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Biomedical subjects

J Vilaseca

Publications and source records attributed to J Vilaseca.

At least 37 records · Page 2Linked to original sources
PubMed1998

Association between strong inflammatory response and low risk of developing visual loss and other cranial ischemic complications in giant cell (temporal) arteritis.

OBJECTIVE: To identify clinical and biochemical parameters that have good predictive value for identifying giant cell (temporal) arteritis (GCA) patients who are at high or low risk of developing cranial ischemic events. METHODS: In this multicenter study, records of patients at 3 university hospitals in Barcelona were reviewed retrospectively. Two hundred consecutive patients with biopsy-proven GCA were studied. RESULTS: Thirty-two patients developed irreversible cranial ischemic complications. The duration of clinical symptoms before diagnosis was similar in patients with and those without ischemic events. Patients with ischemic complications less frequently had fever (18.8% versus 56.9%) and weight loss (21.9% versus 62%) and more frequently had amaurosis fugax (32.3% versus 6%) and transient diplopia (15.6% versus 3.6%). Patients with ischemic events had lower erythrocyte sedimentation rates (ESR) (82.7 mm/hour versus 104.4 mm/hour) and higher concentrations of hemoglobin (12.2 gm/dl versus 10.9 gm/dl) and albumin (37.4 gm/liter versus 32.7 gm/liter). Clinical inflammatory status and biologic inflammatory status were defined empirically (clinical: fever and weight loss; biologic: ESR > or =85 mm/hour and hemoglobin < 11.0 gm/dl). Patients not showing a clinical and biologic inflammatory response were at high risk of developing ischemic events (odds ratio [OR] 5, 95% confidence interval [95% CI] 2.05-12.2). The risk was greatly reduced among patients with either a clinical (OR 0.177, 95% CI 0.052-0.605) or a biologic (OR 0.226, 95% CI 0.076-0.675) inflammatory reaction. No patient with both a clinical and a biologic response developed ischemic events. CONCLUSION: The presence of a strong acute-phase response defines a subgroup of patients at very low risk of developing cranial ischemic complications. Our findings provide a rationale for testing less aggressive treatment schedules in these individuals. Conversely, a low inflammatory response and the presence of transient cranial ischemic events provide a high risk of developing irreversible ischemic complications and require a prompt therapeutic intervention.

Aged↗
PubMed1998

Antitumor necrosis factor therapy in rat chronic granulomatous colitis: critical dose-timing effects on outcome.

Inhibition of tumor necrosis fact (TNFalpha) is of potential benefit in the treatment of chronic inflammatory conditions. However, TNFalpha plays an important role in host defenses against infection, and blocking TNFalpha production may also have adverse effects. We tested the efficacy and safety of anti-TNFalpha therapy in experimental colitis induced by trinitrobenzenesulfonic acid. We cultured colonic wall specimens for bacterial growth and measured native TNFalpha protein synthesis in colonic tissue at days 0, 1, 4, 10 and 18 after induction of colitis. Anti-TNFalpha therapy (monoclonal g1 immunoglobulin, 15 mg/kg i.p., every third day) was started on either day 4 or day 10 after induction of colitis. On day 18, we measured the release of inflammatory mediators and scored colonic lesions. In acute lesions, several species of the common flora were grown, including Streptococcus, Staphylococcus, Bacteroides, clostridia and enterobacteria. In chronic lesions, only enterobacteria, clostridia and lactobacilli were isolated. TNFalpha production by inflamed colonic tissue was increased in both acute and chronic lesions. Anti-TNFalpha therapy induced a significant decrease in the release of inflammatory mediators and histopathological remission when treatment started on day 10. However, anti-TNFalpha therapy increased eicosanoid release and lesion scores when treatment started on day 4. In conclusion, acute colonic lesions showed polymicrobial infection. Anti-TNFalpha therapy induced remission of chronic intestinal inflammation, but early treatment did not prove effective.

Animals↗
PubMed1997

Incrimination of anaerobic bacteria in the induction of experimental colitis.

Commensal bacteria may participate in the pathogenesis of bowel inflammation. We studied the role of bacteria from the rat colonic flora on transmural inflammation induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS). First, bacterial translocation to the colonic wall after induction of colitis was assessed by microbiological and histological methods. Second, rats with a colonic segment excluded from fecal transit were prepared for recolonization with preselected bacteria and used to test the effects of different species on inflammation (eicosanoid release, tissue myeloperoxidase) and damage (histology). Six strains (three aerobes and three anaerobes) were identified in colonic tissue 24 h after induction of colitis. Acridine staining showed bacteria in necrotic areas of the mucosa and invading the submucosa. Rats with excluded colon and sterile culture of luminal washings showed mild inflammation and low mucosal damage in response to TNBS. Rats colonized with anaerobes showed significantly higher eicosanoid release than rats colonized with aerobes only. Moreover, submucosal-lesions were mostly observed in rats with anaerobes. Our findings suggest that colonic anaerobes play a key role in transmural inflammation.

Animals↗
PubMed1996

Von Willebrand factor in the outcome of temporal arteritis.

OBJECTIVE: To determine fluctuation in circulating von Willebrand factor (vWF) in the outcome of patients with temporal arteritis. METHODS: Plasma vWF antigen concentrations were measured in 65 patients with biopsy proven temporal arteritis at different disease activity stages, in 12 with isolated polymyalgia rheumatica, and in 16 controls. Fourteen temporal arteritis patients underwent serial determinations during the course of their disease. RESULTS: vWF concentrations were significantly raised in temporal arteritis (mean 220 [arbitrary units], range 96 to 720) and in polymyalgia rheumatica (mean 196, range 103 to 266) compared with healthy controls (mean 98, range 75 to 137) (P < 0.05). Although vWF values tended to be higher in temporal arteritis, no significant differences were found between temporal arteritis and polymyalgia rheumatica patients nor between temporal arteritis patients with ischaemic complications (mean 269, range 130 to 720) and those who presented with polymyalgia rheumatica or constitutional symptoms only (mean 179, range 140 to 220). The highest levels were obtained in patients with associated, mainly infectious, diseases (mean 631, range 240 to 1680). Raised vWF values found in active temporal arteritis patients (mean 220, range 96 to 720) persisted within the first two years after the beginning of treatment (mean 244, range 102 to 510) but tended to normalise in patients in long term remission (mean 143, range 50 to 260). CONCLUSIONS: Persistent elevation of vWF during early remission of temporal arteritis might represent an endothelial activation status induced by a remaining inflammatory microenvironment rather than a marker of endothelial cell injury. In long term remission, decreasing vWF concentrations might reflect progression of inflammatory lesions to a healing stage.

Acute Disease↗
PubMed1996

Toxic dilatation of colon in a rat model of colitis is linked to an inducible form of nitric oxide synthase.

The contribution of nitric oxide (NO) to the altered colonic contractility of acute colitis was investigated in the 2,4,6-trinitroben-zenesulfonic acid model. NO synthase was measured in colonic tissue; the effects of NO synthase inhibition on colonic contractility were studied in vitro and in vivo. Inducible NO synthase was not detected in normal colons, whereas inflamed colons showed high activity. Acute inflammation was associated with enlarged colonic perimeter. NO synthase inhibitors or selective inhibitors of the inducible enzyme prevented colonic dilatation. In vitro, contractile responses to KCl were lower in muscle from colitic than control rats. After NO synthase inhibition, however, no difference was observed between colitic and control muscle contractility. In vivo, intracolonic pressure was lower in colitic than in control rats. Selective inhibition of inducible NO synthase increased intracolonic pressure in colitic but not in control rats. In conclusion, NO generation by inducible enzymes impairs smooth muscle contractility in colitis and may be involved in the pathogenesis of toxic dilatation of the colon.

Animals↗
PubMed1996

Bacterial peptides enhance inflammatory activity in a rat model of colitis.

Bacterial products released within the gut lumen may alter the course of inflammatory bowel lesions. The effect of intraluminal N-formyl methionyl-leucyl-phenylalanine on mucosal release of inflammatory mediators was investigated in normal and colitis rats (at 1 and 7 days after induction of colitis by trinitrobenzenesulfonic acid). Under anesthesia, the distal colon was perfused using an isosmotic solution with or without synthetic N-formyl methionyl-leucyl-phenylalanine (100 nmol/ml). Effluents were assayed for eicosanoid (PGE2, TXB2 and LTB4) concentration. Myeloperoxidase activity was measured in colonic wall homogenates. In normal rats, peptide perfusion did not change mucosal release of PGE2, TXB2 and LTB4. Colitic rats showed high baseline release of eicosanoids. The peptide did not further increase PGE2 and TXB2 release, but significantly stimulated LTB4 both on days 1 and 7 after induction of colitis. Rats with high myeloperoxidase activity in the colonic wall showed a marked LTB4 response to the peptide. Finally, peptide perfusion increased tissue myeloperoxidase activity in colitis at day 7 but not in colitis at day 1 or in normal rats. In conclusion, bacterial products may activate inflammation. This mechanism of lumen-wall interaction might be involved in the perpetuation of inflammatory lesions of the colonic mucosa.

Animals↗
PubMed1995

Induction of chronic cholangitis in the rat by trinitrobenzenesulfonic acid.

We investigated the effects of the hapten trinitrobenzenesulfonic acid instilled into the rat biliary tree. The study included three groups of animals that received a single intracholedochal injection of either saline, 10% ethanol or 10 mg trinitrobenzenesulfonic acid dissolved in 10% ethanol. A fourth group of rats was subjected to common bile duct ligation and was used as control for biliary obstruction. Liver and biliary tract dysfunction was assessed 1, 10, 20 and 30 days after treatment by serum aspartate aminotransferase, alkaline phosphatase and bilirubin, and by histopathological examination of liver slices. By day 10, saline- or ethanol-treated rats did not show changes in the biochemical parameters, and light microscopy revealed no alterations. In contrast, rats treated with trinitrobenzenesulfonic acid showed significant increases in all serum markers throughout the study period. Inflammatory cell infiltrates were seen in portal areas and around bile ducts, indicating pericholangitis. Some rats presented with dilatation of extrahepatic biliary ducts; ductal proliferation and thin porto-portal fibrotic septa were observed in these cases. Bile duct ligation also induced ductal proliferation and fibrosis in all cases, but pericholangitis was not prominent. Retrograde cholangiograms in trinitrobenzenesulfonic acid rats showed distortion of the intra- and extrahepatic biliary tree. In conclusion, chronic cholangitis may be consistently induced in rats by a single intracholedochal administration of trinitrobenzenesulfonic acid.

Alkaline Phosphatase↗
PubMed1995

Efficacy of intravenous cyclosporine for steroid refractory attacks of ulcerative colitis.

The use of cyclosporine in refractory ulcerative colitis (UC) is still controversial. An 8-year-long retrospective review open-label treatment with intravenous cyclosporine in 21 patients with steroid-refractory UC is therefore in order. Intravenous cyclosporine, 5 mg/kg-1 day, was added to ongoing drug therapy. Those who responded were switched to oral cyclosporine for a mean 8.4-month period, and steroids were discontinued when possible. Sixteen out of 21 patients improved (76%). Mean latency time to onset of improvement was 9 days. Five did not improve: three underwent urgent surgery, one was switched to methotrexate, and the remainder died. While on oral cyclosporine, 10 out of 16 maintained remission and seven could discontinue steroids, five relapsed, and one went on continuous mild activity. One patient died of a Pneumocystis carinii pneumonia, while in remission. Five reversible episodes of hepatobiliary toxicity were recorded. Intravenous cyclosporine effectively and rapidly induces improvement of acute steroid-refractory flare-ups of UC and helps to prevent urgent surgery. However, major adverse events may limit its usefulness.

Adolescent↗
PubMed1995

Eosinophilic gastroenteritis presenting as ascites and splenomegaly.

A 25-year-old man with a 1 year history of episodic abdominal pain presented with splenomegaly, eosinophilic ascites and peripheral eosinophilia. Full-thickness biopsies from his gastrointestinal tract revealed intense eosinophilic infiltration involving both muscular and serosal layers and extending from his stomach to his ileum. When given oral steroids, the patient's condition improved and he was discharged without symptoms. Eighteen months later, he remains asymptomatic and without recurrence of ascites or splenomegaly. This report adds to the scarce data on extraintestinal involvement in eosinophilic gastroenteritis. Special attention is drawn to the differential diagnosis of eosinophilic ascites and to the optimal approach to its management.

Adult↗
PubMed1994

Role of intestinal microflora in chronic inflammation and ulceration of the rat colon.

Bacteria and their products stimulate inflammatory responses. The effects of different antimicrobial regimens (amoxicillin/clavulanic acid, tobramycin, imipenem, vancomycin, metronidazole) were investigated on the course of experimental colitis induced by trinitrobenzenesulphonic acid (TNB) in the rat. On day 7 and 21 after the induction of colitis, matched groups of control and antibiotic treated rats were subjected to colonic dialysis to measure eicosanoid release, and killed for morphological assessment of the colonic lesions (macro and microscopic scores). Stool samples were cultured. Selective antibiotic treatment against Gram positive, Gram negative or anaerobic bacteria had no effect on colonic lesion scores. By contrast, certain broad spectrum antibiotics (amoxicillin/clavulanic acid or the association of imipenem plus vancomycin) significantly reduced macro and microscopic scores. Rats receiving these antibiotics did not develop chronic colitis as shown by the virtual absence of colonic strictures, adhesions, fibrosis, and granulomas. On day 21 after TNB, the intracolonic release of prostaglandin E2, thromboxane B2, and leukotriene B4 was significantly higher in control than in antibiotic treated rats. Control stool cultures showed abundant colony forming units of both aerobic and anaerobic bacteria. Amoxicillin/clavulanic acid and imipenem plus vancomycin induced appreciable reductions in luminal bacteria. In conclusion, certain broad spectrum antibiotics prevent chronic colitis. The normal colonic flora seems to play an important pathogenetic part in the progression of inflammatory colonic lesions to chronicity.

Animals↗
PubMed1994

[The percutaneous dissolution treatment of gallstones. Our initial experience].

OBJECTIVE: To describe our initial experience in direct contact dissolution of cholesterol gallstones with methyl-tert-butyl ether, a non surgical approach for high risk patients. PATIENTS: Twenty symptomatic patients were preselected. They all had radiolucent stones in functioning gallbladders. Patients rejected elective surgery or were considered to be of high risk for anesthesia. Computerized tomography scan was performed to evaluate stone calcium content and liver-gallbladder anatomy. In selected patients, contact stone dissolution was carried out after transhepatic gallbladder catheterization. RESULTS: Ten patients were excluded due to poor gallbladder contact to the liver (two patients) or stone density greater than 70 Hounsfield Units. Percutaneous transhepatic positioning of the catheter into the gallbladder was achieved in seven patients. Stone dissolution was complete in five patients and partial in one. Mean perfusion time was 6.15 hours (3.45-7.5); however, mean hospitalization stay was 7 days (4-10) mainly due to inexperienced management coordination. While on treatment, all patients experienced nausea, burning or abdominal discomfort that were easily controlled. Complications were related to catheter placement (intraperitoneal biliary leakage, external fistula) and in five patients to the dissolution procedure (severe abdominal pain, biliary colic, cholecystopancreatitis). Complications were all handled with non surgical treatment. CONCLUSIONS: Percutaneous gallstone dissolution with methyl-tert-butyl ether is a rapid and efficacious procedure that can, nevertheless, induce relevant secondary effects and complications.

Adult↗
PubMed1992

Dietary manipulation in experimental inflammatory bowel disease.

Eicosanoids are major mediators of defensive and inflammatory processes of the gut mucosa. The activity of the eicosanoid system is modulated by neural and hormonal pathways, but local factors acting within the gastrointestinal lumen may also be involved. We have studied the influence of dietary fatty acids on eicosanoid synthesis by the gastrointestinal mucosa. Since omega-3 fatty acids compete with the omega-6 as precursors of eicosanoid synthesis, we compared the effects of dietary supplementation with either sunflower or cod liver oil as sources of omega-6 or omega-3 fatty acids, respectively. Rats fed with the cod-liver-oil-supplemented diet for four weeks showed high omega-3 and low omega-6 plasma fatty acid levels compared to rats fed with the sunflower oil diet. Synthesis of arachidonic-acid-derived eicosanoids (6-keto-PGF1 alpha, PGE2, TXB2, LTB4, and LTC4) by gastric and intestinal mucosa was found to be lower in the cod liver group as compared to the sunflower group. However, significant generation of eicosapentaenoic-acid-derived eicosanoids (PGE3 and LTC5) was observed only in the cod liver group. We used the (trinitrobenzenesulphonic acid) TNBS model of inflammatory colitis to test the effect of the dietary fat on the development of inflammatory lesions of the bowel. A single intracolonic instillation of the hapten TNBS dissolved in 10% ethanol induces chronic granulomatous lesions of the colonic mucosa that persist for up to 8 weeks. Luminal release of eicosanoid mediators, as measured by intracolonic dialysis, was lower in the cod liver group than in the sunflower group, particularly during the chronic stage of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Participation of thromboxane and other eicosanoid synthesis in the course of experimental inflammatory colitis.

Eicosanoids, as modulators of inflammation, may be involved in the pathogenesis of inflammatory bowel disease. We investigated their potential role in a rat model of chronic granulomatous colonic inflammation induced by trinitrobenzene sulphonic acid. Luminal eicosanoid release was quantified in vivo using a dialysis bag placed into the distal colon. We tested the effect of drugs known to modify inflammatory activity or arachidonic acid metabolism. Three days after intracolonic injection of trinitrobenzene sulphonic acid at different dose levels, the dialysates showed a highly significant increase of prostaglandin E2, 6-keto-prostaglandin F1 alpha, thromboxane B2 (TXB2), and leukotriene B4, compared with levels in controls not subjected to the toxic agent. Remarkably, the release of TXB2 continued to increase during the stage of chronic inflammation (up to day 21), whereas the levels of the remainder eicosanoids declined. Treatment with prednisone or 5-aminosalicylic acid reduced TXB2 levels in the chronic stage of the inflammatory disease and improved the morphological damage as assessed macroscopically and histologically. Moreover, two selective thromboxane synthetase inhibitors, OKY 1581 and R70416, significantly reduced the development of chronic inflammatory lesions in the colon while inhibiting the release of TXB2. Our results indicate that (1) luminal release of thromboxane increases in the chronic stage of colonic inflammation, (2) anti-inflammatory treatment reduces tissue damage and thromboxane release, and (3) selective thromboxane synthetase inhibition improves the course of the disease in our experimental model.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Dietary fish oil reduces progression of chronic inflammatory lesions in a rat model of granulomatous colitis.

Eicosanoids are modulators of defensive and inflammatory processes in the gut mucosa, and may be involved in the pathogenesis of chronic inflammatory lesions of the bowel. As omega-3 fatty acids compete with the omega-6 as precursors of eicosanoid synthesis, we compared the effects of dietary supplementation with either sunflower (source of omega-6) or cod liver (source of omega-3) oil on the development of chronic granulomatous lesions in the rat colon. After four weeks on the supplemented diets, plasma omega-6 fatty acid content was significantly higher in the sunflower group, while omega-3 fatty acids predominated in the cod liver group. Inflammatory colitis was then induced by intracolonic administration of trinitrobenzene sulphonic acid. Luminal eicosanoid release, as measured by radioimmunoassay of intracolonic dialysis fluid, increased significantly after the challenge in both groups. Generation of prostaglandin E2 (PGE2) and leucotriene B4 (LTB4) peaked by day 3 and thereafter declined; thromboxane B2 (TXB2), instead, continued to increase from day 3 to 20 in sunflower fed rats, whereas this change was blunted in cod liver animals. The rats were killed 20, 30, or 50 days after the induction of colitis, and the colonic lesions were scored macroscopically (adhesions to surrounding tissues, strictures, ulcerations, and wall thickness) and histologically (ulceration, inflammation, depth of the lesions, and fibrosis). In cod liver animals, the damage score was markedly reduced by day 30, and inflammation and ulceration were almost absent by day 50. In conclusion, a fish oil diet prevents the increase in thromboxane in the chronic state of inflammation and shortens the course of the colonic disease by diminishing both the severity of the lesions and their progression to chronicity.

Animals↗