Thesis (MMedVet (Med))--University of Pretoria, 2001. / Includes bibliographical references.

Dogs with pituitary-dependent hyperadrenocorticism (PDH) are at increased risk of thromboembolic disease (TED); however the pathogenesis of thrombosis in these patients is poorly characterized. Thromboelastography (TEG®) is a whole blood hemostatic test that has recently been shown to be capable of detecting hypercoagulability in veterinary patients. A modification of TEG, PlateletMappingTM (TEG-PM) measures platelet response to the agonists arachidonic acid (MAAA) and adenosine diphosphate (MAADP), and compares this to fibrin clot strength in the absence of platelet activation (MAfibrin). This prospective study evaluated dogs with PDH for hypercoagulability using TEG-PM as well as conventional plasma-based coagulation tests (prothrombin time [PT], activated partial thromboplastin time [aPTT], fibrinogen concentration). Hemostatic testing was performed in 40 healthy dogs, 19 dogs with untreated PDH, 16 of the dogs with PDH after 3 months’ treatment and 15 dogs after 6 months’ treatment. Systolic blood pressure (SBP) was also measured in all the dogs with PDH before and during treatment. In addition, urine protein to creatinine ratio (UPCR) and antithrombin activity [AT] were measured in some dogs with PDH. PT was significantly decreased in the dogs with PDH compared to controls, however all of the dogs with PDH had results within the reference interval. Dogs with PDH were hyperfibrinogenemic compared to healthy dogs; fibrinogen concentrations reduced with treatment of PDH but remained significantly elevated. AT activity in the PDH dogs was not significantly decreased despite the majority of dogs tested having significant proteinuria. Approximately half of the dogs with untreated PDH were hypertensive, and blood pressure did not change significantly following resolution of hypercortisolemia. Serum cholesterol was increased in dogs with untreated PDH but normalized following control of PDH. TEG-PM revealed decreased κ, increased α-angle and increased MAthrombin in dogs with PDH in comparison to healthy dogs. Platelet response to AA was significantly increased in dogs with untreated PDH. Following treatment of PDH, the majority of TEG-PM parameters (with the exception of MAthrombin) did not change significantly. In conclusion, dogs with PDH had evidence of hypercoagulability and hypertension, which persisted despite medical treatment of PDH. These factors may explain the association between hyperadrenocorticism and TED. / OVC Pet Trust Fund, Vetoquinol

Objective: To evaluate pressor sensitivity to catecholamines in dogs after induction of iatrogenic hyperadrenocorticism (I-HAC) by serial arterial blood pressure measurements during infusions of increasing dose rates of norepinephrine. Animals: Eight dogs with I-HAC induced by administration of oral hydrocortisone at a mean dose of 3.3 mg/kg PO TID for 42-49 days and 8 control dogs which received empty gelatin capsules PO TID for 42-49 days. Procedure: Systolic, diastolic, mean blood pressure and heart rate measurements were recorded after sequential administration of increasing dose rates of norepinephrine (0.1, 0.125, 0.2, 0.3, 0.4, 0.6 and 0.8 mg/kg/min) for 10 minutes. The changes in systolic, diastolic, mean blood pressure and heart rate were compared between control dogs and dogs with I-HAC. Results: Dogs in the I-HAC group had a more pronounced pressor response to norepinephrine infusions than control dogs. The infusions were not completed in 7 of the 8 dogs in the I-HAC group versus 3 dogs in the control group due to severe elevations in systolic blood pressure. The mean change in systolic blood pressure was consistently higher in dogs in the I-HAC group. The difference was statistically significant at the 0.2 mg/kg/min norepinephrine dose rate. The mean change in heart rate was consistently lower in the I-HAC group, a difference that was significant at the 0.2 mg/kg/min norepinephrine dose rate. Conclusions and clinical relevance: Increased pressor sensitivity or decreased baroreceptor response to norepinephrine was seen in dogs with I-HAC suggesting that this mechanism is involved in the development of hypertension in canine hyperadrenocorticism. / Master of Science

O hiperadrenocorticismo é uma das endocrinopatias mais comuns em cães, sendo caracterizado pela exposição excessiva de glicocorticóides secretados pelas adrenais. A hipercortisolemia crônica pode promover várias complicações, incluindo hipertensão sistêmica e glomerulonefrite. A glomerulonefrite pode desencadear variáveis graus de proteinúria e uma tendência de evolução para doença renal crônica. A perda de proteínas na urina, principalmente da albumina, é uma característica das doenças glomerulares e a determinação de variáveis laboratoriais, como a razão proteína:creatinina urinária (RPC), albuminúria (teste de ELISA) e eletroforese das proteínas urinárias, são recomendadas para a elucidação do diagnóstico. Assim, o objetivo do estudo é avaliar a relação entre proteinúria e hipertensão arterial sistêmica em cães com hiperadrenocorticismo e verificar, pela avaliação da albuminúria e do peso molecular das proteínas urinárias, o segmento do néfron que foi comprometido ou lesado. Foram avaliados 30 cães com diagnóstico de hiperadrenocorticismo, subdivididos em 13 cães com hipertensão arterial sistêmica (grupo I) e 17 cães normotensos (grupo II). Foram determinados a razão proteína:creatinina urinária (RPC); a albuminúria pela avaliação da albumina normalizada e razão albumina: creatinina urinária (RAC) e a eletroforese de proteínas pela técnica em gel de poliacrilamida, contendo dodecil sulfato de sódio (SDS - PAGE). Os resultados foram comparados com os dados obtidos de 30 cães clinicamente saudáveis e foi constatado que não houve influência da hipertensão arterial sistêmica nos cães com hiperadrenocorticismo em relação à quantificação da albuminúria, determinada pelo método ELISA, e nem na qualidade e quantidade das bandas de proteínas de baixo (< 60 kDa) e de alto peso molecular (> 60 kDa) determinada pela eletroforese. No entanto foi determinado que cães com hiperadrenocorticismo podem desenvolver lesões glomerulares e tubulares, caracterizadas pela presença de albuminúria e de proteínas de alto e de baixo pesos moleculares, independentemente da presença de hipertensão arterial sistêmica. Concluindo que os métodos laboratoriais, a eletroforese de proteína urinária em gel de poliacrilaminda associada à avaliação quantitativa da proteína total, como a determinação quantitativa da albuminúria, são passíveis de serem empregadas para a avaliação dos segmentos dos néfrons comprometidos que causaram as perdas de proteínas na urina. / Hyperadrenocorticism is a common endocrinopathie in dogs characterized by excessive glucocorticoid expousure secondary to adrenal secretion. Chronic hypercortisolemia may promote several complications, including sistemic hypertension and glomerulonephritis. Glomerulonephritis may lead to different proteinuria degrees and chronic renal disease. Urine protein loss, specially albumin, is characteristic in glomerular diseases. Laboratorial determination by the urinary protein/creatinin ratio (PCR), albuminuria (ELISA test) and urinary protein electrophoresis are recommended for diagnosis. The aim of this study is to evaluate the relationship between proteinuria and sistemic arterial hypertension in dogs with hyperadrenocorticism and to identify the nephron injured segment by evaluating albuminuria and urinary protein molecular weight. Thrithy dogs with hyperadrenocorticism were subdivided in 2 groups as following: 13 dogs with sistemic arterial hypertension (group I) and 17 normal dogs (group II). Urinary protein/creatinin ratio (PCR); albuminuria using the evaluation of normalized albumin and urinary albumin/creatinin ratio (ACR); and protein electrophoresis using polyacrylamide gel with sodium dodecil sulfate (SDS - PAGE) were performed. Results were compared with data of 30 clinically healthy dogs. No influence of sistemic arterial hypertension in dogs with hyperadrenocorticism was noticed in albuminuria magnitude using the ELISA method, nor in the quality and quantity of low (<60 kDa) and high (> 60 kDa) molecular weight bands observed in electrophoresis. However, dogs with hyperadrenocorticism can develop glomerular and tubular lesions, characterized by albuminuria and by the presence of high and low molecular weight proteins in urine independently of sistemic arterial hypertension. Furthermore, urinary protein electrophoresis in polyacrylaminde gel associated to quantitative evaluation of total protein such as the quantitative determination of the albuminuria, may be used in evaluating committed nephrons segments that caused urine protein loss.

O hiperadrenocorticismo é uma das endocrinopatias mais comuns em cães, sendo caracterizado pela exposição excessiva de glicocorticóides secretados pelas adrenais. A hipercortisolemia crônica pode promover várias complicações, incluindo hipertensão sistêmica e glomerulonefrite. A glomerulonefrite pode desencadear variáveis graus de proteinúria e uma tendência de evolução para doença renal crônica. A perda de proteínas na urina, principalmente da albumina, é uma característica das doenças glomerulares e a determinação de variáveis laboratoriais, como a razão proteína:creatinina urinária (RPC), albuminúria (teste de ELISA) e eletroforese das proteínas urinárias, são recomendadas para a elucidação do diagnóstico. Assim, o objetivo do estudo é avaliar a relação entre proteinúria e hipertensão arterial sistêmica em cães com hiperadrenocorticismo e verificar, pela avaliação da albuminúria e do peso molecular das proteínas urinárias, o segmento do néfron que foi comprometido ou lesado. Foram avaliados 30 cães com diagnóstico de hiperadrenocorticismo, subdivididos em 13 cães com hipertensão arterial sistêmica (grupo I) e 17 cães normotensos (grupo II). Foram determinados a razão proteína:creatinina urinária (RPC); a albuminúria pela avaliação da albumina normalizada e razão albumina: creatinina urinária (RAC) e a eletroforese de proteínas pela técnica em gel de poliacrilamida, contendo dodecil sulfato de sódio (SDS - PAGE). Os resultados foram comparados com os dados obtidos de 30 cães clinicamente saudáveis e foi constatado que não houve influência da hipertensão arterial sistêmica nos cães com hiperadrenocorticismo em relação à quantificação da albuminúria, determinada pelo método ELISA, e nem na qualidade e quantidade das bandas de proteínas de baixo (< 60 kDa) e de alto peso molecular (> 60 kDa) determinada pela eletroforese. No entanto foi determinado que cães com hiperadrenocorticismo podem desenvolver lesões glomerulares e tubulares, caracterizadas pela presença de albuminúria e de proteínas de alto e de baixo pesos moleculares, independentemente da presença de hipertensão arterial sistêmica. Concluindo que os métodos laboratoriais, a eletroforese de proteína urinária em gel de poliacrilaminda associada à avaliação quantitativa da proteína total, como a determinação quantitativa da albuminúria, são passíveis de serem empregadas para a avaliação dos segmentos dos néfrons comprometidos que causaram as perdas de proteínas na urina. / Hyperadrenocorticism is a common endocrinopathie in dogs characterized by excessive glucocorticoid expousure secondary to adrenal secretion. Chronic hypercortisolemia may promote several complications, including sistemic hypertension and glomerulonephritis. Glomerulonephritis may lead to different proteinuria degrees and chronic renal disease. Urine protein loss, specially albumin, is characteristic in glomerular diseases. Laboratorial determination by the urinary protein/creatinin ratio (PCR), albuminuria (ELISA test) and urinary protein electrophoresis are recommended for diagnosis. The aim of this study is to evaluate the relationship between proteinuria and sistemic arterial hypertension in dogs with hyperadrenocorticism and to identify the nephron injured segment by evaluating albuminuria and urinary protein molecular weight. Thrithy dogs with hyperadrenocorticism were subdivided in 2 groups as following: 13 dogs with sistemic arterial hypertension (group I) and 17 normal dogs (group II). Urinary protein/creatinin ratio (PCR); albuminuria using the evaluation of normalized albumin and urinary albumin/creatinin ratio (ACR); and protein electrophoresis using polyacrylamide gel with sodium dodecil sulfate (SDS - PAGE) were performed. Results were compared with data of 30 clinically healthy dogs. No influence of sistemic arterial hypertension in dogs with hyperadrenocorticism was noticed in albuminuria magnitude using the ELISA method, nor in the quality and quantity of low (<60 kDa) and high (> 60 kDa) molecular weight bands observed in electrophoresis. However, dogs with hyperadrenocorticism can develop glomerular and tubular lesions, characterized by albuminuria and by the presence of high and low molecular weight proteins in urine independently of sistemic arterial hypertension. Furthermore, urinary protein electrophoresis in polyacrylaminde gel associated to quantitative evaluation of total protein such as the quantitative determination of the albuminuria, may be used in evaluating committed nephrons segments that caused urine protein loss.

As enfermidades endócrinas, notadamente o hiperadrenocorticismo, têm grande importância dentre os quadros mórbidos que acometem a espécie canina. A produção excessiva de ACTH pode, nas adrenais, estimular o aumento não só de glicocorticóides, mas também de hormônios sexuais. Os objetivos do presente estudo foram: avaliar as concentrações séricas dos hormônios esteroidais sexuais (progesterona, 17-hidroxiprogesterona, testosterona e androstenediona), em cães com hiperadrenocorticismo de decurso natural (não iatrogênico) e em cães hígidos; e correlacionar as alterações do perfil esteroidal sexual em cães com hiperadrenocorticismo às manifestações clínicas tegumentares e sistêmicas. Foram utilizados 14 cães com hiperadrenocorticismo endógeno e 15 cães hígidos, os quais compuseram o Grupo controle. O Grupo 1 (animais com hiperadrenocorticismo) foi submetido às determinações bioquímicas, hematimétricas, exame de urina, ultra- sonografia abdominal e ao teste de supressão com dexametasona em dose baixa com colheita basal e oito horas após supressão. Tanto os animais doentes (Grupo 1) quanto aqueles hígidos do (Grupo 2) foram submetidos ao teste de estimulação com ACTH com determinação dos esteróides sexuais no momento zero e após uma hora da administração do fármaco. Os achados mais freqüentes nos animais doentes foram: polidpsia, poliúria, polifagia, cansaço fácil, intolerância ao exercício, abdômen abaulado, hepatomegalia e alterações dermatológicas. As alterações laboratoriais encontradas nos cães com hiperadrenocorticismo foram: hiperfosfatasemia alcalina, hipertrigliceridemia, hipercolesterolemia, leucocitose por neutrofilia, linfopenia, eosinofilia, monocitose, hipercortisolismo basal e após supressão com dexametasona. No exame de urina evidenciou-se hipostenúria, bacteriúria e glicosúria. Na ultra- sonografia, adrenomegalia e hepatomegalia foram os achados mais freqüentes. As determinações dos esteróides sexuais foram realizadas nos dois grupos e os valores detectados nos animais hígidos serviram de comparação com aqueles enfermos onde foram observados, no momento basal, aumentos de testosterona (três cães) e 17-hidroxiprogesterona (um cão). Após o estímulo com ACTH observou-se aumento da testosteronemia em três cães, da 17-OHP em cinco animais e em um hiperprogesteronemia. / The endocrine disorders, especially hyperadrenocorticism, has notorious importance among all the diseases that affect the canine species. The high production of ACTH can stimulate the adrenals to produce highly amount of glicocorticoid and sexual hormones. The aim of this study were: determine the serum concentration of sexual hormones (progesterone, 17-hydroxyprogesterone, testosterone and androstenedione) in dogs with natural hyperadrenocorticism (not iatrogenic) and in health dogs, and correlate the alterations between sexual steroids in dogs with hyperadrenocorticism and the clinical manifestations of skin and systemic. It was selected 14 dogs with natural hyperadrenocorticism and 15 healthy dogs that were the control group. The group 1 (dogs with hyperadrenocorticism) were submitted to bioquimical determination, CBC, urine test, abdominal ultrasonography and the low dose of dexamethasone suppression test, with two gather, basal and eight hours after use of dexamethasone. Both Group 1 and 2 were submitted to ACTH stimulation test with determination of sexual steroids at first moment (zero moment) and after one hour of ACTH. The most often find on group 1 (dogs with hyperadrenocorticism) were: polydpsia, polyuria, polyphagia, high exhaustion exercise intolerance, pot belly abdomen, hepatomegaly and the dermatologic alterations. The laboratorial alterations on Group 1 were: high alkaline phosphatase, high triglycerides, high cholesterol, leukocytosis, neutrofilia, linfopenia, eosinofilia, monocytosis, high basal cortisol and after suppression with dexamethasone. At the urine test hypostenuria, high prevalence of bacteria and glicosúria. At ultrasonography adrenomegaly and hepatomegaly were most frequently finds. The sexual steroids rating were done in both groups and the results of healthy dogs (Group 2) were used of reference values of comparison with sickness dogs (Group 1), at zero moment were seen the rise of values of testosterone (tree dogs) and 17-hydroxyprogesterone (one dog). After stimulations of ACTH were seen the rise of testosterone on tree dogs, the 17-hydroxyprogesterone in five dogs e the progesterone in one dog.

As enfermidades endócrinas, notadamente o hiperadrenocorticismo, têm grande importância dentre os quadros mórbidos que acometem a espécie canina. A produção excessiva de ACTH pode, nas adrenais, estimular o aumento não só de glicocorticóides, mas também de hormônios sexuais. Os objetivos do presente estudo foram: avaliar as concentrações séricas dos hormônios esteroidais sexuais (progesterona, 17-hidroxiprogesterona, testosterona e androstenediona), em cães com hiperadrenocorticismo de decurso natural (não iatrogênico) e em cães hígidos; e correlacionar as alterações do perfil esteroidal sexual em cães com hiperadrenocorticismo às manifestações clínicas tegumentares e sistêmicas. Foram utilizados 14 cães com hiperadrenocorticismo endógeno e 15 cães hígidos, os quais compuseram o Grupo controle. O Grupo 1 (animais com hiperadrenocorticismo) foi submetido às determinações bioquímicas, hematimétricas, exame de urina, ultra- sonografia abdominal e ao teste de supressão com dexametasona em dose baixa com colheita basal e oito horas após supressão. Tanto os animais doentes (Grupo 1) quanto aqueles hígidos do (Grupo 2) foram submetidos ao teste de estimulação com ACTH com determinação dos esteróides sexuais no momento zero e após uma hora da administração do fármaco. Os achados mais freqüentes nos animais doentes foram: polidpsia, poliúria, polifagia, cansaço fácil, intolerância ao exercício, abdômen abaulado, hepatomegalia e alterações dermatológicas. As alterações laboratoriais encontradas nos cães com hiperadrenocorticismo foram: hiperfosfatasemia alcalina, hipertrigliceridemia, hipercolesterolemia, leucocitose por neutrofilia, linfopenia, eosinofilia, monocitose, hipercortisolismo basal e após supressão com dexametasona. No exame de urina evidenciou-se hipostenúria, bacteriúria e glicosúria. Na ultra- sonografia, adrenomegalia e hepatomegalia foram os achados mais freqüentes. As determinações dos esteróides sexuais foram realizadas nos dois grupos e os valores detectados nos animais hígidos serviram de comparação com aqueles enfermos onde foram observados, no momento basal, aumentos de testosterona (três cães) e 17-hidroxiprogesterona (um cão). Após o estímulo com ACTH observou-se aumento da testosteronemia em três cães, da 17-OHP em cinco animais e em um hiperprogesteronemia. / The endocrine disorders, especially hyperadrenocorticism, has notorious importance among all the diseases that affect the canine species. The high production of ACTH can stimulate the adrenals to produce highly amount of glicocorticoid and sexual hormones. The aim of this study were: determine the serum concentration of sexual hormones (progesterone, 17-hydroxyprogesterone, testosterone and androstenedione) in dogs with natural hyperadrenocorticism (not iatrogenic) and in health dogs, and correlate the alterations between sexual steroids in dogs with hyperadrenocorticism and the clinical manifestations of skin and systemic. It was selected 14 dogs with natural hyperadrenocorticism and 15 healthy dogs that were the control group. The group 1 (dogs with hyperadrenocorticism) were submitted to bioquimical determination, CBC, urine test, abdominal ultrasonography and the low dose of dexamethasone suppression test, with two gather, basal and eight hours after use of dexamethasone. Both Group 1 and 2 were submitted to ACTH stimulation test with determination of sexual steroids at first moment (zero moment) and after one hour of ACTH. The most often find on group 1 (dogs with hyperadrenocorticism) were: polydpsia, polyuria, polyphagia, high exhaustion exercise intolerance, pot belly abdomen, hepatomegaly and the dermatologic alterations. The laboratorial alterations on Group 1 were: high alkaline phosphatase, high triglycerides, high cholesterol, leukocytosis, neutrofilia, linfopenia, eosinofilia, monocytosis, high basal cortisol and after suppression with dexamethasone. At the urine test hypostenuria, high prevalence of bacteria and glicosúria. At ultrasonography adrenomegaly and hepatomegaly were most frequently finds. The sexual steroids rating were done in both groups and the results of healthy dogs (Group 2) were used of reference values of comparison with sickness dogs (Group 1), at zero moment were seen the rise of values of testosterone (tree dogs) and 17-hydroxyprogesterone (one dog). After stimulations of ACTH were seen the rise of testosterone on tree dogs, the 17-hydroxyprogesterone in five dogs e the progesterone in one dog.

Trilostane is a synthetic steroid analog used to treat canine hyperadrenocorticism. For small dogs, the dose found in commercially available dosage forms of trilostane is sometimes too high. Compounding trilostane in a liquid diluent provides an option for more precise dosing and adjustments, and can be easier to administer, versus a tablet or capsule. Trilostane suspends well in cod liver oil, which is generally palatable to dogs. The stability of a compounded trilostane suspension in cod liver oil stored at room temperature was investigated for 90 days. Compounded trilostane retained stability, defined as maintaining 90–105% labeled value, for 60 days when stored in amber glass bottles. However, drug potency fell >10% below the labeled value when stored in amber plastic bottles after 7 days.

Cette étude avait comme objectif d’évaluer la coagulation par l’utilisation de la thrombélastographie (TEG®) et de la génération de thrombine (GT) chez des beagles en santé recevant de la prednisone ainsi que chez des chiens atteints d’hyperadrénocorticisme (HAC). Dans un premier temps, six beagles adultes en santé ont été évalués dans une étude prospective longitudinale au courant de laquelle chaque individu recevait 1 mg/kg/jour de prednisone par la voie orale pendant 2 semaines. Après un arrêt de traitement d’une durée de 6 semaines, ils ont finalement reçu 4 mg/kg/jour de prednisone pour encore 2 semaines. Les tracés TEG® et les mesures de la GT ont été obtenus au temps 0, à la fin des 6 semaines d’interruption de traitement, ainsi qu’à la suite des 2 dosages de prednisone. Suite aux 2 traitements avec la prednisone, des résultats significatifs,lorsque comparés aux valeurs de base, ont été obtenus pour la cinétique du caillot (« clot kinetics » ou K), l’angle alpha (α) et l’amplitude maximale (« maximal amplitude » ou MA). La GT avait augmenté de manière significative mais seulement après la dose de 1 mg/kg/jour de prednisone. Dans un deuxième temps, 16 chiens atteints d’HAC ont été évalués avant l’initiation d’un traitement pour leur condition. Quinze chiens ont été évalués par TEG® et 15 par GT. Les données obtenues ont ensuite été comparées aux valeurs normales. L’analyse par TEG® a démontré que 12/15 chiens avaient au moins un paramètre suggérant un état d’hypercoagulabilité. L’analyse par GT a démontré que 4/15 chiens avaient des changements compatibles avec un état d’hypercoagulabilité. Un test t-pairé pour des valeurs de variance inégales a démontré que le groupe de chiens atteints d’HAC avait des tracés hypercoagulables et un potentiel endogène de thrombine (« endogenous thrombin potential » ou ETP) plus élevé, lorsque comparé à la population de référence. / The purpose of this study was to use thrombelastography (TEG®) and thrombin generation (TG) to evaluate coagulation in healthy beagles receiving oral prednisone as well as client-owned dogs diagnosed with hyperadrenocorticism (HAC).Six healthy adult beagles were used in a prospective ongitudinal study whereby all dogs received 1 mg/kg of prednisone orally once daily for two weeks, followed by a 6-week washout period and then 4 mg/kg of prednisone orally once daily for two weeks. TEG® tracings and TG measurements were obtained at baseline, at the end of the washout period and at the end of both corticosteroid trials. Significant results as compared to baseline were obtained for clot kinetics (K), alpha angle (α)and maximum amplitude (MA), with tracings compatible with a hypercoagulable profile following both corticosteroid trials. Thrombin generation resulted in a significant increase in endogenous thrombin potential (ETP) after the 1 mg/kg/day trial only. Secondly, sixteen dogs affected by HAC were evaluated. Fifteen dogs were evaluated by TEG® and 15 dogs were evaluated by TG before treatment and compared to the normal reference values. For the TEG® analysis, 12/15 dogs had at least one parameter that suggested hypercoagulability. A paired t test for values with unequal variance was used to compare the HAC dogs to the healthy dogs and found that HAC dogs have hypercoagulable TEG® tracings. The same results were found when TG was used with the ETP elevated in the HAC dogs. However, when dogs were evaluated individually, only 4/15 had hypercoagulable TG results.

Cette étude avait comme objectif d’évaluer la coagulation par l’utilisation de la thrombélastographie (TEG®) et de la génération de thrombine (GT) chez des beagles en santé recevant de la prednisone ainsi que chez des chiens atteints d’hyperadrénocorticisme (HAC). Dans un premier temps, six beagles adultes en santé ont été évalués dans une étude prospective longitudinale au courant de laquelle chaque individu recevait 1 mg/kg/jour de prednisone par la voie orale pendant 2 semaines. Après un arrêt de traitement d’une durée de 6 semaines, ils ont finalement reçu 4 mg/kg/jour de prednisone pour encore 2 semaines. Les tracés TEG® et les mesures de la GT ont été obtenus au temps 0, à la fin des 6 semaines d’interruption de traitement, ainsi qu’à la suite des 2 dosages de prednisone. Suite aux 2 traitements avec la prednisone, des résultats significatifs,lorsque comparés aux valeurs de base, ont été obtenus pour la cinétique du caillot (« clot kinetics » ou K), l’angle alpha (α) et l’amplitude maximale (« maximal amplitude » ou MA). La GT avait augmenté de manière significative mais seulement après la dose de 1 mg/kg/jour de prednisone. Dans un deuxième temps, 16 chiens atteints d’HAC ont été évalués avant l’initiation d’un traitement pour leur condition. Quinze chiens ont été évalués par TEG® et 15 par GT. Les données obtenues ont ensuite été comparées aux valeurs normales. L’analyse par TEG® a démontré que 12/15 chiens avaient au moins un paramètre suggérant un état d’hypercoagulabilité. L’analyse par GT a démontré que 4/15 chiens avaient des changements compatibles avec un état d’hypercoagulabilité. Un test t-pairé pour des valeurs de variance inégales a démontré que le groupe de chiens atteints d’HAC avait des tracés hypercoagulables et un potentiel endogène de thrombine (« endogenous thrombin potential » ou ETP) plus élevé, lorsque comparé à la population de référence. / The purpose of this study was to use thrombelastography (TEG®) and thrombin generation (TG) to evaluate coagulation in healthy beagles receiving oral prednisone as well as client-owned dogs diagnosed with hyperadrenocorticism (HAC).Six healthy adult beagles were used in a prospective ongitudinal study whereby all dogs received 1 mg/kg of prednisone orally once daily for two weeks, followed by a 6-week washout period and then 4 mg/kg of prednisone orally once daily for two weeks. TEG® tracings and TG measurements were obtained at baseline, at the end of the washout period and at the end of both corticosteroid trials. Significant results as compared to baseline were obtained for clot kinetics (K), alpha angle (α)and maximum amplitude (MA), with tracings compatible with a hypercoagulable profile following both corticosteroid trials. Thrombin generation resulted in a significant increase in endogenous thrombin potential (ETP) after the 1 mg/kg/day trial only. Secondly, sixteen dogs affected by HAC were evaluated. Fifteen dogs were evaluated by TEG® and 15 dogs were evaluated by TG before treatment and compared to the normal reference values. For the TEG® analysis, 12/15 dogs had at least one parameter that suggested hypercoagulability. A paired t test for values with unequal variance was used to compare the HAC dogs to the healthy dogs and found that HAC dogs have hypercoagulable TEG® tracings. The same results were found when TG was used with the ETP elevated in the HAC dogs. However, when dogs were evaluated individually, only 4/15 had hypercoagulable TG results.