Tumeurs du foie et des voies biliaires

Les tumeurs du foie et des voies biliaires ne représentent qu’une partie relativement faible de toutes les tumeurs du chien et du chat. Cependant, leur présentation clinique souvent fruste est parfois déroutante. Une démarche diagnostique rigoureuse permet d’en déterminer la nature : en effet, le pronostic et le traitement sont différents suivant l’espèce et le type de tumeur. Les objectifs de cet article sont de présenter les différentes tumeurs primitives ou secondaires pouvant affecter le foie des carnivores domestiques, avant d’en aborder la présentation clinique, ainsi que les aspects diagnostiques et thérapeutique

Comparaison de l’exactitude du dosage du sodium et du potassium sanguins chez le chien par les analyseurs ECS 2000 et Vitros 250

La mesure des concentrations plasmatiques de sodium et de potassium est un besoin important en médecine vétérinaire, notamment lors des soins intensifs aux animaux choqués ; les résultats doivent donc être obtenus de façon rapide, précise et simple. L’objectif de cette étude a été de comparer chez le chien les résultats obtenus avec un analyseur de laboratoire validé et soumis à un contrôle de qualité, le Vitros 250, à ceux donnés par l’ECS 2000, récemment mis sur le marché. Soixante et onze plasmas héparinés canins ont été analysés par les deux appareils ; les résultats obtenus sur sang total et plasma par l’ECS 2000 ont été comparés sur 36 spécimens. La corrélation entre les résultats des deux analyseurs a été excellente pour le dosage du potassium (KECS = 0,90 x KVitros + 0,29 ; r = 0,96) et satisfaisante pour le dosage du sodium (NaECS = 1,19 x NaVitros - 24,38 ; r = 0,79). Les natrémies mesurées par l’ECS 2000, avec une imprécision de 1,2%, ont été significativement plus élevées que celles obtenues par le Vitros 250 avec un biais proportionnel, allant de 0,6 à 4,9 mmol/L. Les kaliémies mesurées par l’ECS 2000, avec une imprécision de 1,6%, ont été modérément mais significativement plus faibles qu’avec le Vitros 250 et le biais était également proportionnel, allant de 0,11 à 0,44 mmol/L. La discrimination clinique des résultats “ normaux ” vs. “ élevés ” ou “ bas ”, selon des intervalles de référence du Vitros 250, a été la même dans 94% des cas pour le sodium et 90% pour le potassium. Aucune différence significative entre les mesures réalisées avec l’ECS 2000 sur sang total et sur plasma n’a été mise en évidence pour la kaliémie, alors que les natrémies déterminées sur sang total ont été significativement plus faibles que celles déterminées sur plasma. Néanmoins, les dosages de K+ et Na+ effectués sur sang total était très fortement corrélés à ceux effectués sur plasma. La centrifugation du spécimen n’augmente donc pas la qualité analytique de l’appareil et cet analyseur, rapide et facile d’utilisation, constitue une bonne alternative aux analyseurs plus onéreux et techniquement plus délicats pour les cliniques vétérinaires

Pharmacokinetics and pharmacodynamics of a therapeutic dose of unfractionated heparin (200 U/kg) administered subcutaneously or intravenously to healthy dogs

Objectives: To evaluate the effects of 200 U/kg of sodium unfractionated heparin (UFH) on coagulation times in dogs after IV and SC administration and to compare these effects with plasma heparin concentrations assessed by its anti Xa activity. Methods: 200 U/kg of UFH were administered Intravenously (IV) and Subcutaneously (SC) to five healthy adult Beagle dogs with a wash out period of at least 3 days. Activated Partial Thromboplastin Time (APTT), Prothrombin Time (PT) and plasma anti-factor Xa (aXa) activity were determined in serial blood samples. Results: After IV injection, PT remained unchanged except for a slight increase in one dog; APTT was not measurable (> 60 s) for 45 to 90 min, then decreased regularly and returned to baseline values between 150 and 240 min. High plasma heparin concentrations were observed (C max = 4.64±1.4 aXa U/mL) and decreased according to a slightly concave-convex pattern on a semi-logarithmic curve but returned to baseline slightly more slowly (t240 to t300 min). After SC administration, APTT was moderately prolonged (mean±SD prolongation: 1.55±0.28 x APTT t0, range [1.35-2.01]) between 1 and 4 hours after administration. Plasma anti-factor Xa activity reached a maximum of 0.56±0.20 aXa U/mL, range: [0.42 - 0.9] after 132±26.8 min and this lasted for 102±26.8 min. Heparin concentrations were grossly correlated to APTT; prolongation of APTT of 120 to 160% corresponded to plasma heparin concentrations range of 0.3-0.7 aXa U/mL, considered as the therapeutic range in human medicine. Conclusions: As in human, pharmacokinetic of UFH in dogs is non linear. Administration of 200 U/kg of UFH SC in healthy dogs results in sustained plasma heparin concentrations in accordance with human recommendations for thrombosis treatment or prevention, without excessively increased bleeding risks. In these conditions, APTT can be used as a surrogate to assess plasma heparin concentrations. This has to be confirmed in diseased animals

Fibrinogen deficiency in a dog - a case report

Abstract Background Among coagulation disorders, primary fibrinogen deficiency is very rare in dogs. It is divided into hypofibrinogenemia, afibrinogenemia and dysfibrinogenemia. Afibrinogenemia has been described in three dogs. There are, however, no published case reports of primary hypofibrinogenemia in dogs. Case presentation A 1.5 year-old male German Pointer dog was evaluated for a locked-jaw syndrome associated with eye protrusion which appeared after a minor head trauma. Three months before the trauma, a persistent increase in coagulation times was detected by the referring veterinarian after a strong suspicion of snake envenomation. Apart for the primary complaint, physical examination was normal. A complete hemostatic profile revealed a moderately increased prothrombin time, activated partial thromboplastin times and a dramatically decreased fibrinogen concentration (0.34 g/L, reference interval [1.3–4.8 g/L]). Platelet count, plasma D-dimers and antithrombin, were all within the reference intervals and not consistent with a disseminated intravascular coagulation. Other possible causes of hypofibrinogenemia such as chronic hemorrhage and liver failure were excluded by laboratory work-up and imaging studies. Finally, antifibrinogen circulating anticoagulants were excluded using a dilution of citrated plasma from the pooled plasma of healthy dogs. These results supported a diagnosis of congenital fibrinogen deficiency and secondary retrobulbar hematoma and/or cellulitis. The dog’s condition improved rapidly after symptomatic treatment with corticosteroids and antibiotics. At the 1 year follow-up, the dog was clinically normal but a persistent hypofibrinogenemia (≤ 0.8 g/L) remained. Conclusions Various clinical presentations may occur in canine primary hypofibrinogenemia which should be included in the list of coagulation disorders. Diagnosis should include fibrinogen determination by coagulometric and non-coagulometric methods to differentiate from dysfibrinogenemia. There is no specific treatment but care should be taken to prevent bleeding and trauma. Emergency management of bleeding episodes with cryoprecipitate is the treatment of choice

Evaluation of benazepril in cats with heart disease in a prospective, randomized, blinded, placebo‐controlled clinical trial

International audienceBackground:Heart disease is an important cause of morbidity and mortality in cats,but there is limited evidence of the benefit of any medication. Hypothesis:The angiotensin-converting enzyme inhibitor benazepril would delaythe time to treatment failure in cats with heart disease of various etiologies. Animals:One hundred fifty-one client-owned cats. Methods:Cats with heart disease, confirmed by echocardiography, with or withoutclinical signs of congestive heart failure, were recruited between 2002 and 2005and randomized to benazepril or placebo in a prospective, multicenter, parallel-group, blinded clinical trial. Benazepril (0.5-1.0 mg/kg) or placebo was administeredPO once daily for up to 2 years. The primary endpoint was treatment failure. Ana-lyses were conducted separately for all-cause treatment failure (main analysis) andheart disease-related treatment failure (supportive analysis). Results:No benefit of benazepril versus placebo was detected for time to all-causetreatment failure (P= .42) or time to treatment failure related to heart disease(P= .21). Hazard ratios (95% confidence interval [CI]) from multivariate analysis forbenazepril compared with placebo were 1.00 (0.57-1.74) for all-cause failure, and0.99 (0.50-1.94) for forward selection and 0.93 (0.48-1.81) for bidirectional selec-tion models for heart disease-related failure. There were no significant differencesbetween groups over time after administration of the test articles in left atriumdiameter, left ventricle wall thickness, quality of life scores, adverse events, orplasma biochemistry or hematology variables. Conclusions and Clinical Relevance:Benazepril was tolerated well in cats withheart disease, but no evidence of benefit was detecte