hospital for both groups after beginning treatment was 12 days.
Response to treatment was monitored by a simple activity index in preference to the Crohn’s disease activity index proposed by the National Cooperative Crohn’s Disease Group. A similar simple activity index was used in three other controlled trials. The Crohn’s disease activity index depends largely on subjective variables such as general wellbeing and pain, each given different weightings, and includes as the sole laboratory investigation measurement of the packed cell volume, which bears little relation to disease activity. Concentrations of acute phase proteins, serum albumin value, and sedimentation rate are more reliable laboratory indices of disease activity. The simple index correlates well with the complex Crohn’s disease activity index. Other reports of the use of elemental diet in Crohn’s disease were uncontrolled and anecdotal. The principal difficulty of using an elemental diet is its unpalatability. But with encouragement from dietetic, nursing, and medical staff the patients do adapt, particularly when they note subjective improvement, and only two of our patients were unable to tolerate the diet; one of these was given a nasogastric line. We have monitored other patients receiving an elemental diet for six to 12 months. Although the products cost between £9 and £13 a day, the clinical improvement, greater wellbeing, and productivity of the patient provide an excellent cost: benefit ratio. Nutritional improvements are unlikely to be responsible for alleviating the symptoms of Crohn’s disease because clinical improvement starts long before positive nitrogen balance develops. Alterations in bacterial flora in the gut lumen do occur in patients taking an elemental diet, and this might have a beneficial effect. We have been unable to find any difference in faecal flora before and after treatment. The nitrogen source of Vivonex is simple amino acids. By contrast, other liquid diets contain peptides with variable length chains, and all contain come oligopeptides, which may be allergenic. Vivonex may be beneficial in one or two ways: as the components of the diet are absorbed mainly in the upper small bowel, it may act simply as a medical bypass, preventing the dietary contents and digestive enzymes having access to the inflamed, ulcerated gut, Alternatively there may be a secondary immune reponse in Crohn’s disease to exogenous protein which gains access to the gut wall through the ulcerated mucosa. This is likely because antibodies to a wide range of foreign proteins are detectable in the serum of these patients. Possibly this inflammatory immune response to exogenous protein perpetuates chronic inflammation of areas in which the mucosa is breached by acute insults which would otherwise resolve spontaneously. Elemental dietary treatment of acute exacerbations Crohn’s disease offers a therapeutically effective non-toxic alternative to conventional surgery and drugs. It merits serious consideration as the treatment of choice of acute Crohn’s disease.

Another study conducted by Teahon K, Smethurst P, Pearson M, Levi AJ, Bjarnason from Medical Research Council Clinical Research Centre, Harrow, Middlesex, England, confirmed that elemental diet is important for inflammation and also intestinal permeability.
This study examines whether treatment of acute Crohn's disease with an elemental diet improves intestinal integrity and inflammation as assessed by a 51Cr-labeled ethylenediaminetetraacetatic acid (EDTA) permeability test and the fecal excretion of 111In-labeled autologous leukocytes, respectively. Thirty-four patients with active Crohn's disease completed a 4-week treatment course with an elemental diet. Active disease was characterized by increased intestinal permeability [24-hour urineexcretion of orally administered 51Cr-EDTA, 6.4% +/- 0.6% (mean +/- SE); normal, less than 3.0%] and by high fecal excretion of 111In-labeled leukocytes (14.2% +/- 1.1%; normal, less than 1.0%). Twenty-seven (80%) went into clinical remission, usually within a week of starting treatment. After 4 weeks of treatment, there was a significant decrease in both the urine excretion of 51Cr-EDTA (to 3.4% +/- 0.5%; P less than 0.01) and the fecal excretion of 111In (to 5.7% +/- 1.0%; P less than 0.001), indicating that such treatment is not just symptomatic. A framework for the mechanism by which elemental diet works, centering around the importance of the integrity of the intestinal barrier function, is proposed, and also appears to provide a logical explanation for some relapses of the disease

Diet is not only important during the acute fase. Thirty-two patients with Crohn’s disease were treated with a fibre-rich, unrefined-carbohydrate diet in addition to conventional management and followed for a mean of four years and four months. Their clinical coursa was compared retrospectively with that of 32 matched patients who had received no dietary instruction. Hospital admission were significantly fewer and shorter in the hospital compared with 533 days in the non-diet-treated control group. Whereas five of the controls required intestinal operation, only one diet-treated patient needed surgery. This is in strong contrast to general experience with this disease. Treatment with a fibre-rich, unrefined-carbohydrate diet appears to have a favourable effect on the course of Crohn’s disease and does not lead to intestinal obstruction.

Diet is also involved in maintenance of remission.
Twenty patients with Crohn's disease took part in a controlled trial in which remission was maintained by either an unrefined carbohydrate fibre rich diet or a diet which excluded specific foods to which a patient was intolerant. 7 out of the 10 patients on the exclusion diet remained in remission for 6 months compared with none out of the 10 on an unrefined carbohydrate fibre rich diet (p<0•05, Fisher's exact test). In an uncontrolled study an exclusion diet allowed 51 out of 77 patients to remain well on the diet alone for periods of up to 51 months, and with an average annual relapse rate of less than 10%.
The incidence of Crohn’s disease is increasing in industrialised nations, but the condition is almost unknown is developing countries. Food is major factor affecting the intestinal environment, and the considerable change in dietary habits during this century may explan why Crohn’s disease has become more common. In 1976 workes in Marburg and Düsseldorf reported that before developing Crohn’s disease patients had eaten more refined sugar and food containing it than matched controls. In these studies dietary data were collected up to 12 years after diagnosis. It is doubtful whether people recall their eating habits of many previously with any accuracy. Furtheromore, neither study included information on dietary fibre, although a low-fibre diet has been suggested as causal factor. In view of continuing ignorance about the cause of Crohn’s disease, J. R. Thornton, P. M. Hemmet and K. W. Eaton decided to investigate the possible role of dietary fibre and at the same time to see if these German result could be confirmed with improved methods. Thirty consecutive newly diagnosed patients was studied. The diagnosis of Crohn’s disease was made by experience gastroenterologists and supported by tipical radiogical changes and often by histological examination of tissue. All patients were interviewed within three months of diagnosis. The median duration of symptoms before diagnosis was five months. A single dietitian used the dietary history method to question each patient about his or her habitual, pre-illess diet. Using a specially designed questionnaire, she determined the frequency of consumption and the size of helpings of each of a comprehensive range of food and drinks. Special care was taken with items containing refined sugar or dietary fibre. Refined sugar was defined as any fibre-depleted sugar, including brown sugar. These data were analysed by computer, using a programme specially compiled from the recent edition of McCance and Widdowson’s food tables, to determine the average daily intake of different food components. These tables are the first to contain values for dietary fibre as opposed to crude fibre, which is an accurate measurement. Control subject were otherwise healthy people who had recently attended the fracture clinic with minor fractures or orthopaedic conditions. They were matched for age ( 5 years), sex, social class, and marital status, and were closely similar to the patients in height and weight. The controls were interviewed about their diet in the same manner as the patients. Neither group was informed of the purpose or possible findings of the study. The statistiscal significance of differences was calculated by Student’s t test or the Wilcoxon rank sum test for paired data, as appropriate. The patients’ intake of refined sugar (median 122 g/day) was considerably grater than the controls’ (median 65 g/day, P <0.002; fig 1). Table II shows that the patients consistently took more sugar in both food and drinks. Intake was higher in both sexes and with all sites of disease. Sugar consumption was similar in patients whose symptoms had lasted for more and less than 12 months before diagnosis (median 112 and 128 g/day respectively). The patients ate more carbohydrate than the controls but this difference was almost entirely due to their greater consuption of sugar. The two groups ate almost identical quantities of protein and fat. Dietary fibre intake in the patients (17.3  0.6 g/day) slightly lower than in the control (19.2  0.9 g/day, P < 0.05), and the patients ate considerably raw fruit and vegetable fibre (median 0.6 g/day * 2.3 g/day in controls; P < 0.001). As with sugar, this finding was independent of sex, the site of disease, or the duration of symptoms. Thus median raw fibre intakes in patients who had had symptoms for more and less than 12 months before diagnosis were 0.6 and 0.7 g/day respectively. Intakes of cereal fibre and cooked fruit and vegetable fibre were similar in patients and controls. There was no significant difference in the drinking of alcohol or the consumption of conrflakes. This study confirm that people who develop Crohn’s disease habitually eat more refined sugar than healthly people and also shows that they eat less raw fruit and vegetables. Data should be more reliable than those from previous studies since they are derived from newly diagnosed patients. Moreover, the patients’ symptoms were usually of only a few months’ duration. The differences are unlikely to be due to atypical dietary habits in the control subject. Their median sugar intake of 65 g/day is identical to that obtained in a recent survey of randomly selected, Cambridgeshire villagers, using weighed measurements of food intake (when adjusted to the appropriate sex ratio). The National Food Survey estimated that the average refined sugar intake of the British population is 79 g/day. Similarly, dietary fibre intake averaged 19.9 g/day in the villagers and 20.4 g/day in the National Food Survey, whereas our controls are 19.2 g/day. It might be argued that patients may gradually modify their diets in the months and years before their symptoms become troublesome, eating more sugar to try and counteract weight loss or lassitude and eating less raw food to counteract loose stools. But the data do not support this suggestion. There was no difference in the intake of sugar or of raw fruit and vegetables between patients with recent and longer-lasting symptoms. The German studies found that after the onset disease patients ate less, not more, sugar. These eating habits therefore seem to precede the disease. Data lend some support to suggestions that the development of Crohn’s disease is favoured by a low intake of dietary fibre. The difference in total fibre intakes was relatively slight (and there was no difference in cereal fibre), but there was a pronounced difference in the consumption of fibre from raw fruit and vegetables. This is consistent with the idea that a low intake of raw fruit and vegetables is a causal factor. It has been reported that patients with Crohn’s disease eat signifantly more cornflakes at breakfast than controls. In common with three other studies, this study could not confirm this finding. How eating habits, such as those identified in this study, predispose to Crohn’s disease is uncertain and will remain so until the pathogenesis of the disease is understood. A role for diet does not exclude the involvement of a virus or bacterium. Dietary influences may alter the milieu of the intestinal lumen of modify the intestinal flora and so promote the growth of an infective agent or its invasion of the gut wall. The dietary tendencies shown in this study may help to explain the recent emergence of the disease and its rarity in communities eating simple, traditional diets. At a pratical level, reversing these eating habits might be helpful in the management of this intractable condition.

BIBLIOGRAFY
The Lancet, Volume 326, Issue 8448, Pages 177 - 180, 27 July 1985
Gastroenterology. 1988 Mar;94(3):603-10.
Gastroenterology. 1981 Jan;80(1):10-5.
Pubmed
British Medical Journal, Volume 288.

Mycobacterium avium subsp. paratuberculosis, Genetic Susceptibility to Crohn's Disease, and Sardinians: the Way Ahead [Journal of Clinical Microbiology, October 2005]

The present study was performed to determine what proportion of people in Sardinia with or without Crohn's disease were infected with Mycobacterium avium subspecies paratuberculosis and had a preponderance of allelic variants of Nod2, an intracellular protein involved in Crohn's disease susceptibility.

Detection and Isolation of Mycobacterium avium subspecies paratuberculosis from intestinal mucosal biopsies of patients with and without Crohn's disease in Sardinia.[Am J Gastroenterol. 2005 Jul;100(7):1529-36]

Sardinia is an island community of 1.6 million people. There are also about 3.5 million sheep and one hundred thousand cattle in which Johne's disease and Mycobacterium avium subspecies paratuberculosis infection are endemic. The present study was designed to determine what proportion of people in Sardinia attending for ileocolonoscopy with or without Crohn's disease were infected with this pathogen.

ursodeoxycholic and silimarin?

ursodeoxycholic acid and Crohn's disease

Inflamm Bowel Dis. 2010 Mar;16(3):518-24.
Potential for amino acids supplementation during inflammatory bowel diseases. 2010
Coëffier M, Marion-Letellier R, Déchelotte P.

Appareil Digestif Environnement Nutrition (ADEN EA4311), Institute for Biomedical Research, European Institute for Peptide Research (IFRMP 23), Rouen University and Rouen University Hospital, Rouen, France. moise.coeffier@univ-rouen.fr
Abstract
The pathophysiology of inflammatory bowel diseases (IBDs) is multifactorial and involves interactions of gut luminal content with mucosal barrier and especially immune cells. Malnutrition is a frequent issue during IBD flares, especially in Crohn's disease (CD) patients, and nutritional support is frequently used to treat malnutrition but also in an attempt to modulate intestinal inflammation. The use of oral or enteral nutrition intervention in IBDs may be effective, alone or in combination with drugs, to achieve and maintain remission. However, standard diets are less effective than new-generation biotherapies and could be improved by supplementation with specific immunomodulatory amino acids. Experimental studies evaluating glutamine, the preferential substrate for enterocytes, are promising. Some clinical studies with oral glutamine in CD are until now disappointing, but new formulations and targeting could enhance glutamine efficacy at the site of mucosal lesions. The role of arginine, involved in nitric oxide and polyamines synthesis, still remains debated. However, the effects of these amino acids in IBD have been poorly documented in humans. Other candidates like glycine, cysteine, histidine, or taurine should also be evaluated in the future.

Morbo di Crohn, stenosi e ostruzioni ricorrenti
Fra i pazienti con morbo di Crohn che vengono sottoposti ad intervento chirurgico per la comparsa di stenosi, il numero di stenosi e di plastiche effettuate può predire la probabilità di ostruzioni recidivanti. Questa osservazione si deve probabilmente a fattori correlati alla malattia. La presenza di un maggior numero di stenosi intestinali di per sé non porta ad un aumento delle recidive delle ostruzioni, ma probabilmente rappresenta un marcatore della presenza di una forma patologica più grave o avanzata. E' necessario approfondire gli studi per comprendere meglio le ragioni alla base di queste associazioni, ed identificare potenziali interventi per ridurre i tassi di recidiva. (J Am Coll Surg 2009; 208: 1065-70)

Crohn per 60mila italiani. Molti i giovani
Morbo di Crohn, una patologia cronica infiammatoria del tratto gastrointestinale che colpisce un milione di persone in Nord America e in Europa, compresi 60mila italiani. Di questi, 35mila devono fare i conti con forme gravi. Ne sono affetti individui di tutte le età, ma in particolare il Crohn riguarda i giovani adulti: solitamente i primi sintomi si avvertono prima dei 40 anni. Si tratta di diarrea, crampi e dolori addominali ricorrenti, accompagnati da perdita di peso, febbre e in alcuni casi emorragie. Tra le complicazioni l'ostruzione intestinale, fistole e denutrizione. Durante il decorso della malattia il 75% dei pazienti va incontro a un intervento chirurgico causato da tali complicazioni o dalla resistenza alla terapia. Dei malati che sono costretti ad affrontare un'operazione per rimuovere una parte dell'intestino, circa la metà registra una ricaduta nel corso dei cinque anni successivi. Numeri non certo tranquillizzanti, che hanno spinto alcuni dei più eminenti esperti italiani a riunirsi per un incontro, organizzato a Parigi, dal titolo "Crohn's Diseases: Achieving Patients' Benefits": in breve, come ottenere benefici per i pazienti. E per ora la risposta è: con i farmaci, soprattutto, per tenere a bada i sintomi. Perché a oggi non esistono soluzioni terapeutiche definitive. "Si può dire che la comunità scientifica, di fronte a questa malattia - ha detto ai giornalisti intervenuti all'evento Francesco Pallone, presidente della Società italiana di Gastroenterologia - si trovi ancora ai tempi della preistoria. Sappiamo che le cause sono genetiche, ma è solo da poco tempo che abbiamo compreso il meccanismo di insorgenza del Crohn: quando si è scoperto che l'Helicobacter pylori causa l'ulcera, era diventato di gran moda tentare di trovare lo stesso tipo di stimolo patologico che potesse trovarsi alla base del morbo di Crohn".