References of "Leclercq, P"
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See detailSpondylodiscite compliquée d'un abcès du psoas
Leclercq, P.; Loly, Catherine ULg; Giot, Jean-Baptiste ULg et al

in Revue Médicale Suisse (2007), 3(101), 620-621

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See detailLe medicament du mois. Etoricoxib (Arcoxia)
Leclercq, P.; Malaise, Michel ULg

in Revue Médicale de Liège (2004), 59(5), 345-349

Etoricoxib (Arcoxia) is a novel non steroidal anti-inflammatory drug (NSAID) that selectively inhibits the inducible form of cyclo-oxygenase (COX), COX-2. Etoricoxib has a higher COX-1/COX-2 selectivity ... [more ▼]

Etoricoxib (Arcoxia) is a novel non steroidal anti-inflammatory drug (NSAID) that selectively inhibits the inducible form of cyclo-oxygenase (COX), COX-2. Etoricoxib has a higher COX-1/COX-2 selectivity ratio than the other COX-2-selective NSAIDs as rofecoxib, valdecoxib or celecoxib. Tablets of 60, 90 and 120 mg are available. The recommended dosage of etoricoxib is 60 mg/day for osteoarthritis, 90 mg/day for rheumatoid arthritis and 120 mg/day for acute gouty arthritis. Etoricoxib's efficacy has been widely studied in comparative studies, showing the same efficacy as non-COX-2 selective NSAID, with fewer gastro-intestinal adverse effects. [less ▲]

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See detailFièvre méditerranéenne familiale
Leclercq, P.; Hermesse, A.; Malaise, Michel ULg

in Revue Médicale de Liège (2004), 59(5), 320-325

Familial Mediterranean Fever (FMF) is an hereditary disease that especially affects people living around the Mediterranean sea. It is characterized by recurring fever and abdominal pain, eventually ... [more ▼]

Familial Mediterranean Fever (FMF) is an hereditary disease that especially affects people living around the Mediterranean sea. It is characterized by recurring fever and abdominal pain, eventually associated with localised pleuritis, synovitis or skin inflammation. The most serious complication is amyloidosis, which can lead to terminal renal failure. The attacks and complications can be avoided by life long administration of colchicine. Two independent French and American teams discovered the gene responsible for the disease in 1997. It encodes for a protein named pyrin/marenostrin involved in the homeostasis the inflammatory mechanisms. The main mutations have been identified and are henceforth accessible for molecular screening. [less ▲]

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See detailLa goutte
Leclercq, P.; Malaise, Michel ULg

in Revue Médicale de Liège (2004), 59(5), 274-280

In the presence of a clinical acute monoarthritis, a differential diagnosis has to be made between septic arthritis, gout and diffuse chondrocalcinosis. Gout comes from a purine nucleotide metabolism ... [more ▼]

In the presence of a clinical acute monoarthritis, a differential diagnosis has to be made between septic arthritis, gout and diffuse chondrocalcinosis. Gout comes from a purine nucleotide metabolism disorder leading to serum urate level elevation. This hyperuricemia can lead to the deposition of monosodium urate crystals in the joints, causing acute attacks. After long-term evolution, others tissues as the kidneys can be involved: it is chronic gout. The definite diagnosis is based on the presence of monosodium urate crystals in the joint fluid. The diagnosis of gout should prompt a search for associated medical conditions that may affect both urate levels and longevity. These include alcoholism, various nephropathies, myeloproliferative disorders, and hypertension. [less ▲]

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See detailMassive Ketonuria During Sedation with Propofol in a 12 Year Old Girl with Severe Head Trauma
Canivet, Jean-Luc ULg; Gustad, K.; Leclercq, P. et al

in Acta Anaesthesiologica Belgica (1994), 45(1), 19-22

Severe ketonuria developed during sedation with propofol in a 12 year old girl with brain injury. Deep sedation with propofol (5.1 mg/kg/h) was required because of agitation and severe intracranial ... [more ▼]

Severe ketonuria developed during sedation with propofol in a 12 year old girl with brain injury. Deep sedation with propofol (5.1 mg/kg/h) was required because of agitation and severe intracranial hypertension; as a part of our management protocol, glucose intake was restricted to 5 Kcal/h. After 18 hours of propofol infusion there was intense ketonuria (8+ by Ketostix) without any evidence of metabolic acidosis (pH, HCO3- and anion gap were within normal values). At this time, indirect calorimetry (Deltatrac) confirmed that energy expenditure was principally based on fat consumption (70% of energy expenditure). Lowering the propofol infusion rate and increasing glucose intake reduced fat consumption to 39% within 8 hours: at this time, Ketostix was negative for ketone bodies. This case illustrates a potential risk of ketonuria during prolonged sedation with propofol (a 10% solution of intralipid), particularly if glucose intake is restricted. Monitoring urinary ketone bodies is recommended under these circumstances. [less ▲]

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