CT小肠造影影像对结肠型克罗恩病与溃疡性结肠炎的诊断价值

目的  探究CT小肠造影（CTE）对结肠型克罗恩病与溃疡性结肠炎的诊断及鉴别诊断价值。方法  选取蚌埠医学院第一附属医院和南京中医药大学附属江苏省中医院于2019年1月~2022年1月收治的结肠型克罗恩病患者36例和溃疡性结肠炎患者36例行CTE检查,分别观察两组影像特征,结合实验室指标、临床表现对克罗恩病和溃疡性结肠炎患者进行回顾性分析。结果  36例克罗恩病患者中,CTE影像示肠壁不均匀增厚21例、肠道狭窄22例、瘘管形成7例及累及升结肠21例,均高于溃疡性结肠炎患者,差异有统计学意义（P < 0.05）;36例溃疡性结肠炎患者,粘液便18例及血便22例高于克罗恩病患者（P < 0.05）,溃疡性结肠炎患者平均发病年龄较结肠型克罗恩病患者平均发病年龄大（P < 0.05）。克罗恩病患者与溃疡性结肠炎患者的C反应蛋白及红细胞沉降率含量均值分别为28.17 mg/L vs 17.67 mg/L、32.25 mm/h vs 22.95 mm/h;C反应蛋白及红细胞沉降率含量的平均值对克罗恩病与溃疡性结肠炎的鉴别无统计学意义（P > 0.05）。结论  通过CTE影像特征更直观地对结肠型克罗恩病与溃疡性结肠炎进行鉴别,结合临床、内镜表现及病理诊断,为治疗方案设计提供更可靠的依据。     

Enhanced synthesis of neutrophil-activating peptide-1/interleukin-8 in active ulcerative colitis.

1. We studied neutrophil-activating peptide-1/interleukin-8 in inflammatory bowel disease. 2. Mucosal levels of neutrophil-activating peptide-1/interleukin-8 were significantly higher in patients with active ulcerative colitis [median 74.5 (range 17.7-450.8) pg/mg] than in patients with active Crohn's disease [10.4 (4-46.9) pg/mg; P less than 0.002] or in normal control subjects [10.4 (4-16.6) pg/mg; P less than 0.002]. 3. Circulating neutrophil-activating peptide-1/interleukin-8 was generally undetectable but there were higher levels of anti-neutrophil-activating peptide-1/interleukin-8 antibodies in patients with active ulcerative colitis [62.9 (3.4-239) ng/ml] than in patients with active Crohn's disease [5.9 (2.1-18.10) ng/ml; P less than 0.001] or in control subjects [6.1 (3.2-15.8) ng/ml; P less than 0.001]. 4. Neutrophil-activating peptide-1/interleukin-8 may be of specific functional importance in mediating inflammation in ulcerative colitis.     

C-reactive protein as an aid in the differentiation of functional and inflammatory bowel disorders

Eighty-two patients were investigated on their first visit to the outpatient department of St. Mark's Hospital, London, for the assessment of abdominal symptoms. In addition to the clinical examination, a rectal biopsy, routine tests and appropriate special investigations, blood was taken from each patient for the determination of erythrocyte sedimentation rate, C-reactive protein and alpha-1-acid glycoprotein. Nineteen patients were finally diagnosed as having Crohn's disease, twenty-two ulcerative colitis, and forty-one functional bowel disorders. All the patients with Crohn's disease had an elevated erythrocyte sedimentation rate and C-reactive protein level as had 11 (50%) of the patients with ulcerative colitis, but none with functional disorders. All cases of ulcerative colitis could be diagnosed by rectal biopsy. Measurement of alpha-1-acid glycoprotein provided no additional diagnostic information. A combination of rectal biopsy, and measurement of the erythrocyte sedimentation rate and C-reactive protein successfully distinguishes between inflammatory disease of the large and small bowel and functional bowel syndrome.     

Serum amyloid A protein compared with C-reactive protein, alpha 1-antichymotrypsin and alpha 1-acid glycoprotein as a monitor of inflammatory bowel disease

The serum concentrations of serum amyloid A protein (SAA), C-reactive protein (CRP), alpha 1-antichymotrypsin (alpha 1-ACT) and alpha 1-acid glycoprotein (alpha 1-AGP) have been measured in eighty-six patients with Crohn's disease, twenty-five patients with ulcerative colitis and twenty-two patients with the irritable bowel syndrome. In the Crohn's and ulcerative colitis group significant increases in concentration were observed in all four proteins, which parallelled disease severity as defined by other conventional laboratory parameters formulated into a simple activity index. In the irritable bowel group no significant changes were seen. Serum amyloid A and CRP concentrations were significantly lower in ulcerative colitis than in Crohn's disease when mild, but did not differ significantly when severe. Serum amyloid A correlated well with CRP (r = 0.83) and alpha 1-ACT (r = 0.80), but less well with alpha 1-AGP (r = 0.65). Serum amyloid A was the most sensitive protein (77%) but had the lowest specificity (74%). C-reactive protein was less sensitive (58%) than SAA but had greater specificity (100%). Alpha 1-ACT had a sensitivity and specificity similar to CRP and, therefore, provided little or no additional information. Alpha 1-AGP, although also 100% specific, had the lowest sensitivity (34%) and, therefore, is probably the least useful acute phase monitor of inflammatory bowel disease. The role, and associated problems, of SAA measurements are discussed.     

Human chorionic gonadotropin and alpha chain of glycoprotein hormones in patients with inflammatory bowel disease

In twenty patients with Crohn's disease and ten patients with ulcerative colitis serum levels of human chorionic gonadotropin and the common alpha-subunit of glycoprotein hormones were determined by radioimmunoassay. In contrast to published data, all serum samples except one revealed levels within the normal range of 148 controls (human chorionic gonadotropin levels up to 3.9 IU/l, alpha-subunit up to 3.8 micrograms/l). Neither the serum levels of human chorionic gonadotropin nor of the alpha-subunit differed significantly between patients with Crohn's disease (median/maximum: 0.9/4.4 IU/l; 0.7/3.6 micrograms/l) and ulcerative colitis (1.0/3.4 IU/l; 0.8/2.2 micrograms/l). Furthermore, the serum levels studied in patients with active (0.9/3.0 IU/l; 0.7/3.5 micrograms/l) and inactive (0.9/4.4 IU/l; 0.8/3.6 micrograms/l) Crohn's disease and in patients with active (1.1/3.4 IU/l; 0.9/2.2 micrograms/l) and inactive (0.9/2.9 IU/l; 0.8/1.3 micrograms/l) ulcerative colitis were not significantly different. There was no relationship of the duration of the disease or a bowel resection to the serum levels of human chorionic gonadotropin or the alpha-subunit. It is concluded that both parameters are not useful as markers in patients with Crohn's disease or ulcerative colitis. The normal serum levels found in patients with inflammatory bowel diseases indicate human chorionic gonadotropin as a highly specific marker for malignant diseases.     

Zinc status in inflammatory bowel disease

1. The zinc contents of plasma, erythrocytes, polymorphonuclear leucocytes and mononuclear leucocytes from 18 normal control subjects, 31 patients with Crohn's disease and 15 patients with ulcerative colitis were measured. 2. Plasma zinc levels were low in Crohn's disease, particularly in malnourished patients, and related to plasma albumin concentrations, but were normal in ulcerative colitis. 3. Erythrocyte zinc levels were normal in both Crohn's disease and ulcerative colitis. 4. Mean polymorphonuclear leucocyte zinc levels were normal in Crohn's disease and ulcerative colitis. Ten per cent of Crohn's disease patients had subnormal levels, which were associated with inactive disease, while 10% had elevated levels, which were associated with active disease. Seven per cent of ulcerative colitis patients had subnormal levels. Mononuclear leucocyte zinc levels were normal in Crohn's disease and in ulcerative colitis. 5. Tissue zinc depletion occurs in only a few patients with Crohn's disease and ulcerative colitis.     

Serum lysozyme, serum proteins, and immunoglobulin determinations in nonspecific inflammatory bowel disease

The serum levels of lysozyme, serum electrophoresis, and serum immunoglobulins were determined prospectively in 101 patients with ulcerative colitis, ulcerative proctitis, Crohn's disease, or nonclassifiable nonspecific inflammatory bowel disease. Although the mean serum lysozyme concentration of patients with Crohn's disease (10.5 +/- 6.8 microgram/ml) and ulcerative colitis (9.6 +/- 4.1 microgram/ml) performed by a standardized lysoplate method was significantly greater than normal controls (6.0 +/- 1.5 microgram/ml), the results did not correlate with the diagnosis nor with the degree of disease activity. Individually separated protein fractions and serum immunoglobulins also did not correlate with the serum lysozyme levels. This study indicates that measurement of the level of serum lysozyme in individual patients is not helpful in determining the cause or degree of activity of nonspecific inflammatory bowel disease.     

Demonstration and characterization of immunosuppressive factors in sera from patients with Crohn's disease

The effect of sera from 17 patients with Crohn's disease, 8 with ulcerative colitis or 5 with intestinal tuberculosis on the proliferative response of mouse spleen cells induced by phytohemagglutinin (PHA) was studied. Sera from patients with Crohn's disease markedly suppressed the blastogenesis of mouse spleen cells (S.I. = 6.8 +/- 2.0, % suppression = 83%), as compared with normal sera (S.I. = 41.0 +/- 5.2, p less than 0.001, % suppression = 0). Conversely, ulcerative colitis sera did not suppress the blastogenesis of mouse spleen cells (S.I. = 43.5 +/- 8.7, % suppression = -6%), nor the sera of intestinal tuberculosis (S.I. = 38.9 +/- 4.0, % suppression = 6%). Thus, we confirmed the possible existence of immunosuppressive factors in Crohn's disease. Moreover, immunosuppressive factors in Crohn's disease were characterized for biochemical properties. The approximate molecular weight is 45,000 estimated by diafiltration and gel filtration on a Sephadex G-75 column. Analytical isoelectric focusing showed an increased amount of acidic protein in fractionated sera (m.w. ranging 30,000-50,000) from patients with Crohn's disease and ulcerative colitis, in comparison with that in normal sera. Furthermore, the main peak of this acidic protein in Crohn's disease was an isoelectric point (pI) of 2.8, while the pI of that from ulcerative colitis was 3.0. These results suggest that qualitative differences of such acidic protein may serve to discriminate between the sera of Crohn's disease and ulcerative colitis.     

Serum antibodies from patients with Crohn's disease and from their household members react with murine lymphomas induced by Crohn's disease tissue filtrates

Injection into athymic nude mice (nu/nu) of filtrates of Crohn's disease tissue produces lymphoid hyperplasia and lymphomas, which react with serum antibody from other patients with Crohn's disease. We examined for such antibodies in sera of 14 patients with Crohn's disease and 25 of their household members and compared results with sera from 36 healthy unselected controls and from 14 patients with ulcerative colitis and 19 of their household members. Sera from all patients with Crohn's disease and ulcerative colitis and household members were collected in Michigan, coded, and examined by an indirect immunofluorescence assay against two primary nu/nu lymphomas and one transmitted lymphoma produced by three Crohn's disease tissue filtrates. Seven patients with Crohn's disease had antibodies against antigen(s) in the Crohn's disease lymphomas. Seven household members of patients with Crohn's disease and no household members of patients with ulcerative colitis (P less than 0.05) reacted with Crohn's disease lymphomas. However, none of the patients with ulcerative colitis (P less than 0.01) and no control healthy subjects (P less than 0.005) demonstrated immunoreactivity against nu/nu lymphomas. None of the sera reacted with a control nu/nu lymphoma. Five household members who had positive assay results were first-degree blood relatives, and the other two were spouses of patients with Crohn's disease. These results suggest that a common environmental factor may be associated with Crohn's disease, that there is a familial association in Crohn's disease, and that nu/nu mice are an important model to study the pathogenesis of Crohn's disease.     

Macrophage migration inhibitory factor in the sera and at the colonic mucosa in patients with ulcerative colitis: clinical implications and pathogenic significance

BACKGROUND: Inflammatory cytokines produced by activated macrophages are implicated in the pathogenesis of ulcerative colitis (UC). With the theory that macrophage migration inhibitory factor (MIF) may have a role in the accumulation of macrophages, we studied MIF in UC. MATERIALS AND METHODS: A total of 27 patients with UC, 14 patients with Crohn's diseases (CD), 11 patients with other forms of colitis and 26 normal controls were enrolled in the study. The levels of MIF in the sera and culture supernatant were measured by an enzyme-linked immunosorbent assay. MIF, macrophages and T cells were localized at the colonic mucosa by immunohistochemistry. RESULTS: The levels of MIF in the sera were significantly higher in UC than in normal controls (P < 0.05), in serum C-reactive protein (CRP) -positive cases with UC than in CRP-negative cases with UC (P < 0.05), and in patients with severe colitis with UC than in mild colitis with UC (P < 0.05). There was a positive relationship between serum MIF levels with the CRP levels and activities of colitis. However, the levels of MIF in patients with CD and other forms of colitis were not significantly different from their levels in normal controls and UC. Infiltrating cells at the colonic mucosa in UC and CD expressed MIF. CONCLUSIONS: These data suggest a role of MIF in the pathogenesis of UC. MIF may be used as a marker of disease activity in UC and control of MIF production may have therapeutic implications.     

Platelet factor 4 and beta-thromboglobulin in inflammatory bowel disease and giant cell arteritis

BACKGROUND: As platelet factors are important in the inflammatory response, we examined the course of platelet factor 4 and beta-thromboglobulin in relation to disease activity in inflammatory bowel disease and in giant cell arteritis. PATIENTS AND METHODS: In a prospective study, the platelet count, platelet factor 4 and beta-thromboglobulin were measured in 20 patients with Crohn's disease, 18 with ulcerative colitis and 19 with giant cell arteritis, during active and inactive disease, as well as in 51 controls without inflammation. RESULTS: Platelet counts were significantly higher in active vs. inactive Crohn's disease, ulcerative colitis and giant cell arteritis. Levels of platelet factor 4 and beta-thromboglobulin were significantly higher in active inflammatory bowel disease and giant cell arteritis, as well as in inactive inflammatory bowel disease and giant cell arteritis, than in the non-inflammatory controls. A positive correlation was found between the Crohn's disease activity index and the platelet count, platelet factor 4 and beta-thromboglobulin. Also, a positive correlation was found between the ulcerative colitis activity index and beta-thromboglobulin. However, even after 12 months of follow-up, in Crohn's disease and ulcerative colitis the mean levels of platelet factor 4 and beta-thromboglobulin were significantly higher than the levels of the controls. CONCLUSION: Platelet factors were correlated with inflammatory bowel disease activity. Levels of platelet factor 4 and beta-thromboglobulin, however, were markedly raised for a long time in clinically inactive inflammatory bowel disease, which might point to a pre-thrombotic state of disease.     

Chromium 51-ethylenediaminetetraacetate test: a useful test in the assessment of inflammatory bowel disease

We evaluated the usefulness of urinary excretion values in assessing mucosal damage in inflammatory bowel disease after administration of chromium 51-labeled EDTA either orally or rectally. In the oral study, 19 controls, 18 patients with Crohn's disease, and 13 patients with ulcerative colitis were given 100 microCi 51Cr-EDTA by mouth. The amount of 51Cr-EDTA in a 24-hour urine collection was expressed as a percentage of the ingested dose. The patients with Crohn's disease of the small bowel excreted 6.3% +/- 4.3%, which was significantly (P less than 0.001) higher than the percentage in patients with ulcerative colitis (1.7% +/- 1.1%) and controls (1.4% +/- 0.6%). In the enema study, 19 patients with ulcerative colitis, two with Crohn's disease, two with radiation colitis, and four controls (spastic colitis, lactose intolerance) were given 100 microCi 51Cr-EDTA by retention enema. The patients with active colonic inflammation excreted 8.4% +/- 3.9% of the dose given by enema, which was significantly (P less than 0.01) higher than in other controls (1.9% +/- 0.91%) or patients with inactive colitis (2.2% +/- 1.9%). The 51Cr-EDTA excretion test is a safe, inexpensive test useful in evaluating patients with inflammatory bowel disease. It can be given orally to screen patients with abdominal complaints who are suspected of having Crohn's disease involving the small intestine, and when given by enema it provides additional objective assessment of idiopathic ulcerative colitis or proctitis.     

Simultaneous assessment of intestinal permeability and lactose tolerance with orally administered raffinose, lactose and L-arabinose

1. In order to develop an improved differential sugar absorption test for simultaneously assessing intestinal permeability and lactose intolerance, methods were established for determining raffinose, lactose and L-arabinose in human urine. Using NAD(P)H-coupled enzymatic assays and fluorimetry, each sugar was measurable over a concentration range of approximately 3-300 mumol/l in diluted urine specimens. 2. After an overnight fast, 40 normal volunteers drank an iso-osmotic solution containing raffinose, lactose and L-arabinose. The median 5 h urinary sugar excretion was 0.26% of the ingested raffinose, 0.05% of lactose and 17.5% of L-arabinose. 3. In 143 patients with gastrointestinal disease, excretion of both ingested raffinose and lactose was significantly increased in coeliac disease in relapse or in partial remission and in Crohn's disease, but not in the irritable bowel syndrome, coeliac disease in remission or ulcerative colitis. Excretion of lactose, but not raffinose, was increased in patients with mucosal lactase deficiency, whereas excretion of L-arabinose was reduced in all disease groups except ulcerative colitis. 4. Discrimination between diseases was poor when based on individual sugar recoveries, but improved dramatically when excretion was expressed relative to that of L-arabinose. The raffinose/L-arabinose excretion ratio, an index of intestinal permeability, was greater than 0.08 in 15/15 untreated coeliac patients but less than 0.06 in all normal subjects and in 9/9 lactase-deficient patients, 15/16 recovered coeliac patients, 5/6 patients with ulcerative colitis, 13/16 patients with Crohn's disease and 61/62 patients with irritable bowel syndrome.     

Ultrasound findings in Crohn's disease and ulcerative colitis: a prospective study

In a prospective study, 118 patients with Crohn's disease, 51 patients with ulcerative colitis, and 72 patients with no disease of the intestine proximal to the rectum were evaluated by ultrasound. In Crohn's disease, thickening of the bowel wall and inflammatory masses were detected in 72.0% of the patients. With a transducer having optimal imaging properties in the near range, these findings were detected in 87.2% of a group of 47 patients. In ulcerative colitis, bowel wall thickening was detected in 52.9% of all patients. Thickening of the bowel wall was more marked in Crohn's disease than in ulcerative colitis. Most pathologic findings in Crohn's disease were located in the right lower abdomen, whereas those in ulcerative colitis were in the left abdomen, in particular in the lower quadrant. The frequency of wall thickening was correlated to the activity of the disease in ulcerative colitis but not in Crohn's disease. Considerably increased wall thickness, when localized in the right lower quadrant and found in combination with inflammatory masses or an abscess, suggests Crohn's disease.     

Low S-adenosylmethionine concentrations found in patients with severe inflammatory bowel disease.

BACKGROUND: S-adenosylmethionine is a methyl donor in many cellular reactions including detoxification of constantly produced hydrogen sulphide in the colon. A reduced capacity to detoxify hydrogen sulphide may be implicated in the pathogenesis of inflammatory bowel disease. S-adenosylmethionine could be low if this assumption is correct. We compared S-adenosylmethionine concentrations in whole blood in patients with severe and moderate inflammatory bowel disease with healthy reference persons. METHODS: S-adenosylmethionine concentrations in whole blood were measured using high-pressure liquid chromatography. Patients with Crohn's disease (n=21), ulcerative colitis (n=7) and healthy age-matched reference persons (or controls) (n=17) were studied. RESULTS: S-adenosylmethionine concentrations were significantly decreased in patients with severe inflammatory bowel disease (mean 1.10 mg/l) as compared to patients with moderate Crohn's disease and ulcerative colitis (mean 1.83 mg/l) and reference persons (mean 1.84 mg/l). Statistically significant inverse correlations were found between S-adenosylmethionine concentration and activity index (p<0.01 and R2=0.86) as well as Crohn's disease activity index (p<0.01 and R2=0.50) scores. CONCLUSIONS: Low concentrations of S-adenosylmethionine were found in patients with severe inflammatory bowel disease. Future studies will show whether S-adenosylmethionine is a marker for disease activity and a possible tool for investigation of sulphur toxicity as a causative mechanism in inflammatory bowel disease.     

Clinical features, morbidity and mortality of Scottish children with inflammatory bowel disease

From the Scottish Hospitals in-patients statistics for the years 1968-1983 all children and teenagers (a total of 1257) admitted to a National Health Service hospital with Crohn's disease or ulcerative colitis were identified. Case records of samples of patients with onset of symptoms at or before age 16 years were examined to establish the features, morbidity and mortality of unselected cohorts of young patients with inflammatory bowel disease. Median delay in diagnosis was less than six months. Anatomical distribution for Crohn's disease was similar to that in adults (small bowel 30 per cent; large bowel 28 per cent; small and large bowel 38 per cent) and almost half the patients with ulcerative colitis had extensive colitis. The morbidity was substantial in both. In-patient days for Crohn's disease ranged from seven to 322, median 64 days and for ulcerative colitis one to 275, median 30 days. At diagnosis, 11 of 40 young children with Crohn's disease but none of 14 with ulcerative colitis, were below the third centile for height. Despite treatment with corticosteroids 72 per cent of patients with Crohn's disease and 30 per cent of patients with ulcerative colitis required surgical treatment. Seventeen per cent have a permanent stoma. There were only six deaths, all before 1978.     

Analysis of direct tissue isoelectric focused protein profiles of resected intestinal mucosa and endoscopic biopsies from patients with inflammatory bowel disease.

Direct tissue isoelectric focusing was used as a procedure to analyze differences in soluble tissue protein profiles of resected intestinal segments and endoscopic biopsies from patients with ulcerative colitis, Crohn's disease, and colonic cancer. Extraction of tissue proteins was accomplished by electrophoresis of mucosal cryostat sections on agarose gels across a broad pH gradient. The inflamed colonic mucosa from Crohn's disease patients showed similar isoelectric focusing protein patterns. Small bowel mucosa from a patient with both colonic diverticular disease and Crohn's disease showed protein patterns identical with that of the mucosa from a patient with only Crohn's disease. The inflamed mucosae from ulcerative colitis patients revealed identical protein patterns but were distinct from those of non-inflamed ulcerative colitis mucosa and from the inflamed mucosae from Crohn's disease patients. Non-inflamed small bowel mucosae from cancer, ulcerative colitis, and Crohn's disease patients showed distinct protein patterns which were absent in the non-inflamed large bowel mucosae. The inflamed resected ileum of a Crohn's disease patient exhibited protein patterns similar to those of the biopsy of an inflamed mid-transverse large bowel. Mucosal biopsies from inflamed sigmoid colon of a Crohn's disease patient showed different protein patterns than those in biopsies from the inflamed mid-transverse colon. Thus, distinctive isoelectric focusing protein patterns may be useful in differentiating Crohn's colitis and ulcerative colitis when granulomata are absent, and in resolving indeterminant colitis to one of these classic inflammatory bowel diseases.     

Increased arachidonic acid levels in phospholipids of human colonic mucosa in inflammatory bowel disease

1. Colonic mucosa from 19 patients with ulcerative colitis, eight with Crohn's disease and 14 controls were analysed for arachidonic acid (C20:4), linoleic acid (C18:2), oleic acid (C18:1), stearic acid (C18:0) and palmitic acid (C16:0). 2. Gas-liquid chromatography of lipid extracts showed that arachidonic acid was significantly higher in ulcerative colitis (19 +/- 4) and Crohn's disease (20 +/- 3) than in controls (13 +/- 5 micrograms/mg of protein) (means +/- SD). Neither the degree of inflammation nor treatment with sulphasalazine or prednisolone appeared to influence the fatty acid concentrations. 3. Seventy-five to ninety-five per cent of the arachidonic acid was found in the phospholipid fraction after separation by thin-layer chromatography. There were no significant changes in the concentrations of the other fatty acids measured, although oleic acid was lower in inflammatory bowel disease. The ratios of oleic acid to stearic acid and to palmitic acid were lower in inflammatory bowel disease. 4. The alteration in the fatty acid profile may partly explain the increased synthesis of eicosanoids in colonic mucosa in inflammatory bowel disease.     

Tumor necrosis factor-alpha antagonism improves endothelial dysfunction in patients with Crohn's disease

This study assessed the presence of endothelial dysfunction in patients with inflammatory bowel diseases (IBDs) and evaluated the possible role of tumor necrosis factor (TNF)-alpha in the pathophysiology of this abnormality. Similar elevations in circulating markers of inflammation (C-reactive protein and interleukin-6) were observed in Crohn's disease and ulcerative colitis compared to controls. Endothelium-dependent vasodilation to acetylcholine was impaired in Crohn's disease, but not in ulcerative colitis. Endothelium-independent vasodilation to sodium nitroprusside, by contrast, was not different among the three groups. The TNF-alpha neutralizing antibody, infliximab, enhanced the responsiveness to acetylcholine, but not to nitroprusside, in Crohn's disease, without modifying vascular responses to both drugs in ulcerative colitis. In conclusion, despite comparable degrees of systemic inflammation in the two IBDs, endothelial dysfunction is a selective feature of Crohn's disease and is beneficially affected by intravascular TNF-alpha neutralization. These findings underscore the role of selective cytokine targeting in improving endothelial function in patients with Crohn's disease.     

Antibodies to Cathepsin G in Crohn''s disease

Antibodies directed against antigens in human neutrophils have proved to be of great diagnostic value in certain systemic vasculitides. Recent reports have focused the attention on these antigens as targets of antibodies in sera of patients with inflammatory bowel disease. We investigated the sera drawn from 60 patients suffering from biopsy proven Crohn's disease and 15 patients with active ulcerative colitis. Using sensitive enzyme-linked immunosorbent assays with purified antigens and Western blotting the following antibodies could be demonstrated: cathepsin G (cat-G) antibodies IgG 38.3%, IgM 13.3%, IgA 23.3% and antibodies against human leucocyte elastase (HLE) IgG, IgA, IgM 3.3%. Low but significant correlations could be found for cat-G antibodies (IgG) and the van HEES index of activity. 73.9% of the cat-G (IgG) positive patients had colon involvement. In the sera of patients with ulcerative colitis no antibodies to cat-G or HLE were detectable. Only 8.3% of the patients with Crohn's disease had antibodies against proteinase 3 (C-ANCA). Our data indicate that cat-G among other myeloid lysosomal enzymes seems to be an important target antigen of antibodies in sera of patients with Crohn's disease. Cat-G antibodies might be helpful to distinguish Crohn's disease from ulcerative colitis.