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See detailPathophysiologic study of 3-methylindole-induced pulmonary toxicosis in immature cattle
Lekeux, Pierre ULg; Hajer, R.; van den Ingh, TSGAM et al

in American Journal of Veterinary Research (1985), 46(8), 1629-1631

In 5 Friesian calves given 3-methylindole (3-MI) (100 mg/kg once a week for 8 weeks, except calf 4, given a 50 mg/kg dose on weeks 3 to 8), pulmonary function (PF) values and arterial blood gas tensions ... [more ▼]

In 5 Friesian calves given 3-methylindole (3-MI) (100 mg/kg once a week for 8 weeks, except calf 4, given a 50 mg/kg dose on weeks 3 to 8), pulmonary function (PF) values and arterial blood gas tensions (PaO2 and PaCO2) were measured 24 hours after dosing was done and were correlated with clinical, biochemical, and pathologic changes. Three of the calves (No. 1, 2, and 3) showed acute respiratory distress syndrome 24 hours after the first 3-MI treatment, with a large increase in respiratory frequency, minute viscous work, and PaCO2 and a large decrease in tidal volume, dynamic lung compliance, and PaCO2. They died 36, 38, and 84 hours after dosing. Pulmonary function changes were compatible with the severe pulmonary edema and alveolar damage observed at necropsy. The 2 other calves, after they were given the 1st dose, showed only subacute respiratory distress syndrome with less severe changes in PF values recorded at 24 hours. Furthermore, they became progressively more tolerant to the 2nd, 3rd, and 4th weekly treatments, and showed base-line PF values after the 5th weekly treatment. Pathologic changes were not observed in lung biopsy material from these 2 animals at 2 and at 12 weeks after the 8th (or last) 3-MI treatment. [less ▲]

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See detailPathophysiological changes occurring during Escherichia coli endotoxin and Pasteurella multocida challenge in piglets: relationship with cough and temperature and predicitive value for intensity of lesions.
Halloy, David J; Bouhet, Sandrine; Oswald, Isabelle P et al

in Veterinary Research (2004), 35(3), 309-324

The aims of this study were (1) to correlate cough and body temperature (BT) with the severity of bronchopneumonia in pigs, (2) to determine whether these clinical signs can be used to early diagnose ... [more ▼]

The aims of this study were (1) to correlate cough and body temperature (BT) with the severity of bronchopneumonia in pigs, (2) to determine whether these clinical signs can be used to early diagnose bronchopneumonia and (3) to assess the predictive values of cough and BT regarding lung lesions. Bronchopneumonia was induced by administering E. coli endotoxin (LPS) combined with Pasteurella multocida type A (PmA) in the trachea of 13 piglets. Saline-instilled negative controls (n = 8), PmA inoculated (n = 6) and LPS instilled (n = 5) groups were also constituted. Cough and BT were recorded daily while the bronchopneumonia severity was assessed using bronchoalveolar lavage fluid (BALF) cytology, cytokines and measurement of lung lesion volume. Changes in expiratory breathing pattern were also measured (Penh). The combination of LPS and PmA induced a subacute bronchopneumonia characterised by macrophage, neutrophil, and lymphocyte infiltration, changes in Penh and an increase in the mRNA level of IFN-gamma while IL8, IL-18 and TNF-alpha mRNA levels remained unchanged. The daily body weight gain of infected animals was significantly reduced. Cough and BT changes were proportional to the intensity of the lung inflammatory process, functional respiratory changes and to the extent of macroscopic lesions. When comparing the individual values of cough and BT to thresholds defined for both parameters, an early diagnosis of pneumonia was possible. Considering the pooled data of each group, it was possible to define thresholds allowing an early segregation between the groups of diseased and healthy piglets. The daily values of cough and BT were predictive for the volume of lung lesions recorded at the end of the trial. In conclusion, cough and BT appear as potential indicators for the intensity and the evolution of the respiratory disease. They also seem to be good predictors for the magnitude of lung lesions and weight gain recorded at the study endpoint. [less ▲]

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See detailPathophysiological mechanisms of dominant and recessive GLRA1 mutations in hyperekplexia.
Chung, Seo-Kyung; Vanbellinghen, Jean-François ULg; Mullins, Jonathan G L et al

in Journal of Neuroscience (2010), 30(28), 9612-20

Hyperekplexia is a rare, but potentially fatal, neuromotor disorder characterized by exaggerated startle reflexes and hypertonia in response to sudden, unexpected auditory or tactile stimuli. This ... [more ▼]

Hyperekplexia is a rare, but potentially fatal, neuromotor disorder characterized by exaggerated startle reflexes and hypertonia in response to sudden, unexpected auditory or tactile stimuli. This disorder is primarily caused by inherited mutations in the genes encoding the glycine receptor (GlyR) alpha1 subunit (GLRA1) and the presynaptic glycine transporter GlyT2 (SLC6A5). In this study, systematic DNA sequencing of GLRA1 in 88 new unrelated human hyperekplexia patients revealed 19 sequence variants in 30 index cases, of which 21 cases were inherited in recessive or compound heterozygote modes. This indicates that recessive hyperekplexia is far more prevalent than previous estimates. From the 19 GLRA1 sequence variants, we have investigated the functional effects of 11 novel and 2 recurrent mutations. The expression levels and functional properties of these hyperekplexia mutants were analyzed using a high-content imaging system and patch-clamp electrophysiology. When expressed in HEK293 cells, either as homomeric alpha1 or heteromeric alpha1beta GlyRs, subcellular localization defects were the major mechanism underlying recessive mutations. However, mutants without trafficking defects typically showed alterations in the glycine sensitivity suggestive of disrupted receptor function. This study also reports the first hyperekplexia mutation associated with a GlyR leak conductance, suggesting tonic channel opening as a new mechanism in neuronal ligand-gated ion channels. [less ▲]

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See detailPathophysiological response of bovine diaphragm function to gastric distension
Desmecht, Daniel ULg; Linden, Annick ULg; Lekeux, Pierre ULg

in Journal of Applied Physiology (1995), 78

Because of the anatomic association of an exceptionally bulky stomach with a striking compartmentation of the chest wall, leading to the most cranial insertion of the diaphragm among mammals, gastric ... [more ▼]

Because of the anatomic association of an exceptionally bulky stomach with a striking compartmentation of the chest wall, leading to the most cranial insertion of the diaphragm among mammals, gastric overdistension in the bovine species offers a unique pathophysiological condition for the diaphragm. The purpose of the present study was to determine whether increased intragastric pressure (Pga) (1, 2, 3, 4, and 5 kPa) leads to perturbations of respiratory and diaphragm function in calves. Changes in diaphragmatic strength and inspiratory action followed a biphasic pattern: 1) transdiaphragmatic pressure (Pdi) in response to constant bilateral maximal phrenic nerve stimulation at 30 Hz increased with moderate gastric distension and then fell abruptly as Pga continued to rise and 2) the magnitude of the ratio of the fall in pleural pressure to total Pdi was maintained up to a Pga amounting to 2 kPa but declined at higher pressures. We conclude that gastric distension in the bovine species provokes physiologically significant alterations of the diaphragm excitation-to-pressure generation coupling as well as of its capacity to convert Pdi into useful inspiratory pleural pressure. We suggest that these perturbations resulted from the combination of 1) altered tension-generating capacity due to compromised perfusion, 2) altered diaphragm geometry capable of altering tension-to-pressure generation coupling, and 3) modified coupling of the diaphragm with the chest wall that reduced its ability to drive inspiration [less ▲]

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See detailPathophysiological response of bovine pulmonary function to gastric distension
Desmecht, Daniel ULg; Linden, Annick ULg; Lekeux, Pierre ULg

in Journal of Comparative Pathology (1995), 112

The purpose was to determine whether gastric overdistension leads to lifethreatening perturbations of pulmonary gas exchange in healthy calves. Six animals were studied with normal (0 kPa) and increased ... [more ▼]

The purpose was to determine whether gastric overdistension leads to lifethreatening perturbations of pulmonary gas exchange in healthy calves. Six animals were studied with normal (0 kPa) and increased (1, 2, 3, 4 and 5 kPa) intragastric pressure (IGP). Changes in pleural pressures and peak expiratory flow paralleled those of IGP. Inspiratory pressure-time index remained stable throughout the insufflation process. Pulmonary function values were characterized by abrupt changes with increasing IGP. Tidal volume declined as IGP increased and, along with inspiratory flow, decreased abruptly with the highest pressure (5 kPa). Respiratory rate progressively increased up to an IGP of 4 kPa, then decreased by 30%, due to breath-holding at the end of inspiration. Minute volume increased with IGP up to 4 kPa, but dramatically declined at 5 kPa. Total pulmonary resistance remained stable throughout the insufflation process, whereas lung dynamic compliance fell abruptly to one-half of its baseline value at IGPs of 1 kPa and above. Arterial oxygen tension was maintained at an IGP of 1 kPa, slightly diminished at 2–3 kPa, and markedly decreased at 4–5 kPa. Hypercapnia and respiratory acidosis developed progressively with increasing IGP. Changes in arterial gases were probably due to a combination of (1) alveolar hypoventilation, caused by altered tidal to dead space volume ratio, inadequate central nervous system “drive”, altered effectiveness of inspiratory muscle action, or end-inspiratory breath-holding, and (2) ventilation to perfusion mismatch, caused by perfusion of collapsed lung units. In the range of IGPs used, standardized arterial pH did not decline below the control value, which suggests that perfusion of peripheral tissues remained sufficient, and that respiratory failure rather than cardiovascular failure may be the principal physiopathological effect of increased gastric pressure [less ▲]

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See detailPathophysiologie der durch den extrakorporalen Kreislauf bedingten entzündlichen Reaktion im Kindesalter
SEGHAYE, Marie-Christine ULg

Thèse d’agrégation de l’enseignement supérieur (1996)

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See detailPathophysiology and prevention of postoperative peritoneal adhesions.
Arung, Willy; Meurisse, Michel ULg; DETRY, Olivier ULg

in World Journal of Gastroenterology (2011), 17(41), 4545-53

Peritoneal adhesions represent an important clinical challenge in gastrointestinal surgery. Peritoneal adhesions are a consequence of peritoneal irritation by infection or surgical trauma, and may be ... [more ▼]

Peritoneal adhesions represent an important clinical challenge in gastrointestinal surgery. Peritoneal adhesions are a consequence of peritoneal irritation by infection or surgical trauma, and may be considered as the pathological part of healing following any peritoneal injury, particularly due to abdominal surgery. The balance between fibrin deposition and degradation is critical in determining normal peritoneal healing or adhesion formation. Postoperative peritoneal adhesions are a major cause of morbidity resulting in multiple complications, many of which may manifest several years after the initial surgical procedure. In addition to acute small bowel obstruction, peritoneal adhesions may cause pelvic or abdominal pain, and infertility. In this paper, the authors reviewed the epidemiology, pathogenesis and various prevention strategies of adhesion formation, using Medline and PubMed search. Several preventive agents against postoperative peritoneal adhesions have been investigated. Their role aims in activating fibrinolysis, hampering coagulation, diminishing the inflammatory response, inhibiting collagen synthesis or creating a barrier between adjacent wound surfaces. Their results are encouraging but most of them are contradictory and achieved mostly in animal model. Until additional findings from future clinical researches, only a meticulous surgery can be recommended to reduce unnecessary morbidity and mortality rates from these untoward effects of surgery. In the current state of knowledge, pre-clinical or clinical studies are still necessary to evaluate the effectiveness of the several proposed prevention strategies of postoperative peritoneal adhesions. [less ▲]

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See detailPathophysiology of a fall in arterial oxygen saturation during sputum induction.
Cataldo, Didier ULg

in CHEST (2000), 117(6), 1818-9

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See detailPathophysiology of adult respiratory distress syndrome
Lamy, Maurice ULg; Fallat, R. J.; Koeniger, E. L. et al

in Acta Anaesthesiologica Belgica (1975), 26

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See detailPathophysiology of insulin secretion.
Scheen, André ULg

in Annales d'Endocrinologie (2004), 65(1), 29-36

Defects in pancreatic islet beta-cell function play a major role in the development of diabetes mellitus. Type 1 diabetes is caused by a more or less rapid destruction of pancreatic beta cells, and the ... [more ▼]

Defects in pancreatic islet beta-cell function play a major role in the development of diabetes mellitus. Type 1 diabetes is caused by a more or less rapid destruction of pancreatic beta cells, and the autoimmune process begins years before the beta-cell destruction becomes complete, thereby providing a window of opportunity for intervention. During the preclinical period and early after diagnosis, much of the insulin deficiency may be the result of functional inhibition of insulin secretion that may be at least partially and transiently reversible. Type 2 diabetes is characterized by a progressive loss of beta-cell function throughout the course of the disease. The pattern of loss is an initial (probably of genetic origin) defect in acute or first-phase insulin secretion, followed by a decreasing maximal capacity of insulin secretion. Last, a defective steady-state and basal insulin secretion develops, leading to almost complete beta-cell failure requiring insulin treatment. Because of the reciprocal relation between insulin secretion and insulin sensitivity, valid representation of beta-cell function requires interpretation of insulin responses in the context of the prevailing degree of insulin sensitivity. This appropriate approach highlights defects in insulin secretion at the various stages of the natural history of type 2 diabetes and already present in individuals at risk to develop the disease. To date none of the available therapies can stop the progressive beta-cell defect and the progression of the metabolic disorder. The better understanding of the pathophysiology of the disease should lead to the development of new strategies to preserve beta-cell function in both type 1 and type 2 diabetes mellitus. [less ▲]

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See detailThe Pathophysiology of Migraine: A Review Based on the Literature and on Personal Contributions
Schoenen, Jean ULg

in Functional Neurology (1998), 13(1, Jan-Mar), 7-15

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See detailPathophysiology of type 2 diabetes.
Scheen, André ULg

in Acta Clinica Belgica (2003), 58(6), 335-41

Type 2 diabetes mellitus is a heterogeneous syndrome characterized by abnormalities in carbohydrate and fat metabolism. The causes of type 2 diabetes are multi-factorial and include both genetic and ... [more ▼]

Type 2 diabetes mellitus is a heterogeneous syndrome characterized by abnormalities in carbohydrate and fat metabolism. The causes of type 2 diabetes are multi-factorial and include both genetic and environmental elements that affect beta-cell function and tissue (muscle, liver, adipose tissue, pancreas) insulin sensitivity. Although there is considerable debate as to the relative contributions of beta-cell dysfunction and reduced insulin sensitivity to the pathogenesis of diabetes, it is generally agreed that both these factors play important roles. However, the mechanisms controlling the interplay of these two impairments are unclear. A number of factors have been suggested as possibly linking insulin resistance and beta-cell dysfunction in the pathogenesis of type 2 diabetes. A majority of individuals suffering from type 2 diabetes are obese, with central visceral adiposity. Therefore, the adipose tissue should play a crucial role in the pathogenesis of type 2 diabetes. Although the predominant paradigm used to explain this link is the portal/visceral hypothesis giving a key role in elevated non-esterified fatty acid concentrations, two new emerging paradigms are the ectopic fat storage syndrome (deposition of triglycerides in muscle, liver and pancreatic cells) and the adipose tissue as endocrine organ hypothesis (secretion of various adipocytokins, i.e. leptin, TNF-alpha, resistin, adiponectin, implicated in insulin resistance and possibly beta-cell dysfunction). These two paradigms constitute the framework for the study of the interplay between insulin resistance and beta-cell dysfunction in type 2 diabetes as well as between our obesogenic environment and diabetes risk in the next decade. [less ▲]

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See detailLe pathos francophone : francodoxie, argumentation et émotions
Provenzano, François ULg

in Galatanu, Olga; Cozma, Ana-Maria; Marie, Virginie (Eds.) Sens et signification dans les espaces francophones. La construction discursive du concept de francophonie (2013)

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See detailA Pathway closely related to the D-tagatose pathway of Gram-Negative Enterobacteria Identified in the Gram-Positive Bacterium Bacillus licheniformis
Van Der Heiden, Edwige ULg; Delmarcelle, Michaël ULg; Lebrun, Sarah ULg et al

Poster (2013, June)

We report the first identification of a gene cluster involved in d-tagatose catabolism in Bacillus licheniformis. The pathway is closely related to the d-tagatose pathway of the Gram-negative bacterium ... [more ▼]

We report the first identification of a gene cluster involved in d-tagatose catabolism in Bacillus licheniformis. The pathway is closely related to the d-tagatose pathway of the Gram-negative bacterium Klebsiella oxytoca, in contrast to the d-tagatose 6-phosphate pathway described in the Gram-positive bacterium Staphylococcus aureus. [less ▲]

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See detailA Pathway closely related to the D-tagatose pathway of Gram-Negative Enterobacteria Identified in the Gram-Positive Bacterium Bacillus licheniformis
Van Der Heiden, Edwige ULg; Delmarcelle, Michaël ULg; Lebrun, Sarah ULg et al

in Applied and Environmental microbiology (2013), 79(11), 3511-3515

We report the first identification of a gene cluster involved in d-tagatose catabolism in Bacillus licheniformis. The pathway is closely related to the d-tagatose pathway of the Gram-negative bacterium ... [more ▼]

We report the first identification of a gene cluster involved in d-tagatose catabolism in Bacillus licheniformis. The pathway is closely related to the d-tagatose pathway of the Gram-negative bacterium Klebsiella oxytoca, in contrast to the d-tagatose 6-phosphate pathway described in the Gram-positive bacterium Staphylococcus aureus. [less ▲]

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See detailPathways of Human T-Lymphotropic Virus type I for viral entry
Boulanger, F.; Rodriguez, Sabrina ULg; Willems, L.

Scientific conference (2011, June 06)

Pathways of Human T-Lymphotropic Virus type I for viral entry Boulanger Fanny N.J., Rodriguez Sabrina and Willems Luc Cellular and Molecular Epigenetics, GIGA-Research, Liège The Human T-Lymphotropic ... [more ▼]

Pathways of Human T-Lymphotropic Virus type I for viral entry Boulanger Fanny N.J., Rodriguez Sabrina and Willems Luc Cellular and Molecular Epigenetics, GIGA-Research, Liège The Human T-Lymphotropic Virus type I (HTLV-1), the first discovered human retrovirus, infects an estimated number of 20 million people worldwide. HTLV-1 is the causative agent of Adult T-cell Leukemia/Lymphoma (ATL) and a neurodegenerative disease called HTLV associated myeolopathy / tropical spastic paraparesis (HAM/TSP). We have been interested in the early steps of HTLV entry into cells. Infection requires interaction of the viral envelope glycoproteins (SU and TM) with the cell membrane. Three molecules are required for binding and entry into cells: heparan-sulfate proteoglycans (HSPGs), the VEGF-165 receptor Neuropilin 1 (NRP-1) and the ubiquitous glucose transporter GLUT-1. Consecutive steps of HTLV-1 entry are poorly characterized. These could involve phagocytosis/macropinocytosis, caveolae pathway, clathrin-mediated endocytosis, and several mechanisms independent of these two organelles but mediated by dynamin. To identify the endocytic pathways of HTLV-1 entry, we used two complementary strategies based either on pharmacological inhibition or on dominant-negative proteins expression. First, we evaluated the effect of a series of pharmacological inhibitors to interfere with main endocytic pathways. We used wortmannin and cytochalasin D to interfere with phagocytosis and macropinocytosis through their action on phosphatidyl-inositol-3 kinase and on the actin network, respectively. Clathrin-mediated endocytosis was blocked with chlorpromazine and with a polyclonal anti-clathrin antibody as a direct competitor for the formation of clathrin-coated pits. The caveolar function was disrupted with the sterol-binding drug nystatin and the protein tyrosine-kinase inhibitor genistein. Finally, dynamin was competed with a peptide (Dynamin Inhibitory Peptide) or inhibited by dynasore. Since pharmacological inhibitors may have off-target effects, we also used an alternate approach based on dominant-negative proteins expressed by lentivirus-derived vectors. An AP-2-binding site from Eps15 (Epidermal Growth Factor Receptor Substrate 15) was used to interfere with clathrin-mediated endocytosis. A N-terminally GFP-tagged caveolin-1 construct acted as an inhibitor of the caveolae pathway. A dominant-negative GTP-binding mutant of dynamin2(aa) was used to interfere with dynamin-dependant internalization pathways. Lentiviruses expressing these dominant-negative proteins were transduced into several cell lines or primary cells (T-lymphocytes and dendritic cells). These transduced cells were then infected by co-cultivation with HTLV-1-infected T-lymphocytes (MT2) or with free particles. These different approaches will thus allow identifying the pathways involved in cell entry by HTLV-1. [less ▲]

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See detailPatient assessment using standardized bone mineral density values and a national reference database: implementing uniform thresholds for the reimbursement of osteoporosis treatments in Belgium
Boonen, S.; Kaufman, J. M.; Reginster, Jean-Yves ULg et al

in Osteoporosis International (2003), 14(2), 110-115

Dual-energy X-ray absorptiometry (DXA) devices from the three main manufacturers provide different bone mineral density (BMD) values, due in part to technical differences in the algorithms for bone ... [more ▼]

Dual-energy X-ray absorptiometry (DXA) devices from the three main manufacturers provide different bone mineral density (BMD) values, due in part to technical differences in the algorithms for bone mineral content (BMC) and area measurements and in part to the use of different manufacturer-derived reference databases. As a result, significant differences exist between Hologic, Lunar and Norland systems in the reported young normal standard deviation scores or T-scores. In a number of European countries, including Belgium, a T-score below -2.5 is one of the key criteria for reimbursement of osteoporosis treatments. This paper addresses the first attempt to implement a nationwide, uniform expression of BMD in patients, in order to harmonize drug reimbursement. To this end, measures were taken to implement a uniform expression of BMD in Belgian patients, by converting each manufacturer's absolute BMD to standardized BMD (sBMD) values and by establishing a single national reference range. [less ▲]

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See detailLe patient cancéreux ambulatoire traité par radiothérapie
Vanderick, JEAN ULg

in Revue Médicale de Bruxelles (1998), 18(4), 221-225

Le peu de connaissances en radiothérapie acquises par le médecin généraliste au cours de sa formation le rendent souvent désarmé face à un patient qui lui pose de nombreuses questions quant aux effets ... [more ▼]

Le peu de connaissances en radiothérapie acquises par le médecin généraliste au cours de sa formation le rendent souvent désarmé face à un patient qui lui pose de nombreuses questions quant aux effets secondaires du traitement ou le consulte en urgence suite à la survenue brutale de réactions imprévues. Quelle attitude adopter face à une dermite, une mucite, une leucopénie, une alopécie, sur radiothérapie ? Sans se montrer exhaustif, cet article vise à expliquer la pathogénie des réactions aiguës ou chroniques les plus fréquentes rencontrées lors des traitements ambulatoires, à aider à leur reconnaissance précoce, à envisager leur suivi en commun avec le radiothérapeute, leur pronostic et si nécessaire leur traitement en première ligne. [less ▲]

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See detailPatient coronarien avec co-morbidites: integrer indications et contre-indications dans le raisonnement pharmaco-therapeutique.
Scheen, André ULg

in Revue Médicale de Liège (2010), 65(7-8), 476-81

A patient with abdominal obesity, type 2 diabetes, arterial hypertension and dyslipidaemia is exposed to a high risk of coronary artery disease, congestive heart failure and/or renal insufficiency. The ... [more ▼]

A patient with abdominal obesity, type 2 diabetes, arterial hypertension and dyslipidaemia is exposed to a high risk of coronary artery disease, congestive heart failure and/or renal insufficiency. The management of such a patient requires different medications, which should be prescribed by taking into account both (relative and absolute) indications and contra-indications to improve overall prognosis. The present clinical case report illustrates the therapeutic reasoning leading to an appropriate pharmacological polytherapy, combined with life-style changes. [less ▲]

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