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PubMed1993

Antibodies to human recombinant lipocortin-I in inflammatory bowel disease.

1. Corticosteroid drugs are widely employed for the treatment of active inflammatory bowel disease. Not all patients receiving corticosteroid treatment, however, respond satisfactorily, their disease either remaining active in spite of continued treatment, or relapsing upon corticosteroid withdrawal. Raised levels of autoantibodies to lipocortin-I, a corticosteroid-inducible protein with anti-inflammatory activity in vitro, in patients receiving chronic oral corticosteroid therapy have been associated with poor clinical response in rheumatoid arthritis. 2. To determine whether a similar mechanism is responsible for the variable clinical response to corticosteroids in inflammatory bowel disease, we have measured circulating lipocortin-I antibody levels in sera from affected patients and related them to disease activity, treatment and subsequent outcome. 3. IgM, but not IgG, lipocortin-I antibody levels were elevated in patients with ulcerative colitis and Crohn's disease compared with healthy control subjects. In patients with Crohn's disease not taking corticosteroids, IgM lipocortin-I antibody levels were directly related to disease activity scored clinically. 4. IgM lipocortin-I antibody levels were higher in patients receiving sulphasalazine or no treatment and in patients receiving corticosteroids who responded to treatment within 2 months (steroid responders) than in those patients undergoing long-term corticosteroid therapy because of continued disease activity or repeated relapse on corticosteroid withdrawal (steroid non-responders). 5. The high levels of IgM lipocortin-I antibodies in patients with inflammatory bowel disease not taking corticosteroids provides further evidence of disturbed immunity in inflammatory bowel disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Imbalanced secondary mucosal antioxidant response in inflammatory bowel disease.

Intestinal mucosal damage in the inflammatory bowel diseases (IBD) Crohn's disease (CD) and ulcerative colitis (UC) involves reactive oxygen metabolites (ROMs). ROMs are neutralized by endogenous antioxidant enzymes in a carefully balanced two-step pathway. Superoxide dismutases (SODs) convert superoxide anion to hydrogen peroxide (H(2)O(2)), which is subsequently neutralized to water by catalase (CAT) or glutathione peroxidase (GPO). Remarkably changed expression levels of the three isoforms of SOD in paired non-inflamed and inflamed mucosae from CD and UC patients have been previously reported in comparison to normal control mucosa. Most notable was the strong up-regulation of Mn-SOD in inflamed epithelium. It was hypothesized that in order to provide optimal protection against ROM-mediated damage, these changes should be coordinately counterbalanced by an increased H(2)O(2)-neutralizing capacity. Therefore, the same tissue samples were used to assess the levels, activities, and/or localization of the most prominent mucosal H(2)O(2)-related antioxidants CAT, GPO, glutathione (GSH), myeloperoxidase (MPO), and metallothionein (MT). Quantitative measurements showed that in both CD and UC patients, intestinal inflammation was associated with increased activities of CAT, GPO, and MPO, whereas the mucosal GSH content was unaffected and the concentration of MT was decreased. Despite this overall increase in mucosal H(2)O(2)-metabolizing enzyme capacity, immunohistochemical analysis revealed a differentially disturbed antioxidant balance in IBD epithelium and lamina propria. In the lamina propria, the risk of direct H(2)O(2)-mediated damage seemed to be restrained by the increasing numbers of CAT- and MPO-positive monocytes/macrophages and neutrophils that infiltrated the inflamed areas. On the other hand, MPO overexpression might increase the lamina propria levels of hypochlorous acid, a stable ROM with multiple pro-inflammatory effects. In the epithelium, the number of cells that expressed CAT remained unchanged during inflammation and GPO was found in only a very low and constant number of epithelial cells. In addition, the inflamed epithelium displayed decreased expression of the hydroxyl radical (OH(*)) scavenger MT. In view of the high epithelial SOD levels in inflamed IBD epithelium, it is speculated that the efficient removal of excess H(2)O(2) is hampered in these cells, thereby increasing not only the risk of detrimental effects of H(2)O(2) directly, but also those of its extremely reactive derivatives such as OH(*). Taken together, the results suggest an imbalanced and inefficient endogenous antioxidant response in the intestinal mucosa of IBD patients, which may contribute to both the pathogenesis and the perpetuation of the inflammatory processes.

Adult↗
PubMed1986

Immunoelectron microscopic localization of HLA-DR antigen in control small intestine and colon and in inflammatory bowel disease.

We have elucidated the distribution of I2 (HLA-DR) antigen in control and inflammatory bowel disease specimens, using immunoelectron microscopic methods. Control small intestinal epithelium and inflammatory bowel disease epithelium expressed 12 antigen, while control colonic epithelium did not. I2 expression by enterocytes was more frequent on the lateral and basal surface than on the microvillus surface. Two of three M cells in control ileum expressed I2 antigen. I2-positive intraepithelial lymphocytes were rarely detected in both control and disease specimens. I2-positive lamina propria lymphocytes were significantly increased in inflammatory bowel disease, while I2-positive lamina propria lymphocytes were virtually absent in control specimens. I2-positive mononuclear cells in the intestinal lamina propria were largely macrophages and monocytes in both control and inflammatory bowel disease specimens. I2-positive mononuclear cells resembling dendritic cells were not detected in control or disease specimens. Furthermore, there were no significant morphological differences in I2-positive or -negative macrophages and monocytes in control and disease specimens. The expression of I2 antigen on Schwann cells was detected more frequently in disease specimens than in control specimens. Capillary endothelia of both control and disease specimens expressed I2 antigen. We demonstrate that I2 expression is present on surface membranes of both immune and nonimmune cells of the intestine and colon and show that this expression is more prominent in inflammatory bowel disease than in control intestine and colon. Further studies are required to determine whether this finding is meaningful in terms of antigen presentation and whether this apparent "immune activation" is involved in the pathogenesis of inflammatory bowel disease.

Antibodies, Monoclonal↗
PubMed2006

Inflammatory bowel diseases as secondary causes of osteoporosis.

Inflammatory bowel disease (IBD), comprising Crohn's disease and ulcerative colitis, is associated with an increased risk of osteoporosis and bone fractures. Initial studies suggested very high rates of osteoporosis in IBD, but more recent studies have suggested that bone mineral density (BMD) is often normal in patients with IBD and typically changes little over time. Nonetheless, IBD is associated with an increased risk of fractures. Doctors managing patients with IBD must consider a variety of risk factors, not just BMD measurements, in assessing fracture risk. Advances have been made in exploring the pathogenesis of osteoporosis in IBD. The evolution of knowledge regarding receptor for activated factor of nuclear factor kappaB (RANK), its ligand RANKL, and osteoprotegerin (OPG), which serves as a decoy receptor, has enhanced the understanding of both osteoporosis and T-cell immunobiology. Recent clinical studies in patients with IBD have revealed that serum OPG levels may be elevated and inflamed intestinal tissue secretes increased amounts of OPG. It is suspected that OPG levels are elevated as a counterregulatory response to low BMD, as serum OPG levels in IBD have been found to be inversely associated with BMD. Finally, in animal models of IBD, exogenous OPG has reversed both the osteopenia and the enterocolitis, suggesting that it may have a therapeutic role in human IBD.

Humans↗
PubMed1993

Familial empirical risks for inflammatory bowel disease: differences between Jews and non-Jews.

The Jewish population has an increased frequency of inflammatory bowel disease compared with their non-Jewish neighbours. Genetic factors have been implicated in the aetiology of this disorder and may contribute to ethnic differences. This study determined the familial empirical risks for inflammatory bowel disease in the first degree relatives of inflammatory bowel disease probands (for both Jews and non-Jews) for the purpose of accurate genetic counselling and genetic analysis. A total of 527 inflammatory bowel disease patients from Southern California (291 Jews and 236 non-Jews) were questioned about inflammatory bowel disease in their first degree relatives (a total of 2493 individuals). Since inflammatory bowel disease has a variable and late age of onset, age specific incidence data were used to estimate the life time risks and to make valid comparisons between the different groups. In the first degree relatives of non-Jewish probands, the life time risks for inflammatory bowel disease were 5.2% and 1.6% when probands had Crohn's disease and ulcerative colitis respectively. These values were consistently lower than the corresponding risks for relatives of Jewish patients -7.8% and 4.5% for Crohn's disease and ulcerative colitis probands respectively (p value for comparison between Jews and non-Jews: 0.028; between ulcerative colitis and Crohn's disease: 0.005). These data provide the requisite basis for genetic counselling for these disorders in the white American population. In addition, these different empirical risks for relatives of Jewish and non-Jewish probands allow rejection of single Mendelian gene models for inflammatory bowel disease, but are consistent with several alternative genetic models.

Adolescent↗
PubMed1993

Psychopathology and relationship measures in children with inflammatory bowel disease and their parents.

Children with inflammatory bowel disease and their parents were assessed for DMS-III diagnoses, maternal attachment, marital relationship, life stresses, illness severity and cognitive/affective profile. Eleven of 15 children and 21 of 27 parents had psychiatric diagnoses. Three children were suicidal. Thirteen of 15 mothers had insecure attachment. Marital difficulties and medical severity correlated with life stress. The higher prevalence of psychiatric disorders than epidemiologically and of insecure attachment suggest at-risk relationships.

Adolescent↗
PubMed1999

Increased prevalence of methylenetetrahydrofolate reductase C677T variant in patients with inflammatory bowel disease, and its clinical implications.

BACKGROUND: Inflammatory bowel disease (IBD) is associated with an increased incidence of thromboembolic disease. Hyperhomocysteinaemia (hyper-tHcy), a condition associated with the C677T variant of 5, 10-methylenetetrahydrofolate reductase (MTHFR), is linked with an increased incidence of thromboembolic disease. Hyper-tHcy has been reported in patients with IBD. AIMS: To assess the prevalence of the C677T MTHFR genotype and the contribution of this genotype to hyper-tHcy in patients with IBD. METHODS: Patients with established IBD (n=174) and healthy controls (n=273) were studied. DNA samples were genotyped for the MTHFR (C677T) mutation. Subjects were categorised as homozygous for the thermolabile variant (TT), heterozygous for wild type and variant (CT), or homozygous for the wild type (CC). RESULTS: Plasma homocysteine concentrations were significantly higher in patients with IBD than in healthy controls. A total of 17.5% of ulcerative colitis and 16.8% of Crohn's disease patients were homozygous for the C677T variant compared with 7.3% of controls. Homozygosity (TT) for the variant was associated with higher plasma tHcy levels in patients with IBD and in healthy controls. When all subjects who were TT for the variant were excluded, median plasma tHcy was still significantly higher in IBD than controls. Plasma vitamin B(12) levels were lower in patients with IBD irrespective of MTHFR genotype. CONCLUSIONS: There is an association between the thermolabile MTHFR C677T variant and IBD. This accounts in part for the raised plasma tHcy found in patients with IBD and may contribute to the increased incidence of thromboembolic complications. All patients with IBD should receive low dose folic acid and vitamin B(12) therapy to protect against the thromboembolic complications of raised tHcy.

Adolescent↗
PubMed2006

A pilot study on chemospecific duodenal visceral sensitivity in inflammatory bowel disease in remission.

BACKGROUND: Patients with inflammatory bowel disease (IBD) in remission frequently experience symptoms resembling irritable bowel syndrome (IBS). In IBS altered motility and visceral sensitivity are found throughout the whole gastrointestinal tract. We aimed to study chemospecific antroduodenal sensitivity in IBD patients. METHODS: Antroduodenal manometry was performed in 10 IBD patients in remission and 13 controls. Small volumes of nutrients and acid were administered intraduodenally. Motility variables and sensation scores were compared before and after each infusion. RESULTS: Acid and lipid infusion decreased the number of antral pressure waves in both groups (p < 0.05). After acid infusion the number of duodenal pressure waves in the sideholes just distal to the infusion port increased in IBD patients compared to the controls (p < 0.05). Lipid infusion increased the number of duodenal propagated pressure waves in both groups, but in controls they were also increased over longer distances (p < 0.005). None of the infusions significantly affected the sensation scores. CONCLUSION: Subtle alterations in chemospecific responses to lipids and acid in IBD patients in remission were observed, affecting duodenal motor activity but not duodenal perception. These changes are indicative of changes at the chemoreceptor level in the duodenal wall in this patient group.

Analysis of Variance↗
PubMed2005

Probiotics in arthralgia and spondyloarthropathies in patients with inflammatory bowel disease. Prospective randomized trials are necessary.

Arthralgias and spondyloarthropathies of the peripheral and axial joints are common in inflammatory bowel disease. Evidence for a strong association between these clinical manifestations and diseases of the joints has been provided by several clinical and epidemiological studies. Immunological studies have shown the presence of shared inflammatory cells both in the gut and the synovium in spondyloarthropathies. Genetic factors play a crucial role in the pathogenesis of spondyloarthropathies and inflammatory bowel disease. The role of the ubiquitous bacterial flora and pathogenic microorganisms present in the intestinal lumen may induce these joint diseases in patients with inflammatory bowel disease. In this review we will focus on the pathogenesis of spondyloarthropathies and arthralgia in patients suffering from inflammatory bowel disease. Based on preliminary clinical observations in patients with arthralgia and IBD, we put forward the hypothesis that probiotics may be helpful in the management of common extraintestinal manifestations such as arthralgia in patients with ulcerative colitis and Crohn's disease.

Arthralgia↗
PubMed1998

Neuroendocrine neoplasms arising in inflammatory bowel disease: a report of 14 cases.

Inflammatory bowel disease (IBD), particularly ulcerative colitis (UC), is a premalignant condition, because these patients are at increased risk of adenocarcinoma. Neuroendocrine neoplasms (NENs) have rarely been described in this setting. We evaluated 14 cases of NEN arising in a setting of IBD. All of the tumors arose in areas involved by IBD, and all showed immunohistochemical or ultrastructural evidence of neuroendocrine differentiation. The cohort included seven men and seven women (range, 28-71 yr; median, 43 yr). Eight patients had Crohn's disease (CD), and six had UC. Duration of disease ranged from 4 months to 50 years (median, 15 yr), with one of unknown duration. Of the eight patients with CD, five had ileocolitis, one had ileitis, one had colitis, and in one case, the extent of disease was unknown. Of the six patients with UC, four had extensive UC, one had left-sided UC, and the extent of UC was unknown in one case. Reasons for surgery included CD complications (five patients), refractory disease (three patients), dysplasia/carcinoma (five patients), and incontinence (one patient). The NENs were well differentiated in 11 cases and poorly differentiated mixed adenocarcinoma/small cell carcinomas in 3 cases. Tumor sites included the rectum (six cases), appendix (four cases), small bowel (two cases), and sigmoid colon (two cases). High-grade dysplasia was present in adjacent mucosa in four cases, and low-grade dysplasia was present in distant mucosa in two cases. Two patients with poorly differentiated NENs died from the disease at 3 and 11 months after tumor excision. All of the other patients were alive without tumor as of last follow-up. We concluded that NENs rarely arise in a setting of IBD. Most are well-differentiated tumors and are clinically indolent. Dysplasia is found in adjacent mucosa in more than one-third of cases, suggesting that neuroendocrine differentiation might evolve from multipotential cells in dysplastic epithelium.

Adult↗
PubMed2005

Increased risk for demyelinating diseases in patients with inflammatory bowel disease.

BACKGROUND & AIMS: Reports of multiple sclerosis (MS), demyelination, and optic neuritis (ON) associated with anti-tumor necrosis factor alpha therapy resulted in warnings on prescribing instructions for infliximab, etanercept, and adalimumab. However, the underlying relationship between IBD and these neurologic conditions has not been established. METHODS: We performed a retrospective cohort study and a retrospective cross-sectional study using 1988 to 1997 data from the General Practice Research Database. A total of 7988 Crohn's disease and 12,185 ulcerative colitis patients were matched for age, sex, and primary care practice to 80,666 randomly selected controls. In the cohort study, incident cases of MS, demyelination, and/or ON (MS/D/ON) had to occur at least 1 year after registration with the physician and after the diagnosis of IBD. In the cross-sectional study, the diagnosis of MS/D/ON could either precede or follow the IBD diagnosis. RESULTS: In the cohort study, the incidence of MS/D/ON was higher in patients with Crohn's disease and ulcerative colitis compared with their matched controls, reaching statistical significance for ulcerative colitis (ulcerative colitis incidence rate ratio [IRR], 2.63; 95% confidence interval, 1.29-5.15; Crohn's disease IRR, 2.12; 95% confidence interval, .94-4.50). In the cross-sectional study, MS/D/ON was more prevalent in patients with Crohn's disease and ulcerative colitis compared with their matched controls (Crohn's disease odds ratio, 1.54; 95% confidence interval, 1.03-2.32; ulcerative colitis odds ratio, 1.75; 95% confidence interval, 1.28-2.39). CONCLUSIONS: Demyelinating diseases occur more commonly among patients with IBD than among non-IBD patients. Future studies should clarify whether treatment with tumor necrosis factor alpha blockers results in further increased incidence of MS/D/ON among IBD patients.

Adult↗
PubMed2000

Does cyclosporin A worsen liver function in patients with inflammatory bowel disease and total parenteral nutrition?

OBJECTIVE: inflammatory bowel disease (IBD), total parenteral nutrition (TPN) and immunosuppressive treatment with cyclosporin A (CsA) are well known factors in hepatobiliary disorders. Their association, however, has been little studied. METHOD: we retrospectively analyzed the results of liver function tests (transaminases, AST. ALT), total bilirubin, alkaline phosphatase, and gamma-glutamyltransferase (GGT) in a consecutive series of 50 patients (29 men, 21 women, mean age 32 years, range 16-78 years) hospitalized for a severe attack of IBD between January 1992 and July 1997. Basal laboratory values in all patients were normal. Thirty-eight patients had ulcerative colitis (UC) and 12 had Crohn's disease (CD), which debuted in 28% of the patients. All patients were treated with methylprednisolone (MP) (0.75-1.0 mg/kg daily i.v., and received TPN. 42% (21/50) required additional treatment with CsA (5 mg/kg daily i.v.) at the beginning or during the first week of TPN and during 7-24 days, because on nonresponse to steroid treatment. Two study groups were defined according to treatment: Group I consisted of 29 patients given MP + TPN, and group II comprised 21 patients who received MP + TPN + CsA. The groups were otherwise similar in all other variables analyzed. Liver function tests were done weekly until the end of the study period. RESULTS: 62% of the patients (31/50) showed hepatobiliary dysfunction, defined previously as a 2-fold or greater elevation of two or more parameters. There was no statistically significant difference between the two groups in the incidence of dysfunction (15/29 vs 16/21, n.s.). The parameters that showed the greatest alterations were GGT and ALT; the greatest elevation appeared during the third week of immunosuppressive treatment, and did not exceed 6-fold the normal value. The alterations disappeared once TPN and immunosuppressive treatment were discontinued. CONCLUSIONS: the hepatobiliary dysfunction in patients treated with both TPN and CsA was no more severe than associated with TPN alone.

Adult↗
PubMed1992

[Chronic inflammatory bowel diseases in childhood. Case contribution and critical considerations].

The term "inflammatory bowel disease" describes 2 major categories of chronic disease: Crohn's disease and ulcerative colitis. Non specific chronic colitis and allergic colitis in childhood can usually be distinguished by clinical and histopathologic criteria. This study regards a retrospective analysis of 23 patients suffering from chronic inflammatory bowel disease. Clinical manifestations began between 4 and 18 years of age. The Authors report remarkable frequency in pediatric age and common diagnostic delay, especially in Crohn's disease. The possibility of extraintestinal symptoms (erythema nodosum, arthritis, iridocyclitis) is also showed. Moreover they analyse present diagnostic proceedings: in childhood the employ of 99 mTc-HmPAO-labelled granulocytes is a new and non invasive test useful in the follow-up of the patients. In the treatment corticosteroids and sulfasalazine are used in various combinations associated with general supportive measures. Finally the Authors confirm that chronic inflammatory bowel disease may cause, especially in childhood, remarkable involvement on the growth and several psychological disorders.

Adolescent↗
PubMed2025

Multi-ancestry genome-wide and transcriptome-wide association analyses identified new risk loci and genes for inflammatory bowel disease.

To advance genetic understanding of inflammatory bowel disease (IBD), we conducted genome-wide association meta-analyses of 63,415 IBD cases of European and East Asian descendants and identified 90 previously unknown risk loci. Integrating multi-ancestry transcriptome-wide association studies (TWAS), cell type-specific TWAS, alternative splicing (AS-WAS), and alternative polyadenylation (APA-WAS) analyses using RNA-seq data from normal colon tissues of 707 European and 364 East Asian individuals, we uncovered 506 high-confidence IBD risk genes, including 384 not previously reported. These genes converge on immune regulation, microbial interaction, and other pathways central to IBD pathogenesis, with over half showing transcriptional dysregulation supported by single-cell and spatial omics analyses. Notably, 46 risk genes are targeted by 225 drugs that have been approved or in Phase II/III trials, including sulfasalazine already used in IBD therapy. Our study findings deepen the understanding of IBD genetics and support the development of precision medicine for its prevention and treatment.

GWAS↗
PubMed1999

Relatives' expressed emotion and the course of inflammatory bowel disease.

Thirty-one relatives of inflammatory bowel disease (IBD) patients referred to a specialist unit were assessed with the Camberwell Family Interview, and ratings of expressed emotion (EE) were made. These relatives were significantly less critical than relatives of psychiatric patients in previous studies (p<0.001). Outcome was assessed over a 12-month follow-up period by a clinician blinded to the EE ratings. Most patients in this study had a poor outcome, and 11 (38%) needed surgery. A significantly higher proportion of patients with low EE relatives were in the surgery outcome group (p = 0.02). Excluding the surgery group, there was a nonsignificant trend for patients with high EE relatives to have a worse outcome. Patterns of response suggested better tolerance by relatives of the more ill patients. In the group overall there was no relationship between psychiatric status and physical health, either initially or at follow-up. There was considerable agreement among relatives as to the "typical" IBD personality. A number of key findings concerning the IBD patient, patterns of relatives' EE, and how they relate to the course of the illness remain to be verified by more systematic assessment.

Adult↗
PubMed1998

Differential lamina propria cell migration via basement membrane pores of inflammatory bowel disease mucosa.

BACKGROUND & AIMS: In active inflammatory bowel disease (IBD), the intestinal mucosa is infiltrated by polymorphonuclear cells (PMNs), lymphocytes, and monocytes from the systemic circulation. Using an ex vivo model, we have investigated luminally directed migration of cells out of the lamina propria. METHODS: Fresh untreated and deepithelialized mucosal samples were studied by electron microscopy. Cells migrating out of the lamina propria were investigated by immunohistochemistry and fluorescence-activated cell sorter analysis. RESULTS: In intact IBD mucosal samples, tunnels containing cells were prominent in the lamina propria matrix, and PMNs, but not other cell types, were prominent in the epithelium. In deepithelialized mucosal samples, the basement membrane was either destroyed or contained numerous large pores. During culture of deepithelialized mucosal samples, many cells (3.3 [+/-0.8] x 10(5) . g tissue-1 . h-1) migrated out of the lamina propria via basement membrane pores. PMNs and eosinophils were prominent during the first 3 hours of culture, but T cells predominated thereafter. Macrophages also migrated, but B cells were the minority population (<2%) at all times. CONCLUSIONS: In active IBD mucosa with an intact epithelium, luminally directed migration of lamina propria cells is restricted mainly to PMNs. After loss of the epithelium, other cell types also migrate into the lumen via numerous, large, basement membrane pores.

Basement Membrane↗
PubMed2004

Inflammatory bowel diseases in pediatric and adolescent patients: clinical, therapeutic, and psychosocial considerations.

Inflammatory bowel diseases (Crohn's disease and ulcerative colitis) primarily affect young adults, but in 15%-25% of cases, the initial disease starts in childhood. Many aspects of inflammatory bowel disease, including initial evaluation, nutritional support, medical and surgical intervention, and the direction of future research, are encountered in both adult and pediatric patients. However, it is important to delineate issues specific to pediatric patients, especially growth velocity impairment, derangements in and treatment of abnormal bone mineralization, and transitional care issues; the lack of extensive randomized, controlled pediatric therapeutic trials is also a concern. This article reviews the epidemiology of pediatric inflammatory bowel disease incidence and prevalence worldwide, clinical issues (including impairments of growth velocity and bone density), diagnostic and therapeutic interventions, and psychosocial issues unique to pediatric patients. Future research directions defined by the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition and opportunities provided by existing pediatric research databases are highlighted.

Adolescent↗
PubMed1996

Factor XIII in chronic inflammatory bowel diseases.

Severe acute inflammation in chronic inflammatory bowel disease is associated with large wound areas and ulcerations that show spontaneous hemorrhage or marked friability. Therefore, an enormous potential of hemostasis and wound healing is required. Coagulation studies demonstrate a deficiency of factor XIII that is important for both clot formation and wound healing. Consequently, the substitution of factor XIII may be beneficial; the first case reports present favorable clinical results. In a prospective pilot study, we treated 12 patients with therapy-resistant ulcerative colitis. The colitis activity index (CAI) and the endoscopic score (ES) according to Rachmilewitz were elevated; all patients suffered from hematochezia. After substitution therapy with factor XIII concentrate (1,250 U/d) the stool frequency dropped and no further hematochezia was detected. The CAI and the ES declined highly significantly. Because of these encouraging results two placebo-controlled multicenter trials have been initiated. In the first study, patients with acute stage of ulcerative colitis associated with severe intestinal blood loss are treated with two different dosages of factor XIII concentrate (1,250 and 500 U/d, respectively) or placebo for 10 days. In the second trial, patients with therapy-resistant ulcerative colitis with a lack of remission in spite of a consequent therapy for 2 weeks are included; factor XIII concentrate or placebo is administered for 10 days. The aim of both trials is an end of intestinal bleeding and the fostering of a more effective wound-healing process.

Adult↗