Monitoring Cortisol Levels During Treatment of Hyperadrenocorticism

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-08-11

Key Takeaways

• The ACTH stimulation test is the gold standard for monitoring trilostane and mitotane therapy, assessing adrenal cortisol reserve by measuring post-stimulation cortisol levels. For trilostane, testing 4-6 hours post-dose is critical to capture peak drug effect, with target post-ACTH cortisol generally between 55-250 nmol/L (2-9 µg/dL).
• Mitotane therapy requires more intensive monitoring due to its adrenocorticolytic mechanism, with an induction phase targeting post-ACTH cortisol of 55-165 nmol/L (2-6 µg/dL) and a maintenance phase requiring periodic ACTH stimulation tests every 3-6 months.
• Basal cortisol measurements are useful adjuncts, particularly for screening for iatrogenic hypoadrenocorticism with trilostane (below 28 nmol/L or 1 µg/dL with clinical signs) or for assessing induction progress with mitotane. However, basal cortisol alone is insufficient for confirming adequate suppression.
• Urine cortisol to creatinine ratio (UCCR) is not recommended for routine monitoring due to high sensitivity to stress and inability to distinguish adequate suppression from over-treatment, making it unsuitable for dose adjustment decisions.
• Clinical signs, such as resolution of polyuria/polydipsia or onset of lethargy/vomiting, are paramount and must be integrated with biochemical monitoring; biochemical targets are secondary to the patient's overall well-being and absence of adverse effects.
• Overtreatment leading to iatrogenic hypoadrenocorticism is the most significant risk, necessitating immediate drug withdrawal and supportive care if post-ACTH cortisol falls below critical thresholds (e.g., < 55 nmol/L or 2 µg/dL for trilostane) or if basal cortisol is critically low with compatible signs.

This article addresses the practical use of serial cortisol measurement to guide medical therapy for canine hyperadrenocorticism (HAC), with emphasis on trilostane and mitotane protocols. The intended reader is the practicing veterinarian who has already established the diagnosis and now needs a structured framework for biochemical monitoring, dose adjustment, and recognition of over-treatment. The clinical questions answered here are: which test to use at which time point, what target ranges define adequate control, how to interpret discordant results, and when to intervene in suspected iatrogenic hypoadrenocorticism.

The scope excludes initial diagnostic testing, including low-dose dexamethasone suppression and baseline ACTH measurement, except where those tests inform monitoring decisions. The evidence base for monitoring protocols derives largely from consensus guidance and pharmacokinetic studies instead of randomized trials, and the clinician should expect to individualize intervals and targets within published frameworks.

At a Glance

Physiologic Basis of Cortisol Monitoring

The hypothalamic-pituitary-adrenal (HPA) axis operates as a closed negative feedback loop. In pituitary-dependent HAC, a functional or structural pituitary lesion drives excess ACTH secretion, which in turn stimulates adrenal cortical production of cortisol. In adrenal-dependent HAC, an adrenal tumor autonomously secretes cortisol, suppressing pituitary ACTH. Both forms result in chronic glucocorticoid excess, and both are treated by suppressing or ablating adrenal cortisol production.

Therapeutic monitoring exploits the axis's feedback sensitivity. Trilostane inhibits 3-beta-hydroxysteroid dehydrogenase, blocking cortisol synthesis at the adrenal level. The drug does not destroy adrenal tissue, and its effect is reversible and duration-limited. Mitotane, by contrast, is adrenocorticolytic, destroying the zona fasciculata and zona reticularis while sparing the zona glomerulosa at appropriate doses. The two drugs therefore demand different monitoring philosophies: trilostane requires assessment of peak drug effect relative to dosing, while mitotane requires assessment of cumulative adrenal destruction.

Cortisol is secreted in a pulsatile pattern with diurnal variation in dogs, although the circadian amplitude is less pronounced than in humans. A single baseline cortisol measurement reflects only a moment in that pulsatile pattern and is poorly correlated with integrated daily cortisol exposure. This limitation underlies the preference for dynamic testing, particularly the ACTH stimulation test, which measures the adrenal's maximal secretory capacity at the time of testing. The test's value in monitoring rests on the assumption that adrenal responsiveness to exogenous ACTH correlates with the degree of HPA suppression or destruction achieved by therapy.

The ACTH Stimulation Test in Monitoring

The ACTH stimulation test remains the standard biochemical monitor for both trilostane and mitotane therapy. The test measures the adrenal cortex's capacity to respond to supraphysiologic ACTH stimulation, providing an integrated assessment of functional adrenal reserve. In treated HAC patients, the post-stimulation cortisol concentration reflects the residual functional capacity of the adrenal cortex after drug-induced suppression or destruction.

For trilostane, the test must be timed to capture the drug's peak effect. Trilostane's duration of action is approximately 8 to 12 hours, and the maximal cortisol suppression occurs 4 to 6 hours after oral administration. Testing at this window assesses whether the dose achieves adequate suppression during the period of greatest drug effect. Testing at other times may overestimate control if performed near the end of the dosing interval, or underestimate it if performed before the drug reaches peak concentration.

The American Society for Veterinary Clinical Pathology provides quality assurance guidance for endocrine testing, including reference interval validation and assay performance standards that apply to cortisol measurements in monitoring protocols. Clinicians should confirm that their laboratory's cortisol assay is validated for canine samples and that the reference intervals used for monitoring targets are appropriate for the specific assay platform. Assay variation between laboratories can shift absolute cortisol values, and monitoring decisions should be made with awareness of the laboratory's established performance characteriztics.

Urine Cortisol to Creatinine Ratio

The urine cortisol to creatinine ratio (UCCR) offers a noninvasive measure of integrated cortisol secretion over the period of urine accumulation, typically 8 to 12 hours for an early morning sample. The test has established utility in initial diagnosis of HAC, where a normal UCCR effectively excludes the disease. Its role in monitoring treated patients is more limited.

The UCCR is highly sensitive to stress. Environmental disturbance, hospitalization, or even the anticipation of sampling can elevate cortisol and produce falsely high ratios. A study of dogs transferred to novel kennels demonstrated that urinary cortisol to creatinine ratios increased significantly upon introduction to the new environment, remained elevated for weeks in non-habituated animals, and showed poor correlation with behavioral indicators of stress. These findings illustrate the test's vulnerability to contextual confounding, a limitation that becomes critical when monitoring therapy where the clinical question is whether cortisol production is adequately suppressed.

For monitoring purposes, the UCCR cannot distinguish between adequate suppression and over-treatment with the precision required for dose adjustment. A low UCCR may reflect appropriate suppression or may signal impending hypoadrenocorticism, and the test does not provide the dynamic information that the ACTH stimulation test offers. The UCCR is therefore not recommended as the primary monitoring tool for treated HAC patients. It may have a role in specific situations where ACTH stimulation testing is impractical, but results must be interpreted with caution and in conjunction with clinical signs.

Hair Cortisol Analysis

Hair cortisol analysis measures cortisol deposited into the growing hair shaft over weeks to months, providing a retrospective calendar of integrated HPA activity. The method has been validated in several species, including non-human primates, where segmental analysis of hair can reconstruct cortisol exposure over defined time periods. In orang-utans, hair cortisol concentrations were higher in animals with documented stressful periods and showed close correspondence between segmental results and keeper reports of stress exposure.

The potential appeal of hair cortisol in monitoring HAC treatment is the ability to assess long-term cortisol exposure without repeated blood sampling. However, the method has not been validated for monitoring therapeutic response in canine HAC. Hair growth rates, coat cycling, and the lag between cortisol deposition and hair sampling introduce uncertainty about which treatment period a given segment represents. The technique remains a research tool in this context, and the practicing clinician should not substitute hair cortisol for ACTH stimulation testing when making dose adjustments.

Trilostane Monitoring: Protocol and Targets

Trilostane suppresses cortisol synthesis reversibly by inhibiting 3-beta-hydroxysteroid dehydrogenase. Monitoring therefore measures drug effect instead of drug concentration, and the goal is to identify the dose that maintains post-treatment cortisol within a targeted therapeutic window while avoiding both under-treatment and iatrogenic hypoadrenocorticism.

The standard monitoring tool is the ACTH stimulation test, performed 4 to 6 hours after the morning trilostane dose. This timing captures the peak suppressive effect of the drug. The test is performed by measuring baseline cortisol, administering synthetic ACTH, and measuring cortisol again 60 minutes later. The post-ACTH cortisol concentration is the value used for dose decisions.

The widely cited therapeutic target for trilostane-treated dogs is a post-ACTH cortisol concentration between 41 and 138 nmol/L (approximately 1.5 to 5.0 micrograms/dL). Values below 41 nmol/L indicate excessive suppression and carry risk of iatrogenic hypoadrenocorticism, particularly if accompanied by clinical signs. Values above 138 nmol/L suggest inadequate suppression and typically warrant a dose increase. These thresholds are derived from clinical experience and are cited in standard references such as the MSD Veterinary Manual, and practitioners should confirm current recommendations against the most recent literature and product labeling.

The first recheck is scheduled 10 to 14 days after initiating therapy or after any dose change. This interval allows the drug to reach steady-state effect and gives the owner time to observe clinical response. At this visit, the clinician performs an ACTH stimulation test and adjusts the dose based on the result. If the post-ACTH cortisol is within target and clinical signs are improving, the next recheck is scheduled at 30 days. Thereafter, rechecks occur at 3 to 6 month intervals, with the exact frequency determined by clinical stability and owner compliance.

Dose adjustments follow a simple rule. If post-ACTH cortisol exceeds 138 nmol/L and clinical signs persist, the dose is increased by approximately 25 to 50 percent. If post-ACTH cortisol falls below 41 nmol/L, the dose is decreased by a similar proportion, and the clinician should inquire about lethargy, vomiting, diarrhea, or inappetence. If the dog shows signs consistent with hypoadrenocorticism and the post-ACTH cortisol is below 41 nmol/L, trilostane should be withheld and a basal cortisol measured. A basal cortisol below 28 nmol/L (approximately 1.0 microgram/dL) in a dog with compatible signs supports a diagnosis of iatrogenic hypoadrenocorticism, and the drug should be discontinued until clinical signs resolve, then restarted at a lower dose.

Clinical response should be assessed at every recheck. Polydipsia and polyuria typically resolve within the first 1 to 2 weeks of effective therapy, while dermatologic changes such as alopecia and calcinosis cutis improve over 3 to 6 months. The owner's report of water intake and urination frequency is a sensitive indicator of under-treatment and should be solicited at each visit. Resolution of clinical signs in the face of a post-ACTH cortisol slightly above the target range may be acceptable, and the clinician can elect to maintain the dose and recheck sooner instead of chase a laboratory value.

Mitotane Monitoring: Protocol and Targets

Mitotane causes progressive adrenocortical necrosis, and monitoring serves a different purpose than with trilostane. The goal is to achieve a partial adrenocortical destruction that leaves sufficient functional tissue to maintain basal cortisol production while abolishing the excessive secretion seen in hyperadrenocorticism. The margin between adequate control and permanent hypoadrenocorticism is narrower than with trilostane, and monitoring is correspondingly more intensive.

Mitotane therapy proceeds in two phases: an induction phase and a maintenance phase. During induction, mitotane is administered daily and the dog is monitored closely for the development of clinical signs of hypoadrenocorticism, including lethargy, vomiting, diarrhea, and inappetence. An ACTH stimulation test is performed at day 7 to 10 of induction, or earlier if clinical signs develop. The induction target is a post-ACTH cortisol concentration between 28 and 138 nmol/L (approximately 1.0 to 5.0 micrograms/dL). Once this target is reached, induction is stopped and maintenance dosing begins.

The distinction between the trilostane and mitotane targets is clinically important. The lower bound of the mitotane target, 28 nmol/L, is below the trilostane lower bound of 41 nmol/L. This reflects the fact that mitotane-treated dogs are maintained with less functional adrenocortical reserve, and the clinician accepts a lower cortisol value as long as the dog is clinically well. A post-ACTH cortisol below 28 nmol/L during induction indicates excessive adrenocortical destruction, and mitotane should be stopped immediately. The dog is then reassessed clinically and with serial basal cortisol measurements to determine whether permanent hypoadrenocorticism has developed.

During maintenance, mitotane is given at a lower frequency, typically once weekly, and the dog is rechecked at 1, 3, and 6 months after induction, then every 6 months thereafter. Maintenance monitoring relies on clinical assessment and periodic ACTH stimulation tests. A post-ACTH cortisol that rises above 138 nmol/L during maintenance, with recurrence of clinical signs, indicates that the remaining adrenocortical tissue is regenerating and that a second induction course may be required. Conversely, a post-ACTH cortisol below 28 nmol/L in a clinically normal dog warrants continued observation, but the clinician should instruct the owner to watch closely for signs of hypoadrenocorticism.

Basal Cortisol as a Monitoring Adjunct

Basal cortisol measurement has a limited but useful role in monitoring. In a dog receiving trilostane, a basal cortisol below 28 nmol/L in the presence of clinical signs supports a diagnosis of iatrogenic hypoadrenocorticism and can be used to make an immediate management decision without waiting for an ACTH stimulation test. However, basal cortisol alone cannot confirm adequate suppression, because a normal basal cortisol can coexist with an elevated post-ACTH cortisol. Basal cortisol should therefore be used as a screening tool for over-suppression, not as a substitute for ACTH stimulation testing.

In mitotane-treated dogs, basal cortisol is more informative. During induction, a basal cortisol below 28 nmol/L is a strong indicator that the induction target has been reached or exceeded, and many clinicians use this value to decide when to perform a confirmatory ACTH stimulation test. During maintenance, a rising basal cortisol can signal escape from suppression before clinical signs become apparent.

Monitoring Parameters and What Each Detects

The ACTH stimulation test detects the functional capacity of the adrenal cortex to respond to exogenous stimulation. In trilostane-treated dogs, it measures the degree of enzymatic blockade at the time of peak drug effect. In mitotane-treated dogs, it measures the mass of functional adrenocortical tissue remaining after necrosis. The test does not distinguish between these two mechanisms, and the clinician must interpret the result in the context of the drug being used.

Clinical signs detect the integrated physiologic effect of cortisol excess or deficiency. Polydipsia and polyuria are the earliest signs to resolve with effective treatment and the earliest to recur with under-treatment. Lethargy, vomiting, and inappetence are the earliest signs of over-treatment and should prompt immediate evaluation regardless of the scheduled recheck interval.

The urine cortisol to creatinine ratio has no role in routine monitoring of treated dogs. It is too insensitive to detect the transition from adequate suppression to over-suppression, and it cannot distinguish between the effects of trilostane and mitotane. Its use is confined to initial diagnosis, as discussed in the preceding section. Similarly, hair cortisol analysis is not validated for monitoring the rapid dose adjustments required during trilostane or mitotane therapy, because it reflects integrated cortisol secretion over weeks to months instead of the current state of adrenal suppression, as described in research on hair cortisol as a retrospective biomarker.

Documentation and Recheck Scheduling

Every monitoring visit should be documented with the date, the drug and dose, the time of the last dose relative to the ACTH stimulation test, the baseline and post-ACTH cortisol values, the clinical signs reported by the owner, and the dose decision made. This record allows the clinician to track trends over time and to distinguish a transient aberration from a progressive loss of adrenal function.

Recheck intervals should be adjusted to the individual patient. A dog that has been stable on a constant dose for more than 12 months may be rechecked every 6 months, while a dog that has required multiple dose adjustments may need rechecks every 4 to 6 weeks until stability is achieved. Owner reliability is a practical consideration. If the owner cannot reliably administer medication or observe for signs of over-treatment, more frequent rechecks are warranted.

The choice between trilostane and mitotane is influenced by drug availability, cost, and regional practice norms, and the monitoring protocol must be adapted accordingly. In regions where trilostane is the only licensed option, the monitoring schedule described above applies directly. Where mitotane is used, the more intensive induction monitoring is mandatory. The American Veterinary Medical Association practice resources provide general guidance on professional standards, but specific monitoring protocols should be based on current product labeling and peer-reviewed literature.

Recognized Complications and Failure Modes

Overtreatment is the most consequential failure in monitoring hyperadrenocorticism therapy. With trilostane, iatrogenic hypoadrenocorticism can develop rapidly, sometimes within days of a dose increase. The earliest biochemical indicator is a pre-trilostane cortisol below the reference interval, often accompanied by a blunted ACTH stimulation response. Clinical signs such as lethargy, inappetence, vomiting, or diarrhea may lag behind the biochemical change, so the clinician should act on the cortisol result alone instead of waiting for clinical deterioration. When the pre-pill cortisol falls below the laboratory reference interval, the drug should be withheld and the patient reassessed, even if the owner reports no visible change.

With mitotane, the corresponding failure mode is irreversible adrenocortical necrosis. The induction phase carries the highest risk, and monitoring relies on the ACTH stimulation test performed after each phase of treatment. A post-ACTH cortisol that drops below 2 µg/dL during induction signals adequate adrenocortical destruction and mandates immediate cessation of the induction protocol, regardless of whether clinical signs have resolved. Continuing mitotane beyond this point risks permanent hypoadrenocorticism requiring lifelong mineralocorticoid and glucocorticoid replacement.

Under-treatment presents a different diagnostic challenge. Persistent polydipsia, polyuria, and polyphagia with a pre-trilostane cortisol above the therapeutic target suggest an inadequate dose, but the clinician must first confirm owner compliance and correct timing of drug administration relative to the blood sample. Trilostane should be given with food to optimize absorption, and the sample should be drawn 4 to 6 hours after the morning dose. A sample drawn at the wrong interval produces a misleading result and may prompt an unnecessary dose adjustment.

A second failure mode is the development of a pituitary macrotumour in a dog whose cortisol is well controlled. Neurologic signs such as stupor, circling, or behavioral change in a treated dog warrant advanced imaging instead of endocrine testing. The cortisol assay will not detect this complication, and the clinician should maintain a low threshold for referral when neurologic signs emerge.

Common Monitoring Errors

The most frequent error in trilostane monitoring is interpreting a single cortisol value without reference to the clinical picture. A pre-pill cortisol within the therapeutic range does not guarantee adequate control if the owner reports persistent polyuria, and a low value does not always indicate overtreatment if the dog is clinically normal. The two must be reconciled at every recheck.

A second error is adjusting the dose on the basis of a single marginally high cortisol without repeating the test. Cortisol secretion varies from day to day, and a single value near the upper boundary of the target range may reflect inter-day variation instead of genuine loss of control. Repeating the ACTH stimulation test or pre-pill cortisol within 1 to 2 weeks provides a more reliable basis for dose adjustment.

A third error involves the urine cortisol to creatinine ratio. This test has no role in monitoring treatment response because it cannot distinguish adequate suppression from overtreatment. Its use in the monitoring phase produces confusing results and should be discouraged. The test remains useful only for initial diagnosis, and even there it is confounded by stress, as demonstrated in kennelled dogs where the ratio rose significantly upon introduction to a novel environment Rooney et al., behavioral and glucocorticoid responses of dogs to kennelling.

A fourth error is failing to recheck electrolytes when a dog on trilostane develops vomiting or weakness. Hyponatraemia and hyperkalemia may precede a dramatic fall in cortisol, and the electrolyte panel is faster and cheaper than an ACTH stimulation test. The clinician should run both when iatrogenic hypoadrenocorticism is suspected.

Limitations of the Evidence and Divergent Expert Opinion

The evidence base for monitoring protocols rests largely on expert consensus and retrospective case series instead of prospective randomised trials. Published target ranges for trilostane monitoring differ between sources, and the MSD Veterinary Manual presents target values that are broadly accepted but not universally applied. Some specialists advocate tighter control with lower cortisol targets, while others accept a wider therapeutic window to reduce the risk of overtreatment. This divergence reflects the absence of outcome data linking specific cortisol values to long-term survival or complication rates.

Hair cortisol analysis, while validated in several species as a retrospective measure of integrated HPA activity Meyer and Novak, minireview of hair cortisol as a biomarker of HPA activity, has not been established as a monitoring tool for treated canine hyperadrenocorticism. Its slow turnover makes it unsuitable for detecting acute changes in cortisol status, and no published data define target hair cortisol concentrations for treated dogs. The technique remains a research tool in this context.

When to Refer or Consult

Referral is warranted when a dog fails to respond to escalating doses of trilostane despite documented post-pill cortisol suppression, when neurologic signs develop during treatment, or when the clinician cannot stabilize a patient within three recheck cycles. Specialist consultation is also appropriate when the diagnosis is uncertain, such as when the ACTH stimulation test and low-dose dexamethasone suppression test yield discordant results.

Laboratory involvement is indicated when assay results seem inconsistent with the clinical picture. The ASVCP quality assurance guidelines emphasize that reference intervals are method-specific, and a cortisol value interpreted against the wrong reference interval can lead to incorrect dose decisions. The clinician should confirm that the laboratory's reference intervals apply to the assay platform in use and should question results that conflict with clinical expectations.

Regulatory reporting is rarely relevant to cortisol monitoring in companion animal practice. It becomes relevant only if a drug is suspected to be defective or if an adverse reaction meets the reporting criteria of the relevant national pharmacovigilance scheme. The AVMA practice resources provide guidance on adverse event reporting obligations in the United States, and the WOAH terrestrial animal health standards address reporting obligations in an international context, though these apply primarily to production animal and notifiable disease scenarios.

Frequently Asked Questions

How should I proceed if the reference laboratory cannot run an ACTH stimulation test today?

When same-day ACTH stimulation testing is unavailable, delay the test instead of substitute a basal cortisol sample for dose adjustment decisions. Basal cortisol correlates poorly with treatment adequacy and cannot distinguish controlled from over-treated patients. If clinical signs suggest impending hypoadrenocorticism, such as weakness, vomiting, or collapse, do not wait for laboratory confirmation. Discontinue the drug, initiate supportive care, and submit samples once the laboratory can process them. For routine monitoring, schedule the test when laboratory services are operational. The MSD Veterinary Manual provides guidance on interpreting stimulation results in the context of clinical presentation.

What monitoring approach is reasonable when the owner has severe financial constraints?

A single basal cortisol measurement can serve as a screening test, but it cannot confirm adequate control. If the owner cannot afford ACTH stimulation testing, discuss the inherent risk of undetected over-treatment. The urine cortisol to creatinine ratio is not a suitable substitute during treatment because it does not distinguish controlled disease from iatrogenic hypoadrenocorticism. Some clinicians use clinical signs and serial basal cortisol values below 1.0 µg/dL as a pragmatic warning of possible over-treatment, but this approach lacks validation. Document the financial limitation in the record and schedule the most affordable test at the interval that balances risk against cost. Referral may be appropriate if the owner cannot sustain any laboratory monitoring.

How does monitoring differ when treating a dog with atypical or food-borne hyperadrenocorticism?

The same monitoring principles apply because treatment targets cortisol production regardless of the underlying cause. Dogs with food-borne hyperadrenocorticism may require higher trilostane doses, but the ACTH stimulation targets remain identical. The key difference is that these dogs often have less severe clinical signs at diagnosis, so owners may be less vigilant in reporting potential over-treatment. Emphasize the warning signs of hypoadrenocorticism more explicitly and consider a slightly shorter interval before the first recheck. The American Society for Veterinary Clinical Pathology quality assurance guidelines support consistent laboratory standards across testing scenarios.

What should I record in the medical record after each monitoring visit?

Record the drug and dose administered on the morning of testing, the exact timing of drug administration relative to the ACTH stimulation test, the pre- and post-ACTH cortisol values, and the laboratory reference interval. Note the clinical signs reported by the owner, body weight, and any adverse events since the last visit. Document the dose adjustment made and the planned date for the next recheck. If the owner declined a recommended test, record that discussion and the reason. This level of detail allows accurate dose titration across multiple visits and protects against errors when a different clinician assumes the case.

How do I explain the need for repeated testing to a frustrated owner?

Frame monitoring as the mechanism that prevents both undertreatment and dangerous over-treatment. Explain that the dose is individualised and that the only way to find the correct dose is to measure the drug's effect on cortisol production. Use a concrete analogy, such as adjusting a thermostat based on the room temperature instead of guessing. Acknowledge the cost and time burden directly, then state the consequence of skipping tests: the dog may remain symptomatic or develop life-threatening adrenal insufficiency. The AVMA practice resources offer communication guidance for discussing diagnostic recommendations with clients.

Is hair cortisol analysis useful for monitoring trilostane or mitotane therapy?

No. Hair cortisol reflects integrated cortisol deposition over weeks to months, as described in the review of hair cortisol as a biomarker of hypothalamic-pituitary-adrenocortical activity. It cannot detect the acute changes in cortisol that occur after a dose adjustment, nor can it identify iatrogenic hypoadrenocorticism developing over days. The same temporal limitation applies to the hair cortisol calendar validated in orang-utans. Hair analysis may have research applications for assessing chronic stress, but it has no role in therapeutic drug monitoring for hyperadrenocorticism. Continue to rely on ACTH stimulation testing for dose decisions.

Related Clinical & Scientific Guides

• Peripheral Blood Smear Evaluation: A Step-by-Step Guide
• Reticulocyte Counts in Veterinary Medicine: Clinical Utility and Interpretation
• Cerebrospinal Fluid Analysis in Veterinary Neurology: Collection and Interpretation

References and Further Reading

• Behavioral and glucocorticoid responses of dogs (Canis familiaris) to kennelling: Investigating mitigation of stress by prior habituation.. 2007.
• Neural monitoring of vasovagal syncope.. 1997.
• Hair as a long-term retrospective cortisol calendar in orang-utans (Pongo spp.): new perspectives for stress monitoring in captive management and conservation.. 2014.
• Minireview: Hair cortisol: a novel biomarker of hypothalamic-pituitary-adrenocortical activity.. 2012.
• The association between heart rate, heart rate variability, endocrine and behavioral pain measures in horses suffering from laminitis.. 2004.
• Validation of a behavioral observation tool to assess pig welfare.. 2006.
• American Society for Veterinary Clinical Pathology Guidelines. American Society for Veterinary Clinical Pathology.
• MSD Veterinary Manual, Professional Edition. MSD Veterinary Manual.
• American Veterinary Medical Association Practice Resources. American Veterinary Medical Association.

Related Articles

• Monitoring Thyroid Hormone Levels During Treatment of Hypothyroidism
• Monitoring Pancreatic Enzyme Levels in Acute Pancreatitis
• Serial Cytology for Treatment Response Assessment in Lymphoma
• Monitoring Inflammatory Markers in Chronic Enteropathy
• Laboratory Monitoring of Anemia: Reticulocyte Response and Beyond

This article is educational professional reference material for veterinary audiences. It is not a substitute for veterinary diagnosis, individual clinical judgment, current product labeling, or applicable regulatory requirements.