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PubMed1987

[Severe epithelio-exfoliative colitis in infants. Anatomical data].

Amongst the uncommon forms of congenital severe colitis, we wish to draw attention to a peculiar and probably previously never described condition that we propose calling provisionally, epithelio-exfoliative colitis. This condition appears to be characterized by the following features: its early beginning within the first weeks of life; the smooth, glossy appearance of the mucosa, without ulcerations visible to the naked eye; the prevalent degenerative changes of the epithelial cells which become vacuolated, break away prematurely from the basement membrane and finally exfoliate within the glandular lumens; the distension and rupture of the glands, the mucous contents of which intrude into the lamina propria and induce a localized, mild and non suppurative inflammatory reaction; accessory reactive traits: intense mucus production actively regenerating epithelium (high mitotic activity, syncytial cells) and increase of the cholinergic fibers within the lamina propria. Although patchily distributed, these lesions involve the colon exclusively. The cause of epithelio-exfoliative colitis is unknown. However, the ultrastructural studies and immunocytochemical investigations using anti-collagen IV, antilaminin, anti-fibronectin antibodies disclose in some glands localized thinning and rupture of the basement membrane. These data suggest a primary disorder within the molecular arrangement of either the basement membrane itself or the proteins which anchor the glandular cells to the basement membrane.

Colitis↗
PubMed1991

Contaminated fistula following J-pouch ileoanal reservoir. Treatment with a collagen sponge containing gentamicin and metronidazole. Case report.

In a 55-year-old woman, a 1 x 5 cm fistula developed in the ileoanal anastomosis after restorative proctocolectomy with J-pouch ileoanal reservoir and temporary ileostomy for intractable ulcerative colitis. The fistula extended between the pouch and the sacral bone. Lasting closure was achieved by intrafistular placement of a collagen sponge containing gentamicin and soaked in metronidazole solution and pouch drainage through a transanal Foley catheter.

Anal Canal↗
PubMed2004

[28-year-old woman with Goodpasture's syndrome and nonspecific colitis].

Goodpasture's syndrome usually becomes manifest with progressive glomerulonephritis and pulmonary hemorrhage. The diagnostic hallmark is the demonstration of anti-basement membrane anti-alpha3 type IV collagen antibodies (anti-GMB antibodies) in patient sera. Herein is reported the case of 28-year-old woman with Goodpasture's syndrome who developed the acute symptoms of nonspecific colitis which required surgical intervention. Immunosuppression along with plasmapheresis was successful in the treatment of life-threatening pulmonary hemorrhage, but not for the improvement of renal function.

Abdomen, Acute↗
PubMed2005

Systemic administration of the chemokine macrophage inflammatory protein 1alpha exacerbates inflammatory bowel disease in a mouse model.

INTRODUCTION: Exacerbations of inflammatory bowel disease are thought to be related to concurrent infections. As infections are associated with elevated local and serum concentrations of chemokines, we have determined whether systemic administration of the CC chemokine macrophage inflammatory protein 1alpha (MIP-1alpha) exacerbates colitis in a mouse model. METHODS: Colitis was induced in Balb/c mice using trinitrobenzene sulfonic acid (TNBS). Starting four days later, animals received daily intraperitoneal injections of recombinant MIP-1alpha. On day 7, mice were killed and pieces of colon taken for immunohistology and polymerase chain reaction analysis. The direct effects of MIP-1alpha on mucosal T cells and fibroblasts in vitro were also investigated. RESULTS: Systemic administration of MIP-1alpha markedly enhanced colitis with mice developing large transmural ulcers filled with granulation tissue. Treatment resulted in increased numbers of CD4 cells infiltrating the colonic lamina propria, increased interferon gamma (IFN-gamma) levels, and increased transcripts for tumour necrosis factor alpha (TNF-alpha) and matrix metalloproteinase 3 (MMP3). Isolated lamina propria lymphocytes from mice with TNBS colitis contained increased numbers of IFN-gamma and TNF-alpha transcripts when stimulated with MIP-1alpha in vitro. Colonic lamina propria fibroblasts also responded to MIP-1alpha with increased proliferation and decreased collagen 1 synthesis but fibroblast proliferation was not seen in vivo. CONCLUSIONS: These experiments show that increasing serum concentrations of a chemokine, MIP-1alpha, exacerbates immune mediated colitis. The effect seems to be due to the ability of MIP-1alpha to boost Th1 responses in the gut wall. Our findings also suggest a potential pathway by which peripheral infections can exacerbate inflammatory bowel disease.

Animals↗
PubMed2005

Oxytocin ameliorates oxidative colonic inflammation by a neutrophil-dependent mechanism.

UNLABELLED: Oxytocin (OT), a nonapeptide produced in the paraventricular and the supraoptical nuclei in the hypothalamus has a wide range of effects in the body. However, the role of OT on the gastrointestinal (GI) tract has to be settled. OT may participate in the regulation of motility, secretion, blood flow, cell turnover and release of neurotransmitters and/or peptides in the GI tract, possesses antisecretory and antiulcer effects, facilitates wound healing and is involved in the modulation of immune and inflammatory processes. The present work was conducted to assess the possible therapeutic effects of OT against the acetic acid-induced colonic injury in the rat. METHODS: Colitis was induced by intracolonic administration of acetic acid (5%) in Sprague-Dawley rats (200-250 g). Either saline or OT (0.5 mg/kg) was injected subcutaneously, immediately after the induction of colitis and repeated two times a day for 4 days. On the 4th day, rats were decapitated and distal 8 cm of the colon were removed for the macroscopic and microscopic damage scoring, determination of tissue wet weight index (WI), malondialdehyde (MDA) levels, an end product of lipid peroxidation; glutathione (GSH) levels, a key antioxidant; and myeloperoxidase (MPO) activity, as an indirect index of neutrophil infiltration. Colonic collagen content, as a fibrosis marker was also determined. Lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-alpha) levels were assayed in serum samples. In the acetic acid-induced colitis, macroscopic and microscopic damage scores, WI, MDA and MPO levels were significantly increased, while GSH levels were decreased when compared to control group (p <0.05-<0.001). Treatment with OT abolished the colitis-induced elevations in damage scores, WI, MDA and MPO levels and restored the GSH levels (p <0.05-0.001). Similarly, acetic acid increased the collagen content of colonic tissues and OT-treatment reduced this value to the level of the control group. Serum LDH and TNF-alpha levels were also elevated in the acetic acid-induced colitis group as compared to control group, while this increase was significantly decreased by OT treatment. The results suggest that OT, which improves the antioxidative state of the colonic tissue and ameliorates oxidative colonic injury via a neutrophil-dependent mechanism, requires further investigation as a potential therapeutic agent in colonic inflammation.

Acetic Acid↗
PubMed2004

Is the mucosal route of administration essential for probiotic function? Subcutaneous administration is associated with attenuation of murine colitis and arthritis.

BACKGROUND: We and others have reported the prophylactic efficacy of oral consumption of probiotic lactobacilli in the interleukin 10 knockout (IL-10 KO) model of colitis. It has not been demonstrated that the oral route is essential for probiotic efficacy. AIMS: (i) To determine the effect of parenteral administration (subcutaneous) of Lactobacillus salivarius 118 on colitis of IL-10 KO mice; and (ii) to determine if observed responses are disease specific. METHODS: (i) IL-10 KO mice were injected subcutaneously with L salivarius 118 or saline over 19 weeks. At sacrifice, the bowels were histologically scored. Isolated splenocytes were cultured in vitro and cytokine levels measured. (ii) In the collagen induced arthritis model, DBA/1 mice were injected subcutaneously with the probiotic or saline. At sacrifice, paw thickness was measured and joints were histologically scored. RESULTS: (i) Colonic inflammatory scores were significantly decreased in IL-10 KO mice injected with L salivarius 118 compared with controls (p<0.05). Proinflammatory cytokine production from stimulated splenocytes was significantly lower for the probiotic group whereas stimulated transforming growth factor beta (TGF-beta) levels were significantly increased (p<0.05). (ii) Scoring of arthritis and paw thickness were significantly improved in the group of mice injected with L salivarius 118 compared with controls. CONCLUSIONS: (1) Subcutaneous administration of L salivarius 118 significantly attenuated colitis in the IL-10 KO model and suppressed collagen induced arthritis, suggesting that the oral route may not be essential for probiotic anti-inflammatory effects and that responses are not disease specific. (2) The probiotic effect was associated with reduced production of proinflammatory (T helper 1) cytokines and maintained production of anti-TGF-beta.

Animals↗
PubMed1992

Mucosal capillary thrombi in rectal biopsies.

We studied the initial rectal biopsy from 46 patients in whom subsequent follow-up established the diagnosis of either self-limited colitis or inflammatory bowel disease. An additional 12 non-inflamed rectal biopsies were also studied. There was between 2 and 8 years of follow-up in each of these cases. Staining for fibrin (MSB, fibrinogen), platelets (factor XIIIA, Y2/51), and capillary basement membrane (reticulin, collagen 4) was performed to identify thrombotic material within capillaries. Mucosal capillary thrombi were best identified by staining for factor XIIIA; thrombi were observed in 8/13 cases of ulcerative colitis, 4/10 cases of Crohn's disease, 1/3 cases of unspecified inflammatory bowel disease and 5/20 cases of self-limited colitis. The presence of capillary thrombi was not related to the severity of inflammation, but none of the control biopsies showed capillary thrombi. Their presence seems of little diagnostic value in distinguishing inflammatory bowel disease from self-limited colitis. The pathogenetic significance of these mucosal capillary thrombi is uncertain.

Adult↗
PubMed1999

Cutaneous necrotizing vasculitis. Relation to systemic disease.

Cutaneous necrotizing vasculitis (CNV) is a complex multisystem disease generally involving the skin and mucous membranes, often accompanied by renal, gastrointestinal, pericardial, neurological, and articular signs and symptoms. CNV may be idiopatical or occur in association with a drug, infection, or underlying disease. CNV has been shown in patients with chronic infections (viral, bacterial, protozoa, helminthic), serum sickness, a variety of collagen vascular diseases (systemic lupus erythematous, Sjögren's syndrome, rheumatoid arthritis, Behçet's disease) hyperglobulinemic states, cryoglobulinemia, bowel bypass syndrome, ulcerative colitis, cystic fibrosis, primary biliary cirrhosis and HIV infection. Association with malignancies is not frequent. Lymphoproliferative disorders (Hodgkin's disease, mycosis fungoides, lymphosarcoma, adult T-cell leukemia, multiple mieloma) and solid tumors (lung cancer, colon carcinoma, renal, prostate, head and neck cancer and breast cancer) may be associated with CNV. Whenever possible, treatment is directed at the elimination of the cause. In other cases after adequate laboratory screening local and systemic therapy are recommended.

Arthritis, Rheumatoid↗
PubMed2005

Acute colitis induced by dextran sulfate sodium progresses to chronicity in C57BL/6 but not in BALB/c mice: correlation between symptoms and inflammation.

Exposure to dextran sulfate sodium (DSS) induces acute colitis, which is normally resolved after DSS removal. To study chronicity, mice are typically subjected to three to five cycles of weekly DSS exposures, each followed by a 1- to 2-wk rest period. Here, we describe a novel and convenient way of inducing chronic, progressive colitis by a single exposure to DSS. C57BL/6 mice exposed to DSS for 5 days developed acute colitis that progressed to severe chronic inflammation. The plasma haptoglobin levels remained high during the chronic phase, showing that the inflammation was active. Surprisingly, the mice regained their original weight along with the progression of colitis, and the only apparent symptom was loose feces. Histopathological changes 4 wk after DSS removal were dense infiltrates of mononuclear cells, irregular epithelial structure, and persistent deposits of collagen. A progressive production of the cytokines IL-1beta, IL-12 p70, and IL-17 correlated with the extensive cellular infiltration, whereas high IFN-gamma production was mainly found late in the chronic phase. Similar to C57BL/6 mice, BALB/c mice exposed to 5 days of DSS developed acute colitis as previously described. The acute colitis was accompanied by elevated plasma levels of haptoglobin and increased colonic levels of IL-1alpha/beta, IL-6, IL-18, and granulocyte colony-stimulating factor. However, soon after DSS removal, BALB/c mice recovered and were symptom free within 2 wk and completely recovered 4 wk after DSS removal in terms of histopathology, haptoglobin levels, and local cytokine production. In summary, these data stress the effect of genetic background on the outcome of DSS provocation. We believe that the present protocol to induce chronic colitis in C57BL/6 mice offers a robust model for validating future therapies for treatment of inflammatory bowel disease.

Acute Disease↗
PubMed2006

Increased aggregation response of platelets in patients with inflammatory bowel disease.

BACKGROUND: Platelets play an important role in hemostatic and inflammatory responses. To evaluate any potential enhancement of platelet activity in patients with inflammatory bowel disease (IBD), we measured the platelet aggregation responses to various stimuli. METHODS: Twenty-two healthy controls, 24 patients with ulcerative colitis (UC) and 25 patients with Crohn's Disease (CD) were studied. The aggregation responses induced by three agonists (epinephrine, collagen, and ADP) were measured by an 8-channel aggregometer. The platelet-derived microparticles (PDMP) levels were measured by an enzyme-linked immunosorbent assay. RESULTS: Twenty-one out of the 22 healthy controls did not respond to epinephrine (0.1 microg/ml), collagen (0.2 microg/ml), or ADP (1.0 microM). Eight out of the 12 active UC patients were sensitive to all agonists, and 4 patients showed increased sensitivity to epinephrine/collagen or epinephrine/ADP. Three out of the 12 inactive UC patients were normal, but 9 of these patients showed increased sensitivity, mainly to epinephrine. Ten out of the 12 active CD patients were sensitive to all agonists, and 2 active CD patients were sensitive to epinephrine/collagen or epinephrine/ADP. Eight out of the 13 inactive CD patients were sensitive to two or all agonists. Even after remission, almost all of the UC and CD patients showed some increased sensitivity to the agonists. The platelet number and the plasma PDMP levels were significantly higher in the active IBD patients than in the control group. CONCLUSIONS: Platelet aggregation responses are enhanced in IBD, even in inactive-phase patients. This increased sensitivity of the platelets may play an important role in the pathophysiology of IBD.

Adenosine Diphosphate↗
PubMed1977

[Disorders of the blood circulation in the gastrointestinal tract].

Blood flow disturbances in the gastrointestinal tract can lead to serious illness. They can be acute or chronic, their cause may be arterial or venous occlusion or hypotonia. Lesions of the gastrointestinal tract caused by ischemia depend on localisation, acuteness and degree of the blood flow disturbance. They may reach from focal and segmental ischemic lesions to extensive necroses of the entire intestinal tubes. The most serious ischemic disease is the embolic and thrombotic occlusion of the arteria mesenterica superior due to previous arterosclerotic damage. Infarction of a large part of the intestines and peritonitis can be the consequence. These patients' only chance of survival is early diagnosis--as a rule exclusively via angiography--and immediate surgery. Chronic occlusion of the arteria mesenterica superior leads to angina abdominalis which mainly occurs after food intake and can last for hours. The reason may also be a general arteriosclerosis. Men are affected more frequently and at a younger age than women. As a consequence of lowered intestinal blood flow these patients suffer from malabsorption and heavy weight loss. Conservative therapy is not effective. These patients, too, will have to be treated surgically after previous angiography. Vascular disease with decreased blood flow as its consequence can be found in a number of inflammatory diseases, in malign hypertensian, in collagen disease and in other more rare diseases as pseudoxanthoma elasticum or Ehlers-Danlos-syndrome. In the case of ischemic colitis arterial and more rarely venous occlusions cause decreased blood flow in the big bowel. A frequent consequence is colitis in the left colon which is characterized by acuteness, pain in the left side of the abdomen and by heavy rectal bleeding. Diagnosis is established by means of endoscopy, barium enema and angiography. Primarily therapy of ischemic colitis is of the conservative type. In severe cases with gangrene and peritonitis the colon has to be resected.

Acute Disease↗
PubMed2006

Acutely administered melatonin is beneficial while chronic melatonin treatment aggravates the evolution of TNBS-induced colitis.

The aim of this study was to evaluate the effects of melatonin on the inflammatory response and hydroxyproline production in an experimental acute and chronic model of trinitrobenzene sulfonic (TNBS) acid-induced colitis in Wistar rats. In the acute model, melatonin (0.5, 1, and 2 mg/kg, i.p.) was applied 48, 24, and 1 hr prior to the induction of colitis and 24 and 48 hr after; the severity of colitis was less evident in melatonin-treated animals with significant response in the group treated with 2 mg/kg. All doses investigated significantly reduced the myeloperoxidase activity (MPO). In the chronic studies, melatonin (1 and 2 mg/kg, i.p.) was administered daily 24 hr before hapten instillation and for 7 or 21 days after TNBS; melatonin (2 mg/kg) worsened colitis evolution in the 21-day study with a significant increase in MPO activity and tumor necrosis factor-alpha production with respect to TNBS group. Histological slides were in concordance with macroscopic data where areas of extensive necrosis and edema, fibrosis, and absence of regenerated epithelium were observed. Moreover, the hydroxyproline determination, used as indicator of collagen production and fibrosis, also showed a marker increase. The results obtained in this experimental model showed that short-term administration is protective while in the long term it negatively influences evolution of inflammatory colitis; therefore, the immunostimulatory effect of melatonin in some situations when given chronically, such as during inflammatory bowel disease, might lead to negative consequences.

Animals↗
PubMed2000

Deficiency of epithelial basement membrane laminin in ulcerative colitis affected human colonic mucosa.

Imbalances in epithelium-matrix interactions have been discussed as a pathomechanism in ulcerative colitis, causing a colonic mucosal barrier dysfunction. Laminin, the major noncollagenous component of the basement membrane, plays a role in epithelial basal lamina formation and promotes differentiation of human enterocytes. We therefore investigated the distribution of laminin in ulcerative colitis affected colonic tissues. Tissue specimens from both affected and nonaffected colonic regions were obtained from ten patients with ulcerative colitis during colonoscopies or operations. Healthy tissue from five patients with colorectal cancer was used as control. After histological classification, the localization and distribution of the basement membrane associated extracellular matrix proteins were determined by immunohistochemistry. Paraffin-embedded sections were incubated with antibodies against laminin and type IV and V collagen. No positive immunoreactivity against laminin was found in most of the epithelial basement membranes surrounding the crypts in affected colonic tissues, without involvement of the subendothelial structures. In contrast, a type IV and V collagen accumulation occurred in all these tissue samples. The lack of laminin in combination with an overexpression of type IV and V collagen, as reported for the first time in this paper, leads to changes in basement membrane structure. These findings indicate that the three-dimensional network of the colonic epithelial basement membrane and its function are seriously disturbed in exacerbating ulcerative colitis. This provides new insights into the importance of cell-matrix interactions for physiological and pathological mechanisms in the etiology of ulcerative colitis.

Adolescent↗
PubMedDate not supplied

Seasonal pattern of onset in lymphocytic colitis.

BACKGROUND: The etiology of lymphocytic colitis, a microscopic colitis syndrome, has remained elusive. Because 1) many infectious enteritides exhibit seasonal variability in incidence and 2) a few investigators have proposed some infectious mechanism in lymphocytic colitis, our aim was to determine if any variability in symptom onset existed among lymphocytic colitis patients diagnosed at our institution. STUDY: We identified 71 nonduplicated, consecutive patients with lymphocytic colitis over a 4-year period using rigorous clinicopathologic inclusion criteria: 1) chronic watery diarrhea, 2) endoscopically normal colon, 3) no evidence for celiac sprue or drug-induced colitis, 4) diffuse colitis with increased intraepithelial lymphocytes of at least 10 lymphocytes per 100 epithelial cells, 5) evidence of surface epithelial damage, and 6) no significant neutrophilic infiltrates, architectural distortion of the mucosa, or subepithelial collagen deposits. The date of diagnosis was corrected for month of onset of symptoms. RESULTS: The distribution of month of onset of symptoms showed a statistically significant (chi test of homogeneity, P = 0.0008) temporal variability and seasonal incidence pattern with excess cases during summer and fall and a paucity of cases during colder months. CONCLUSIONS: To our knowledge, this is the first study to examine systematically and report a significant seasonal incidence pattern of lymphocytic colitis. Our observations may support a potential link to an infectious source in lymphocytic colitis.

Adult↗
PubMed1975

Studies of rectal mucosal catecholamines in ulcerative colitis.

Rectal mucosal biopsies from six patients suffering from ulcerative colitis were studied by estimating the catecholamine (CA) content and by fluorescence microscopy. Adrenergic nerve fibres were relatively scanty both in diseased and control patients. The adrenergic structures seem well preserved in the affected areas of the colon, although the nonspecific collagenous autofluorescence makes interpretation difficult. There was a significant rise in the noradrenaline (NA) content compared with the seven control patients (p smaller than 0.01). This may be a compensatory phenomenon to inhibit increased intestinal motility. The increased NA level may be due to the intense perivascular adrenergic plexus typical for ulcerative colitis. In both groups there were varying amounts of fluorescing enterochromaffin cells probably without relation to the diagnosis.

Adult↗
PubMed2006

Frequency of rheumatic diseases in patients with autoimmune thyroid disease.

We aimed to investigate the frequency of rheumatic diseases in patients suffering from autoimmune thyroid diseases (ATD). Sixty-five patients (56 F, 9 M), who were followed by diagnosis of ATD, were questioned and examined for the presence of rheumatic disease. Basic laboratory tests and antithyroid antibodies, antinuclear antibody and rheumatoid factor (RF) levels were also measured by appropriate methods. Various rheumatic diseases were detected in 40 (62%) of patients with ATD. The most frequent rheumatic conditions were fibromyalgia, recurrent aphthous stomatitis, osteoarthritis, keratoconjunctivitis sicca and xerostomia and carpal tunnel syndrome which were detected in 20 (31%), 13 (20%), 10 (15%), 9 (14%) and 8 (12%) of patients, respectively. Autoimmune diseases, except Sjogren's syndrome, which were detected in ten patients with ATD, are as follows-vitiligo: two; autoimmune hepatitis: two; oral lichen planus: one, ulcerative colitis: one, inflammatory arthritis in four patients (two of them had rheumatoid arthritis, one had psoriasis and psoriatic arthritis and one had mixed collagen tissue disease). RF was positive in two patients, one of them had rheumatoid arthritis and FANA was positive in six (9%) patients; all of them had hypothyroidism. The frequency of rheumatic diseases seems to be higher in patients suffering from ATD. Initial evaluation and a regular checking for rheumatic diseases in patients suffering from ATD were recommended.

Adolescent↗
PubMed1993

ANCA in systemic vasculitides, collagen vascular diseases, rheumatic disorders and inflammatory bowel diseases.

It was the aim of this study to reevaluate the diagnostic significance and clinical implication of ANCA after testing sera from 13,606 patients for the presence of ANCA. Our data confirm the high specificity (97%) and sensitivity (80%) of cANCA for Wegener's granulomatosis. pANCA were found in renal vasculitides (60%), collagen vascular diseases (SLE 20%, Sjögren's syndrome 26%, polymyositis 16%) and rheumatic disorders (Felty's syndrome 50%, rheumatoid arthritis 20%). A third fluorescence pattern in sera of patients with inflammatory bowel disease (ulcerative colitis 28/72, Crohn's disease 6/84), here called xANCA, was seen. Target antigens of granule proteins from PMN and monocytes (proteinase 3, myeloperoxidase, elastase, cathepsin G, lactoferrin, lysozyme) were identified.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1980

Inflammatory bowel disease in children and adolescents.

Ulcerative colitis and Crohn's disease are significant childhood illnesses. With their many extraintestinal manifestations, they may masquerade as fever of unknown etiology, arthritis, anorexia nervosa, growth hormone deficiency, collagen-vascular disease, idiopathic growth retardation and even irritable bowel syndrome of childhood. In any child who presents with growth failure and/or chronic abdominal pain with fever or weight loss, the diagnosis of inflammatory bowel disease must be considered. As in any other chronic disease of childhood, long-term management will often challenge the physician emotionally and intellectually. As the etiology is yet unknown and a definitive cure is lacking, proper treatment depends on optimal medical and surgical management and supportive care.

Adolescent↗