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H Mielants

Publications and source records attributed to H Mielants.

At least 181 records · Page 10Linked to original sources
PubMedDate not supplied

Gut mucosal T cell lines from ankylosing spondylitis patients are enriched with alphaEbeta7 integrin.

OBJECTIVE: An intriguing link between gut and synovial inflammation exists in patients with spondyloarthropathy (SpA), illustrated by the high frequency of microscopically inflammatory gut lesions observed in these patients. We hypothesise that aberrant homing of mucosal T cells might play a role in the induction/perpetuation of arthritis in SpA. Here, we analyse the expression of the homing molecules alpha4beta7 and alphaEbeta7 on mucosal T cells from patients with ankylosing spondylitis (AS) and controls, in view of the critical role of these receptors in the homing of mucosal lymphocytes. METHODS: Colonic biopsy specimens were obtained from patients with AS (n = 23) and controls (n = 30). Biopsy specimens were immunostained, treated for extraction of intraepithelial lymphocytes (IEL) and lamina propria lymphocytes (LPL) or cultured in the presence of IL-2. The expression of the beta7 integrins was investigated. RESULTS: In situ no differences were observed in alphaEbeta7 and alpha4beta7 integrin expression in isolated IEL and LPL, whether determined by flow cytometry or by immunohistochemical staining. In gut mucosal T cell lines, alphaEbeta7 expression was significantly higher in the mucosa of patients with AS compared with controls. Alpha4beta7 was highly expressed on T cells in both groups studied. Mucosal T cells either expressed only the alpha4beta7 integrin or co-expressed the alpha4beta7 and alphaEbeta7 integrins. Almost none of them expressed only the alphaEbeta7 integrin. CONCLUSION: In gut mucosal T cell lines from patients with AS an increased expression of alphaEbeta7 was observed.

Adolescent↗
PubMedDate not supplied

Influence of the gut and cytokine patterns in spondyloarthropathy.

Clinical and histological studies have previously shown that spondyloarthropathy (SpA) patients can have subclinical gut inflammation. This gut inflammation is related to enterocolitis in Crohn's disease (CD) and may evolve to overt inflammatory bowel disease in a subset of these patients. Moreover, there is an intriguing clinical link between gut inflammation and peripheral joint inflammation. In order to explore immunologically these concepts, recent studies have characterized phenotypically and functionally the inflammatory cells in both the gut and the synovium of SpA patients and have provided a number of new insights. Firstly, they confirm histological and pre-histological alterations of the gut immune system in SpA, which are redundant of CD and which are linked to alterations of the peripheral joints. Secondly, both the acquired and the innate immune system contribute to these alterations, with an important role for both T cells and macrophages and their cytokines. Thirdly, interpretation of these data support the hypothesis that gut and joint inflammation in SpA are induced by the combination of an impaired anti-bacterial host defence and an uncontrolled pro-inflammatory response of the innate immune system. The insights provided by the study of the gut immunology in SpA have contributed to develop new therapeutic strategies, with TNFalpha blockade as prototype.

Cytokines↗
PubMedDate not supplied

[Relationship between avascular necrosis and lipid and purine metabolisms].

The serum levels of uric acid, triglycerides, cholesterol, and lipoproteins were determined in 35 patients suffering from primary avascular necrosis. The results were compared with those of a control group and with those of patients suffering from gout. The frequency distribution of the results in the three groups was of the log-normal type and statistical calculations were made on logarithmic transformations of the serum values. In comparison with the control group, significant increases in the levels of triglycerides, cholesterol, pre-beta-lipoproteins, and uric acid were observed in patients presenting an avascular necrosis. No significant differences were observed between these patients and patients with gout in the levels of lipids and lipoproteins. Uricaemia was higher in the gout patients. Contrary to observations made on the gout patients, there was no correlation in the avascular necrosis patients between the uric acid level and the serum levels of lipids or lipoproteins. In an earlier study the authors put forward an hypothesis according to which the close relationship between the lipid and purine metabolisms in gout patients was due to a genetic linkage based on a common enzyme defect, which directly affected the two metabolisms. In avascular necrosis there is no common enzyme defect; the initial event is a disturbance in the lipid metabolism. The authors conclude with data which tend to show that the bone necrosis observed in patients using steroids or alcohol is not directly induced by these substances, but that once again the initial event is a disturbance in the lipid metabolism.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Osteomyelitis in a patient with a chronically infected arterial graft and longstanding hypertrophic osteoarthropathy of the leg.

A patient is reported with hypertrophic osteoarthropathy of the right leg who developed an osteomyelitis; this appeared to be related to an infected aortic bifurcation prosthesis with increased uptake on leukocyte scan and chronic gas formation at the proximal aortic anastomosis on computed tomography. There have been previous reports of hypertrophic osteoarthropathy as a sign of arterial prosthesis infection. In this patient antibiotic therapy was successful in controlling the osteomyelitis but eradication of the arterial prosthesis infection could not be confirmed and an elective arterial operation involved too great a risk.

Blood Vessel Prosthesis↗
PubMedDate not supplied

Ileal mucosal mononuclear cells in patients with seronegative spondylarthropathy.

In order to study local immunoregulatory mechanisms in patients with seronegative spondylarthropathy and histological evidence of asymptomatic intestinal inflammation, we determined mononuclear cells in distal ileal mucosa with an indirect immunoperoxidase technique using a panel of monoclonal antibodies. The number of intraepithelial lymphocytes in inflamed mucosa was not significantly increased. They carried mainly the suppressor-cytotoxic CD8 marker (greater than 80%), less frequently the helper T cell marker CD4 and lacked the pan T epitope CD3 in greater than 50%. There were no intraepithelial B cells or natural killer cells. The lamina propria lymphocytes were T and B cells, the former being more numerous. Helper T cells were more frequent than suppressor-cytotoxic T cells. There were no alterations in the proportion of T cells in inflamed mucosa. Natural killer cells were scarce. They occurred in small numbers in a minority of cases with gut inflammation and spondylarthropathy and rarely in inflammatory bowel disease. It is concluded that although there is an increase of lamina propria monocytes, there is no immunoregulatory imbalance in the ileal mucosa of patients with seronegative spondylarthropathy.

Adolescent↗
PubMedDate not supplied

Destructive lesions of small joints in seronegative spondylarthropathies: relation to gut inflammation.

Destructive lesions of small joints were found in 40 out of 211 patients suffering from seronegative spondylarthropathies (SpA) on whom ileocolonoscopy with biopsies of the ileum and colon were performed. The destructive lesions of small joints, radiologically only distinguishable from rheumatoid arthritis lesions by the pauciarticular and asymmetrical involvement, the rare tendency to fusion and the rare occurrence of periosteal hypertrophy, were observed more frequently in patients presenting subclinical inflammatory gut lesions, predominantly of the chronic type, than in patients without gut inflammation.

Arthritis↗
PubMedDate not supplied

Subclinical involvement of the gut in undifferentiated spondylarthropathies.

In order to evaluate the frequency of subclinical gut involvement in the seronegative spondylarthropathies, ileocolonoscopy with biopsies of the colon, ileocecal valve and ileum were performed on 211 patients with ankylosing spondylitis (AS), reactive arthritis (ReA) and undifferentiated spondylarthropathies. Inflammatory gut lesions were detected in a large number of these patients. It was concluded that the group of undifferentiated spondylarthropathies could be split into fairly equal subgroups: one subgroup suffering from subclinical inflammatory bowel disease associated with peripheral joint symptoms, a second subgroup presenting a form of enterogenic ReA, and a third subgroup in which no relation with the gut could be demonstrated. Ankylosing spondylitis, which has to be considered as a form of undifferentiated seronegative spondylarthropathy, could be subdivided into the same subgroups. These findings confirm the existence of subclinical gut involvement in patients with seronegative spondylarthropathies.

Arthritis↗
PubMedDate not supplied

Salicylate-induced gastrointestinal bleeding: comparison between soluble buffered, enteric-coated, and intravenous administration.

Serum salicylate levels and blood loss in stools were compared in 94 patients after intake of various forms of acetylsalicylate. Four different oral soluble forms, an enteric-coated variety and an intravenous form were evaluated. Analysis of the results of blood loss measurement in stools showed that salicylate users could be divided into "bleeders" and "non-bleeders". Administration of enteric-coated and intravenous forms of salicylates showed less blood less than ingestion of soluble forms. Only after administration of enteric-coated or intravenous forms of salicylates was a relationship between serum salicylate level and blood loss in stools observed in "bleeders". This suggests a similar mode of action of both these preparations on gastric mucosa. We conclude that enteric-coated forms of salicylates cause gastrointestinal bleeding by a systemic action on gastric mucosa.

Aspirin↗
PubMedDate not supplied

Goldsalts, levamisole and D-penicillamine as first choice slow-acting antirheumatic drugs in rheumatoid arthritis--a long-term follow-up study.

In the present study, 345 rheumatoid arthritis patients were treated using goldsalts, D-Penicillamine or levamisole as the slow-acting antirheumatic drug of first choice. Goldsalts were given to 182 patients, levamisole to 139 and D-Penicillamine to 24. At the time of the present evaluation, 83 patients were still on goldsalts (44.6%), 63 on levamisole (45.2%) and 11 on D-Penicillamine (45.9%). Adverse reactions required interruption of treatment in 64 patients on goldsalts (35.2%), in 44 on levamisole (31.7%) and in 5 on D-Penicillamine (20.8%). Inefficacy was responsible for withdrawal of 33 patients receiving goldsalts (18.1%), 30 receiving levamisole (21.6%) and 8 receiving D-Penicillamine (33.3%). The duration of treatment was 4.6 years for goldsalts, 3.6 years for levamisole and 3.6 years for D-Penicillamine. In the present analysis none of the compounds was found to have a definite advantage over the others. The rather favourable treatment continuation rates in this study can be attributed to the fact that the slow-acting antirheumatic drugs were given at an early stage of the disease, preferably before the occurrence of radiological lesions.

Adult↗
PubMedDate not supplied

[Osteopoikilosis].

Explore the source record for details and available documents.

Adolescent↗
PubMedDate not supplied

Levamisole as basic treatment of rheumatoid arthritis: longterm evaluation.

We evaluated longterm levamisole treatment of 201 rheumatoid patients. Fifty-nine patients in their 1st yr of treatment were not analyzed; of the remaining 142, 69 (49%) still took levamisole with benefit. Levamisole was stopped in 32 patients (22%) for inefficacy and for reversible adverse reactions in 37 (26%). Leukotoxic side-effects were the commonest cause of withdrawal (23 patients = 16%). Since June 1977, we administer levamisole on a 1 d/wk schedule (150 mg), with determination of white blood cells 10 h after intake to detect high-risk patients for agranulocytosis. With disease exacerbation during treatment or lack of response after 6 months, the drug is given on a 2nd non-consecutive day. Since June 1977, cases of agranulocytosis have not been observed. Allergic vasculitis did not occur with a 1 d/wk schedule. The absence of nephrotoxicity and hepatotoxicity is stressed. Only 4 patients (3%) were lost to follow-up. Comparison is made with longterm use of gold and D-penicillamine. We conclude that levamisole is a useful slow acting antirheumatic drug.

Agranulocytosis↗
PubMedDate not supplied

Idiopathic inflammatory bowel diseases: immunological hypothesis.

Circumstantial evidence indicates that immunological mechanisms are important in the pathogenesis of inflammatory bowel diseases. In Crohn's disease lesions the naive T cells are reduced and memory T cells are increased in number. Colonocytes of normal mucosa do not express MHC class II molecules but aberrant HLA-DR expression is induced in inflammatory conditions. Also in ileal epithelial cells there is increased MHC class II molecules expression suggesting augmented antigen presentation. Once the initiating event (environmental, dietary, infectious or enterobacterial products) has activated inflammatory cells, an auto-amplifying inflammatory immune cascade is induced by numerous agents such as cytokines, transforming growth factors, leukotrienes, prostaglandins and other mediators. Tissue injury may be caused by oxygen free radicals generated by neutrophils and macrophages. The inflammatory process can be perpetuated by a persistent antigenic stimulus or alternatively, by abnormal regulation of immune and inflammatory responses. This can mean exaggerated activation of inflammatory responses to "normal" stimuli or defective feedback mechanisms of down-regulation. The early lesions of inflammatory bowel disease are patchy necrosis of the surface epithelium, focal accumulations of leukocytes adjacent to crypts and an increased number of intraepithelial lymphocytes. In Crohn's disease the earliest lesions are aphthoid ulcers overlying lymphoid follicles in the terminal ileum. In patients with spondylarthropathy and asymptomatic intestinal inflammation we demonstrated lesions in the top of the follicle associated epithelium. The changes consist of increase in number of membranous (M) epithelial cells, ruptures, fissures and perforations of M cells. Aphthoid ulcers that may occur in the entire gastrointestinal tract are typically found at the M cell level.(ABSTRACT TRUNCATED AT 250 WORDS)

Colitis, Ulcerative↗