Dynamic adrenal function testing in eight dogs with hyperadrenocorticism associated with adrenocortical neoplasia.

The results of adrenocorticotropin (ACTH) stimulation and low-dose dexamethasone suppression tests (LDDST) were evaluated retrospectively in eight dogs with clinical signs of hyperadrenocorticism arising from functional adrenocortical tumours, and compared with the results from 12 dogs with confirmed pituitary-dependent hyperadrenocorticism (PDH). The post-ACTH cortisol concentration in the dogs with adrenocortical tumours ranged from 61 to 345-6 nmol/litre (median 251.5 nmol/litre) and they were within the reference range (150 to 450 nmol/litre) in five and unexpectedly low (< 150 nmol/litre) in three dogs. Both the basal and post-ACTH cortisol concentrations were significantly lower in the dogs with adrenocortical neoplasia than in the dogs with PDH. Eight hours after the LDDST, only two of six dogs with adrenocortical tumours had a cortisol concentration above 30 nmol/litre, and the median resting, three, and eight-hour cortisol concentrations were 31.5, 23.0, and 22.7 nmol/litre respectively. There was no significant cortisol suppression during the LDDST, although interpretation was complicated by the low cortisol concentrations, but two dogs showed a pattern of apparent suppression. Two dogs with adrenal tumours showed a diagnostically significant increase in 17-OH-progesterone concentration in response to ACTH although their cortisol concentrations did not increase greatly. These results differ from previous reports of the response of functional adrenal tumours to dynamic endocrine tests.     

Effects of administration of glucocorticoids and feeding status on plasma leptin concentrations in dogs

OBJECTIVE: To investigate effects of short- and long- term administration of glucocorticoids, feeding status, and serum concentrations of insulin and cortisol on plasma leptin concentrations in dogs. ANIMALS: 20 nonobese dogs. PROCEDURE: For experiment 1, plasma leptin concentrations and serum concentrations of insulin and cortisol were monitored for 24 hours in 4 dogs administered dexamethasone (0.1 mg/kg, IV) or saline (0.9% NaCl) solution for fed and nonfed conditions. For experiment 2, 11 dogs were administered prednisolone (1 mg/kg, PO, q 24 h for 56 days [7 dogs] and 2 mg/kg, PO, q 24 h for 28 days [4 dogs]) and 5 dogs served as control dogs. Plasma leptin and serum insulin concentrations were monitored weekly. RESULTS: For experiment 1, dexamethasone injection with the fed condition drastically increased plasma leptin concentrations. Furthermore, injection of saline solution with the fed condition increased plasma leptin concentrations. These increases in plasma leptin concentrations correlated with increases in serum insulin concentrations. Dexamethasone injection with the nonfed condition increased plasma leptin concentrations slightly but continuously. Injection of saline solution with the nonfed condition did not alter plasma leptin concentrations. For experiment 2, prednisolone administration at either dosage and duration did not alter plasma leptin concentrations in any dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Dexamethasone injection and feeding increased plasma leptin concentrations in dogs. In addition, dexamethasone administration enhanced the effect of feeding on increases in plasma leptin concentrations. Daily oral administration of prednisolone (1 or 2 mg/kg) did not affect plasma leptin concentrations in dogs.     

The use of 17-hydroxyprogesterone in the diagnosis of canine hyperadrenocorticism

A number of dogs are seen with clinical signs consistent with hyperadrenocorticism (HAC), supporting CBC and biochemical findings, but the disease cannot be confirmed with either the ACTH stimulation test or the low-dose dexamethasone suppression test (LDDST). Therefore, another screening test is required to aid diagnosis in these atypical cases of HAC. The aim of this study was to investigate whether measuring 17-hydroxyprogesterone (OHP) concentrations could be used in this role. Plasma cortisol and OHP concentrations were measured in dogs with clinical signs suggestive of HAC before and after administration of exogenous ACTH. In dogs with HAC, plasma OHP showed an exaggerated response to ACTH stimulation. This was seen in both typical cases of HAC with a positive cortisol response to ACTH administration and in atypical cases with negative screening test results. The test can be performed on plasma already taken for a conventional ACTH stimulation test. Post-ACTH OHP concentrations decreased after treatment with mitotane or adrenalectomy. These results suggest that OHP measurements can be used as an aid to diagnose and manage canine HAC.     

Effects of single intravenous doses of dexamethasone on baseline plasma cortisol concentrations and responses to synthetic ACTH in healthy dogs

The duration of adrenocortical suppression resulting from a single IV dose of dexamethasone or dexamethasone sodium phosphate was determined in dogs. At 0800 hours, 5 groups of dogs (n = 4/group) were treated with 0.01 or 0.1 mg of either agent/kg of body weight or saline solution (controls). Plasma cortisol concentrations were significantly (P less than 0.01) depressed in dogs given either dose of dexamethasone or dexamethasone sodium phosphate by posttreatment hour (PTH) 2 and concentrations remained suppressed for at least 16 hours. However, by PTH 24, plasma cortisol concentrations in all dogs, except those given 0.1 mg of dexamethasone/kg, returned to control values. Adrenocortical suppression was evident in dogs given 0.1 mg of dexamethasone/kg for up to 32 hours. The effect of dexamethasone pretreatment on the adrenocortical response to ACTH was studied in the same dogs 2 weeks later. Two groups of dogs (n = 10/group) were tested with 1 microgram of synthetic ACTH/kg given at 1000 hours or 1400 hours. One week later, half of the dogs in each group were given 0.01 mg of dexamethasone/kg at 0600 hours, whereas the remaining dogs were given 0.1 mg of dexamethasone/kg. The ACTH response test was then repeated so that the interval between dexamethasone treatment and ACTH injection was 4 hours (ACTH given at 1000 hours) or 8 hours (ACTH given at 1400 hours). Base-line plasma cortisol concentrations were reduced in all dogs given dexamethasone 4 or 8 hours previously.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of long-term phenobarbital treatment on the thyroid and adrenal axis and adrenal function tests in dogs

Phenobarbital can interfere with the thyroid axis in human beings and rats by accelerating hepatic thyroxine metabolism because of enzyme induction. In human beings, it also can interfere with the low-dose dexamethasone suppression test (LDDST) used to assess adrenal function by accelerating dexamethasone metabolism. This effect can cause a lack of suppression of pituitary ACTH and subsequent adrenal cortisol release after dexamethasone administration. The effects of phenobarbital on the thyroid axis, the adrenal axis, and adrenal function tests were prospectively investigated in 12 normal, adult dogs. Phenobarbital was administered at 5 mg per kilogram of body weight (range, 4.8–6.6 mg/kg) PO q12h for 29 weeks, resulting in therapeutic serum concentrations (20–40 μg/mL). Serum total thyroxine (TT4), free thyroxine (FT4) by equilibrium dialysis, total triiodothyronine (TT3), thyrotropin (TSH), and cholesterol were determined before and during phenobarbital treatment. LDDST, ACTH stimulation tests, and ultra-sonographic evaluation of the adrenal glands were performed before and during treatment. TT4 and FT4 decreased significantly ( P ≤ .05), TT3 had minimal fluctuation, TSH had only a delayed compensatory increase, and cholesterol increased during phenobarbital treatment. The delayed increase in TSH, despite persistent hypothyroxinemia, suggests that accelerated hepatic thyroxine elimination may not be the only effect of phenobarbital on the thyroid axis. There was no significant effect of phenobarbital on either of the adrenal function tests. With the methods employed, we did not find any effects of the drug on the hormonal equilibrium of the adrenal axis.     

Effects of single intravenously administered doses of dexamethasone on response to the adrenocorticotropic hormone stimulation test in dogs

The effects of single IV administered doses of dexamethasone on response to the adrenocorticotropic hormone (ACTH) stimulation test (baseline plasma ACTH, pre-ACTH cortisol, and post-ACTH cortisol concentrations) performed 1, 2, and 3 days (experiment 1) or 3, 7, 10, and 14 days (experiment 2) after dexamethasone treatment were evaluated in healthy Beagles. In experiment 1, ACTH stimulation tests were carried out after administration of 0, 0.01, 0.1, 1, and 5 mg of dexamethasone/kg of body weight. Dosages greater than or equal to 0.1 mg of dexamethasone/kg decreased pre-ACTH plasma cortisol concentration on subsequent days, whereas dosages greater than or equal to 1 mg/kg also decreased plasma ACTH concentration. Treatment with 1 or 5 mg of dexamethasone/kg suppressed (P less than 0.05) post-ACTH plasma cortisol concentration (on day 3 after 1 mg of dexamethasone/kg; on days 1, 2, and 3 after 5 mg of dexamethasone/kg). In experiment 2, IV administration of 1 mg of dexamethasone/kg was associated only with low (P less than 0.05) post-ACTH plasma cortisol concentration in dogs on day 3. In experiment 2, pre-ACTH plasma cortisol and ACTH concentrations in dogs on days 3, 7, 10, and 14 and post-ACTH plasma cortisol concentration on days 7, 10, and 14 were not affected by dexamethasone administration. The results suggest that, in dogs, a single IV administered dosage of greater than or equal to 0.1 mg of dexamethasone/kg can alter the results of the ACTH stimulation test for at least 3 days. The suppressive effect of dexamethasone is dose dependent and is not apparent 7 days after treatment with 1 mg of dexamethasone/kg.(ABSTRACT TRUNCATED AT 250 WORDS)     

Determination of thyroxine, triiodothyronine, and cortisol changes during simultaneous adrenal and thyroid function tests in healthy dogs

Changes in thyroxine (T4), triiodothyronine (T3), and cortisol during a combined adrenal (dexamethasone suppression/adrenocorticotrophic hormone response test) and thyroid function tests (thyroid-stimulating hormone [TSH] response test) were determined in 20 healthy hospitalized pet dogs. The effect of dexamethasone on T4 and T3 changes was evaluated during a simultaneous TSH response/dexamethasone suppression adrenocorticotrophic hormone response test. Greater ranges in basal cortisol concentrations and slower changes after dexamethasone was administered were observed in healthy pet dogs kenneled in a hospital setting than those reported for conditioned laboratory dogs. Pet dogs were observed to demonstrate cortisol suppression more reliably at 4 hours than at 2 hours after dexamethasone was administered. Dexamethasone had no effect on the response to TSH as assessed by T4 and T3 assays, thus supporting the validity of combining adrenal and thyroid response tests in a 5-hour period.     

Evaluation of a focused assessment with sonography for trauma protocol to detect free abdominal fluid in dogs involved in motor vehicle accidents

OBJECTIVE: To establish a focused assessment with sonography for trauma (FAST) protocol in dogs, determine whether FAST can be performed by veterinary clinicians without extensive ultrasonographic experience, and assess the frequency of free fluid (as determined via FAST) in the abdominal cavity of dogs following motor vehicle accidents (MVAs). DESIGN: Prospective study. ANIMALS: 100 client-owned dogs evaluated within 24 hours of an MVA. PROCEDURE: Dogs were placed in lateral recumbency for the FAST examination. To detect fluid in the abdomen, 2 ultrasonographic views (transverse and longitudinal) were obtained at each of 4 sites (just caudal to the xiphoid process, on the midline over the urinary bladder, and at the left and right flank regions). RESULTS: In the 100 dogs evaluated via FAST, free abdominal fluid was detected in 45 dogs. In 40 of those 45 dogs, abdominocentesis was performed; hemoperitoneum and uroperitoneum were diagnosed in 38 and 2 dogs, respectively. Compared with dogs that had no free abdominal fluid detected via FAST, dogs that had free abdominal fluid detected via FAST had significantly higher heart rates and serum lactate concentrations and significantly lower PCVs and total solid concentrations. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate that FAST is a simple and rapid technique that can be performed on dogs in an emergency setting to detect intra-abdominal free fluid and can be performed by veterinary clinicians with minimal previous ultrasonographic experience.     

Effect of low doses of cosyntropin on serum cortisol concentrations in clinically normal dogs

OBJECTIVE: To determine the lowest of 5 doses of cosyntropin (1.0, 0.5, 0.1, 0.05, or 0.01 microg/kg) administered IV that stimulates maximal cortisol secretion in clinically normal dogs. ANIMALS: 10 clinically normal dogs. PROCEDURES: 5 dose-response experiments were performed in each of the dogs. Each dog received 5 doses of cosyntropin (1.0, 0.5, 0.1, 0.05, and 0.01 microg/kg) IV in random order (2-week interval between each dose). Serum samples for determination of cortisol concentrations were obtained before (baseline) and at 10, 20, 30, 40, 50, 60, 120, and 240 minutes after cosyntropin administration. RESULTS: Compared with baseline values, mean serum cortisol concentration in the study dogs increased significantly after administration of each of the 5 cosyntropin doses. Mean peak serum cortisol concentration was significantly lower after administration of 0.01, 0.05, and 0.1 microg of cosyntropin/kg, compared with findings after administration of 0.5 and 1.0 microg of cosyntropin/kg. After administration of 0.5 and 1.0 microg of cosyntropin/kg, mean peak serum cortisol concentration did not differ significantly; higher doses of cosyntropin resulted in more sustained increases in serum cortisol concentration, and peak response developed after a longer interval. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of cosyntropin IV at a dose of 0.5 microg/kg induced maximal cortisol secretion in healthy dogs. Serum cortisol concentration was reliably increased in all dogs after the administration of each of the 5 doses of cosyntropin. These data should be useful in subsequent studies to evaluate the hypothalamic-pituitary-adrenal axis in healthy and critically ill dogs.     

Comparison of two low-dose dexamethasone suppression protocols as screening and discrimination tests in dogs with hyperadrenocorticism

Two low-dose dexamethasone suppression test protocols were evaluated in 18 dogs with hyperadrenocorticism (14 dogs with pituitary-dependent hyperadrenocorticism [PDH] and 4 dogs with adrenocortical tumor) and in 5 healthy control dogs. Blood was obtained immediately before and 2, 4, 6, and 8 hours after IV administration of either 0.01 mg of dexamethasone sodium phosphate/kg of body weight or 0.015 mg of dexamethasone polyethylene glycol/kg. At 8 hours after dexamethasone administration, 18 of 18 (100%) dogs with hyperadrenocorticism given the sodium phosphate preparation and 16 of 18 (89%) affected dogs given the polyethylene glycol preparation failed to have suppression of plasma cortisol concentration (less than 1.4 micrograms/dl). Plasma cortisol concentration was suppressed to less than 1.4 micrograms/dl at 2, 4, and/or 6 hours after administration of either dexamethasone preparation in 5 of 14 dogs with PDH and to less than 50% of baseline cortisol concentration in 10 of 14 dogs with PDH. Suppression, as identified by these 2 criteria, was not observed at 2, 4, 6, or 8 hours after administration of either dexamethasone preparation in dogs with adrenocortical tumor. For both protocols, the 8-hour plasma cortisol concentration was suppressed to less than 1.4 micrograms/dl and to less than 50% of baseline in the 5 control dogs. Both protocols were comparable for use as screening tests in establishing a diagnosis of hyperadrenocorticism. Suppression of plasma cortisol concentration to less than 50% of baseline (or less than 1.4 micrograms/dl) during the test was consistent with diagnosis of PDH. Failure to have such suppression, however, was observed in dogs with PDH as well as in those with adrenocortical tumor.     

Secretion of sex hormones in dogs with adrenal dysfunction

OBJECTIVE: To evaluate adrenal sex hormone concentrations in response to ACTH stimulation in healthy dogs, dogs with adrenal tumors, and dogs with pituitary-dependent hyperadrenocorticism (PDH). DESIGN: Prospective study. ANIMALS: 11 healthy control dogs, 9 dogs with adrenal-dependent hyperadrenocorticism (adenocarcinoma [ACA] or other tumor); 11 dogs with PDH, and 6 dogs with noncortisol-secreting adrenal tumors (ATs). PROCEDURE: Hyperadrenocorticism was diagnosed on the basis of clinical signs; physical examination findings; and results of ACTH stimulation test, low-dose dexamethasone suppression test, or both. Dogs with noncortisol-secreting ATs did not have hyperadrenocorticism but had ultrasonographic evidence of an AT. Concentrations of cortisol, androstenedione, estradiol, progesterone, testosterone, and 17-hydroxyprogesterone were measured before and 1 hour after i.m. administration of 0.25 mg of synthetic ACTH. RESULTS: All dogs with ACA, 10 dogs with PDH, and 4 dogs with ATs had 1 or more sex hormone concentrations greater than the reference range after ACTH stimulation. The absolute difference for progesterone, 17-hydroxyprogesterone, and testosterone concentrations (value obtained after ACTH administration minus value obtained before ACTH administration) was significantly greater for dogs with ACA, compared with the other 3 groups. The absolute difference for androstenedione was significantly greater for dogs with ACA, compared with dogs with AT and healthy control dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Dogs with ACA secrete increased concentrations of adrenal sex hormones, compared with dogs with PDH, noncortisol-secreting ATs, and healthy dogs. Dogs with noncortisol-secreting ATs also have increased concentrations of sex hormones. There is great interdog variability in sex hormone concentrations in dogs with ACA after stimulation with ACTH.     

Use of a flow-mediated vasodilation technique to assess endothelial function in dogs

OBJECTIVE: To develop and assess the reproducibility of a protocol to noninvasively test endothelial function in dogs on the basis of the flow-mediated vasodilation (FMD) procedure used in humans. ANIMALS: 5 healthy spayed female dogs. PROCEDURES: Luminal arterial diameter and blood flow velocity in the brachial and femoral arteries were measured with ultrasonography. The within-dog reproducibility of these ultrasonographic measurements was tested. An occlusion period of 1, 3, or 5 minutes with an inflatable cuff was used to create the FMD response. Measurements made at 15, 30, and 60 seconds following release of the occlusion were compared with measurements made immediately prior to each occlusion to assess the FMD response. RESULTS: Within-dog reproducibility of measurements revealed moderate to high correlations. Change from baseline in luminal arterial diameter was most substantial when measured at 30 seconds following release of occlusion, whereas blood flow velocity changes were maximal when measured at 15 seconds following release. The brachial imaging site provided a larger number of significant FMD responses than the femoral site. The 3-minute occlusion period provided equal or better responses than the 5-minute occlusion period. CONCLUSIONS AND CLINICAL RELEVANCE: Ultrasonographic measurement of the FMD responses was a feasible and reproducible technique and significant changes from baseline were detected. The FMD responses in dogs were most substantial when performed at the brachial artery with blood flow velocity and luminal arterial diameter changes from baseline measured at 15 and 30 seconds, respectively, following release of a 3-minute occlusion period.     

Adrenocortical suppression associated with topical otic administration of glucocorticoids in dogs

Commercial otic preparations that contained dexamethasone or triamcinolone acetate were applied twice daily to both ears of 2 groups of dogs (n = 8). Marked adrenocortical suppression, reflected by low serum cortisol concentrations, was observed in all dogs. Results of ACTH response tests were blunted after 7 days of treatment. Twenty-one days after treatment, serum cortisol concentrations still were suppressed in all dogs, compared with pretreatment control concentrations. Fourteen days after cessation of otic treatment, 5 of 8 dogs still had inadequate release of cortisol in response to ACTH.     

Effects of exercise-induced stress and dexamethasone on plasma hormone and glucose concentrations and sedation in dogs treated with dexmedetomidine

OBJECTIVE: To compare the effects of pretreatment with dexamethasone, physical stress (exercise), or both on sedation and plasma hormone and glucose concentrations in dogs treated with dexmedetomidine (DEX). ANIMALS: 6 healthy purpose-bred Beagles. PROCEDURE: Dogs received 4 treatments each in a randomized order prior to i.v. administration of DEX (5 fLg/kg). Pretreatments were as follows: (1) i.v. administration of saline (0.9% NaCI) solution and no exercise (control group); (2) IV administration of dexamethasone (0.05 mg/kg) and no exercise (DM group); (3) i.v. administration of saline solution and exercise (EX group; 15 minutes of trotting on a treadmill at a speed of 2 m/s); and (4) i.v. administration of dexamethasone and exercise (DM+EX group). RESULTS: Following DEX administration, all dogs had similar times to recumbency and sedation index values, irrespective of pretreatment with values, irrespective of pretreatment with dexam-d ethasone or exercise. Plasma catecholamine concentrations decreased after DEX administration. Compared with control group dogs, plasma cortisol concentrations were higher in EX-group dogs prior to DEX administration and lower in DM- and DM+EX-group dogs following DEX administration. Administration of DEX decreased plasma cortisol concentration in EX-group dogs only. Plasma glucose concentration was not influenced by exercise or dexamethasone administration was lower than baseline concentrations at 30 minutes after DEX administration and returned to baseline values by 90 minutes. Heart and respiratory rates and rectal temperature increased during exercise. After DEX administration, these values decreased below baseline values. The decrease in heart rate was of shorter duration in dogs that underwent pretreatment with dexamethasone, exercise, or both than in control group dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Pretreatment with dexamethasone, moderate physical stress (exercise), or both did not influence sedation or cause adverse effects in healthy dogs treated with DEX.     

Measurement of Faecal Cortisol Metabolites in Cats and Dogs: A Non-invasive Method for Evaluating Adrenocortical Function

The aim of this comparative study was to gain more information about the metabolism and excretion of glucocorticoids in cats and dogs in order to establish non-invasive methods for evaluating stressful conditions. Therefore, in a first experiment, [¹⁴C]cortisol was administered intravenously to 8 animals (two of each sex and species). Over a period of 6 days, faeces and urine were collected immediately after spontaneous defecation and urination. Marked species differences were found, as cats mainly excreted cortisol in the faeces (82%±4% of the total recovered radioactivity), whereas in dogs only a small portion was found there (23%±4%). The highest urinary radioactivity was observed after 9±3 h in cats and 3±1 h in dogs. Peak concentrations in the faeces occurred after 22±6 h in cats and after 24±4 h in dogs. Most of the radioactivity was not extractable with diethyl ether, indicating that the metabolites excreted in urine and faeces were mainly of the conjugated or polar unconjugated types. This was confirmed by RP-HPLC, which also revealed marked differences between cats and dogs concerning the metabolites formed. In addition, the immunoreactivity of the metabolites was tested in cortisol, corticosterone and 11-oxoaetiocholanolone EIAs. The latter, measuring 11,17-dioxoandrostanes (11,17-DOA) detected the highest quantities of immunoreactive metabolites in cats, but not in dogs. In a second experiment, the adrenal cortex of both species was stimulated by ACTH and, three weeks later, suppressed by dexamethasone. In this study, only faeces were collected over a period of 7 days. In both species, inter-animal variability in the basal and maximal/minimal faecal cortisol metabolite concentrations and the time course was observed. The 11-oxoaetiocholanolone EIA in cats and the cortisol EIA in dogs proved best suited for monitoring changes in adrenocortical activity. ACTH injections resulted in an increase above baseline values of 355% (median) in 11,17-DOA concentrations in cats and of 702% in the concentrations of cortisol equivalents in dogs by about 25 h and 22 h (median) after injection, respectively. Minimal concentrations after dexamethasone administration were about 17% in cats and 31% in dogs (in relation to baseline values) and were reached in 66 h and 72 h, respectively. It was concluded that measuring cortisol metabolites in faeces should be a useful non-invasive tool for monitoring stress in carnivores.     

Effects of low dosages of intravenous dexamethasone on serum cortisol concentrations in the normal cat

The suppressive effects of three different low dosages of dexamethasone (5, 10 and 15 micrograms kg-1) on serum cortisol concentrations were evaluated in 10 normal cats. On four different days, serum was collected before and at two, four, six and eight hours after the intravenous administration of saline or dexamethasone. Following the administration of saline, no significant difference in mean serum cortisol concentrations was noted between the basal or postinjection values. In contrast, mean serum cortisol concentrations decreased significantly (P less than 0.05) by two hours and remained significantly below mean basal values eight hours after injection of all three dosages of dexamethasone. The degree of cortisol suppression became progressively greater as the dosages of dexamethasone were increased. After administration of the highest dose of dexamethasone (15 micrograms kg-1), serum cortisol decreased to below 5 ng ml-1 by two to four hours and remained suppressed (under 5 ng ml-1) eight hours after injection in all cats. In contrast, two of the 10 cats showed a slight escape from cortisol suppression by eight hours after injection of dexamethasone at the dosage of 10 micrograms kg-1, whereas a dosage of 5 micrograms kg-1 failed to suppress cortisol concentrations below 10 ng ml-1 at any of the sampling times in one cat and was associated with increasing serum cortisol concentrations at eight hours after injection in three cats.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of multiple intramuscular injections and doses of dexamethasone on plasma cortisol concentrations and adrenal responses to ACTH in horses

Adrenocortical function was assessed in horses given multiple IM doses of dexamethasone to determine the duration of adrenocortical suppression and insufficiency caused by 2 commonly used dosages of dexamethasone (0.044 and 0.088 mg/kg of body weight). Dexamethasone was administered at 5-day intervals for a total of 6 injections. Daily blood samples were collected. The plasma was frozen and later assayed for cortisol. An ACTH response test was determined 2 days before the first injection of dexamethasone and again 8 days after the last dexamethasone injection. Maximum suppression of plasma cortisol was observed in horses given both dosages of dexamethasone (0.044 and 0.088 mg/kg). Plasma cortisol concentrations returned to base-line values in all horses by 4 days after dexamethasone injection. Normal ACTH responses observed after 6 dexamethasone injections given at 5-day intervals indicated that measurable adrenal atrophy did not develop under the conditions of this study.     

Canine Hyperadrenocorticism Due to Adrenocortical Neoplasia: Pretreatment Evaluation of 41 Dogs

This retrospective study identifies parameters that might separate dogs with hyperadrenocorticism caused by adrenocortical tumors from dogs with pituitary-dependent hyperadrenocorticism. Further, an attempt was made to identify factors that could separate dogs with adrenocortical adenomas from dogs with carcinomas. The records of 41 dogs with hyperadrenocorticism caused by adrenocortical neoplasia were reviewed. The history, physical examination, urinalysis, hemogram (CBC), chemistry profile adrenocorticotrophic hormone (ACTH) stimulation and low dose dexamethasone test results were typical of the nonspecific diagnosis of hyperadrenocorticism. The preceding information on the 41 dogs with adrenocortical tumors was compared with that from 44 previously diagnosed pituitary-dependent hyperadrenocorticoid dogs. There was no parameter which aided in separating these two groups of dogs. Thirty dogs with adrenocortical tumors were tested with a high-dose dexamethasone test and none had suppressed plasma cortisol concentrations 8 hours after IV administration of 0.1 mg/kg of dexamethasone. In 29 of the 41 adrenal tumor dogs, plasma endogenous ACTH was not detectable on at least one measurement (less than 20 pg/ml). The remaining 12 dogs from this group had nondiagnostic concentrations (20-45 pg/ml). Thirteen of 22 dogs (59%) with adrenocortical carcinomas had adrenal masses identified on abdominal radiographs and seven of 13 dogs (54%) with adrenocortical adenomas had radiographically visible adrenal masses. Thirteen of 17 adrenocortical carcinomas (76%) and five of eight adenomas (62%) were identified with ultrasonography. Radiographs of the thorax and ultrasonography of the abdomen identified most of the dogs (8 of 11) with metastatic lesions.(ABSTRACT TRUNCATED AT 250 WORDS)     

TECHNIQUE FOR ULTRASOUND‐GUIDED INTRAARTICULAR CERVICAL ARTICULAR PROCESS INJECTION IN THE DOG

Ultrasound‐guided intraarticular injection of cervical articular process joints is a well‐established procedure in both humans and horses for neck pain resulting from osteoarthritis, but the technique has not been described in dogs. Aims of this study were to describe the ultrasonographic anatomy and landmarks for cervical articular process joint injections in the dog, develop a technique for articular process joint injections using these landmarks, and determine the accuracy of injections and factors that may influence it. Eleven canine cadavers were used and bilateral joint spaces from C2–3 to C7‐T1 were injected under ultrasound guidance with a blue radiopaque solution. A computed tomographic scan was acquired following each injection, and an injection score was assigned and compared with other patient‐specific factors. Of the 132 injections performed, 110 (83.3%) were intraarticular, 20 (15.1%) were periarticular within 5 mm, and 2 (1.5%) were periarticular beyond 5 mm from the joint. There was no significant difference in mean scores between dogs. Only C2–3 had a significantly lower mean score than any other joint. There was no significant correlation between injection score and any other factors measured. The transverse processes of the cervical vertebrae served as excellent ultrasonographic landmarks for identifying the cervical articular process joints in dogs regardless of the size of the dog or location along the vertebrae. Accuracy of ultrasound‐guided intraarticular process joint injection was 83% in dogs and similar to published techniques in horses. Further studies are needed to examine the safety and efficacy of this procedure in live animals.     

Interpretation of laboratory tests for canine Cushing's syndrome

Hypercortisolism (HC) is a common disease in dogs. This article will review the laboratory tests that are available for diagnosis of HC and laboratory tests for differentiating between causes of HC. An emphasis will be made on the clinical process that leads to the decision to perform those tests and common misconceptions and issues that arise when performing them. To choose between the adrenocorticotropic hormone (ACTH)-stimulation test and the low-dose dexamethasone suppression test (LDDST), the advantages and disadvantages of both tests should be considered, as well as the clinical presentation. If the index of suspicion of HC is high and other diseases have been appropriately ruled out, the specificity of the ACTH stimulation test is reasonably high with an expected high positive predictive value. Because of the low sensitivity, a negative result in the ACTH stimulation test should not be used to rule out the diagnosis of HC. The LDDST is more sensitive but also less specific and affected more by stress. A positive result on the urine cortisol:creatinine ratio does not help to differentiate HC from other diseases. A negative result on the urine cortisol:creatinine ratio indicates that the diagnosis of HC is very unlikely. The LDDST is useful in differentiating pituitary-dependent HC from an adrenal tumor in about two thirds of all dogs with HC. Differentiation of HC from diabetes mellitus, liver diseases, and hypothyroidism cannot be based solely on endocrine tests. Clinical signs, imaging studies, histopathology, and response to treatment should all be considered.