An unusual endoscopic diagnosis for acute epigastric pain

Chemotactic, phagocytic, and oxidative metabolic activity of exudative leukocytes was measured in patients with Crohn's disease (n = 20) and with ulcerative colitis (n = 20). Unstimulated and casein-stimulated migration in Boyden chambers did not differ from that of healthy controls (n = 21). Patients with Crohn's disease had reduced serum-independent phagocytosis compared with healthy controls (p < 0.01) and patients with ulcerative colitis (p < 0.01). Serum-dependent phagocytosis by leukocytes from patients with Crohn's disease did not differ from that in controls but was slightly increased in patients with ulcerative colitis (p < 0.02). Unstimulated leukocytes showed increased oxidative metabolic activity in both patient groups compared with controls (p < 0.01), which was negatively correlated with the disease activity in Crohn's disease (p < 0.02). The study shows that mobilized leukocytes from patients with Crohn's disease differ from those mobilized in ulcerative colitis and supports the concept of an abnormal inflammatory reaction in Crohn's disease.     

Diminished neutrophil function in Crohn's disease and ulcerative colitis identified by decreased oxidative metabolism and low superoxide dismutase content.

Features of the neutrophil oxidative metabolism and enzyme activity in peripheral blood neutrophils were studied in 43 patients with Crohn's disease, 13 with ulcerative colitis and 33 healthy controls. The production of superoxide anion (O2-.) by phorbol-myristate-acetate stimulated neutrophils from patients with Crohn's disease and ulcerative colitis was significantly diminished compared with controls mean (SE) = 47.1 (3.6) and 38.0 (3.8) v 67.4 (7.5) nmol/10(7) cells/min, p less than or equal to 0.02, respectively, while the production of hydrogen peroxide was normal. The neutrophil content of superoxide dismutase (SOD), a cytoprotective enzyme, was also markedly diminished in Crohn's disease mean (SE) = 7.11 (0.23) ng SOD/micrograms DNA, p less than 0.05, and ulcerative colitis mean (SE) = 5.74 (0.42) compared with controls 7.84 (0.27), p less than 0.001. In contrast, the concentration of neutrophil elastase, a neutral protease, was found to be normal when compared with neutrophils from controls. The neutrophil O2-. production and the SOD concentrations were significantly and negatively correlated with the disease activity in Crohn's disease and ulcerative colitis. The results indicate diminished neutrophil function in peripheral blood of patients with Crohn's disease and ulcerative colitis as illustrated by a diminished oxidative system, which correlates with the disease activity.     

Adhesion molecules in inflammatory bowel disease.

The ability of leucocytes to adhere to endothelium is essential for leucocyte migration into inflammatory sites. Some of these adhesion molecules are released from the cell surface and can be detected in serum. The soluble adhesion molecules intercellular adhesion molecule 1 (ICAM-1), E selectin, and vascular cell adhesion molecule 1 (VCAM-1) were studied in the serum of patients with Crohn's disease, ulcerative colitis, and healthy controls. A second blood sample was taken from patients with active disease after one month of treatment and a third two months after remission was achieved. Tissue expression of the same adhesion molecules was studied by immunohistology. Circulating VCAM-1 concentrations were significantly higher in patients with active ulcerative colitis (n = 11, median = 165 U/ml) compared with patients with inactive ulcerative colitis (n = 10, median = 117 U/ml, p < 0.005), active Crohn's disease (n = 12, median = 124 U/ml, p < 0.02), and controls (n = 90, median = 50 U/ml, p < 0.0001). Within each disease group there were no significant differences in E selectin or ICAM-1 concentrations between the active and inactive states, however, patients with active Crohn's disease had significantly higher ICAM-1 concentrations (n = 12, median = 273 ng/ml) than controls (n = 28, median = 168, p < 0.003). VCAM-1 concentrations fell significantly from pretreatment values to remission in active ulcerative colitis (p < 0.01). In Crohn's disease there was a significant fall in ICAM-1 both during treatment (p < 0.01) and two months after remission (p < 0.02). Vascular expression of ICAM-1 occurred more often and was more intense in inflamed tissue sections from patients with ulcerative colitis and Crohn's disease than from controls. Vascular labelling with antibody to E selectin also occurred more often in patients with active inflammatory bowel disease. In conclusion, increased circulating concentrations of selected adhesion molecules are associated with inflammatory bowel disease. There is also evidence of local upregulation, particularly of ICAM-1. Differential expression of adhesion molecules in tissue may play a part in the initiation of leucocyte migration and local inflammation; the function of circulating adhesion molecules is unknown, but may play a physiological part in blocking adhesion.     

Influence of inflammatory bowel disease on intestinal microflora.

The microflora of the jejunum, ileum, and colon has been studied from operative samples in Crohn's disease (n = 30), ulcerative colitis (n = 15), and controls (n = 40). There was no significant difference in the flora of patients with ulcerative colitis compared with controls. In Crohn's disease there was a significant increase in E. coli (P less than 0.001) and B. fragilis (P less than 0.001) in the ileum and of E. coli (P less than 0.001) and lactobacilli (P less than 0.01) in the colon. The abnormal ileal flora in Crohn's disease was unrelated to serological evidence of disease activity (indices: ESR, serum albumin, serum seromucoids), diameter of the ileum, or excision of the ileocaecal valve. The abnormal colonic flora in Crohn's disease was not related to presence of macroscopic colitis.     

T lymphocyte subsets in inflammatory bowel disease: peripheral blood

Peripheral blood T lymphocytes and T lymphocyte subsets have been quantified in 28 patients with ulcerative colitis and 26 with Crohn's disease by an indirect immunofluorescence technique using monoclonal antibodies: OKT3, which detects all peripheral blood T lymphocytes; OKT4 (T cells of helper phenotype); and OKT8 (T cells of supressor-cytotoxic phenotype). Eighteen normal subjects and 16 patients with a variety of non-inflammatory gastrointestinal disorders were studied as controls. No significant differences were found between patient and control groups in the proportions of circulating T lymphocytes or their subsets. When compared with normal subjects, absolute numbers of T lymphocytes were reduced in patients with active ulcerative colitis or Crohn's disease (p less than 0.05). OKT4+ T cell numbers were reduced in ulcerative colitis, whether active (p less than 0.02) or inactive (p less than 0.05) and in active Crohn's disease (p less than 0.05) Numbers of OKT8+ T cells were reduced in active Crohn's disease (p less than 0.01). There were no differences in T lymphocyte numbers between the patient groups and the disease control subjects. The OKT4+:OKT8+ ratio in patients with inflammatory bowel disease did not differ from that in controls. No relation was found between any of the parameters studied and disease activity, site, or extent of disease, or treatment with sulphasalazine or corticosteroids. The presence of Ia-like, HLA-DR antigens on T cells was detected using a double marker immunofluorescence technique. In control subjects up to 7% of OKT3+ cells were HLA-DR+. In only three patients was the proportion of HLA-DR+ cells greater than in controls. These results indicate that the pathogenesis of ulcerative colitis or Crohn's disease does not depend upon an alteration in the proportion of circulating T lymphocytes nor upon an imbalance of T lymphocyte subsets as defined by monoclonal antibodies. The reduction in T lymphocyte numbers may result from mucosal infiltration. The findings also suggest that circulating T lymphocytes are not activated.     

Abnormal small intestinal permeability to sugars in patients with Crohn's disease of the terminal ileum and colon

The absorption of lactulose and mannitol in 20 patients with Crohn's disease limited to the ileum or colon was studied, and lactulose/mannitol excretion ratios were calculated. The results were compared to those from 16 normal controls and 6 patients with ulcerative colitis. The 13 patients with ileal Crohn's disease had significantly higher lactulose/mannitol excretion ratios than the controls (p less than 0.01) or ulcerative colitics (p less than 0.01). Similarly, the 7 patients with Crohn's disease limited to the colon had significantly higher excretion ratios than the controls (p less than 0.01) or ulcerative colitics (p less than 0.01). The results provide support for the concept that Crohn's disease may be more extensive than is apparent macroscopically.     

Leucocyte function in ulcerative colitis. Quantitative leucocyte mobilisation to skin windows and in vitro function of blood leucocytes.

Leucocyte function was evaluated by the in vivo mobilisation to skin windows with chambers and by the chemotactic, phagocytic, and nitro blue tetrazolium reducing capacity of blood leucocytes from 20 patients with ulcerative colitis. The total number of leucocytes mobilised to the chambers after 12 hours did not differ from those in 21 healthy volunteers. After 24 and 48 hours reduced number of leucocytes were mobilised by patients with ulcerative colitis (p less than 0.01). Correspondingly, the leucocyte migration rates were normal initially but were reduced after 18 hours Mobilisation in vivo was positively correlated to the blood neutrophil count (Rho:0.5549 po less than 0.02) but unrelated to clinical activity. Blood leucocytes showed reduced random migration in vitro as well as chemotactic response to casein (p less than 0.01). Serum independent and dependent phagocytosis did not differ from healthy volunteers. Nitro blue tetrazolium reduction by resting leucocytes was increased (p less than 0.01) in ulcerative colitis compared with controls. Our findings suggest altered in vivo mobilisation and in vitro migration of leucocytes in ulcerative colitis with increased spontaneous nitro blue tetrazolium reduction reflecting increased generation of potentially tissue damaging agents. The findings probably reflect changes secondary to the disease but which may be important in maintaining the inflammatory process.     

Ulcerative colitis--a disease characterised by the abnormal colonic epithelial cell?

The leakiness of the cell membranes of colonic epithelial cells isolated by the collagenase/Dispase technique from normal or diseased colons was assessed in a 4 h 51Cr release assay. Cells from normal, adenoma bearing or cancer bearing colons showed 51Cr release of 8% or less in almost all of 46 cell populations tested. In contrast, cells from mucosa affected by ulcerative colitis [11.9 (4.3%) n = 23] or Crohn's disease [8.4 (2.7%) n = 18] released significantly more 51Cr than the non-inflamed groups. Values are expressed as mean (SD). Overall, release values were greater in ulcerative colitis than Crohn's disease (p less than 0.01). In Crohn's disease, cells obtained from histologically inflamed mucosa released significantly more 51Cr [9.7 (2.5%) n = 11] than those from non-inflamed mucosa [6.4 (1.5%) n = 7, p less than 0.02] whereas, in ulcerative colitis, abnormal release values were found in 8 of 13 cell populations isolated from mucosa showing no histological evidence of active disease. In five patients with distal ulcerative colitis, cells from mucosa not apparently involved demonstrated normal 51Cr release in four of five studies despite abnormal release from cells from involved mucosa suggesting that a diffuse abnormality of the colonic epithelial cell is not usually present. These data indicate that chronic mucosal inflammation per se is associated with abnormalities of the colonic epithelial cell but that, in ulcerative colitis, the abnormality remains in many patients with quiescent disease. Identification of the local factors responsible for such an abnormality may contribute to an understanding of the pathogenesis of ulcerative colitis.     

Functional, morphological and biochemical study of the jejunal mucosa in cryptogenetic colitis

The function of the jejunum has been assessed in patients with ulcerative colitis (n = 23) and Crohn's disease of the colon (n = 20) by measurement of serum folate levels, oral folic acid and D-xylose absorption. Forty-six normal subjects served as controls. The mean serum folate level was 4.5 +/- 2.0 ng/ml in patients with the disease and 7.8 +/- 1.7 ng/ml in controls (p less than 0.001) and was similarly decreased in both ulcerative colitis and Crohn's disease patients. It was lower in patients under sulphasalazine therapy (n = 15) than in those untreated: 3.5 +/- 1.5 vs. 4.8 +/- 2.1 ng/ml (p less than 0.05). Serum folate correlated with disease activity in the latter only. The peak serum folate obtained during the oral absorption test was decreased in patients: 38.9 +/- 12.9 vs. 60.8 +/- 19.3 ng/ml in controls (p less than 0.001); this decrease was similar in ulcerative colitis and Crohn's disease, in treated and untreated patients and was independent of disease activity. Basal serum folate did not correlate with peak serum folate in any patient group. D-xylose absorption was normal in every case. Jejunal biopsies were performed in 23 patients, 13 of whom had folic acid malabsorption (13 with ulcerative colitis, 10 with Crohn's disease of the colon). The crypt height/villus height ratio was abnormal (greater than 0.6) in only 2 patients and borderline in 9 others. The fragility of enterocyte brush-borders and lysosomes, as assessed by biochemical methods, was normal in all cases.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intestinal permeability in gastrointestinal disorders

This study examined intestinal permeability in gastrointestinal disorders by measuring urinary recovery following oral administration of [99mTc]DTPA in 117 subjects. The mean percent of the ingested dose excreted in a 24-hr urine sample was 2.8 +/- 1.6% in 11 healthy controls, 10.8 +/- 10.2% (P less than 0.001) in 21 ulcerative colitis patients, 8.0 +/- 4.7% (P less than 0.001) in 35 Crohn's disease patients, 5.1 +/- 2.9% (P less than 0.01) in 17 patients with heterogeneous digestive disease diagnoses, and 3.2 +/- 4.7% (P greater than 0.05) in 33 patients with hepatobiliary diagnoses. Among ambulatory patients, Crohn's disease subjects, but not ulcerative colitis patients, had greater urinary recovery than the controls (P less than 0.05). The Crohn's disease activity index correlated positively with the radionuclide recovery in Crohn's subjects (r = 0.455, P less than 0.02). In a heterogeneous sample of subjects simultaneous ingestion of [99mTc]DTPA and [51Cr]EDTA produced urinary levels that were correlated positively (r = 0.556, P less than 0.001). Increased absorption of [99mTc]DTPA relative to [51Cr]EDTA, however, was noted in ulcerative colitis patients (P less than 0.05). In conclusion, increased intestinal permeability has been demonstrated by utilizing [99mTc]DTPA in Crohn's disease and ulcerative colitis patients. Although this observation appears to be a nonspecific indicator of injury, the test provides a simple objective means of establishing disease activity, which possibly may be utilized for therapeutic and investigative studies.     

Toxic oxygen metabolite production by circulating phagocytic cells in inflammatory bowel disease.

To investigate the possibility that the oxidative capacity of phagocytic cells may be defective in inflammatory bowel disease, toxic oxygen metabolite production by circulating neutrophils and monocytes has been measured by luminol dependent chemiluminescence. Neutrophils from patients with Crohn's disease and ulcerative colitis produced significantly lower chemiluminescent responses after chemotactic stimulation with formylmethionylleucylphenylalanine (fMLP) than neutrophils from control patients, p = 0.018 and 0.043 respectively. Chemiluminescent responses of neutrophils from patients with inflammatory bowel disease, however, were similar to control responses when cells were stimulated with latex beads or phorbol myristate acetate. Monocytes from patients with Crohn's disease produced significantly greater levels of chemiluminescence than control monocytes when stimulated with either fMLP (p less than 0.002), phorbol myristate acetate (p less than 0.0005) or latex beads (p less than 0.002). Monocytes from patients with ulcerative colitis also produced significantly greater levels of chemiluminescence than controls when stimulated with latex beads (p less than 0.5) or phorbol myristate acetate (p less than 0.0005), although there was no difference in the level of chemiluminescence in response to fMLP. These results exclude a generalised defect in phagocytic cell oxidase activity in inflammatory bowel disease and suggest that circulating monocytes are 'activated'.     

Antineutrophil cytoplasm autoantibodies against bactericidal/permeability-increasing protein in inflammatory bowel disease.

BACKGROUND: Bactericidal/permeability-increasing protein (BPI), a constituent of primary neutrophil granules, is a potent natural antibiotic and an antineutrophil cytoplasm antibody (ANCA) antigen in cases of vasculitis in which the target antigen is neither myeloperoxidase (MPO) nor proteinase-3 (PR3). AIM: To investigate BPI as a possible target antigen for ANCAs in inflammatory bowel disease. METHODS: ANCAs were detected by routine immunofluorescence (IIF) and solid phase enzyme linked immunosorbent assay (ELISA) performed for antibodies to the purified neutrophil granule proteins; MPO, PR3, cathepsin-G, lactoferrin, and BPI in serum samples from 88 patients with inflammatory bowel disease (36 with Crohn's disease, 52 with ulcerative colitis). Thirty patients with bacterial enteritis acted as controls. RESULTS: Significantly more patients with ulcerative colitis were ANCA positive by IIF (60%) than patients with Crohn's disease (28%) or infectious enteritis (23%) (p < 0.001). IgG anti-BPI antibodies were present in 29% of patients with ulcerative colitis, 14% of patients with Crohn's disease, and 23% of patients with infectious enteritis, occurring in 44% of those patients with inflammatory bowel disease who were ANCA positive by IIF. Antibodies to other ANCA antigens were rare. The presence of ANCAs was not related to either disease activity or extent; presence of anti-BPI antibodies was significantly related to both a lower serum albumin concentration (p = 0.001) and a higher erythrocyte sedimentation rate (p = 0.02) in patients with ulcerative colitis, and to colonic involvement in patients with Crohn's disease (p = 0.01). CONCLUSION: BPI is a significant minority target antigen for ANCAs in inflammatory bowel disease that seems related to colonic Crohn's disease and disease activity in ulcerative colitis. Anti-BPI antibodies occur in infectious enteritis.     

Plasma polyunsaturated fatty acid pattern in active inflammatory bowel disease.

Plasma fatty acid patterns were assessed by gas liquid chromatography in 73 patients with active inflammatory bowel disease and 107 healthy controls. The influence of the disease activity on fatty acid profile was also investigated. Plasma fatty acid patterns in patients with ulcerative colitis and Crohn's disease were similar. Plasma C18:3n3 and C22:6n3 were significantly higher in active ulcerative colitis (p = 0.0143 and p < 0.00001 respectively) and in Crohn's disease (p < 0.00001 for both) than in controls, whereas C20:3n6 was significantly lower in patients than in controls, both in ulcerative colitis (p = 0.0001) and in Crohn's disease (p = 0.0041). In more severe disease, plasma polyunsaturated fatty acid concentrations fell with a significant stepwise decrease in the desaturation index (p = 0.0031 in ulcerative colitis and p = 0.0355 in Crohn's disease). Even in patients with severe disease, however, plasma n3 fatty acids (C18:3n3 and C22:6n3) never fell below those of healthy controls. These findings suggest that in active inflammatory bowel disease, an increased biosynthesis might coexist with an increased consumption of polyunsaturated fatty acids. These observations may be of relevance in the pathogenesis of the disease as polyunsaturated fatty acids are involved in tissue eicosanoid synthesis and cellular membrane function, including that of immunocompetent cells. These results also question the rationale of using n3 polyunsaturated fatty acids in the treatment of inflammatory bowel disease.     

Mean platelet volume: a useful marker of inflammatory bowel disease activity

OBJECTIVES: We investigated whether the mean platelet volume would be a useful marker in the evaluation of inflammatory bowel disease activity. METHODS: Complete blood count, C-reactive protein, erythrocyte sedimentation rate, serum thrombopoietin and erythropoietin, plasma beta-thromboglobulin, and platelet factor 4 were measured in 93 patients with ulcerative colitis, 66 patients with Crohn's disease, and 38 healthy blood donors. Disease activity was assessed by the Clinical Colitis Activity Index in patients with ulcerative colitis and by the Crohn's Disease Activity Index in patients with Crohn's disease. RESULTS: Mean platelet count was increased in patients with active compared to inactive ulcerative colitis (p < 0.05), and in patients with active compared to inactive Crohn's disease (p = 0.0002) or healthy controls (p < 0.0001). On the other hand, mean platelet volume was significantly decreased in patients with active compared to inactive ulcerative colitis (p = 0.02) or healthy controls (p < 0.0001), and in patients with active compared to inactive Crohn's disease (p = 0.0005) or healthy controls (p < 0.0001). Mean platelet volume was inversely correlated with the white blood cell count (r = -0.17, p = 0.02), C-reactive protein (r = -0.46, p = 0.009) and erythrocyte sedimentation rate (r = -0.28, p = 0.008). No significant correlations were found between mean platelet volume and serum thrombopoietin or erythropoietin levels; however, a strong negative correlation between mean platelet volume and beta-thromboglobulin (r = -0.34, p < 0.0001) and platelet factor 4 (r = -0.30, p = 0.0002) was observed. CONCLUSIONS: Mean platelet volume is significantly reduced in active inflammatory bowel disease and is negatively correlated with the known inflammatory bowel disease activity markers and the platelet activation products. We propose that mean platelet volume provides a useful marker of activity in inflammatory bowel disease.     

Histochemical demonstration of desialation and desulphation of normal and inflammatory bowel disease rectal mucus by faecal extracts.

Experiments were carried out to assess the susceptibility of normal and inflammatory bowel disease rectal mucus to desulphation and desialation by faecal extracts and by bacterial sialidase. The effects were assessed histochemically using a combined high iron diamine (HID) and alcian blue (AB) stain for sulphomucins and sialomucins. Rectal mucus in biopsies from controls (irritable bowel syndrome) and patients with ulcerative colitis or Crohn's disease was resistant to desialation by Clostridium perfringens sialidase, but susceptible to desialation and desulphation by bacteria-free extracts of normal faeces. Periodic acid-Schiff (PAS) staining of adjacent sections similarly treated showed retention of neutral mucus. One faecal extract selectively desulphated all 42 biopsies, causing the goblet cells to change from HID positive to AB positive, suggesting that most, or all HID positive cells also contain sialomucins. This alters the interpretation of previous histochemical studies. Faecal extracts from patients with active ulcerative colitis (n = 6) had desialating and desulphating effects similar to faecal extracts from normal subjects (n = 6). Ulcerative colitis (n = 21), Crohn's disease (n = 18), and control (irritable bowel syndrome) (n = 17) rectal biopsies all showed similar susceptibility to desulphation by a pooled normal faecal extract, but rectal biopsies from patients with Crohn's disease proved more resistant to desialation than control or ulcerative colitis biopsies (p less than 0.02). These studies imply that colonic mucus undergoes continual desulphation and desialation in vivo as a result of faecal enzyme activity that is probably mainly of bacterial origin. Altered susceptibility of colonic mucus to this may be important in the pathogenesis of colonic disease.     

Urinary excretion of N-methylhistamine as a marker of disease activity in inflammatory bowel disease

OBJECTIVE: Mast cells are thought to participate in the pathogenesis of inflammatory bowel disease (IBD). In this study, urinary excretion of N-methylhistamine (UMH), a stable metabolite of the mast cell mediator histamine, was evaluated as an indicator of disease activity in patients with IBD. METHODS: Urinary excretion of UMH (microg/mmol creatinine x m2 body surface area) was measured by radioimmunoassay in 55 controls, 56 patients with Crohn's disease, and in 36 patients with ulcerative colitis. Excretion rates were correlated with clinical, serological, and endoscopic disease activity, disease extent, and location. RESULTS: Urinary excretion of UMH was found to be significantly elevated in IBD. Patients with active Crohn's disease (7.1 +/- 4.2, p = 0.002 vs controls) and active ulcerative colitis (8.1 +/- 4.8, p = 0.02 vs controls) had higher rates of UMH excretion than patients in remission (6.3 +/- 3.8 and 5.2 +/- 2.3, respectively) or controls (4.6 +/- 1.9). In Crohn's disease and ulcerative colitis, a significant correlation of UMH excretion with clinical disease activity was obtained (Crohn's Disease Activity Index r2 = 0.58, Clinical Activity Index r2 = 0.57, p < 0.0001). Serologically, orosomucoid showed the best positive correlation with disease activity (Crohn's Disease Activity Index r2 0.80, Clinical Activity Index r2 = 0.86, p < 0.0001), but UMH excretion was found to reflect disease activity more accurately than C-reactive protein (Crohn's Disease Activity Index r2 = 0.46, Clinical Activity Index r2 = 0.42, p < 0.0001). No association between UMH excretion and disease type or localization could be found in Crohn's disease. However, UMH excretion correlated strongly with endoscopic severity of inflammation in Crohn's disease (Crohn's Disease Endoscopic Index of Severity r2 = 0.70, p < 0.0001) or disease extent in ulcerative colitis. CONCLUSIONS: Urinary excretion of the histamine metabolite UMH is enhanced in IBD. It appears to represent an integrative parameter to monitor clinical and endoscopic disease activity in IBD, which appears to be influenced most likely by mediators released from histamine-containing cells, such as intestinal mast cell subtypes.     

Increased in vitro release of soluble interleukin 2 receptor by colonic lamina propria mononuclear cells in inflammatory bowel disease.

Increased concentrations of the soluble form of the interleukin 2 receptor have been observed in the sera of Crohn's disease and ulcerative colitis patients. In this study we have observed the spontaneous release of soluble interleukin 2 receptor by unstimulated, isolated normal and inflammatory bowel disease colonic lamina propria mononuclear cells. Lamina propria mononuclear cells from Crohn's disease patients (median = 204 U/ml (interquartile range 126-396, n 17) secreted significantly (p less than 0.01) more soluble interleukin 2 receptor than normal controls (median = 124.5 U/ml (108-131), n 12). No statistically significant differences were seen between ulcerative colitis (median = 135 U/ml (92-196), n 20) and normal controls. Moreover, significantly (p less than 0.01) increased amounts of soluble interleukin 2 receptor were secreted by colonic diverticulitis lamina propria mononuclear cells (median = 259 U/ml (149-282), n 15) which were used as disease specificity controls. Time course experiments showed that the majority of soluble interleukin 2 receptor was released by isolated lamina propria mononuclear cells in the first six days of culture. Upon stimulation with pokeweed mitogen, Crohn's disease (median = 2258 U/ml (1435-3584), n 14), normal control (median = 2622 U/ml (2030-3180), n 14) and diverticulitis lamina propria mononuclear cells (median = 2745 U/ml (1733-3192), n 10) reached similar maximal soluble interleukin 2 receptor secretion levels, while ulcerative colitis lamina propria mononuclear cells secreted significantly (p less than 0.005) less soluble interleukin 2 receptor (median = 912 U/ml (494-1259), n 17). These results suggest that enhanced shedding/secretion of soluble interleukin 2 receptor by intestinal lymphocytes may account in part for increased serum soluble interleukin 2 receptor concentrations during chronic intestinal inflammatory reactions.     

活动性炎症性肠病患者蛋白质和脂代谢的变化

目的 比较炎症性肠病患者及正常对照者之间蛋白质和脂代谢的差异,研究这些差异与疾病活动性及病变部位的关系.方法 回顾性研究1995至2007年溃疡性结肠炎(UC)195例、克罗恩病(CD)76例及正常对照者97名的蛋白质和脂代谢资料.同时评价临床疾病活动指数,红细胞沉降率(ESR)和C-反应蛋白(CRP)水平.性别分层分析蛋白质和脂代谢指标的改变,同时分析蛋白质和脂代谢的改变与疾病活动性及病变部位的关系.结果 UC患者的ESR与血清白球比呈负线性相关(β=-0.521,P＜0.01),与α2-球蛋白呈正线性相关(β=0.319,P＜0.01);CD患者血清球蛋白与ESR(β=0.558,P＜0.01)以及cRP(β=0.424,=P0.01)呈正线性相关.UC患者间因病变部位不同,血清白球比、白蛋白和总胆固醇水平存在显著差异,其中直乙结肠炎患者该三项显著高予其他类型的UC患者(P值分别=0.003、0.005、0.038).CD患者间亦因病变部位不同,血清球蛋白水平存在显著差异,仅累及结肠者的血清球蛋白水平显著高于单纯小肠受累者(P=0.029).结论 UC患者血清白球比和α2-球蛋白的异常程度可作为炎症活动性的预测因素;CD患者血清球蛋白增高预示疾病严重程度活动性增加,累及小肠的CD患者相对仅累及结肠的CD患者而言存在更为严重的营养缺失.     

Rectal wall thickness measured by ultrasound in chronic inflammatory diseases of the colon

Rectal wall thickness was measured ultrasonically by means of a 7-MHz transducer. 2 mm in diameter. In eight autopsy cases differences between ultrasonic and slide gauge measurements varied from -0.7 mm to 0.2 mm, with a median of 0.05 mm. Patients studies were carried out in 19 control subjects, showing a median rectal wall thickness of 2.6 mm, in 33 patients with ulcerative colitis with a median wall thickness of 2.8 mm, and in 18 patients with colonic Crohn's disease with a median wall thickness of 3.2 mm. These differences were not statistically significant. Subgroups of ulcerative colitis patients showed increasing wall thickness with increasing clinical activity (p less than 0.02), with increasing proctoscopic changes (p less than 0.01), and with increasing histologic activity (p less than 0.05). Corresponding correlations could not be demonstrated within the group of colonic Crohn's disease. It is concluded that even though the method could not distinguish between patients with ulcerative colitis and Crohn's disease of the colon, further studies concerning application of the measuring principle in gastroenterological endoscopy are indicated.     

Circulating human leucocyte elastase in patients with inflammatory bowel disease.

The plasma concentration of human leucocyte elastase (HLE), measured by enzyme immunoassay as the complex with alpha 1-proteinase inhibitor, was determined in 94 patients with active and inactive inflammatory bowel disease. In Crohn's disease and in ulcerative colitis human leucocyte elastase levels were raised significantly above normal when the disease was active, and fell on remission. The mean human leucocyte elastase level in 31 cases of active Crohn's disease was significantly greater than the mean human leucocyte elastase level in 23 patients with active ulcerative colitis (p = 0.013). The values of human leucocyte elastase correlated significantly with Crohn's disease activity index scores (p = 0.05) and with the circulating concentration of C-reactive protein (p less than 0.05 and p less than 0.01 for ulcerative colitis and Crohn's disease respectively), but not with the erythrocyte sedimentation rate. These results indicate that the concentration of human leucocyte elastase in the plasma of patients with inflammatory bowel disease reflects the activity of their intestinal disease and suggest that serial measurements of human leucocyte elastase may be useful in the assessment and clinical management of these conditions.