High prevalence of cytotoxin positive Helicobacter pylori in patients unrelated to the presence of peptic ulcers in Japan

Background—It has been reported that infectionwith vacuolating cytotoxin positive Helicobacter pyloristrains is associated with gastroduodenal disease in Western countries.
Aims—To evaluate the prevalence ofcytotoxin producing strains among patients with H pyloriinfection in relation to gastrointestinal diseases in Japan.
Patients—Ninety seven patients undergoing endoscopy.
Methods—A Western blot assay was conducted todetect serum antibodies against the cytotoxin using recombinantcytotoxin (VacA protein) as an antigen. To obtain a purifiedrecombinant cytotoxin, the vacA gene (2233 nucleotides)was cloned into an expression vector to produce the protein (744 aminoacids), which was expressed in Escherichia coli.
Results—Serum IgG antibodies to thecytotoxin were present in 85%, 95%, 95%, and 100% of infectedpatients with gastric ulcer (n=26), duodenal ulcer (n=21), chronicgastritis (n=19), and endoscopically normal mucosa (n=14), respectively.
Conclusion—The western blot method usingrecombinant VacA protein is simple and useful for detecting antibody tovacuolating cytotoxin. This method showed antibodies against cytotoxinwere highly prevalent, even in subjects with endoscopically normal mucosa in Japan, indicating that the cytotoxin may not be anindependent cause of gastrointestinal diseases induced by Hpylori infection.

     

Poor diagnostic value of colonic CD44v6 expression and serum concentrations of its soluble form in the differentiation of ulcerative colitis from Crohn's disease

Background—Increased expression ofCD44v6 on colonic crypt epithelial cells in ulcerative colitis has beensuggested as a diagnostic tool to distinguish ulcerative colitis fromcolonic Crohn's disease.
Aims—To investigate colonicCD44v6 expression and serum concentrations of soluble CD44v6 (sCD44v6)in patients with ulcerative colitis and Crohn's disease.
Methods—Colonic biopsy samples wereobtained from 16 patients with ulcerative colitis, 13 with ileocolonicCrohn's disease, and 10 undergoing polypectomy. Serum samples wereobtained from 15 patients with active ulcerative colitis, 20 withactive Crohn's disease, and 20 healthy donors. Colonic CD44v6expression was evaluated immunohistochemically by monoclonal antibody2F10 and the higher affinity monoclonal antibody VFF18. Serum sCD44v6concentrations were measured by ELISA.
Results—2F10 stained colonicepithelium of inflamed ulcerative colitis and Crohn's disease samplesin 80% and 40% of cases, respectively, and VFF18 in 95% and 87%,respectively. Both monoclonal antibodies displayed a sensitivity andspecificity of 60% and 87% to differentiate ulcerative colitis fromcolonic Crohn's disease. Serum concentrations of sCD44v6 were lower inpatients with ulcerative colitis (median 153 ng/ml; interquartile range(IQR) 122-211) compared with Crohn's disease (219; IQR 180-243) andhealthy donors (221; IQR 197-241 (p=0.002)). Its sensitivity andspecificity to discriminate ulcerative colitis from Crohn's diseasewas 75% and 71%, respectively.
Conclusion—Colonic CD44v6 and serumsCD44v6 concentrations do not facilitate reliable differentialdiagnosis between ulcerative colitis and Crohn's disease.

Keywords:CD44 variant 6; differential diagnosis; immunohistochemistry; soluble CD44v6

     

Increased secretion of pro-inflammatory cytokines by circulating polymorphonuclear neutrophils and regulation by interleukin 10 during intestinal inflammation

Background—Concentrations of pro-inflammatorycytokines are increased in the intestinal mucosa of patients withactive inflammatory bowel disease (IBD). Polymorphonuclear neutrophilgranulocytes (PMN) are the most abundant cell type in intestinallesions in IBD. Interleukin 10 (IL-10) is an importantcontra-inflammatory cytokine which induces downregulation ofpro-inflammatory cytokines.
Aims—To investigate whether PMN from patients withIBD or infectious colitis, respectively, secrete increased amounts ofpro-inflammatory cytokines and can be regulated by IL-10.
Methods—Secretion (ELISA) as well as correspondingmRNA levels (semiquantitative RT-PCR) of pro-inflammatory cytokines(IL-1β, TNF-α) and of IL-1 receptor antagonist were assessed inperipheral PMN.
Results—PMN from patients with IBD are primed tosecrete enhanced amounts of pro-inflammatory cytokines accompanied bydetection of corresponding mRNAs in comparison with normal controls.This finding is not specific for IBD but rather reflects intestinal inflammation in general. IL-10 markedly inhibited pro-inflammatory cytokine secretion as well as corresponding mRNA concentrations.
Conclusions—PMN are an important source ofpro-inflammatory cytokines in patients with intestinal inflammation andcan be downregulated by IL-10.

Keywords:granulocytes; interleukin 1β; interleukin 10; inflammatory bowel disease; intestinal immunity; inflammation; neutrophils; tumour necrosis factor α

     

Generation and molecular characterisation of monoclonal IgG4 rheumatoid factor from a patient with rheumatoid arthritis

OBJECTIVE—To characterise IgG4 rheumatoid factor (RF) at the molecular level from a patient with rheumatoid arthritis.
METHODS—B cells were cloned from the peripheral blood of a patient with rheumatoid arthritis, using EB virus transformation. The supernatants of the clones were screened for IgG RF activity by ELISA. Nucleotide sequences of the expressed immunoglobulin heavy and light chain genes of one IgG RF producing clone were determined by direct sequencing of the products of a polymerase chain reaction.
RESULTS—One clone producing monospecific IgG4 RF was obtained. Sequence analysis of the heavy and light chain genes suggested the accumulation of somatic mutations resulting in amino acid replacement in complementarity determining regions.
CONCLUSIONS—The results may suggest an antigen driven response in the generation of IgG4 RF in rheumatoid arthritis disease processes.

     

Fasting enhances mucosal antigen specific B cell responses in rheumatoid arthritis

OBJECTIVE—To evaluate the influence of fasting on the antigen specific immune responsiveness in patients with rheumatoid arthritis and healthy volunteers.
METHODS—Seven rheumatoid arthritis patients and 17 healthy volunteers were immunised perorally or parenterally with influenza virus vaccine after a three to six day long period of total energy deprivation (water fast). The subsequent antigen specific antibody mediated immune response was recorded in the blood at the single cell level by the ELISPOT method.
RESULTS—Short term starvation induced an enhanced antigen specific mucosa derived B lymphocyte response in rheumatoid arthritis patients and healthy volunteers. In contrast, the systemic B cell responses were not significantly altered by a total energy deprivation.
CONCLUSIONS—Short term starvation increases the mucosa derived B cell responsiveness, while systemic responsiveness is largely unaffected. The similar pattern of response in rheumatoid arthritis patients and healthy volunteers indicates that fasting alters the mucosal immune response independently of medical treatment.

     

Tolerance to oats in dermatitis herpetiformis

Objectives—Recent studies on coeliac diseasehave shown that oats can be included in a gluten-free diet withoutadverse effects on the small bowel. The presence of a rash is also asensitive indicator of gluten ingestion in dermatitis herpetiformis,and this was used to study whether patients with this disease could also tolerate oats.
Patients/Methods—Eleven patients with dermatitisherpetiformis in remission on a gluten-free diet were challenged dailywith 50 g oats for six months. Clinical symptoms were recorded, serum samples taken, and skin and small bowel biopsies performed before andafter the oat challenge. A control group comprised of 11 patients withdermatitis herpetiformis on a conventional gluten-free diet was also studied.
Results—Eight patients challenged with oatsremained asymptomatic, two developed a transient rash, and one withdrewbecause of the appearance of a more persistent but mild rash. Three of the 11 controls also developed a transient rash. IgA endomysial antibodies remained negative in all patients. The small bowel villous architecture, the densities of intraepithelial CD3 and α/βand γ/δ T cell receptor positive lymphocytes and crypt epithelial cell DR expression remained unaltered during the oat challenge.
Conclusions—The results confirm the absenceof oat toxicity on the gluten sensitive small bowel mucosa and suggestthat the rash in patients with dermatitis herpetiformis is notactivated by eating oats.

Keywords:dermatitis herpetiformis; coeliac disease; gluten-free diet; oats

     

Visualising E-selectin in the detection and evaluation of inflammatory bowel disease

Background—Vascular endothelial E-selectin expression is induced by proinflammatory cytokines andcontributes to accumulation of leucocytes in tissues.
Aims—To investigate the role ofE-selectin in inflammatory bowel disease (IBD).
Methods—E-selectin expression wasassessed in patients with ulcerative colitis and Crohn's disease bymeasuring the concentration of circulating soluble E-selectin(sE-selectin) using ELISA, by immunohistochemistry of colonic biopsyspecimens, and by abdominal immunoscintigraphy after injectingradiolabelled F(ab')₂ fragment of a monoclonalanti-E-selectin antibody. The value of scintigraphy usinganti-E-selectin was judged by a prospective comparative study ofautologous leucocyte scanning and E-selectin antibody scanning in 17 patients with IBD.
Results—Circulating sE-selectin waselevated in patients with clinically active disease. Tissue expressionof E-selectin was enhanced in patients with active inflammation, withweak or absent expression in inactive disease and healthy controls.In-111 labelled anti-E-selectin scintiscans were compared with Tc-99mlabelled leucocyte scans performed 24 hours earlier. Twelve patientshad areas of active inflammation on leucocyte scan while 11 patients had positive E-selectin scans. The results of the two scans were concordant in 14 patients, with those positive for both (10/17) showingsimilar disease localisation and extent.
Conclusions—Tissue E-selectinand circulating sE-selectin are increased during active inflammatorybowel disease. Anti-E-selectin imaging with radiolabelled monoclonalantibody identified areas of inflammation in Crohn's disease andulcerative colitis. The technique should prove useful clinically foridentifying the site and extent of disease.

Keywords:E-selectin; inflammatory bowel disease; Crohn'sdisease; ulcerative colitis

     

Transabdominal bowel sonography for the detection of intestinal complications in Crohn's disease

Background—The course ofCrohn's disease is characterised by the occurrence of intestinalcomplications such as strictures, intra-abdominal fistulas, orabscesses. Standard diagnostic procedures may fail to show thesecomplications, in particular fistulas.
Aims—To test the value oftransabdominal bowel sonography (TABS) for the detection of intestinalcomplications in Crohn's disease.
Methods—TABS was prospectivelyperformed in 213 patients with Crohn's disease in a university basedinflammatory bowel disease referral centre. Thirty three underwentresective bowel surgery and were included in this study. The accuracyof TABS to detect strictures, intra-abdominal fistulas, or abscesseswas compared with surgical and pathological findings.
Results—TABS was able to identifystrictures in 22/22 patients and to exclude it in 10/11 patients (100%sensitivity, 91% specificity). Fistulas were correctly identified in20/23 patients and excluded in 9/10 patients (87% sensitivity, 90%specificity). Intra-abdominal abscesses were correctly detected in 9/9patients and excluded in 22/24 patients (100% sensitivity, 92% specificity).
Conclusions—In experienced handsTABS is an accurate method for the detection of intestinalcomplications in Crohn's disease. TABS is thus recommended as aprimary investigative method for evaluation of severe Crohn's disease.

Keywords:Crohn's disease complications; fistula; stricture; abscess; bowel sonography

     

Interstitial cells of Cajal in the human fetal small bowel as shown by c-kit immunohistochemistry

Background—Interstitialcells of Cajal (ICCs) express the tyrosine kinase receptor c-kit, whichis required for their development and spontaneous pacemaker activity inthe bowel. From murine models it has been proposed that ICCs do notdevelop until after birth, but more recent findings indicate that c-kitis expressed early in the embryonic period. The temporal development ofICCs in the human gut remains unknown.
Aim—To investigateICCs in the human fetal small bowel using c-kit immunohistochemistry.
Subjects—Small bowelspecimens were obtained at post mortem examination of 16 fetuses andnine neonates, eight of whom were premature, born at gestational agesof 13 to 41 weeks, without gastrointestinal disorders.
Methods—Immunohistochemicalanalysis was performed on material fixed in formalin and embedded inparaffin. The specimens were exposed to antibodies raised against c-kit(an ICC marker) and neurone specific enolase (a general neuronalmarker). The ABC complex method was used to visualise binding ofantibodies to the corresponding antigens.
Results—c-kitimmunoreactive cells were visualised from 13 weeks of gestation. Theimmunoreactivity was mainly localised in association with the myentericplexus. From about 17-18 weeks of gestation, the ICCs formed a layeralong the myenteric plexus, whereas this layer appeared to be disruptedat 13-16 weeks of gestation.
Conclusions—ICCs arec-kit immunoreactive at least from a gestational age of 13 weeks inthe human fetal small intestine. From 17-18 weeks of gestation untilbirth, they form a continuous layer around the myenteric ganglia.

Keywords:interstitial cells of Cajal; c-kit; myentericplexus; human; fetal; development

     

Crohn's-like reaction in diverticular disease

Background—Diverticulitis and Crohn's diseaseaffecting the colon occur at similar sites in older individuals, and incombination are said to carry a worse prognosis than either disease inisolation. It is possible that diverticulitis may initiate inflammatorychanges which resemble Crohn's disease histologically, but do notcarry the clinical implications of chronic inflammatory bowel disease.
Aims—To evaluate histological features andclinical outcome in individuals initially diagnosed histologically ashaving both Crohn's colitis and diverticulitis.
Patients—Eleven consecutive individuals having acolonic resection showing histological features of both Crohn'sdisease and diverticulitis.
Methods—Retrospective review of histologicalspecimens, case notes, and discharge letters.
Results—In nine patients, the Crohn's-likereaction was confined to the segment bearing diverticula. They had noclinical evidence of Crohn's disease.
Conclusion—A Crohn's-like inflammatory responsecan be a localised reaction to diverticulitis and does not necessarilyindicate chronic inflammatory bowel disease.

Keywords:Crohn's disease; diverticulitis; colitis; histology

     

Rapid modulation of electrolyte transport in Caco-2 cell monolayers by enteropathogenic Escherichia coli (EPEC) infection

Background and aims—The pathophysiology ofenteropathogenic Escherichia coli (EPEC) diarrhoea remainsuncertain. EPEC adhere to enterocytes and transduce signals whichproduce a characteristic "attaching and effacing" (A/E) lesion inthe brush border membrane. The present in vitro study was designed todetermine whether signal transduction by EPEC also influenceselectrolyte transport.
Methods—Caco-2 cell monolayers were rapidlyinfected with wild type EPEC strain E2348/69, or the signaltransduction-defective mutant 14.2.1(1), and mounted in Ussing chambers.
Results—Strain E2348/69 stimulated a rapid buttransient increase in short circuit current (Isc) whichcoincided with A/E lesion formation; this Isc response wasabsent on infection with strain 14.2.1(1). While the initial rise inIsc induced by E2348/69 was partially (~35%) dependenton chloride, the remainder possibly represents an influx of sodium andamino acid(s) across the apical membrane.
Conclusions—The study directly shows that, afterinitial adhesion, EPEC induce major alterations in host cellelectrolyte transport. The observed Isc responses indicatea rapid modulation of electrolyte transport in Caco-2 cells by EPEC,including stimulation of chloride secretion, for which signaltransduction to host cells is a prerequisite.

Keywords:enteropathogenic Escherichia coli; Caco-2 cells; Ussing chambers; electrolyte transport; signaltransduction

     

Interferon γ induces differential upregulation of α and β chemokine secretion in colonic epithelial cell lines

Background—Production of chemoattractant factorsby the intestinal epithelium may contribute to mucosal infiltration byinflammatory cells in inflammatory bowel disease. Secretion of the α chemokine interleukin 8 (IL-8), a neutrophil chemoattractant, has beenwidely studied, but little is known about epithelial secretion of β chemokines, which are preferentially involved in recruiting monocytes.
Aims—To investigate the profiles of α and β chemokine secretion in colonic cell lines and their differentialmodulation by interferon γ (IFN-γ), a product of activated Tlymphocytes and natural killer cells.
Methods and results—HT29-19A, a model of theCl secretory crypt cell, exhibited a parallel secretionof the α chemokines IL-8 and GROα, which could be markedlyupregulated by tumour necrosis factor α (TNF-α) and IL-1β. Thesecells showed no significant expression of the β chemokines RANTES(regulated upon activation T cell expressed and secreted), MIP-1α(macrophage inflammatory protein 1α), and MCP-1 (monocyte chemotacticprotein 1) under these conditions, but IFN-γ in combination withTNF-α caused a dose dependent induction of RANTES and MCP-1secretion. This was accompanied by a marked increase of RANTES mRNA. Incontrast, IFN-γ had no significant effect on TNF-α stimulated IL-8secretion. Caco-2 cells, with features more typical of villusabsorptive cells, were relatively poor secretors of α chemokines butsecreted high levels of MCP-1 in response to IL-1β. IFN-γ did notinfluence α or β chemokine secretion in these cells.
Conclusions—These studies suggest that intestinalepithelial cells may produce chemokines capable of attracting bothneutrophils and monocytes. The ability of IFN-γ to activate theexpression of β chemokines preferentially could facilitate thedevelopment of chronic inflammatory infiltrates.

Keywords:inflammatory bowel disease; RANTES; interferongamma; chemokine

     

The p68 autoantigen characteristic of rheumatoid arthritis is reactive with carbohydrate epitope specific autoantibodies

OBJECTIVE—The autoantigen p68 is a target of autoantibodies as well as autoreactive T cells with a high specificity in rheumatoid arthritis (RA). The binding characteristics of the autoantibodies to their antigen were now analysed biochemically and cytologically.
METHODS—Deglycosylation techniques as well as lectin and sugar competition experiments were performed to p68 to discover if the antibodies detected a glycoepitope. Its antigenicity was investigated applying anti-p68 antibodies derived from RA patients in comparison with polyclonal rabbit anti-p68 antibodies.
RESULTS—p68 specific antibodies from RA patients did not to bind to p68 that had been deglycosylated by alkaline β-elimination, O-glycosidase or periodate treatment. In contrast, binding of p68 specific antibodies raised in rabbit was unaffected by either deglycosylation protocol. Furthermore, lectins specific for the carbohydrate N-acetylglucosamine competed with p68 specific antibodies from RA patients for antigen binding. N-acetylglucosamine by itself also competed with patient derived anti-p68 antibodies for p68 binding. Again, rabbit anti-p68 antibodies did not elicit these competitive effects. Applying cytoimmunofluorescence, p68 was present in the cytoplasm or endoplasmic reticulum and also in low abundance on the cell surface. Under heatshock conditions, p68 was detectable in the nucleus.
CONCLUSIONS—Autoimmunity to p68 during RA is carried by anti-carbohydrate autoantibodies. The carbohydrate modification of p68 appears to be N-acetylglucosamine, which may reflect the regulation of intracellular localisation of the antigen. It is hypothesised that a shift in glycosylation pattern accompanied by an unphysiological localisation of the antigen could trigger antigenicity of p68 during the pathogenesis of RA.

Keywords: carbohydrate epitope; autoantibodies; autoantigen; rheumatoid arthritis     

Compared with parenteral nutrition, enteral feeding attenuates the acute phase response and improves disease severity in acute pancreatitis

Background—In patients with major trauma andburns, total enteral nutrition (TEN) significantly decreases the acutephase response and incidence of septic complications when compared with total parenteral nutrition (TPN). Poor outcome in acute pancreatitis isassociated with a high incidence of systemic inflammatory response syndrome (SIRS) and sepsis.
Aims—To determine whether TEN can attenuate theacute phase response and improve clinical disease severity in patientswith acute pancreatitis.
Methods—Glasgow score, Apache II, computedtomography (CT) scan score, C reactive protein (CRP), serum IgMantiendotoxin antibodies (EndoCAb), and total antioxidant capacity(TAC) were determined on admission in 34 patients with acutepancreatitis. Patients were stratified according to disease severityand randomised to receive either TPN or TEN for seven days and thenre-evaluated.
Results—SIRS, sepsis, organ failure, and ITUstay, were globally improved in the enterally fed patients. The acutephase response and disease severity scores were significantly improvedfollowing enteral nutrition (CRP: 156 (117-222) to 84 (50-141),p<0.005; APACHE II scores 8 (6-10) to 6 (4-8), p<0.0001) withoutchange in the CT scan scores. In parenterally fed patients theseparameters did not change but there was an increase in EndoCAb antibodylevels and a fall in TAC. Enterally fed patients showed no change in the level of EndoCAb antibodies and an increase in TAC.
Conclusion—TEN moderates the acute phaseresponse, and improves disease severity and clinical outcome despiteunchanged pancreatic injury on CT scan. Reduced systemic exposure toendotoxin and reduced oxidant stress also occurred in the TEN group.Enteral feeding modulates the inflammatory and sepsis response in acute pancreatitis and is clinically beneficial.

Keywords:acute pancreatitis; enteral nutrition; bacterialtranslocation; oxidative stress

     

Increased incidence of biliary sludge and normal gall bladder contractility in patients with high spinal cord injury

Background—Patients with spinal cordinjury (SCI) have an increased prevalence of gallstones.
Aims—To study prospectively theincidence of gallstones and gall bladder contractility inpatients with SCI.
Patients and methods—Thirty sixconsecutive patients with SCI were studied: 18 patients with SCI abovethoracic 10 neuronal segment (>T10) and 18 patients with SCI below T10(<T10). An equal number each of disease controls (multiple fractures)and healthy controls were also studied. All patients and controlsunderwent serial ultrasonography to detect development of gallstonesand ultrasonographic measurement of gall bladder contractility.
Results—A significantly higher number(9/18) of patients with SCI >T10 developed biliary sludge comparedwith patients with SCI <T10 (2/18), disease controls (2/18), andhealthy controls (1/18) (p<0.05). No patient developed gallstones. Thegall bladder fasting volume was significantly decreased in patientswith SCI >T10 (20.56 ml; 95% confidence intervals (CI) 19.74 to21.38) compared with that in patients with SCI <T10 (27.33 ml, 95%CI 26.17 to 28.49; p<0.05), disease controls (27.92 ml, 95% CI 26.69to 29.15; p<0.05), and healthy controls (28.35 ml, 95% CI 27.25to29.45; p<0.05). Gall bladder contractility was normal in patients withSCI as shown by normal gall bladder residual volume and emptying time.
Conclusions—Patients with SCI aboveT10 have an increased incidence of biliary sludge and a decreased gallbladder fasting volume. Gall bladder contractility is, however, normal.

Keywords:spinal cord injury; biliary sludge; gall bladder

     

Prevalence of infection with Cryptosporidium parvum and Cyclospora cayetanensis among international travellers

Background—Cryptosporidium parvumand Cyclospora cayetanensis are recognised aspossible pathogens of traveller's diarrhoea.
Aims—To identify the prevalence of C parvumand Cyc cayetanensis in travellers returning fromdeveloping countries.
Patients—Nine hundred and seventy eight stoolsamples were taken from 795 patients returning from developing countries.
Methods—Microscopy (iron-haematoxylinstain, SAF concentration, modified acid fast stain) and a commerciallyavailable enzyme linked immunosorbent assay (ELISA) kit for thedetection of Cryptosporidium antigen in stool.
Results—Of the 795 patients in the study, 469 suffered from diarrhoea. Infection with Cyc cayetanensiscould be detected in five subjects (1.1%) by acid fast stain, and 13 patients (2.8%) were infected with C parvum. Onevaluation, the antigen capture ELISA turned out to be clearly lesssensitive for detection of C parvum than microscopy. Allpatients with either C parvum or Cyccayetanensis infection suffered from watery diarrhoea.
Conclusions—C parvum and Cyccayetanensis are not major causes of diarrhoea in internationaltravellers. In cases of persistent watery diarrhoea, however, thesepathogens should be taken into account in the differential diagnosis.

Keywords:diarrhoea; Cryptosporidium parvum; Cyclospora cayetanensis

     

Bone mineral density and nutritional status in children with chronic inflammatory bowel disease

Background—Osteoporosis has been reported inadult patients with inflammatory bowel disease.
Aims—To evaluate bone mineral density (BMD),nutritional status, and determinants of BMD in children withinflammatory bowel disease.
Patients—Fifty five patients (34 boys and 21 girls, age range 4-18) were studied; 22 had Crohn's disease and 33 ulcerative colitis.
Methods—Lumbar spine and total body BMD, and bodycomposition were assessed by dual energy x rayabsorptiometry (DXA). Results were expressed as standard deviationscores (SDS). Lean body mass was also assessed by bioelectricalimpedance analysis (BIA). Yearly measurements during two years wereperformed in 21patients.
Results—The mean SDS of lumbar spine BMD andtotal body BMD were significantly lower than normal (−0.75 and−0.95, both p<0.001). Height SDS and body mass index SDS were alsodecreased. The decrease in BMD SDS could not be explained by delay inbone maturation. The cumulative dose of prednisolone correlatednegatively with lumbar spine BMD SDS (r=−0.32, p<0.02).Body mass index SDS correlated positively with total body BMD SDS(r=0.36, p<0.02). Patients with Crohn's disease hadsignificantly lower lumbar spine and total body BMD SDS than patientswith ulcerative colitis, even after adjustment for cumulative dose ofprednisolone. In the longitudinal data cumulative dose of prednisolonebetween the measurements correlated negatively with the change inlumbar spine and total body BMD SDS. Lean tissue mass measured by DXAhad a strong correlation with lean body mass measured by BIA(r=0.98).
Conclusions—Children with inflammatory boweldisease have a decreased BMD. Children with Crohn's disease have ahigher risk of developing osteopaenia than children with ulcerativecolitis. Corticosteroid therapy and nutritional status areimportant determinants of BMD in these patients.

Keywords:bone mineral density; inflammatory bowel disease; children; nutritional status; corticosteroid treatment; bodycomposition

     

Anti-Saccharomyces cerevisiae mannan antibodies combined with antineutrophil cytoplasmic autoantibodies in inflammatory bowel disease: prevalence and diagnostic role

^a Service d'Hépato-Gastroentérologie, Hôpital Huriez, ^b Laboratoire de Parasitologie-Mycologie, ^c Service d'Epidémiologie et de Santé Publique, CH et U Lille, ^d Département d'Hématologie-Immunologie-Cytogénétique, CH Valenciennes, France, ^e Division of Gastroenterology and the UCLA Inflammatory Bowel Disease Center, Department of Medicine, UCLA School of Medicine, Los Angeles, California, USA

Correspondence to: Dr J-FColombel, Clinique des Maladies de l'Appareil Digestif et de la Nutrition, Hôpital Huriez, CH et U Lille, 59037 Lille, France.

Accepted for publication 19 January 1998

Background—Perinuclear antineutrophil cytoplasmic autoantibodies (pANCA) are a well recognised marker for ulcerative colitis. Antibodies to oligomannosidic epitopes of the yeast Saccharomyces cerevisiae (ASCA) are a new marker associated with Crohn's disease.
Aims—To assess the value of detecting pANCA and/or ASCA for the diagnosis of ulcerative colitis and Crohn's disease.
Methods—Serum samples were obtained from 100 patients with Crohn's disease, 101 patients with ulcerative colitis, 27 patients with other miscellaneous diarrhoeal illnesses, and 163 healthy controls. Determination of pANCA and ASCA was performed using the standardised indirect immunofluorescence technique and an ELISA, respectively.
Results—The combination of a positive pANCA test and a negative ASCA test yielded a sensitivity, specificity, and positive predictive value of 57%, 97%, and 92.5% respectively for ulcerative colitis. The combination of a positive ASCA test and a negative pANCA test yielded a sensitivity, specificity, and positive predictive value of 49%, 97%, and 96% respectively for Crohn's disease. Among patients with miscellaneous non-inflammatory bowel disorders, three were ASCA positive and two were pANCA positive. One control was ASCA positive. The presence of ASCA in patients with Crohn's disease was associated with small bowel involvement.
Conclusion—ASCA and pANCA are strongly associated with Crohn's disease and ulcerative colitis, respectively. Combination of both tests could help the diagnosis of inflammatory bowel disease.
(GUT 1998;:788-791)

Keywords: Crohn's disease;  ulcerative colitis;  antineutrophil cytoplasmic autoantibodies;  anti-Saccharomyces cerevisiae mannan antibodies

     

Relation between Helicobacter pylori infection and gastrointestinal symptoms and syndromes

Background—Helicobacter pylori is ahuman pathogen that colonises the gastric mucosa and causes permanentgastric inflammation.
Aims—To assess the symptoms of Hpylori infection in an adult unselected population.
Subjects—A random sample of 3589 adult Danes whowere examined in 1982 and 1987 (n=2987).
Methods—Abdominal symptoms within the precedingyear were recorded at both attendances. Circulating IgG antibodiesagainst H pylori in serum samples drawn in 1982 weremeasured by using in-house indirect enzyme linked immunosorbent assays (ELISA).
Results—People with increased levels of IgGantibodies to H pylori were more likely than uninfectedindividuals to report heartburn (odds ratio (OR) = 1.26, 95%confidence interval (CI) 1.03-1.54) and abdominal pain characterisedby daily length (OR= 1.33, 95% CI 0.92-1.91), nocturnal occurrence(OR = 1.62, 95% CI 1.19-2.19), spring aggravation (OR = 1.68, 95% CI0.70-4.05), and no relation to meals (OR = 0.62, 95% CI 0.43-0.91)or stress (OR = 0.69, 95% CI 0.50-0.95). The inclusion of people withincreased levels of IgG antibodies to H pylori, butwithout upper dyspepsia, at study entry significantly increased thelikelihood of reporting upper dyspepsia at follow up (OR = 1.71, 95%CI 1.24-2.36). People with epigastric pain and increased levels of IgMantibodies to H pylori only indicative of acute Hpylori infection were more likely to report nocturnal pain,heartburn, nausea, and vomiting.
Conclusions—H pylori infection mayprecede the development of dyspepsia and is associated with a varietyof gastrointestinal symptoms in people with no history of peptic ulcer disease.

Keywords:epidemiology; Helicobacter pylori;non-ulcer dyspepsia; symptomatology; upper dyspepsia

     

Detection of oncostatin M in synovial fluid from patients with rheumatoid arthritis

OBJECTIVE—To measure oncostatin M (OSM) in synovial fluid from patients with rheumatoid arthritis (RA) and osteoarthritis (OA).
METHODS—20 samples of synovial fluid from patients with RA and 10 samples from patients with OA were examined using an OSM specific sandwich ELISA.
RESULTS—OSM was detected at concentrations ranging from 2.36 to 901.82 pg/ml in 18 (90%) of 20 samples of synovial fluid from RA patients. There was no detectable OSM in synovial fluid from OA patients. In the RA patients, the OSM concentration in synovial fluid correlated significantly with the synovial fluid white blood cell count (r=0.67, p<0.01), but not with other laboratory parameters of disease activity.
CONCLUSION—These findings suggest that OSM may contribute to joint inflammation in RA.