Assessing the immune state of dogs suffering from pituitary gland dependent hyperadrenocorticism by determining changes in peripheral lymphocyte subsets

Abstract

In order to evaluate the immune state of dogs suffering from pituitary-dependent hyperadrenocorticism (PDH), peripheral lymphocyte subsets were examined. Twenty seven PDH dogs and eight healthy control dogs were used in the current study. Eight healthy dogs served as the control group. Twenty seven PDH dogs were categorized into 4 groups based on their post serum cortisol concentrations by ACTH stimulation test: 2-5, excellent control (n = 8); 5-20, fair control (n = 7); >20, poor control (n = 4); and untreated (n = 8). Cell counts were executed with white blood cells (WBC), lymphocytes, CD3(+) (T lymphocytes), CD4(+) (Helper T lymphocytes), CD8(+) (Cytotoxic T lymphocytes), CD21(+) (B lymphocytes) cells in addition to calculating CD4(+)/CD8(+) ratio. Results indicated a significant difference in lymphocyte numbers and lymphocyte subset populations (CD3(+), CD4(+), CD8(+), and CD21(+) cells) between PDH and control dogs. Moreover, comparison of the PDH groups (excellent control; fair control; poor control; untreated) demonstrated that all groups had a significant decrease in lymphocytes numbers (CD3(+), CD4(+) and CD21(+) cell counts) as compared to control group. Meanwhile, no significant differences were observed in WBC counts and CD4(+)/CD8(+) ratio between groups. Furthermore, lymphocyte subset distribution in excellent control PDH dogs without concurrent disease (n = 4) better resembled that of control dogs as compared to PDH dogs with concurrent disease (n = 4). PDH dogs may be suffering from an immuno-depressed state as evidenced by significant differences in lymphocyte subset populations. Furthermore, treatment of both PDH and concurrent disease might improve lymphocyte subset distribution.

Prevalence and impact of cholecystitis on outcome in dogs with gallbladder mucocele

“…Dogs with GBM have a high incidence of concurrent hyperadrenocorticism, hypothyroidism, and hyperlipidemia . These metabolic disturbances cause immune dysregulation in various species and may contribute to the development of, or magnify, cholecystitis (infectious and sterile) in dogs with GBM . Alternatively, it has been suggested that GBMs in dogs may be a consequence of primary chronic cholecystitis .…”

Comparative study of peripheral blood leukocytes in healthy dogs and in dogs with cancer and inflammatory diseases

“…Studies available describe immune status by means of peripheral lymphocyte subsets in dogs with cancer, 6,11,14,17 hyperadrenocorticism, 10 leishmaniosis, 1,9 or ehrlichiosis. 8,16 The data presented in the current study showed that immunophenotype of peripheral blood lymphocytes in diseased dogs may be altered.…”

Characterization and Comparison of Insulin Resistance Induced by Cushing Syndrome or Diestrus against Healthy Control Dogs as Determined by Euglycemic- Hyperinsulinemic Glucose Clamp Profile Glucose Infusion Rate Using an Artificial Pancreas Apparatus

“…Glucocorticoid-induced insulin resistance is mediated by reduced cellular insulin signaling [2,3,11]. A cortisol concentration (after 1 hr ACTH-stimulation) of 2-5 µg/dl, via drug treatment, in CS dogs is considered to be an excellent control state [17]. However, cortisol concentrations, in our 4 dogs suffering from CS, were higher than those of the excellent control level range.…”

“…A cortisol concentration of>20 µg/dl in the sample, obtained 1 hr after ACTH administration, was considered abnormal and consistent with CS. In addition, the adrenal glands were examined using ultrasound (Vivid 7, GE Yokokawa Medical System, Tokyo, Japan), and pituitarydependent hyperadrenocorticism was confirmed on the basis of a bilateral symmetric appearance or bilateral enlargement of the adrenal glands (minor axis; over 6-7 mm) [17]. All CS dogs were treated with trilostane (Adrestane, Kyoritsu Seiyaku Corporation, Tokyo, Japan) or mitotane (Opeprim, Yakuruto Honsha Co., Ltd., Tokyo, Japan) ( Table 1).…”

“…However, cortisol concentrations, in our 4 dogs suffering from CS, were higher than those of the excellent control level range. As such, CS dogs were categorized as a fair control group, taking into account of being under long term treatment [17]. Therefore, we speculate that a major factor fostering insulin resistance, in these dogs, is inadequate glucocorticoid exposure due to inadequate dosage.…”