Michel Lambert
Université catholique de Louvain
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Featured researches published by Michel Lambert.
Lupus | 1995
Frédéric Houssiau; Chantal Lefebvre; M. Vandenberghe; Michel Lambert; Jean-Pierre Devogelaer; Jean-Christophe Renauld
We investigated whether serum titers of interleukin 10 (IL-10), a cytokine known to shift lymphocyte responses towards humoral immunity, reflect disease activity in systemic lupus erythematosus (SLE). Sera from 72 SLE patients, 25 RA patients and 30 healthy controls were tested for IL-10 by ELISA. Low titers of IL-10 were detected in the serum of 37.5% of SLE patients and in 24% of RA patients but in only 3% of healthy controls. Interestingly, serum IL-10 titers in SLE patients were positively correlated with the SLE Disease Activity Index (SLEDAI) and with anti-DNA antibody titers, but negatively with complement fraction C3 levels. These results indicate that serum IL-10 values reflect SLE disease activity and suggest that overexpression of IL-10 might play a pathogenic role in severe lupus disease.
Clinical Endocrinology | 2003
Marie-Laure Delporte; Sonia Brichard; M. P. Hermans; Claire Beguin; Michel Lambert
objective Adiponectin (ApN) is a fat‐derived hormone that enhances insulin sensitivity, controls body weight, prevents atherosclerosis and negatively regulates haematopoiesis and immune functions. In contrast to many proteins secreted by adipose tissue, the circulating level of ApN falls in obesity and insulin resistance states. The influence of starvation‐induced depletion of fat stores on ApN concentrations is yet unknown. We therefore investigated plasma ApN in anorexia nervosa (AN).
Retina-the Journal of Retinal and Vitreous Diseases | 1990
Bernadette Snyers; Michel Lambert; Jean-Paul Hardy
Three patients with systemic lupus erythematosus (SLE) associated with anti-phospholipid antibodies are reported. All three had severe vaso-occlusive disease: the first had an unilateral vaso-occlusive retinopathy, the second an unilateral central retinal venous obstruction, and the third a bilateral ischemic choroidopathy. The association of these occlusive ocular vascular diseases with the presence of the lupus anticoagulant and other associated factors in SLE is discussed.
International Journal of Eating Disorders | 1997
Michel Lambert; Catherine Hubert; G Depresseux; Bruno Vande Berg; Jean-Paul Thissen; Charles Nagant de Deuxchaisnes; Jean-Pierre Devogelaer
OBJECTIVE To assess the relationships between total body fat mass (FM) and hematological abnormalities in anorexia nervosa (AN). METHOD Peripheral blood parameters and body composition were determined in 10 anorectic patients and 19 age- and sex-matched healthy subjects. In patients with AN, magnetic resonance imaging (MRI) studies of bone marrow were also performed. RESULTS Compared with controls, patients with AN had -41% body weight, -81% FM, -18.8% lean tissue mass (LTM), and -22.6% bone mineral content; they also had lower mean total leukocyte (4.52 +/- 0.47 vs. 6.28 +/- 0.33 x 10(3)/microliter, p < .005), neutrophil (2.45 +/- 0.34 vs. 3.46 +/- 0.20 x 10(3)/microliter, p < .005), monocyte (0.24 +/- 0.03 vs. 0.37 +/- 0.03 x 10(3)/microliter, p < .05), and platelet counts (184 +/- 17 vs. 238 +/- 9 x 10(3)/microliter, p < .005). Hemoglobin level was normal and comparable in both groups. In patients with AN, but not in controls, total leukocyte, neutrophil, eosinophil, and monocyte counts as well as hemoglobin level were highly correlated with FM expressed in absolute values or in percentage of body weight, but not with LTM. Moreover, AN patients with signal intensity patterns suggestive of serous atrophy of bone marrow at MRI had not only lower erythrocyte, leukocyte, neutrophil, and platelet counts, but they also had lower FM than AN patients with normal MRI patterns. DISCUSSION Hematological changes in AN, as assessed by peripheral blood parameters and MRI patterns of bone marrow, are correlated with total body FM depletion, suggesting that the reduction of adipose tissue adversely affects hematopoiesis.
The American Journal of Medicine | 1990
Michel Lambert; Francis Zech; Philippe De Nayer; Jean Jamez; Bernard Vandercam
PURPOSE In order to assess the relation of thyroid function tests to human immunodeficiency virus (HIV) infection, we determined the levels of serum thyroid hormones, serum binding proteins [thyroxine-binding globulin (TBG), cortisol-binding globulin (CBG), and sex hormone-binding globulin (SHBG)], and serum tumor necrosis factor (TNF) in HIV-seropositive subjects at different clinical stages. PATIENTS AND METHODS Thirty-seven HIV-seropositive patients were studied: 7 at stage II, 13 at stage III, and 17 at stage IV (eight ambulatory and nine hospitalized) according to the Centers for Disease Controls criteria. RESULTS As compared with stage II and stage III patients, stage IV patients had significantly higher mean TBG and total thyroxine (TT4) values, similar and normal total triiodothyronine (TT3) levels, and similar and abnormally low reverse triiodothyronine (rT3) concentrations. However, stage IV hospitalized patients had significantly lower TT3 values than stage IV ambulatory patients. In contrast to TBG, mean levels of CBG and SHBG were comparable in the three groups and within normal limits. For the whole population of HIV patients, there was a highly significant correlation between the CD4 lymphocyte count and TBG (r = -0.529, p less than 0.001) but not with CBG and SHBG levels. Finally, TNF values higher than 10 pg/mL were detected in six of the 17 stage IV patients and in only one of the 13 stage III patients (p = 0.059); elevated TNF levels correlated with a lower CD4 count (p less than 0.01) but not with serum TBG levels. CONCLUSION The progression of HIV infection is associated with an elevation of serum TNF and TBG, but not of CBG or SHBG. HIV-infected patients have an unexpectedly normal TT3-low rT3 state.
European Respiratory Journal | 2001
Cédric Hermans; M. Petrek; V. Kolek; Birgit Weynand; Michel Lambert; Alfred Bernard
To test the hypothesis that sarcoidosis is associated with an intravascular leakage of lung epithelium secretory proteins, the occurrence and determinants in serum of sarcoid patients of CC16, a small size and readily diffusible lung-specific protein of 16 kDa secreted by bronchiolar Clara cells, was investigated. CC16 was measured by a sensitive latex immunoassay in the serum of 117 patients with established sarcoidosis and of 117 healthy subjects matched for age, sex and smoking status. Stepwise regression analysis was used to identify extrapulmonary variables of CC16 changes in serum. These changes were then compared with biochemical and cellular parameters in bronchoalveolar lavage fluid (BALF) as well as with the number of CC16 immunostaining cells on bronchial or pulmonary biopsy samples. CC16 concentration in serum of sarcoid patients was significantly increased, compared to their matched controls (25.9 +/- 16.2 versus 13.9 +/- 5.2 microg x L(-1)). In nonsmoking patients without significant renal impairment, CC16 in serum increased with the severity of the chest radiograph and computed tomography changes, and was on average 50-100% higher when parenchymal involvement was present. Sarcoid patients had, however, normal levels of CC16 in BALF and an unchanged number of CC16-immunopositive cells in lung biopsy samples, suggesting that an increased secretion of CC16 in the sarcoid lung is very unlikely, and that the elevation of CC16 in sarcoidosis results from an increased intravascular leakage of the protein across the air-blood barrier. The present study suggests that CC16 in serum might provide a useful tool to noninvasively evaluate the damage and increased permeability to proteins of the air-blood barrier associated with sarcoidosis.
Journal of Internal Medicine | 2000
T. Pieters; Benoît Boland; C. Beguin; C. Veriter; D. Stanescu; A. Frans; Michel Lambert
Abstract. Pieters T, Boland B, Beguin C, Veriter C, Stanescu D, Frans A, Lambert M (Cliniques, Universitaires Saint‐Luc, Brussels, Belgium). Lung function study and diffusion capacity in anorexia nervosa. J Intern Med 2000; 248: 137–142.
Journal of Internal Medicine | 1993
Jonathan Unger; Michel Lambert; M. Jonckheer; Pierre Denayer
Amiodarone has been reported as an anti-anginal drug in 19h7 [ 11 and as an anti-arrhythmic drug in 1969 [2]. Thyroid side-effects (hypothyroidism and thyrotoxicosis) were suspected as early as in 1971 [3]. Jonckheer et al. reported in 1973 a series of patients with amiodarone-associated thyrotoxicosis presenting worsening angina and arrhythmia for which the patients were taking the drug [4]. In 1976. Burger et al. demonstrated the effects of arniodarone on the peripheral metabolism of thyroid hormones [5], which were shown in 1978 by Jonckheer et al. to result in a low T, syndrome in patients treated chronically with the drug [h]. In 1982. Lambert et al. showed that amiodarone changes the T, production rate (T, PR) by the thyroid [7]. In 1987. Van Reeth et al. took advagtage of the properties of amiodarone for the treatment of thyrotoxicosis [S]. This review deals with the relationship between arniodarone and thyroid hormone metabolism on the one hand, and the risk of dysthyroidism and the antithyroid properties of the drug on the other. Effects of iodine overload on the thyroid gland
Acta Clinica Belgica | 2011
Astrid Marot; Johann Morelle; Virginie-Anne Chouinard; Michel Jadoul; Michel Lambert; Nathalie Demoulin
Abstract Myopathy, including rhabdomyolysis, is a well-known, albeit rare complication of statin therapy. Predisposing factors include comorbidities and the concomitant use of cytochrome P-450 (CYP) 3A4 inhibitors. We report a case of severe simvastatin-induced rhabdomyolysis triggered by the addition of amiodarone to previously well-tolerated chronic statin therapy. Physicians should be aware of the risk of this potentially severe drug interaction. The dose of simvastatin should be reduced (to 20 mg daily) when concomitant treatment with amiodarone is required, or preference should be given to pravastatin, rosuvastatin or fluvastatin, which are not metabolised by the CYP 3A4.
Clinical Neurology and Neurosurgery | 2011
Eric Constant; Stéphane Adam; Benoit Gillain; Michel Lambert; Etienne Masquelier; Xavier Seron
OBJECT Chronic fatigue syndrome (CFS) patients report usually cognitive complaints. They also have frequently comorbid depression that can be considered a possible explanation for their cognitive dysfunction. We evaluated the cognitive performance of patients with CFS in comparison with a control group of healthy volunteers and a group of patients with MDD. PATIENTS AND METHODS Twenty-five patients with CFS, 25 patients with major depressive disorder (MDD), and 25 healthy control subjects were given standardized tests of attention, working memory, and verbal and visual episodic memory, and were also tested for effects related to lack of effort/simulation, suggestibility, and fatigue. RESULTS Patients with CFS had slower phasic alertness, and also had impaired working, visual and verbal episodic memory compared to controls. They were, however, no more sensitive than the other groups to suggestibility or to fatigue induced during the cognitive session. Cognitive impairments in MDD patients were strongly associated with depression and subjective fatigue; in patients with CFS, there was a weaker correlation between cognition and depression (and no correlation with fatigue). CONCLUSIONS This study confirms the presence of an objective impairment in attention and memory in patients with CFS but with good mobilization of effort and without exaggerated suggestibility.