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PubMed1995

[Frequency of antibiotics-associated colitis in hospitalized patients in 1974-1991 in "Comprehensive Hospital Drug Monitoring", Bern/St. Gallen].

In 3 divisions of internal medicine of teaching hospitals of the Comprehensive Hospital Drug Monitoring (CHDM) Foundation Bern/St Gallen, 42,920 patients consecutively admitted between 1974-1991 were investigated for adverse drug reactions. Of these 16,150 patients (38%) had received at least one systemically administered antibacterial drug during the hospital stay. Antibiotic-associated colitis included the following diagnoses: pseudomembranous colitis, hemorrhagic colitis and milder forms of colitis. We collected the data of these patients by searching for all diagnoses which might represent antibiotic-associated colitis (from the list of WHO adverse drug reaction terminology). 9 individual patients with one episode of probable antibiotic-associated colitis were found. In 5 of these cases, only one drug given during the hospital stay seemed to be implicated. An additional 32 patients were admitted with antibiotic-associated colitis in relation to treatment with the same groups of drugs before hospital admission. Based on the exposure pattern of the 9 patients with antibiotic-associated colitis compared to all patients exposed during hospital stay, we estimated the following frequencies related to the drug groups with at least 1,000 patients exposed: for all antibacterial chemotherapeutics 0.6/1000 (0.25-1.06); all penicillins 0.6/1000 (0.22-1.32), for benzyl-, phenoxy-, ureido-, isoxazolyl penicillins and methicillin 2.0/1000 (0.42-5.92) and aminopenicillin or analogues, with or without clavulanic acid 0.6/1000 (0.18-1.35). For cephalosporins the frequency is 1.4/1000 (0.17-5.12). Under sulfonamides combined with trimethoprim or related substances (5077 exposed patients) and fluoroquinolones (1043 exposed patients) no case was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

First attack of inflammatory bowel disease and infectious colitis. A clinical, histological and microbiological study with special reference to early diagnosis.

To investigate the possibilities of differentiating between inflammatory bowel disease (IBD) and infectious colitis on clinical, microbiological, laboratory and histological grounds, a prospective study of 105 patients with a first attack of colitis was undertaken. Rectal biopsy was performed on four occasions during 1 year. In 56% of the patients who proved to have IBD, the mode of onset of diarrhoeal symptoms was insidious and in 44% it was more acute, while in 81% of those who proved to have infectious colitis the onset was acute. Most patients with infectious colitis presented within 1 week, had early fever, and did not show any histological features characteristic of IBD. In most IBD patients with a non-insidious onset there were clinical warning signs of IBD, such as slight previous bowel symptoms, a late presentation time (> 1 week) and absence of early fever, or histological features characteristic of IBD. Moreover, 62% of the IBD patients with a non-insidious onset fell ill in connection with travelling abroad, gastrointestinal infection or treatment with antibiotics. Travel abroad seemed to be associated with an increased risk of developing IBD. The strongest histological predictor of IBD was basal plasmocytosis, followed by more than two vertical crypt branches/MPF, crypt distortion, villous mucosa, mucosal atrophy, epithelioid granulomas and Paneth cell metaplasia. These signs were rarely or never found among patients with infectious colitis. Their frequency increased with the interval between the initial symptoms and the first biopsy. The presence of focal basal plasmocytosis seems to be the earliest sign of IBD. The frequency of histological signs indicating IBD was maximal (88%) at the 1-week biopsy. During treatment the basal plasmocytosis and villous mucosa decreased, while crypt distortion and mucosal atrophy remained unchanged. Early treatment did not prevent the appearance of any feature. Nor did it prevent relapse. In 21% of the IBD patients microbial findings were positive. The findings consisted in known colitis-causing agents in 14% and other agents, such as viruses, in another 7%. In 78% of the patients with non-relapsing colitis (NRC), colitis-causing agents were found. Haemolytic strains of E. coli were detected more often in IBD. Among the IBD patients, 65% showed positive immunofluorescence reactivity to neutrophil granulocytes, indicating the presence of antineutrophil antibodies (ANCA). The corresponding figure for NRC patients was 5%. Antibodies against beta-glucuronidase were found in 42% of the patients with granulocyte reactivity.

Acute Disease↗
PubMed1993

Clinicopathologic study of dextran sulfate sodium experimental murine colitis.

BACKGROUND: We undertook this study in order to fully characterize the clinical and histopathology features of the dextran sulfate sodium (DSS) model of experimental murine colitis and to discover the earliest histopathologic changes that lead to colitis. EXPERIMENTAL DESIGN: Acute colitis was induced in Swiss-Webster mice by 7 days of oral DSS with animals sacrificed daily. Chronic colitis was induced by: (a) 7 days of oral DSS followed by 7 days of H2O (for 1, 2, and 3 cycles) and (b) 7 days of oral DSS followed by 14 and 21 days of H2O. In each experimental group, the entire colons were examined histologically and correlated with clinical symptoms. RESULTS: Acute clinical symptoms (diarrhea and/or grossly bloody stool) were associated with the presence of erosions and inflammation. More importantly, the earliest histologic changes which predated clinical colitis was loss of the basal one-third of the crypt (day 3), which progressed with time to loss of the entire crypt resulting in erosions on day 5. The earliest changes were very focal and not associated with inflammation. Inflammation was a secondary phenomena and only became significant after erosions appeared. Animals treated with only 7 days of DSS followed by 14 and 21 days of H2O developed a chronic colitis with the following histologic features: areas of activity (erosions and inflammation), inactivity, crypt distortion, florid epithelial proliferation and possible dysplasia. These changes were similar to animals given 3 cycles of DSS. The clinical disease activity index correlated significantly with pathologic changes in both the acute and chronic phases of the disease. CONCLUSIONS: The mechanism of DSS colitis is presently unknown. However, the finding of crypt loss without proceeding or accompanying inflammation suggests that the initial insult is at the level of the epithelial cell with inflammation being a secondary phenomena. This may be a good model to study how early mucosal changes lead to inflammation and the biology of the colonic enterocyte. Chronic colitis induced after only 7 days of DSS may serve as a useful model to study the effects of pharmacologic agents in human inflammatory disease and mechanisms of perpetuation of inflammation. Finally, we believe that this model has the potential to study the dysplasia cancer sequence in inflammatory disease.

Animals↗
PubMed1996

Evidence of genetic heterogeneity in IBD: 1. The interleukin-1 receptor antagonist in the predisposition to suffer from ulcerative colitis.

OBJECTIVE: To investigate a polymorphism within intron 2 of the interleukin-1 receptor antagonist (IL-1ra) gene in a Dutch white population of patients with ulcerative colitis and Crohn's disease. DESIGN: Genotype and allele frequencies of the polymorphic region in the IL-1ra gene were determined in 111 unrelated patients with ulcerative colitis, 92 patients with Crohn's disease, and 86 healthy controls. METHODS: The polymorphic region on the IL-1ra gene was amplified by the polymerase chain reaction (PCR). The resultant products were analyzed by electrophoresis on 2% agarose gels and stained with ethidium bromide. Amplification of the second exon of HLA-DRB1, HLA-DQA1, and HLA-DQB1 genes was performed by PCR, and Dot-blot analysis with biotin-labelled sequence-specific oligonucleotide probes was used for HLA typing. The standard perinuclear antineutrophil cytoplasmic antibodies (pANCA) indirect immunofluorescence assay was performed according to the protocol described by the First International Workshop on ANCA. RESULTS: The frequency of allele 2 of the IL-1ra gene in ulcerative colitis (27.0%) and Crohn's disease patients (25.5%) did not differ significantly from healthy controls (23.8%). However, the estimate of the relative risk for carriers of allele 2 for ulcerative colitis [odds ratio (OR): 1.35, 95%-confidence interval (CI) from 0.73 to 2.49] was in agreement with a previous British study. The exact test for homogeneity of odds ratios provided no evidence for heterogeneity between both populations (P = 0.35) and therefore confirmed the genetic associated between ulcerative colitis and the IL-1ra allele 2 in a different population. Our data confirm that, in ulcerative colitis, the presence of this allele is a genetic marker for severity of the disease. A significant association was demonstrated between the carriership of allele 2 of the IL-1ra gene and the trend over the three localizations in ulcerative colitis (P = 0.023). The same approach for Crohn's disease when compared with healthy controls did not provide evidence for a similar association. The meta-analysis, based on the British data and our data, yielded: OR = 1.06, 95%-CI from 0.71 to 1.59, and P = 0.767. No association between IL-1ra gene polymorphism, and pANCA and the HLA-DR2 allele was found in ulcerative colitis.

Alleles↗
PubMed1997

Indications for operation in ulcerative colitis in the era of the pouch and before.

OBJECTIVE: To find out if the change in the operation of choice for ulcerative colitis from proctocolectomy with conventional ileostomy to restorative proctocolectomy which occurred during the 1980s had any influence on the indications for operation. DESIGN: Retrospective analysis. SETTING: University hospital, Finland. SUBJECTS: 430 consecutive patients who underwent operations for ulcerative colitis: 154 patients during 1976-85, when conventional proctocolectomy was the first choice, and 276 patients in 1986-94, when restorative proctocolectomy was the operation of choice. INTERVENTIONS: Comparison of the main surgical indications between the two periods. MAIN OUTCOME MEASURES: The indication for the first operation for three groups of patients: acute colitis, chronic colitis, and carcinoma (or at risk of cancer). RESULTS: The annual number of patients operated on roughly doubled even though the duration of colitis became longer and the age of patients older. The percentage of patients with "acute colitis" decreased from 29% (45/154) to 20% (55/276) (p = 0.032) and that of "chronic colitis" increased from 52% (80/154) to 65% (179/276) (p = 0.01) during the study period, while patients operated on for risk of carcinoma decreased slightly (19%, 29/154, compared with 15%, (42/276) p = 0.35). CONCLUSION: The adoption of restorative proctocolectomy has not caused any significant changes in indications for operation in ulcerative colitis. On the contrary, the medical control is better than before, but dealing with the risk of cancer remains difficult.

Adolescent↗
PubMed1997

5-Aminosalicylates, sulfasalazine, steroid use, and complications in patients with ulcerative colitis.

OBJECTIVES: The choice between sulfasalazine and 5-aminosalicylate (5-ASA) drugs in the management of patients with ulcerative colitis often depends on idiosyncrasies of drug tolerance and control of the disease in individual patients. We sought to evaluate whether there were population differences in the effect of 5-ASA and sulfasalazine on the occurrence of clinically recognized adverse events. We also attempted to determine whether there were differences in the use of concomitant steroids and in the rates of hospitalization. METHODS: We reviewed a large computerized database drawn from general practices in the United Kingdom. There we found records of 2894 patients in whom general practitioners had diagnosed ulcerative colitis, and who were receiving ongoing medical therapy specific to ulcerative colitis. The period of data availability ran from the beginning of 1990 to the latter part of 1993. The average duration of observation was 2.1 yr per patient. Patient histories were categorized into distinct periods according to the dose of 5-ASAs and sulfasalazine, steroids, and immunosuppressants, and were further separated according to the activity of ulcerative colitis. Within these categories, we examined the initiation and discontinuation of steroids, incidence of new hospitalizations for ulcerative colitis, and clinical mention of adverse events. RESULTS: New clinical mentions of hepatic, pancreatic, renal, and hematological events other than anemia were similar among the 5-ASAs and were very infrequent overall. Hospitalizations for ulcerative colitis occurred with similar frequency (about 15 hospitalizations per 100 patients per year) among users of those drugs. Patients receiving sulfasalazine had lower rates of initiation of prednisolone than did patients receiving 5-ASA, but sulfasalazine was used proportionately less often in patients who had been recently hospitalized, and it may be that sulfasalazine patients were somewhat less sick, overall, than were 5-ASA-using patients. The choice of drug did not affect discontinuation rates for prednisolone among established users. CONCLUSIONS: In the United Kingdom, during the period of this study, serious adverse reactions to drugs were not an important aspect of the management of patients with ulcerative colitis. Renal and pancreatic complications of sulfasalazine and 5-ASA therapy were extremely rare. Sulfasalazine and 5-ASA drugs have similar steroid-sparing properties. Disease-specific hospitalizations are approximately 100 times more common in ulcerative colitis patients than are serious adverse drug effects. Considerations of drug efficacy should therefore dominate the choice between therapeutic agents.

Adolescent↗
PubMed1998

HLA antigens and pANCA define ulcerative colitis as a genetically heterogeneous disorder.

BACKGROUND: Several genetic and subclinical markers have been associated with ulcerative colitis. AIM: To determine whether a significant association with HLA class I and II antigens was present in Italian ulcerative colitis patients considered as a whole population or stratified according to their anti-neutrophil cytoplasmatic antibodies. METHODS: HLA class I and II antigens were studied by serological typing techniques and related to the presence of anti-neutrophil cytoplasmatic antibodies detected by means of indirect immunofluorescence. RESULTS: Patients with ulcerative colitis (n = 45) had a significantly increased frequency of DQ6 (p = 0.04) and DQ7 (p = 0.003) and a decreased frequency of DQ5 (p = 0.03) and DQ8 (p = 0.02) when compared with ethnically matched healthy controls (n = 252 for HLA class I and 173 for HLA class II). No significant difference in HLA I- and DR-antigens was observed. Anti-neutrophil cytoplasmatic antibodies were found in 27/45 (60%) ulcerative colitis patients and in 0/252 controls (p < 0.001). After stratifying ulcerative colitis patients according to their anti-neutrophil cytoplasmatic antibodies status, anti-neutrophil cytoplasmatic antibodies +ve patients had an increased frequency of A19 (p = 0.007), DR2 (p = 0.03), and DR15 (p = 0.006), and a decreased frequency of A1 (p = 0.004) compared with anti-neutrophil cytoplasmatic antibodies -ve ones. CONCLUSIONS: We suggest that specific HLA-class II loci play an important role in the susceptibility to ulcerative colitis in Italy. A subset of ulcerative colitis patients is characterised by the presence of a specific subclinical marker (anti-neutrophil cytoplasmatic antibodies) which seems to be genetically determined as shown by the increased frequencies of HLA-A19 and DR2 observed in anti-neutrophil cytoplasmatic antibodies +ve ulcerative colitis.

Adult↗
PubMed1995

Cytokines in Crohn's colitis.

BACKGROUND: Increasing evidence points to a pathologic role for cytokines in Crohn's colitis. Levels of cytokines are increased in diseased segments of colon in Crohn's colitis, but no one has studied the concentration of cytokines in clinically and histologically nondiseased segments. METHODS: Mucosal biopsies were obtained from 7 patients with active segmental Crohn's colitis and from 7 controls without inflammatory bowel disease. The concentration of Interleukin (IL)-1 beta, IL-2, IL-6, and IL-8 in patients and controls were determined using enzyme linked immunosorbent assay and compared. Histologic sections were also performed to confirm diseased and nondiseased segments of colon. RESULTS: The concentrations of IL-1 beta, IL-6, and IL-8 were significantly higher in the involved segments of colon (10.3 +/- 4.1, 3.7 +/- 1.0, 34.4 +/- 6.9 picograms [pg] per mg) when compared to controls (1.8 +/- 0.5, 1.1 +/- 0.5, 5.3 +/- 1.0 pg/mg). The concentrations of IL-1 beta, IL-2, and IL-8 (8.5 +/- 2.9, 5.3 +/- 1.2, 26.3 +/- 8.8 pg/mg) in normal appearing segments of colon of patients with Crohn's colitis were also significantly higher than in controls, whose IL-2 level was 2.0 +/- 0.5 pg/mg. IL-1 beta and IL-8 were significantly more concentrated in both the involved and uninvolved colonic segments of patients with Crohn's colitis compared to controls. IL-2 and IL-6 were also more concentrated in Crohn's patients than in controls, but not significantly. The differences in interleukin concentrations between involved and uninvolved segments of colon in patients with segmental Crohn's colitis were not significant. CONCLUSIONS: Although Crohn's colitis is often a segmental disease, concentrations of IL-1 beta and IL-8 are increased throughout the entire colon. These observations reinforce the hypothesis that Crohn's colitis involves the whole colon even when this is not apparent clinically or histologically.

Adult↗
PubMed2005

Alpha CD 2 mAb treatment safely attenuates adoptive transfer colitis.

Increased proliferation, defective apoptosis, and cytokine dysregulation of T lymphocytes are thought to be important for the pathogenesis of inflammatory bowel disease. Since these phenomena can be corrected by alpha CD 2 mAb, we asked whether CD2 directed immunotherapy safely prevents and/or ameliorates adoptive transfer colitis. Colitis was induced by transfer of CD4(+) T cell blasts to syngenic RAG 1(-/-) mice or CD 45 RB(high) CD4(+) T cells to SCID mice. The alpha CD 2 mAb 12-15 or rat IgG was given, starting either initially or upon first signs of colitis. Disease activity was assessed by clinical monitoring, microscopic scoring, hemoccult, endoscopy, and blood count analysis. Cytokine production of stimulated LPL was measured by ELISA and cell proliferation by [(3)H]-thymidine incorporation. Parasite control was analyzed in a murine model of infection with Toxoplasma gondii. The alpha CD 2 mAb significantly increased mean survival time when starting at transfer of blasts (survival >35 days: alpha CD 2 69% vs 0% of controls, P<0.001). In the SCID colitis model hematochezia and macroscopic colitis were delayed. When used in established T-cell blast colitis, the benefit was less pronounced, even in combination with dexamethasone (mean survival+/-s.e.m.: alpha CD 2+dexa: 13.5+/-2.9 vs dexa+IgG: 6.3+/-1.0, P<0.05). In the preventive experiment the alpha CD 2 mAb markedly reduced IL-2 secretion and T-cell proliferation. The immune response towards Toxoplasma gondii was not impaired. These studies show for the first time that CD2 directed immunotherapy can attenuate or delay adoptive transfer colitis and ameliorate established colitis. Most likely inhibition of IL-2 secretion and T-cell proliferation are responsible for these effects. Still, immune defence towards T. gondii is maintained.

Adoptive Transfer↗
PubMed2003

Epithelial transport and gut barrier function in colitis.

PURPOSE OF REVIEW: Colitis is an inflammatory bowel disease that is confined to the colon and is characterized by a watery diarrhea that can also be accompanied by blood in the stool. The inflammation associated with colitis is generally confined to the mucosal and submucosal layers, although Crohn's colitis may be transmural. The principal functions of the colonic mucosa are to act as a barrier to the luminal contents of the intestinal tract and to facilitate the bidirectional transport of water and electrolytes. It is well established that barrier and transport defects occur in colitis and may be involved in pathogenesis. Consequently, this review discusses recent evidence of potential mechanisms that may be involved in the perturbation of mucosal transport and barrier functions in colitis and therapeutic advances to counteract these defects. RECENT FINDINGS: Mechanisms responsible for transport dysfunction and barrier defects in colitis are discussed, including decreased activity of transport proteins such as CFTR, bacterial interactions with the epithelium, including understanding of the regulation and function of NOD-2, and altered expression of components of the intestinal barrier, such as mucins and multidrug resistance proteins. SUMMARY: Recent advances in our understanding of how changes in barrier and transport function occur in colitis may illuminate the pathophysiology of this condition. The work discussed may also identify novel targets that are functionally altered in colitis, which potentially can be modulated therapeutically either with existing medications or with newer agents that are in development.

Journal Article↗
PubMed1988

Cytomegalovirus colitis in patients with acquired immunodeficiency syndrome.

Twenty-four AIDS patients, who underwent gastrointestinal evaluation, died from their disease and were autopsied. Seven had Cytomegalovirus colitis (group I) and 17 did not (group II). Clinical manifestations, digestive lesions, and infections were compared in the two groups. Chronic watery diarrhea was present in all the patients with colitis but was also present in 65% of the patients without colitis. Hematochezia was present only in the group with colitis (one of seven patients) but appeared late in the diarrheal course, due to necrotizing colitis. No other difference were noted between the two groups (mean duration of diarrhea, frequency and nature of the other infections). As for group I specifically, colonic ulcerations due to Cytomegalovirus were present in all the patients, varying from punctate and superficial erosions to deep ulcerations, with granular and friable intervening mucosa. Severe colonic lesions appeared during the course of Cytomegalovirus colitis in two patients who developed lethal necrotizing colitis. Finally, the clinical and pathologic features of these seven cases were compared to other reports of Cytomegalovirus infection of the colon.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Safety of urgent restorative proctocolectomy with ileal pouch-anal anastomosis for fulminant colitis.

PURPOSE: Subtotal colectomy with ileostomy is the operation of choice for patients with fulminant colitis. Restorative proctocolectomy (RPC) with ileal pouch-anal anastomosis (IPAA) is preferred for patients who undergo elective surgery for ulcerative colitis. We retrospectively evaluated the safety of RPC with IPAA in patients with a moderate form of fulminant colitis. METHODS: A chart review of 737 patients who underwent RPC with IPAA for ulcerative and indeterminate colitis from 1983 through 1992 was performed. Moderate fulminant colitis was defined as acute disease requiring hospitalization and parenteral steroid therapy, but without hypotension (systolic blood pressure, < 100 mmHg), tachycardia (> 120 beats/min), or megacolon. RESULTS: Twelve patients with moderate fulminant colitis underwent urgent surgery (1.6 percent). They had been treated preoperatively for 5.1 +/- 2.3 days with intravenous high-dose steroids, total parenteral nutrition, and antibiotics. These patients had a shorter length of disease (P = 0.01), lower hemoglobin, hematocrit, and albumin (P = 0.001), and higher temperature (P = 0.002) and leukocyte count (P = 0.007) than patients undergoing elective surgery. No early septic complications occurred, although perianal abscess occurred in one patient and pouch-anal fistula in another patient, 13 and 14 months after surgery, respectively. CONCLUSION: In carefully selected, hemodynamically stable patients with fulminant colitis and without megacolon, RPC with IPAA can be safely performed.

Acute Disease↗
PubMed1977

Perforation of the colon in unsuspected amebic colitis: report of two cases.

Two cases of amebic colitis that resulted in perforation of the colon, an ominous complication, are presented. The first was diagnosed preoperatively as acute ulcerative colitis with toxic megacolon, and the second as peritonitis complicating acute cholecystitis. In both instances the correct diagnosis was made after operation. The first patient recovered after colectomy and antiamebic therapy, but the second patient died in the early postoperative period, in septic shock. Amebic colitis occurs infrequently in the United States, and the diagnosis is rarely considered. In most cases an initial diagnosis of ulcerative or granulomatous colitis is made and the true diagnosis is recognized only after operation for colonic perforation or hepatic abscess. It is suggested that amebic colitis should be considered more frequently in cases of patients who have diarrhea. Stool examination for ova and parasites is often negative in amebic colitis. The IHA is usually positive in emebiasis, and should be performed early in casesof patients who have bloody diarrhea or other clinical symptons when amebiasis is suspected. Rectal biopsy is also a useful diagnostic approach, but failed to reveal amebae in one of our cases. Finally, it is suggested that operation be performed urgently when fulminating amebic colitis is not reversed by antiamebic therapy, when peritonitis occurs even with antiamebic treatment in progess, and for colonic perforation or toxic megacolon even when antiamebic therapy has not been indicated.

Adult↗
PubMed2006

Inhibition of neutrophil elastase prevents the development of murine dextran sulfate sodium-induced colitis.

BACKGROUND: Neutrophil elastase (NE) is a major secretory product from activated neutrophils and a major contributor to tissue destruction. However, little is known about the pathogenic contribution of NE to ulcerative colitis (UC). This study was designed to investigate the contribution of NE by measuring NE activity in plasma and colonic mucosal tissue from UC patients and a murine acute colitis model, and to elucidate the therapeutic effect of the NE-specific inhibitor ONO-5046. METHODS: The NE enzyme activities in plasma and colonic mucosal tissue from UC patients were directly measured using an enzyme-substrate reaction. Acute colitis was induced in mice by administration of 1.5% dextran sulfate sodium (DSS) for 5 days. DSS-induced colitis mice were then treated with ONO-5046 (50 mg/kg body weight) intraperitoneally twice a day. RESULTS: In UC patients, the NE enzyme activity was significantly elevated in both the plasma and colonic mucosal tissue compared with healthy controls. In DSS-induced colitis mice, the NE enzyme activity increased in parallel with the disease development. ONO-5046 showed therapeutic effects in DSS-treated mice by significantly reducing weight loss and histological score. ONO-5046 suppressed the NE enzyme activities in both plasma and culture supernatant of colonic mucosa from DSS-induced colitis mice. CONCLUSIONS: ONO-5046, a specific NE inhibitor, prevented the development of DSS-induced colitis in mice. NE therefore represents a promising target for the treatment of UC patients.

Adult↗
PubMed2002

Amelioration of dextran sulfate sodium-induced colitis by anti-macrophage migration inhibitory factor antibody in mice.

BACKGROUND & AIMS: We investigated the effects of macrophage migration inhibitory factor (MIF) antibodies in experimental colitis-induced dextran sulfate sodium (DSS) and trinitrobenzenesulfonic acid (TNBS) and examined whether plasma levels of MIF were elevated in patients with inflammatory bowel disease (IBD). METHODS: BALB/c or C57BL/6 mice were fed 4% DSS in their drinking water for up to 7 days with and without administration of an anti-MIF antibody every 2 days. The severity of inflammation in the cecum and colon was assessed by clinical signs and histologic scoring. Tissue levels of MIF, tumor necrosis factor (TNF)-alpha, interferon gamma (IFN-gamma), interleukin (IL)-4, and matrix metalloproteinase (MMP)-13 messenger RNA (mRNA) were measured. The effects of anti-MIF antibody on chronic colitis induced by TNBS was assessed in BALB/c mice. Plasma MIF concentrations were assayed in patients with Crohn's disease, ulcerative colitis, and healthy controls. RESULTS: During DSS-induced colitis, colonic MIF mRNA expression was increased. Clinical signs and histopathologic features were significantly improved in animals given anti-MIF antibody. DSS-induced up-regulation of colonic TNF-alpha and IFN-gamma were significantly suppressed in animals given the anti-MIF antibody. Colonic IL-4 was decreased during DSS but restored to baseline by the anti-MIF antibody. The anti-MIF antibody prevented MMP-13 up-regulation by DSS and ameliorated TNBS colitis. Plasma MIF was elevated in patients with Crohn's disease or ulcerative colitis compared with healthy controls. CONCLUSIONS: We conclude that anti-MIF antibodies reduce the severity of experimental colitis and limit the up-regulation of Th1-type cytokines. Anti-MIF antibodies are of potential therapeutic use in IBD.

Animals↗
PubMed1982

Acute infective colitis caused by endemic pathogens in western Europe: endoscopic features.

In a 4-year period 45 patients were admitted to our gastroenterological u nit with acute infective colitis. The endemic pathogens responsible for the colitis were Yersinia enterocolitica (46%), Campylobacter fetus jejuni (20%), common Salmonellae (13%), less virulent strains of Shigella (9%), Entamoeba hystolytica (7%) and Cytomegalovirus (4%). These microorganisms caused very severe disease in 18% of the patients, who were mostly predisposed. While Salmonella- and amoebic colitis always mimicked ulcerative colitis by the presence of diffuse lesions, the other pathogens caused focal colitis, thus necessitating differential diagnosis vis a vis Crohn's colitis. Two patients (4%) died of complications, while 93% of the patients were cured by proper antimicrobial therapy. In the same period 12 patients were admitted with an acute attack of inflammatory bowel disease due to an intercurrent infection with the same pathogens. In most of these patients clinical remission of IBD was achieved by treating the intercurrent infection. These data indicate that in the presence of an acute attack of colitis an infective etiologic agent must always be sought, and that an attack of chronic idiopathic inflammatory bowel disease may be caused by an intercurrent infection.

Adolescent↗
PubMed1983

[Fungus colonization in colitis].

Fungal cultures, unstained smears and histological assessment of endoscopically obtained particles from ulcers in rectum, colon or terminal ileum were obtained in a prospective study of possible fungal infection in 78 patients with colitis of various aetiologies (Crohn's disease - 46; ulcerative colitis - 21; infectious colitis - 5; ischaemic colitis - 2; radiation colitis - 1; non-classifiable colitis - 3). Positive fungal culture was obtained in 13 patients (16.7%). The germ count was low (2--8 colonies per biopsy piece). The demonstrated fungi were almost exclusively Candida or Torulopsis. The potentially pathogenic mycelia phase of the fungi were never seen, either histologically or in unstained preparations. Stool specimens, obtained at the same time, were examined in 54 patients: positive cultures were obtained in 14 (25.9%). Only rarely were there concordance of positive fungal findings in both ulcer particles and faeces. It is concluded that (1) there is little danger of secondary fungal infection in colitis of various aetiologies; (2) positive faecal fungal culture is apparently of no pathogenic significance if the germ count is less than 10(6) per gram stool; (3) in the lower as well as the upper gastro-intestinal tract pathogenic fungal infection can be demonstrated only by endoscopy and biopsy.

Adolescent↗
PubMed1998

A simple clinical colitis activity index.

BACKGROUND: The appropriate medical treatment of patients with ulcerative colitis is determined largely by the severity of symptoms. Hospital assessment of the severity of disease activity includes investigation of laboratory indices and sigmoidoscopic assessment of mucosal inflammation. AIMS: To develop a simplified clinical colitis activity index to aid in the initial evaluation of exacerbations of colitis. METHODS: The information for development of the simple index was initially evaluated in 63 assessments of disease activity in patients with ulcerative colitis where disease activity was evaluated using the Powell-Tuck Index (which includes symptoms, physical signs, and sigmoidoscopic appearance). The new index was then further evaluated in 113 assessments in a different group of patients, by comparison with a complex index utilising clinical and laboratory data, as well as five haematological and biochemical markers of disease severity. RESULTS: The newly devised Simple Clinical Colitis Activity Index, consisting of scores for five clinical criteria, showed a highly significant correlation with the Powell-Tuck Index (r = 0.959, p < 0.0001) as well as the complex index (r = 0.924, p < 0.0001) and all laboratory markers (p = 0.0003 to p < 0.0001). CONCLUSIONS: This new Simple Colitis Activity Index shows good correlation with existing more complex scoring systems and therefore could be useful in the initial assessment of patients with ulcerative colitis.

Acute Disease↗