Systemic hypertension in dogs with hyperadrenocorticismPrevalence, evolution during treatment and influence on survival

  1. Paula García San José
Supervised by:
  1. Carolina Arenas Bermejo Director
  2. María Dolores Pérez Alenza Director

Defence university: Universidad Complutense de Madrid

Year of defence: 2021

  1. Laura Luisa Peña Fernández Chair
  2. Mercedes García-Sancho Téllez Secretary
  3. Yaiza Forcada Committee member
  4. María Luisa Suárez Rey Committee member
  5. Diego Daniel Miceli Committee member
  1. Medicina y Cirugía Animal

Type: Thesis


Canine hyperadrenocorticism (HAC) is one of the most common endocrine diseases in middle aged to old dogs. It is characterized by chronic hypercortisolism, result of an excessive production either of ACTH by a pituitary tumor (pituitary dependent HAC, PDH), or cortisol by an adrenal tumor (adrenal dependent HAC, ADH). Diagnosis is based in the clinical picture, and supported by adrenal function tests. Treatment is focused on the reduction of hypercortisolism either removing the tumour responsible for the disease, or inhibiting the production of cortisol with drugs such as trilostane. In the last years low trilostane doses administered twice daily (0.2-1 mg/kg/12h) have proven to be effective to treat canine HAC. In people with Cushing¿s syndrome (CS), systemic hypertension (SH) is one of the most common complications, which is often persistent even after adequate treatment is provided. Multidrug antihypertensive therapy is commonly needed and SH is associated with higher mortality rates. In dogs with HAC prevalence of SH is also high, but not many studies have focused on SH, its changes during treatment, or its influence on survival. Survival time when using low trilostane doses twice daily has not been studied. Therefore, 4 clinical studies in dogs with HAC were conducted with the aims of describing prevalence and risk factors for SH (clinical study 1), changes in systolic blood pressure (SBP) during the first year of treatment in dogs with PDH (clinical study 2) and ADH (clinical study 3), and survival and prognosis factors using low trilostane doses (clinical study 4). Treatment with trilostane was prescribed at a starting dose of 0.2-1 mg/kg/12h. The clinical study 1 included 66 dogs with HAC, and showed that prevalence of both SH (81%) and severe SH (45%) were high. Higher platelet counts and lower potassium concentrations increased the risk of SH. The relationship between potassium concentrations and SH might suggest a role of an apparent mineralocorticoid excess in the development of SH in dogs with HAC. The clinical study 2 focused on the changes in SBP in 51 dogs with PDH during the first year of trilostane treatment and its relation with disease control, and their response to antihypertensive drugs. Prevalence of SH decreased from 71% at diagnosis (T0) to 46% 12 months after (T12). Multidrug therapy was needed in 50% of the cases to manage SH. Blood pressure was not correlated with the clinical control of the disease, and one third of non-hypertensive dogs at T0 developed SH and required antihypertensive treatment during follow-up. The clinical study 3 evaluated the changes in SBP in 9 dogs with ADH after adrenalectomy or during the first year of trilostane treatment. In dogs with ADH medically treated, prevalence of SH decreased from 100% at T0 to 33% at T12, and in dogs with ADH surgically treated from 67% to 0%. No correlation was observed with the clinical control of the disease, and in most dogs, SH was well managed with a single drug. The clinical study 4 included 91 dogs with PDH treated with trilostane, and 18 dogs with ADH either treated with trilostane or surgically. In dogs with PDH median survival time was 998 days; poor prognosis factors were older age, presence of calcinosis cutis, low body condition score and higher platelet count, but not SH. In dogs with ADH lifelong medical treatment provided a shorter survival time than surgical treatment (237 vs 510 days) and only the presence of pulmonary metastases negatively affected survival. The final trilostane dose was still low both in dogs with PDH and ADH. The results of the present work reinforce the importance of assessing SBP in all dogs with HAC at diagnosis and throughout treatment, regardless of the clinical control of the disease. They also reflect that survival time achieved in dogs with PDH treated with low trilostane doses twice daily is somewhat longer than with other therapeutic protocols, supporting its use.