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J Vilaseca

Publications and source records attributed to J Vilaseca.

At least 19 recordsLinked to original sources
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↗
PubMed1979

[Granulomatous hepatitis. Etiologic study of 107 cases (author's transl)].

An etiologic study was made of 107 cases of granulomatous hepatitis which were observed in a Department of Internal Medicine between January, 1971 and December, 1977 (excluding the hepatobiliary diseases). The most common etiology was tuberculosis (30 cases, 28 percent) followed by sarcoidosis (19 cases, 17.7 percent), Mediterranean exanthematous fever (13 cases, 12.1 percent), brucellosis (8 cases, 7.4 percent) typhoid fever (7 cases, 6.5 percent) and the idiopathic forms (8 cases, 7.4 percent). A lower rate of incidence was among Hodgkin's disease, toxoplasmosis, adenocarcinomas, leprosy, and those of unknown etiology, classified in this way because the study and follow-up of the patients could not be completed. There were, moreover, individual cases caused by mononucleosis, BCG reaction, hypogammaglobulinemia, celiac disease, and temporal arteritis. From a clinical point of view 50 percent of the patients had hepatomegaly and moderate disturbance of the liver enzymes. The most important enzymatic increases were detected in the cases caused by brucellosis; in the cases which were secondary to sarcoidosis the liver enzymes were normal. A comparison is established between the etiologic incidence of the present series and of others published in the literature. The causes and diagnostic problems of this type of lesion are discussed.

Agammaglobulinemia↗
PubMed1979

[Clinical course characteristics of polymyalgia arteritica. Study of 16 cases].

Clinical and biological characteristics are studied in 16 patients with polymyalgia arteritica. 12 of them were diagnosed by biopsy of the temporal artery and the other 4 because they presented clinical, biological data and a high response to corticosteroids. There were no differences according to sex. Most patients (75%) had symptoms since 1-6 months, headache being the most common (75%). Fever (56%), polymyalgia (50%), weight loss (37%), intermittent claudication, loss of vision and arthritis (12%) were the symptoms seen in these patients. ERS was high in all cases, hemoglobin was less than 8 g/100 ml in 8 cases and an increase of alfa-2-globuline was found in 8 patients. Temporal artery palpation was abnormal in 11 patients. Two of 5 patients who presented a normal arterial palpation had a positive biopsy. All patients received 6-metil-prednisolone. 3 are well after 3, 4 and 6 months therapy. 8 are also well but receiving small doses of steroids as treatment.

Aged↗
PubMed1978

[Granulomatous hepatitis: aetiological study of 107 cases (author's transl)].

In this series, the commonest aetiology was tuberculosis (30 cases, 28%), followed by sarcoidosis (18 cases, 17,7%), mediterranean fever (Olmer's disease) (13 cases, 12,1%), brucellosis (8 cases, 7,4%), typhoid fever (7 cases, 6,6%) and idiopathic forms (8 cases, 7,4%). These were followed by Hodgkin's disease, toxoplasmosis, adenosarcoma, and leprosy. Finally, there were single cases due to infectious mononucleosis, B.C.G. reaction, hypogammaglobulinaemia, coeliac disease and temporal arteritis. Half of the patients had hepatomegaly and an increase, in general moderate, in hepatic enzymes (transaminases, alkaline phosphatase). The highest enzyme levels were seen in cases of brucellosis, hepatic enzymes being normal in patients with sarcoidosis.

Alanine Transaminase↗