Tests to diagnose Cushing's syndrome and Cushing's disease
Tests to diagnose Cushing's syndrome
It is important that the diagnosis of Cushing's syndrome is confirmed. First a doctor will test you for Cushing's syndrome. Once glucocorticoid medicines have been ruled out, there are 4 types of tests that are generally used to find out if you have Cushing's syndrome. These tests measure the amount of cortisol in samples of urine, blood, or saliva to determine how much cortisol is circulating in your body. If the tests show that the level of cortisol is too high, it means you have Cushing's syndrome. 1 If the test is not positive for high levels of cortisol, then signs and symptoms should be closely watched. If your symptoms get worse, check back with your doctor in 6 months. 1
In certain cases, doctors recommend specific types of tests based on a person's medical history. Some of these recommendations are included below.
UFC=urine-free cortisol; DST=dexamethasone suppression test; *=No recommendation stated.
Following are brief descriptions of tests that are used to diagnose Cushing’s syndrome. However, complete information about these tests, along with instructions for patients, should be obtained from your doctor.
Urine-free cortisol (UFC) test 1,2
What it measures:
Why it's used:
- Almost all people with Cushing's syndrome have high urine cortisol levels
- The UFC test only measures the type of cortisol that causes Cushing's syndrome, called "circulating, free cortisol." It does not measure "bound" cortisol, which increases in the blood from taking certain medicines such as estrogen, but does not cause Cushing's syndrome
How it's done:
- Urine samples are collected at every opportunity throughout a 24-hour period. The samples are then given to a lab for testing
Special instructions:
- During the 24-hour testing period, don't drink a lot of fluids or use glucocorticoid medicines or products, such as hemorrhoid or skin creams that contain steroids. This test needs to be done up to 3 times to be certain the results are accurate
Late-night salivary cortisol test 1,3
What it measures:
Why it's used:
- Normally, the amount of cortisol in saliva is lowest late at night. However, Cushing's syndrome will cause there to be more cortisol than normal in saliva at this time
How it's done:
- A saliva sample is obtained between 11 PM and midnight on 2 different nights. These are then given to a lab for testing
Special instructions:
- Don't eat licorice, smoke cigarettes, or chew tobacco on the days when samples are obtained
- Avoid situations that create extreme stress or excitement
- If bedtime is usually well past midnight, obtain samples at bedtime
Late-night plasma cortisol test 3,4
What it measures:
Why it's used:
- Normally, the amount of cortisol in blood is lowest late at night. However, Cushing's syndrome will cause there to be more cortisol than normal in blood at this time
How it's done:
- A blood sample is obtained at night while the patient is sleeping in a hospital. 4 This is then given to a lab for testing
Dexamethasone suppression test (DST) 1,3
What it measures:
Why it's used:
- Normally, low doses of dexamethasone will reduce cortisol levels. However, if a person has Cushing's syndrome, these doses will not have an effect on cortisol levels
Overnight DST (short test)
How it's done:
- A 1-mg dose of dexamethasone is taken between 11 PM and midnight
- A blood sample is taken at the doctor's office between 8 AM and 9 AM the next morning
Special instructions:
- Don't drink or eat anything for at least 10 hours before the blood test
48-hour DST (long test)
Why it's used:
- To better distinguish Cushing's syndrome from other conditions that can raise cortisol levels (such as depression, anxiety, morbid, obesity, alcoholism and diabetes) 1
How it's done:
- A 0.5-mg dose of dexamethasone is taken every 6 hours for 48 hours
- A blood sample is taken at the doctor's office 6 hours following the last dose
Special instructions:
- Be sure to take dexamethasone every 6 hours as instructed 2
(Note: The longer DST is considered more accurate in determining whether high cortisol levels are caused by Cushing’s syndrome or some other condition. 1 )
Tests to diagnosis Cushing’s disease
If a patient is diagnosed with Cushing’s syndrome after measuring the level of cortisol in his or her body, the next step is additional testing to diagnose if the cause of excess cortisol is Cushing’s disease (a pituitary tumor) or a different form of Cushing’s syndrome. 1
Tests to diagnose Cushing's disease
ACTH measurement
What it measures:
- Adrenocorticotropic hormone (ACTH) in the blood
How it's done:
- A blood sample is obtained. 4 This is then given to a lab for testing
Why it's used 4,5 :
- If ACTH levels are high, then Cushing's syndrome may be caused by a tumor in the pituitary (Cushing's disease) or somewhere other than the pituitary, most commonly on the lungs (ectopic Cushing's syndrome)
- If ACTH levels are low, then Cushing's syndrome may be caused by a tumor in the adrenal glands or another area of the body
Imaging tests
What it measures:
- Location of the tumor
How it's done:
- Doctors use an MRI* or CT* machine to scan areas of the patient's body to look for a tumor based on ACTH testing
- MRI scan of the pituitary gland if ACTH levels are high
- MRI or CT scan of the adrenal gland if ACTH levels are low 4
Corticotropin-releasing hormone (CRH) stimulation test
What it measures:
- How CRH changes ACTH and cortisol levels 2,4,5
How it's done:
- ACTH and cortisol levels are checked with a blood test, then a CRH intravenous injection is given 2,4
- After the CRH injection, blood tests are repeated several times to recheck ACTH and serum cortisol levels 2,4
- If these levels are higher, this helps to confirm that there is a pituitary tumor 2,4
Why it's used:
- The CRH test can be used to confirm that there is a pituitary tumor if either the ACTH measurement or the pituitary MRI is inconclusive 5
*MRI=magnetic resonance imaging; CT=computerized tomography.
Other testing
If a pituitary tumor is suspected but not found on MRI, it may be because either the tumor is too small to see, or it is not a pituitary tumor, but rather an ACTH-producing tumor in another part of the body. Additional imaging and/or tests are then needed. 2
A test called inferior petrosal sinus sampling (IPSS) test can be used to determine whether an ACTH-producing tumor is in the pituitary gland (Cushing’s disease). 4
Once the doctor knows what is causing the level of cortisol to be too high, then he or she can determine the most appropriate treatment.
References: 1. Nieman LK, Biller BMK, Findling JW, et al. The diagnosis of Cushing’s syndrome: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2008;93:1526-1540. 2. Newell-Price J, Bertagna X, Grossman AB, Nieman LK. Cushing’s syndrome. Lancet. 2006;367:1605-1617. 3. The Hormone Foundation’s patient guide to the diagnosis of Cushing’s syndrome. The Hormone Foundation. http://www.hormone.org/resources/patient_guides/upload/mgmt-cushings-syndrome-070609.pdf. Accessed August 4, 2009. 4. Arnaldi G, Angeli A, Atkinson AB, et al. Diagnosis and complications of Cushing’s syndrome: a consensus statement. J Clin Endocrinol Metab. 2003;88:5593-5602. 5. Nieman LK, Ilias I. Evaluation and treatment of Cushing’s syndrome. Am J Med. 2005;118:1340-1346.
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Acth test hund
Wednesday, March 16, 2011
What's the Best Protocol for ACTH Stimulation Testing in Dogs and Cats?
67 comments:
(this may be a re-resubmit. Not sure if first comment went through).
Giving a larger dose of ACTH (cosyntropin) to your dog will not produce any harm. However, it will be more expensive cost you more money.
Our 12 year old Min-Pin has diabetes/Cushing's Disease. In the past when he has ACTH tests, we have always been told to fast him for 12 hours, give half a dose of insulin (1.5 units) and 10mg of trilostane before he goes for the test. After first result we were told test was too LOW and to change the dosage from 10 mg. daily to 10 mg. once every other day. This last test his readings were 12.1, so now we are instructed to order compounded medicine of 5 mg. to be given once daily. I am just wondering how accurate the tests have been with the fasting, and if the once daily dose is a good idea. I see that twice a day is recommended in some places. I thank you for your help. Jan
First of all, trilostane is a fat-soluble drug and should always be given with food to ensure that it get absorbed. The same is certainly true the morning that you are going to do ACTH stimulation testing to monitor your dog. You do NOT want to fast in that situation, because it's not going to mimic what is going on all the other days of the month(s) between monitoring periods.
Dear Dr Peterson,
I know this is a big problem, which I don't have an answer for in these cases.
Dear Dr. Peterson,
I found this site information very useful. I just realize that there is no agreement among vets on treatment and how this very expensive test is done. I've been treating my little Nina with the very expensive drug Vetoryl for almost a year. I don't see any improvement in "symptoms" other than normalization of her cortisol levels. I have to mention that based on symptoms I read on line she is a very mild case. Her only issue is extreme appetite and large tummy. Nothing else. The medication didn't help reduce her increased appetite, and since starting it she has diarrhea everyday. It's been getting worse with time. She also takes Vetmedin and I read that both medications can cause diarrhea. In addition, she takes enalapril and lasix. Nobody mentioned to be the danger of mixing these medications and I found that it can be dangerous when taken together. I feel like Nina is intoxicated. Her bowel is crashing. I may even consider stopping her Cushing treatment as I sincerely don't see benefits. Her triglycerides are reaching the roof and I also believe it can be a side effect. She's been on H/D diet since diagnosed with heart problems. Any recommendation is greatly appreciated. I heard some dogs do better with lysodren.
I agree with you that your dog maybe should not be on the Vetoryl, especially if there are so many other problems going on and you haven't noticed any improvmement.
Dr. Peterson, you have experience with use of Synacthen Depot for monitoring treatment of hyperadrenocorticism in dogs? The dose may be the same or intravenous larger? Collection with two hours of application, right? Thank you.
We don't have Synacthen depot in the USA. But I do know that most use a dose of 1 vial per dog (half a vial may be enough in very small dogs).
My 4 year old english bulldog was ACTH tested today with Cortrosyn given IV at 8 40 am. She has since developed high sensitivity to low and high lights and appears to loose her vision. But these episodes are short. I am an RVT and have monitored and conducted may of these test through out my career but have never seen such a reaction. Thank you for your insight. Bette
I have not ever seen or heard of such a side effect. The timing, however, would certainly indicate that the Cortrosyn (or saline used to dilute it) is responsible. Talk to your vet about possible short term steroid treatment for an allergic reaction. Also have them do a good eye exam. But I honestly do not know what the pathogenesis of your dog's signs could be.
My vet always asks to fast the night before the acth stim test. so you advise against it?
Only if you are monitoring trilostane therapy. If you fast and give the drug the morning of the test, the trilostane might not be absorbed on an empty stomach.
Sorry, I should have explained better. My min dachshund is on Trilostane, my vet always requests a complete fast (no food, meds, or water).
Well, you cannot monitor the effects of trilostane therapy if you don't give the drug the morning of the text. The drug has a very short half life and will be totally gone from the circulation in 12-18 hours.
My question is, will it be ok to give him trilostane again with food in the morning before the test? That would be like giving him recommended dosage every 12 hr instead of every 24 hr, although it would be just for that day for the test. What would be the best way to get a correct result from the test?
If you are going to use once daily trilostane, it must be given in the morning if you are going to check the peak effect of the drug (3-6 hrs after administration). It makes no sense to give an extra dose on the day of testing -- then you have effectively raised the dose given for that day.
Bottom line is that I do not know the answer.However, I highly doubt that touching, holding or petting a dog that received trilostane could result in enough absorption of the drug to result in infertility. The worry is that this drug will inhibit progesterone secretion if you take or absorb the drug by handling it (see reference). Again, this doesn't seem possible after ingestion by a dog, but I'm not a pharmacologist!
Thank for your quick answer.
Hello. We have a dog with Cushings and am wondering if there is a way to lower the cost of the ACTH Stim test. such as any assistance programs. The Vet bills are overwhelming for our family but we want to help our dog as much as we can. Any suggestions? The test just recently went up and is now $400.00.
Sorry, I do not know of any assistance programs.
,my pom has had cushing for over a year. when my vet confrimed he needed treated, he wanted to give him lysodren. I read on line about side effects of both drugs (trilostane) I did not want lysodren, tried to talk my vet out of it.But had his mind made up. I changed vets and feel so bad,he had taken care of my dog for 7 years. Is trilostane better than lysodren?
No best drug for all dogs. Both drugs nave pros and cons.
I am fostering a shelter dog who is so very fearful that she cannot be groomed or handled by a vet without sedation. She becomes beyond stressed, combatant and bites. I have had cushingoid dogs of my own as well as fostered two rescues with cushing's so when I saw her, the symptoms and her physical appearance were very familar to me. Her symptoms are defintely not mild either. She was constantly hungry, panting, excessive dilute urine, excessive drinking, very thin coat, and very bad skin. Her behavioral problem is not conducive to doing all of the usual screening test but this is a shelter dog whose alternative was euthanasia so we're doing what we can with the information we have. A UC:CR was done with a specimen collected first thing in the morning at home. Results were greater than 100, suggestive of cushing's. She weighs 20 lbs and was started on 10 mg Vetoryl twice a day. The dog was sedated and an acth stimulation test was done at day 16. Results were pre 3.4 ug/dl and post 10.9 ug/dl. I have definitely noted improvement in symptoms so I don't feel an adjustment to dosing should be made at this time. I spoke with a representative at Dechra and asked her if sedation can skew the results of an acth stimulation test and she said she didn't think so. That wasn't very reassuring so I was hoping that you may have a more definitive answer for me. If sedation does skew results, is cortisol normally lower or higher when the dog is sedated. Any guidance you can provide in this very special case would be most appreciated. Thank you for your time.
Stress will increase the basal cortisol concentration but should now affect the post-ACTH cortisol value.
I apologize if I was unclear in my question. The dog had to be sedated in order to even do the stimulation test so she was knocked out completely before starting the acth stimulation test. I apologize but I don't know which sedation was used. My question is are pre and post stimulated results affected by sedation and if so, would you expect them to be lower or higher? Thank you.
Basal cortisol will be increased. Post cortisol should not be affected.
Trilostane being fat soluble, does the fat content of the meal given with the trilostane administration matter to its absorption? My 15-17 y/o beagle is on 40mg q.d., but he eats Purina OM (Overweight Management) Rx kibbles, which are (from what I understand) higher protein, higher fiber, and more medium-to-low in fat than most dog foods. Would it benefit the absorption of trilostane to add something to his breakfast (like, say, 1/2 tsp. of olive oil), or is "fat solubility" more of an internal process of digestion that wouldn't be effected by the lipids in the actual meal?
If your dog is well controlled, I wouldn't worry about it. If not, then added a bit a fat to the food at time of drug administration wouldn't be a bad idea.
I am in an awkward situation and need advise. I am in Florida for the winter and seeing a covering vet until our return home to my regular vet. I have a 7 yr old cocker diagnosed last October. We caught Cushings early and dog's only symptoms was overeating, hair and skin is normal, no overdrinking, etc. He is 32 lbs and taking 30 mg Vetoryl daily and doing great. First ACTH tests were good, pre 2.5, post 10; pre 3.3, post 8.3. Normal ranges are pre 1-5 and post 8-17. But the most recent ACTH was pre <1, post 3.4 which are both low and I am very afraid he will go Addisons and think he should be decreased to 20 mg daily, but vet wants to continue 30 mg. Covering vet told me over the phone that the pre was 1, but when I got the actual written lab report it showed <1. I spoke with my regular vet at home and told him it was 1 and he said to continue with the 30 mg, but he did not know it was lower and is on vacation this week. What do you suggest I do?
If you lower the dose this week and talk to your vet when he or she returns from vacation, that isn't going to hurt anything.
You can't evaluate trilostane treatment if given without food. I have never fasted a dog when retested on this drug. I don't find that feeding produces significant lipidemia to influence cortisol measurement.
Thank you. I hope I didn't offend. I was only looking for more opinions and yours seems highly respected. I do appreciate your taking the time to respond.
My dog was recently diagnosed with Cushing's, started Vetoryl 20 days ago, and underwent her 1st ACTH and electrolyte testing 12 days after start of treatment. Contrary to Vetoryl manufacturing instructions, my vet does not find any benefit of performing interval ACTH testing at the 30, 60, 90 days and 3 mo. from start of treatment. He's suggesting next ACTH wouldn't be necessary for 6 months! I'm shocked and ready to get a 2nd opinion. Any thoughts?
I agree. Find another vet who knows how to monitor dogs treated with this drug!
Dear Dr. Peterson,
My cat has been successfully treated for Cushings' now going on 5 plus years. However, now she is having problems and is declining. Her skin is very loose, her sodium continues to elevate to dangerous levels, and she is very thin.
I'm concerned with how her current Internist does the ACTH stim.
1. He says she doesn't have to wait 4 hours after her Trilostane dose.
2. He only gives one blood test an hour after the ACTH med is administered.
Well, no research has been done to determine the best time to do an ACTH stimulation test to monitor trilostane treatment, or if the ACTH stimulation test even helps with the dosing.
Unfortunately I was so focused on reading the info and risks related to my dog that I managed to miss the warning on the vetoryl information sheet regarding women not handling the medication if trying to become pregnant. I've been handling his pills for nearly a month. Now I'm afraid to try to conceive this cycle and don't know when it's safe to do so. I know for certain I am not pregnant at the moment. As long as I don't handle vetoryl from now on, am I ok to continue trying to conceive or is it recommended I wait a period of time?
You need to speak to your physician about this but trilostane has a very short duration of effect so you should be fine to try to conceive now.
I've just had my four year old dog diagnosed with Cushings using an ACTH stir test and a urine sptest for cortisol production. He has started on Vetoryl at a 2mg/kg SID. Can you please tell me what further tests he will need - most importantly does he need US to look at adrenal glands and/or scan of pituitary glad? I am very concerned he may have a tumour - I would wish to do everything necessary/recommended to ensure his care is the best it can be. Your advice would be very much appreciated.
These days, most vets do an abdominal ultrasound to diagnose or exclude an adrenal tumor. I agree with you. I like to know if the dog has adrenal hyperplasia or adrenal tumor. It's not difficult to do the ultrasound if the operator has experience.
We had to suspend my dog's Vetoryl last week because her ACTH came back very low.
Do we need to test her again using ACTH or how do we know her cortisol level?
I'd do another ACTH stimulation test in 2-4 weeks to see if you need to reinstate the Vetoryl.
So it is not recommended to wait for symptoms to return such as excessive thirst etc?
You want to monitor both labs and clinical signs.
After her ACTH results tomorrow, will her cortisol be high even though she has been off Vetoryl for 2 weeks? If so should we start again or wait for symptoms to return?
If the cortisol levels are high, then the drug should be started at a lower dose.
Good evening Dr.Peterson,
Cortisol M0 3.12 ug/dLL
Cortisol M1 24.16 ug/dLL
Do you believe I should start her tomorrow on 30mg and have another test in 15 days?
Any other recommendation is appreciated.
The Vetoryl needs to be started based on these results. Talk to your vet about the correct dosage. I cannot do that online.
I have had my dog scanned now, and he doesn't have an adrenal tumour. Is the next step wait and see if the symptoms fully resolve on Vetoryl, or do you think there is any merit in an MRI to see if he has an operable pituitary tumour. I'm not keen on surgery, but as a mentioned before, he is only four and if he could be "fixed" permanently it could be worth it. Do you have knowledge of this type of surgery and is it something you would advise/consider? Also, my dog is loosing pigment from around his eyes and nose - - could this be a side affect of Cushings??
Pituitary surgery might be the best, but you need a facility with experience (not many available). I'd talk to your vet about this, but if there aren't any experienced pituitary surgeons nearby, then I'd start the Vetoryl.
Many dogs will need (or at least do better) on twice daily treatment, and that is no way predicts that your dog has an expanding pituitary tumor.
Dr, can you help me. My dog has just been diagnosed with a-typical Cushing which the vet says is good news. Does he need a stim test? He is an older rescue litter doxies approximately 10 years. I only brought him to the vet to get his nails trimmed and I got concerned when he lost half a pound. I asked the vet to run a blood test. He has no Cushing symptoms.
If you think your dog is not symptomatic for anything, I would NOT recommend any further testing or treatments at this time.
My 29lb neutered dog was diagnosed with Cushing's in early December and began a course of Vetoryl 10ml BID. We have steadily increased the dosage to where it is now, 20/20 daily based on Stim testing (five total). Each post test was in the range of 9 to 16; the last one, 13 was higher than the previous one, 12 even though the dose was increased by 5 ml daily. He has had two US's and a blood panel in 12/16. He also has a perianal adenoma; I'm waiting on surgery to try to get his cortisol under control. Should I pursue an MRI of his pituitary? Should we keep bumping the dose? His clinical symptoms are somewhat improved but still lots of trembling, lethargy, drinks somewhat more than he should and needs to go out in the middle of the night. Thank you for your thoughts or ideas.
Make sure you are giving the drug with food. If you are, then I'd switch to Lysodren (also needs to be given with food). Talk to your vet.
Dear Doctor, my vet never warned me that I should not touch vetoryl if I want to get pregnant. Several times he said that i should split capsule of 5 mg becouse there is no such kaopsule. For a long time I can not get pregnant, and I was wondering if I can do some blod test becouse touched a vetoryl and i touched powder inside couple of times I read that is dangerous to humans. Is there a blood test or something that I can do. Thanks in advance and sorry for bad English, I write from Serbia Sofia
If you only touched the powder a couple of times, you should be okay. But please talk to you own doctor and show him the package insert for the drug.
Dr. Peterson, are you familiar with the study; Pre-trilostane and three-hour post-trilostane cortisol to monitor trilostane therapy in dogs conducted by L. Macfarlane, BVMS DipECVIM-CA MRCVS1, T. Parkin, BSc, BVSc, PhD, DipECVPH, FHEA, MRCVS2 and I. Ramsey, BVSc, Phd, DSAM, FHEA, FRCVS, DipECVIM-CA3? The results of this study indicate that this monitoring method shows that the pre-trilostane and three-hour post-trilostane cortisol concentrations were better than the post-ACTH cortisol concentrations at discriminating between dogs with excellent control and those that were undercontrolled. Do you see this as a possible futyure choice to monitor Vetoryl treatment using a simple pre-pill cortisol rather than having to go through the hassle and expense of an ACTH stim test?
Yes, I know the work well and I do think this approach has great promise. Certainly makes more sense thank the ACTH stimulation test!
Thank you Dr. Peterson! I have been moderating canine cushing's support groups for 12 years and there is absolutely no doubt that if this approach becomes established protocol, it can make a huge difference for many pet owners who are financially unable to treat their dogs and afford the acth stimulation tests. I think this could be the best thing since sliced bread. :) You are a trusted expert by many of us who often use this amazing site to educate our members and help them become better advocates for their dogs. You've been my personal go to with questions over the years and you have no idea how many dogs have benefited from your Q & A pages and your personal answers to me and others. It is not uncommon for members to educate their general practice vets, using pages out of your site, so you've also helped provide free continuing education for many, many vets over the years as well. I think I speak for scores of us who are dedicated to helping pet owners and their dogs when I say thank you from the bottom of my heart for being so gracious with your time and knowledge. You rock the canine cushing's world!
Dr. Mark E. Peterson
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Beware of false positives, negatives in canine hyperadrenocorticism testing
Canine hyperadrenocorticism is a commonly diagnosed endocrinopathy in small animal practice.
The diagnosis of canine hyperadrenocorticism using the low dose dexamethasone suppression test or the ACTH stimulation test is usually straightforward, but problems with false positive and false negative test results can be encountered.
Adrenal function testing The effect of nonadrenal illness on the low dose dexamethasone suppression test and the ACTH stimulation test (resulting in false positive test results) is well described. Adrenal function testing should be reserved for dogs with historical and clinical signs consistent with hyperadrenocorticism. Furthermore, the adrenal function testing of sick animals should be avoided if at all possible, and delayed until after the resolution of the nonadrenal illness if suspicion of hyperadrenocorticism remains.
Recent cases Recently, Ristic, Evans and Herrtage (2001 ACVIM Forum Abstract #107) described several dogs with clinical findings consistent with hyperadrenocorticism (such as polyuria, polydipsia, polyphagia, pendulous abdomen, dermatological abnormalities and elevated serum alkaline phosphatase levels), but with normal results on low dose dexamethasone suppression tests and ACTH stimulation tests. Both pituitary-dependent and adrenal tumor cases were described.
All of the cases had elevated post-ACTH serum 17-OH progesterone levels. Treatment with mitotane (Lysodren) resulted in normalization of the 17-OH progesterone levels and resolution of the clinical signs of hyperadrenocortism.
Hill, et al reported on the incidence of elevations of adrenal sex hormones in dogs with pituitary dependent hyperadrenocorticism, adrenal adenocarcinoma and noncortisol-secreting adrenal tumors (2002 ECVIM-CA/ESVIM Congress Abstract; 2003 ACVIM Forum Abstract # 60). Concentrations of testosterone, estradiol, progesterone, 17-OH progesterone and androstenedione were determined before and one hour after administration of ACTH in dogs with pituitary-dependent hyperadrenocorticism, adrenal adenocarcinoma and noncortisol-secreting adrenal tumors.
All of the dogs with adrenal adenocarcinoma, 90 percent of the dogs with pituitary-dependent hyperadrenocorticism and 67 percent of the dogs with noncortisol-secreting adrenal tumors had one or more of the hormones above the reference range after ACTH stimulation.
Dogs with adrenal adenocarcinoma had significantly higher levels of testosterone, progesterone and 17-OH progesterone after ACTH stimulation than the dogs in the other two groups.
Study findings These studies show that dogs with hyperadrenocorticism can have elevations of other adrenal hormones besides cortisol. In the case of 17-OH progesterone, it has been shown that such elevations can result in clinical signs of hyperadrenocorticism in dogs with normal low dose dexamethasone suppression test results and a normal post ACTH cortisol concentration. We have seen several such dogs in our practice.
Historical and clinical signs of Cushing's disease were present, but the standard tests (low dose dexamethasone suppression test and ACTH stimulation test) for Cushing's disease were negative. All of these dogs had elevated 17-OH progesterone concentrations following ACTH stimulation and bilateral adrenomegaly on abdominal ultrasound examination. Treatment using the standard mitotane (Lysodren) protocol for canine pituitary-dependent Cushing's disease (induction dose followed by maintenance therapy) resulted in resolution of the signs of hyperadrenocorticism in the cases we have seen. Measurement of pre- and post- ACTH 17-OH progesterone levels can be recommended in dogs with historical and clinical signs of hyperadrenocorticism and normal low dose dexamethasone test results and a normal post ACTH cortisol concentration.
Should these results also be normal, the clinician could contemplate measuring other adrenal hormone levels before and after ACTH stimulation.
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Diagnosing Canine Cushing's Disease with an ACTH Stimulation Test
Canine Cushing’s disease is a condition where too much cortisol is in the bloodstream. The complex system of pituitary gland, hypothalamus and hormone secretions is broken, making the dog’s body unable to regulate the cortisol production. The elevated cortisol levels in turn have an impact on various body systems including nervous system, cardiovascular system, skeletal muscles, blood sugar levels, fat metabolism, kidney function and immune response. Once diagnosed, Cushing’s disease can be treated, allowing the dog to live a more comfortable life and avoiding the secondary problems caused by the disease. While no single test can properly diagnose Cushing’s disease, the ACTH stimulation test, used in tandem with other diagnostic results, can pinpoint the diagnosis.
ACTH Stimulation Test
The ACTH stimulation test is conducted by comparing baseline blood work against blood work taken 1 to 2 hours after an injection of the ACTH hormone. ACTH is the hormone that is naturally produced in the pituitary gland and triggers the release of cortisol from the adrenals into the dog’s system. If the test results show an extremely elevated level of cortisol in the bloodstream, it is likely the dog has Cushing’s disease. The ACTH stimulation test is often done in conjunction with a low dose dexamethasone suppression test in order to confirm the diagnosis of Cushing’s disease.
Neither of these tests can differentiate between the different causes of Cushing’s disease. In order to do this, a high dose dexamethasone suppression test must be conducted. Baseline blood work is compared to blood work at 4 and 8 hours after the dog has been given a high dose of dexamethasone. The test results will determine the cause of the Cushing’s disease and allow the veterinarian to prescribe the appropriate treatment.
Treatment for Cushing’s Disease
Because most dogs diagnosed with Cushing’s disease are elderly and already being treated for other medical conditions, treatment can be complicated. For Cushing’s caused by adrenal tumors, surgical removal of benign tumors can cure the disease. Malignant adrenal tumors often go unrecognized until the tumor has already attached itself to the liver or lungs. In these cases, non-surgical treatment is often the route taken.
Medicinal treatment for pituitary dependent or for inoperable adrenal-based Cushing’s disease is done, not to cure the disease, but to make the dog’s quality of life more comfortable. Your veterinarian will choose the drugs based upon your dog’s condition, the type of Cushing’s present and other medications your dog may be on.
Iatrogenic Cushing’s is caused by medications that cause overproduction of corticosteroids. Gradual withdrawal of the offending medication will allow the dog’s body to fully recover and return to a non-Cushing’s state.
The ACTH stimulation test allows your veterinarian to determine whether or not your dog’s body is producing excessive amounts of cortisol and creating a toxic situation that can affect a variety of his body’s systems. Once the initial diagnosis is confirmed by additional tests, and the cause of the Cushing’s disease identified, treatment can begin, allowing your dog to live his life more comfortably.
Hond & Cushing
Geplaatst in Cushing bij de hond – behandeling
Wat gek, de uitslagen van de ACTH stimulatietest zijn “omgedraaid”
Is de dosering Vetoryl te hoog?
Vetoryl onderdrukt de aanmaak van cortisol (stresshormoon) in de bijnieren. Wanneer de dosering te hoog is, wordt deze aanmaak teveel onderdrukt. Dit geeft de verschijnselen van de ziekte van Addison (het tegenovergesteld van de ziekte van Cushing).
Dit zijn verschijnselen van de ziekte van Addison:
- Lethargie (futloos, depressief)
- Slechte eetlust
- Braken of voedsel opgeven
- Spierzwakte
- Afvallen
- Diarree
- Veel drinken en plassen
- Spiertrillingen
- Buikpijn
- Bloed bij braaksel of ontlasting
- Dronkenmansgang (ataxie)
- Epileptische aanvallen
- Instorten (shock)
Dit zijn verschijnselen om altijd alert op te zijn, vooral wanneer is gestart met het geven van Vetoryl, of wanneer de dosering onlangs is verhoogd.
Lethargie en slechte eetlust zijn beslist symptomen om direct de Vetoryl te staken en contact op te nemen met de dierenarts. Wanneer je hond instort, dan is de situatie uiteraard kritiek en moet hij met spoed naar een dierenkliniek toe. Het kan zijn dat je hond aan het infuus moet en/of prednison krijgt toegediend om weer op te krabbelen.
Als alles weer normaal is en de hond helemaal hersteld van de Addison verschijnselen kan wellicht een lagere dosering Vetoryl worden ingezet. Dit moet dan vervolgens goed worden gemonitord, hiervoor is de ACTH stimulatietest bedoeld. Dit is een bloedtest die aangeeft of de dosering Vetoryl goed, te hoog of te laag is. Mooie bloeduitslagen zijn een bevestiging dat de dosering goed is ingeregeld, maar het klinisch beeld is minstens zo belangrijk: doet de hond het goed, is hij blij en actief en zijn de Cushing verschijnselen verdwenen of sterk verminderd? Blijft dit zo goed gaan, zonder dat het beeld omslaat in Addison verschijnselen? Dan gaat de dosering goed.
Lees de bijsluiter ook goed door om goed geinformeerd je hond te monitoren. Tot oktober 2014 gaf de bijsluiter van Vetoryl een startdosering per kilo lichaamsgewicht aan, die voor sommige honden te hoog bleek te zijn. Daarom heeft de fabrikant de startdosering verlaagd naar 1 tot 2 mg Vetoryl per kilo lichaamsgewicht. Helaas zijn er nog steeds bijsluiters van voor oktober 2014 in omloop, zowel op papier als op internet. Wees hier alert op en wanneer je twijfelt over de dosering, bespreek dit punt dan met je dierenarts.
Bijsluiter Vetoryl van juni 2015: bijsluiter-vetoryl-2015
Vetoryl combineren met andere medicatie
Ik heb Sara Galac gevraagd om eens in te gaan op de combinatie van Vetoryl met andere medicijnen.
Als voorbeeld gaf ik ook Vasotop (werkzame stof is ramipril) op; dat is een ACE inhibitor tegen hartfalen en het werkt ook positief bij nierfalen, omdat het de doorbloeding verbetert. Dat middel gaat niet samen met Vetoryl, dus dan moeten eigenaren vaak kiezen voor het een of het ander.
Haar reactie op mijn mail was:
Het lijk me nuttig om een korte tekst toe te voegen op het blog, over de combinaties Vetoryl-andere medicaties, maar het kan ook gevaarlijk zijn, want soms zijn de combinaties zeer individueel.
Wat ik wel al nu kan vertellen is het volgende:
– vaccineren mag (moet!)
– pijnstillers: tramadol geen probleem, NSAID`s alleen op de volle maag
– antibiotica: in het algemeen geen probleem
– prednison therapie heeft geen nut in combinatie met de trilostane, want trilostane breekt prednison af. Dus in situaties dat de hond wel steroïden nodig heeft, moet je met de therapie stoppen. Wat vaak gezien wordt is dat een ziekte die met steroïden behandeld zou worden (atopie, voedsel alergie) tijdens onbehandelde Cushing eigenlijk geen klachten veroorzaakt, omdat de lichaam al zelf voldoende steroïden aanmaakt. Pas als Cushing goed onder controle is, komen de klachten van atopie (etc.) tevoorschijn. In zulke situaties is soms verlagen van de dosis van de trilostane voldoende om de klachten onder controle te houden. Maar – puur mijn gevoel – zijn zulke patiënten nooit goed gereguleerd.
Wanneer moet ik Vetoryl verdelen over de dag?
Ik heb Sara Galac, de specialist in Utrecht, vorig jaar eens gevraagd wat een aanwijzing zou zijn om over te stappen op 2 x daags de helft van de Vetoryl te geven i.p.v. 1 x daags de voorgeschreven dosis. Dit was het antwoord:
Er zijn enkele onderzoeken die laten zien dat 2 keer per dag trilostane geven beter is dan een keer per dag. Als endocrinoloog, denk ik ook dat het beter zou zijn om het hormoon cortisol de hele dag te gaan remmen en niet maar enkele uren per dag. Trilostane zou namelijk maar 6 tot 8 uur moeten werken, dus met 1 keer per dag toedienen is de daling van cortisol maar enkele uren. Maar toch hebben wij goede ervaring met 1 keer per dag therapie en omdat dit ook praktisch en `goedkoop` voor de eigenaar is, is het onze standaard om met 1 keer per dag te starten.
Er zijn wel situaties dat de trilostane 2 keer per dag gebruik wordt:
- De hond krijgt al een tijdje trilostane, maar heeft nog steeds klachten van Cushing (veel drinken en plassen, etc.). Dus het idee zou zijn om de dosis te verhogen, maar de ACTH stimulatie test laat zien dat de dosis NIET verhoogd mag worden – anders lopen wij risico op bijwerkingen. In zulke gevallen wordt de conclusie getrokken dat de trilostane zeer waarschijnlijk te kort werkt en wordt het medicijn 2 keer per dag gegeven. Tot nu toe is er nog geen test om te beoordelen hoe lang trilostane werkt. Wij dachten dat de UCCR (urine cortisol:kreatinine ratio) een goede methode zou kunnen zijn, maar dat is niet zo gebleken – tot mijn grote teleurstelling. De vraag is welke dosis gegeven moet worden als je van 1 naar 2 keer per dag gaat. In principe zou de huidige dosis 2 keer per dag gegeven kunnen worden, maar dat kan gauw te veel zijn. Dus wordt de dosis liever gesplitst. Bij voorbeeld: 20 mg 1 keer per dag laat onvoldoende effect zien, dan is de volgende stap 2 keer per dag 10 mg.
- De tweede indicatie om 2 keer per dag trilostane te gaan geven is als de hond ook diabetes heeft. Dan beginnen wij meteen met 2 keer per dag, de dosering is 1 mg/kg 2 keer per dag. Dit omdat de insuline ook 2 keer per dag gegeven wordt en omdat de cortisol spiegel op deze manier stabieler wordt.
Startdosering Vetoryl aangepast per 22 juli 2014
Dechra, de fabrikant van Vetoryl heeft in juli jl. op basis van ervaringsgegevens de startdosering van Vetoryl verlaagd naar 2 mg per kilo lichaamsgewicht. Dit zal ook genoemd worden op de nieuwe bijsluiter.
In dit artikel staat ook een mailadres van Dechra genoemd: technical@dechra.com.
Ik heb het benut om hen maar eens een mailbericht te sturen met het verzoek om meer diversiteit aan te brengen in de dosering van Vetoryl, dat tot op heden alleen verkrijgbaar is in 10 mg, 30 mg, 60 mg en 120 mg. Misschien vind je het zinvol om dit ook te doen; je kunt dan de tekst kopieren en Dechra per mail aanschrijven:
Acth test hund
MYASTHENIA GRAVIS: DIAGNOSTIC TESTS
General Principles of Diagnostic Testing for MG
- Rationale
- As thymectomy or long term immunotherapy may be necessary to treat MG, it is essential to establish a firm diagnosis
- A firm diagnosis avoids inappropriate treatments, and their side effects, in patients who do not have the disease.
- Strategy of diagnostic testing
- As a general rule, a firm diagnosis is based upon
- A characteristic history and physical examination, and
- Two positive diagnostic tests, preferably serological and electrodiagnostic.
- Diagnostic investigations of MG should usually include both
- Testing for serum anti-AChR antibodies
- Repetitive nerve stimulation studies
- As a general rule, a firm diagnosis is based upon
- Tensilon tests
- May be readily performed at the bedside
- Are not as sensitive, or specific, as the serological and electrophysiological studies
- Single fiber EMG: Reserved for selected patients in whom other tests have been negative or equivocal.
Edrophonium (Tensilon) Testing
- Action
- Inhibits acetylcholinesterase
- Prolongs presence of neurotransmitter, acetylcholine, in the NMJ
- Results in enhanced muscle strength
- Duration: Lasts for a few minutes
- Response
- In patients with NMJ dysfunction
- Not specific for MG
- Time course: Minutes; Rapid-onset; Short-acting
- Action
- Initially
- Dosing: 2 mg of edrophonium is administered intravenously as a test dose
- Monitoring heart rate: Bradycardia or ventricular fibrillation may develop
- Follow-up
- After observing for about 2 minutes, if no clear response develops
- Up to 8 additional mg of edrophonium is injected
- A double-blind protocol with a saline injection as placebo has been advocated
- Testing should be performed with patient free of all cholinesterase-inhibitor medications
- Cholinergic side effects of edrophonium
- May include increased salivation and lacrimation, mild sweating, flushing, urgency & perioral fasciculations.
- Atropine should be readily available to reverse effects of edrophonium in case of hemodynamic instability
- Extra precautions are especially important in elderly patients
- Most myasthenic muscles respond in 30 to 45 seconds after injection
- Improvement in strength that may persist for up to 5 minutes
- Requires objective improvement in muscle strength.
- Subjective or minor responses, such as reduction of a sense of fatigue, should not be over interpreted
- Only useful in patients with objective, preferably measurable, findings on physical examination
- Rarely helpful in the diagnostic evaluation of equivocal cases of MG
- Sensitivity for MG is relatively low (60%) compared to other diagnostic tests
- Tensilon testing should not be used to determine adjustments in the dose of pyridostigmine
- False positive results
- Can occur in patients with LES, ALS or even localized, intracranial mass lesions
- Positive testing does not necessarily predict respose to a longer-acting anti-AChE drug
Serum antibodies vs Acetylcholine Receptors
- AChR antibodies: General testing method
- Measurement using immunoprecipitation methodology
- Method: Human nicotinic AChRs from skeletal muscle labeled with 125 I-α-Bungarotoxin
- Antibody properties & types
- Type: IgG1-dominant
- Properties
- Binding
- Modulating
- Blocking
- vs AChR aggregates
- Low affinity
- Targets
- Antibody (IgG) targets in MG: Nicotinic AChRs
- α1-subunit of AChR
- Typical myasthenia gravis
- Epitope location: Main immunogenic region on extracellular tip of α1-subunit
- Main immunogenic region (MIR) features
- Cluster of overlapping epitopes
- Conformation dependent
- Also commonly a target of anti-AChR antibodies in Experimental autoimmune MG (EAMG)
- Cross-linking
- Single bivalent antibody cannot bind to both MIRs on same AChR
- Antibodies can cross-link adjacent AChRs
- Clinical correlation
- e -subunit
- Acquired slow channel syndrome
- Binding to Adult AChRs (containing e -subunit) 1
- 13% of serums with no IgG binding to fetal AChRs
- Increases finding (sensitivity) of anti-AChR antibodies in MG by
3%
- Occur in patients with either ocular or generalized MG syndromes
- γ-subunit
- Neonatal MG (Transient
- Arthrogryposis, Recurrent
- α1-subunit of AChR
- AChR binding antibodies: Measurement of serum IgG (& IgM) antibodies that bind to AChRs
- Antigenic target
- AChRs from human skeletal muscle: Mixed innervated & denervated, or
- Myogenic cell line expressing both adult & fetal AChRs
- Clinical relevance
- Relatively specific & sensitive test for MG
- Other types of AChR testing (Modulating & Blocking): Low specificity
- Anti-AChR antibodies occur in
- Adults with generalized MG: 85 to 90%
- Childhood MG: 50%
- Ocular MG: 50% to 70%
- Lower titers
- Bind best to adult AChRs with e subunit
- MG and thymoma: Nearly 100%
- Some patients taking penicillamine with or without MG
- "False" positives
- Thymoma without MG
- Immune liver disorders
- Older patients (> 70 years): 1% to 3%
- Neuromyotonia
- Antigenic target
- Antibody effects on AChRs: Other
- AChR Modulating Antibodies
- Mechanism
- Anti-AChR antibodies cross-link AChRs on the post-synaptic membrane
- Endocytosis & degradation of AChRs are accelerated
- Test results
- May occur in a rare patient when anti-AChR antibody binding is negative.
- MG: Usual loss = 20% to 90% of AChRs (Normal < 20%)
- MG with thymoma: > 90% loss
- False positives: Common
- Low specificity for MG
- Specific causes: Hemolysis; Muscle relaxant drugs; Serum heating
- Mechanism
- AChR blocking antibodies: Block binding site for ACh on AChR (positive = 26% to 100% blocking).
- Prevalence: Repeated arthrogryposis; 52% of generalized MG; 30% of ocular
- 1% of patients with no binding or blocking antibodies
- Complement binding
- Damage to postsynaptic membrane: Simplification of postsynaptic folds
- Widening of synaptic cleft
- AChR Modulating Antibodies
- Clinical correlations of MG & anti-AChR antibodies
- Absolute titer of AChR binding antibodies
- Among patients: No relation with severity of MG
- In individual patient: Improvement often seen with reduction in titer of > 50%
- Titer of antibody binding to main immunogenic region (MIR) of AChRs 2
- Correlates with disease severity: Ocular vs Generalized
- MIR location: Extracellular end of 2 α subunits of pentameric AChR
- > 50% of MG AChR Abs bind to MIR
- Antibody blocking & modulation of AChRs
- Some correlation with disease severity
- Not diagnostically specific
- Neonatal MG: Transient
- High anti-fetal/anti-adult muscle anti-AChR antibody ratio
- Recurrent arthrogryposis
- IgG vs γ subunit of fetal AChR: Blocks AChR function
- Slow channel syndrome: Acquired
- IgG vs adult AChR
- IgG vs Clustered AChRs 3
- Present in
- "Sero-Negative" ocular or generalized MG patients: 50%
- AChR Ab+ patients: Many
- Complement fixing
- Antibody subclass: IgG1
- Associated with thymic pathology: Lymphocytic infiltrates; Germinal centers
- Present in
- Neuronal AChR: α3 subunit
- Autonomic PN (42%)
- Isaacs (25%)
- LEMS (12%)
- Also see: AChR disorders
- Absolute titer of AChR binding antibodies
- Patients with MG but no anti-AChR antibodies
- Rule out hereditary MG
- Low frequency of thymic pathology & thymoma
- May have antibodies to other neuromuscular junction antigens
Repetitive Nerve Stimulation (RNS): 2 to 3 Hz
Repetitive Nerve Stimulation
- Most frequently used electrodiagnostic test for MG
- Nerve to be studied is electrically stimulated six to ten times at 2 or 3 Hertz
- Compound muscle action potential (CMAP) is recorded with surface electrodes over muscle
- Nerves tested
- At least one proximal & one distal motor nerve
- Innervation of weak muscles
- If decrement present
- Repeat RNS: To ensure decrement is reproducible
- Test for: Post-exercise facilitation (Repair of decrement)
- Perform EMG
- Rule out: Denervating disorder producing decrement
- Look for: Small-short or Unstable motor unit action potentials supportive of NMJ disorder
- If NO decrement at baseline
- Look for post exercise exhaustion: Appearance of decrement after exercise
- Perform: Single fiber EMG
- Normal muscles: No change in CMAP amplitude with repetitive nerve stimulation
- Myasthenia gravis
- Progressive decline in CMAP amplitudes with the first 4 to 5 stimuli
- Caused by failure (Block) of increasing number of NMJs
- Positive RNS test features
- Decrement in CMAP amplitude
- Size: More than 10% in reduction in CMAP amplitude
- Measure from 1st to 4th or 5th potential in train
- Smallest CMAP is often 2nd or 3rd potential in train
- Size: More than 10% in reduction in CMAP amplitude
- Post-tetanic potentiation (Post-exercise facilitation)
- Definition: Reduction in (Repair of) decrement after exercise
- Stimulus: Isometric exercise, brief (10 to 15 sec)
- Time course
- Onset: Immediate
- Duration:
2 minutes
- Degree of repair: Partial or Complete
- Post-exercise exhaustion
- Definition: Post exercise appearance, or exacerbation, of decremental response
- Protocol
- Stimulus: Muscle exercise for 1 minute
- Repeat RNS after 1, 2, 3 and 4 minutes
- Time course
- Onset: Maximal 3 to 5 minutes after exercise
- Disappears by: 10 minutes after exercise
- Decrement in CMAP amplitude
- RNS is positive in about 75% of patients with generalized MG, if:
- Proximal & Clinically involved muscles are tested
- Muscle is warm: Cooling reduces size of decrement
- More than one muscle is tested: Strong muscles often have less decrement
- Diagnostic issues
- Sensitivity of RNS for MG
- Sensitivity in generalized MG
- Overall: 75% to 80%
- Increased
- Proximal & Clinically involved muscles are tested
- Muscle is warm
- More than one muscle is tested
- Reduced
- Only distal muscles are tested
- Cooling: Reduces size of decrement
- Childhood MG
- Acute severe generalized or bulbar MG (≤ 4 weeks of disease): 11% to 40% positive 4
- Often have abnormal jitter
- Strong muscles: Often have less decrement
- Ocular MG: 50%
- Sensitivity in generalized MG
- Diagnostic specificity
- A decremental response to RNS is not specific for MG
- Decrements may also be seen in
- Presynaptic disorders: Such as LEMS
- Motor neuron diseases: Including ALS
- Myopathies: McArdle's; Myotonia
- Sensitivity of RNS for MG
- Progressive decline in CMAP amplitudes with the first 4 to 5 stimuli
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Urine Cortisol
By Kristiina Ruotsalo, DVM, DVSc, Dip ACVP & Margo S. Tant BSc, DVM, DVSc
What is the urine cortisol/creatinine ratio?
Cortisol is a stress hormone that is excreted from the body in the urine. The amount of cortisol in the urine reflects the average cortisol concentration in the blood at the time that the urine was formed. However, this measurement is affected by the concentration of the urine. Creatinine is a product of muscle metabolism and it is normally lost in the urine at a relatively steady rate. Because of this, the ratio of cortisol to creatinine in the urine can be used to account for the effect of urine concentration.
Why is this test done?
The urine cortisol/creatinine ratio is usually evaluated in animals suspected of having Cushing's disease (hyperadrenocorticism). When an animal has hyperadrenocorticism (Cushing's disease or syndrome), it produces an excessive amount of cortisol. This increased blood cortisol concentration results in increased loss of cortisol into the urine. Therefore, the urinary cortisol/creatinine ratio is usually increased in animals with Cushing's disease.
Does an increased urine cortisol/creatinine ratio always mean that Cushing's disease is present?
No, there are other causes of an increased urinary cortisol/creatinine ratio. Simple stress, such as a car ride or a visit to your veterinarian, may cause a mild increase in this ratio. The presence of other illnesses may also result in increased cortisol production by the adrenal glands and thereby increase this ratio.
However, if your pet has appropriate clinical signs and other initial screening tests (CBC, urinalysis, and biochemical profile) are supportive of Cushing's disease, then further confirmatory testing for Cushing's disease is indicated. Additional tests may include the ACTH stimulation test and/or the dexamethasone suppression test.
What does a normal urine cortisol/creatinine ratio mean?
Like any other test, the urine cortisol/creatinine ratio result must always be evaluated along with other clinical information and data. However, if the cortisol/creatinine ratio is not elevated, then it is very unlikely that your pet has Cushing's disease.
"If the cortisol/creatinine ratio is not elevated, then it is very unlikely that your pet has Cushing's disease."
Exactly how is the urine cortisol/creatinine ratio test done?
This test involves the collection of a single urine sample, taken first thing in the morning. Ideally, this sample should be collected at your home, to minimize the effects of stress due to a hospital visit. By collecting a first morning sample, the average amount of cortisol that has been lost into the urine overnight can be assessed. The urine sample is usually sent to a referral lab for analysis.
Antibody Titres
Antibodies are specialized proteins, also called immunoglobulins that are primarily found in the bloodstream. They are produced by specialized white blood cells called plasma cells, a form of lymphocyte.
Bile Acid Test
The bile acid test is a very useful test that helps to determine if the liver is working properly.
Preparing Your Pet for a Blood Test
Having your pet properly prepared before blood collection helps to ensure that test results are as accurate and reliable as they can be. Sometimes abnormal test results say more about how the pet was prepared than about true illness.
©Copyright VCA Hospitals all rights reserved.
Iatrogenic Hyperadrenocorticism in Dogs (Cushing’s Syndrome)
Hyperadrenocorticism in dogs may occur spontaneously or may be iatrogenic from the administration of glucocorticoids (GC) like prednisone (a steroid). Spontaneous hyperadrenocorticism is pituitary dependent (most commonly a pituitary gland adenoma producing ACTH hormone that signals the adrenal gland to produce cortisol hormone without feedback regulation) or adrenal dependent from an adrenal tumor (tumor produces excess cortisol without feedback regulation). The excess cortisol is responsible for the clinical signs and abnormalities seen with hyperadrenocorticism (“Cushing’s Syndrome”).
Iatrogenic hyperadrenocorticism is what veterinary dermatologists see most in the face of GC use for the diseases we manage- allergies (canine atopic dermatitis), autoimmune diseases (pemphigus foliaceus) and other immune mediated skin conditions. The diagnosis of iatrogenic hyperadrenocorticism is made based upon history, exam findings, general laboratory work findings (complete blood count, serum biochemistry test, urinalysis, urine cortisol to creatinine ratio) and tests to evaluate the pituitary adrenocortical axis (ACTH stimulation test, low-dose dexamethasone suppression test). Abdominal ultrasounds may also be done as a screening test.
Iatrogenic hyperadrenocorticism is often seen in toy and small breed dogs, but large breed dogs may also be affected. The average age is 10-14 yrs and the average time on a GC medication is 9.4 months. We see this with oral, injectable, and topical use of GC. It may be seen with both appropriate and excessive use of these medications. Signs may include an enlarged liver upon palpation of the abdomen, a “pot belly” appearance of the abdomen, obesity, muscular atrophy, lethargy, excessive water consumption, excessive urinations, and excessive appetite. Skin changes include thinning of the hair coat and skin, prominent cutaneous vasculature, hair loss that may or may not be symmetrical, hyperpigmentation of skin, scaling, bruising, poor wound healing, and calcinosis cutis (mineralization of the skin).
Related: Treatment for Calcinosis Cutis in Dogs
Secondary infections of the skin may occur with bacteria, yeast and some fungi (dermatophyte) due to impaired immune defenses. A mange, demodex mites, may also be a secondary problem. Laboratory work may reveal elevated liver enzymes, cholesterol, triglycerides, and blood glucose. The urine is usually dilute and there may be a urinary tract infection. Complete blood counts also have characteristic features. A definitive test may be done, ACTH stimulation test, and would be consistent with exogenous use of GC by showing a suppressed cortisol concentration at baseline and poor stimulation of cortisol production 1 hour after ACTH administration. Management of dogs with iatrogenic hyperadrenocorticism involves monitored discontinuation of exogenous GC, treatment of any secondary infections, and monitoring of the laboratory work. Identification and control of the primary disease for which GC were being administered warrants careful review and alternative therapies.
About Northeast Veterinary Dermatology Specialists (NVDS): Northeast Veterinary Dermatology Specialists is a full-service dermatology practice, with a dedicated team of veterinary staff treating diseases involving the skin, hair, ears, and nails. Services, tests and procedures provide the most effective, safe and state-of-the-art care in New York and Connecticut.
Animal dermatology and allergy specialists Dr. Nina Shoulberg and Dr. Lauren Pinchbeck, and their veterinary technicians, treat diseases stemming in part from allergies, bacterial infections, fungal infections, parasitic infestations, endocrine disorders, and immune-mediated diseases.
Services include: intradermal and serum testing for airborne allergens, immunotherapy, the diagnosis and treatment of ear diseases using video otoscopy, and removal of skin tumors using a carbon dioxide laser.
©2018 Northeast Veterinary Dermatology Specialists. All rights reserved.
Hypoadrenocorticism
(Addison disease)
By David Bruyette, DVM, DACVIM, Medical Director, VCA West Los Angeles Animal Hospital
- The Adrenal Glands
- Overview of the Adrenal Glands
- Adrenal Cortex
- Cushing Syndrome (Hyperadrenocorticism)
A deficiency in adrenocortical hormones is seen most commonly in young to middle-aged dogs and occasionally in horses. The disease may be familial in Standard Poodles, West Highland White Terriers, Great Danes, Bearded Collies, Portuguese Water Dogs, and a variety of other breeds. The cause of primary adrenocortical failure usually is unknown, although most cases probably result from an autoimmune process. Other causes include destruction of the adrenal gland by granulomatous disease, metastatic tumor, hemorrhage, infarction, adrenolytic agents ( mitotane ), or adrenal enzyme inhibitors (trilostane).
Clinical Findings:
Many of the functional disturbances of chronic adrenal insufficiency are not highly specific; they include recurrent episodes of gastroenteritis, a slowly progressive loss of body condition, and failure to respond appropriately to stress. Although hypoadrenocorticism is seen in dogs of any breed, sex, or age, idiopathic adrenocortical insufficiency is most common in young female adult dogs. This may be related to its suspected immune-mediated pathogenesis.
A reduction in secretion of aldosterone, the principal mineralocorticoid, results in marked alterations of serum levels of potassium, sodium, and chloride. Potassium excretion by the kidneys is reduced and results in a progressive increase in serum potassium levels. Hyponatremia and hypochloremia result from renal tubular loss. Severe hyperkalemia may result in bradycardia and an irregular heart rate with changes in the ECG. Some dogs develop a pronounced bradycardia (heart rate ≤50 bpm) that predisposes to weakness or circulatory collapse after minimal exertion.
Although the development of clinical signs is often unnoticed, acute circulatory collapse and evidence of renal failure frequently occur. A progressive decrease in blood volume contributes to hypotension, weakness, and microcardia. Increased excretion of water by the kidneys, because of decreased reabsorption of sodium and chloride, results in progressive dehydration and hemoconcentration. Emesis, diarrhea, and anorexia are common and contribute to the animal’s deterioration. Weight loss is frequently severe. Similar clinical signs are seen in cats with hypoadrenocorticism.
Decreased production of glucocorticoids results in several characteristic functional disturbances. Decreased gluconeogenesis and increased sensitivity to insulin contribute to the development of moderate hypoglycemia. In some dogs, hyperpigmentation of the skin is seen because of the lack of negative feedback on the pituitary gland and increased ACTH release. Atypical Addison disease has been reported in dogs and is associated with hypocortisolemia with normal electrolytes. Clinical signs are similar to those seen in dogs with both glucocorticoid and mineralocorticoid insufficiency.
The most common abnormality in dogs is bilateral idiopathic adrenocortical atrophy, in which all layers of the cortex are markedly reduced in thickness. The adrenal cortex is reduced to one-tenth or less of its normal thickness and consists primarily of the adrenal capsule. The adrenal medulla is relatively more prominent and, with the capsule, makes up the bulk of the remaining adrenal glands.
All three zones of the adrenal cortex are involved, including the zona glomerulosa, which is not under ACTH control; however, no obvious pituitary lesions have been seen in dogs with idiopathic adrenal cortical atrophy.
A destructive pituitary lesion that decreases ACTH secretion is characterized by severe atrophy of the inner two cortical zones of the adrenal gland; the zona glomerulosa remains intact.
A presumptive diagnosis is based on the history and supportive (although not specific) laboratory abnormalities, including hyponatremia, hyperkalemia, a sodium:potassium ratio of 11 mEq/L.
Differential diagnoses include primary GI disease (especially whipworm infection), renal failure, acute pancreatitis, and toxin ingestion. For definitive diagnosis, evaluation of adrenal function is required. After obtaining a baseline blood sample, ACTH (gel or synthetic) is administered. Gel preparations are administered IM, and a second blood sample is obtained 2 hr later. Synthetic preparations are administered IM or IV with a second blood sample 1 hr later. Baseline (resting) cortisol concentrations >2.5 mcg/dL effectively exclude the diagnosis of hypoadrenocorticism, whereas values
An adrenal crisis is an acute medical emergency. An IV catheter should be inserted, and an infusion of 0.9% saline begun. If the dog is hypoglycemic, the saline should include 2.5%–5% dextrose. The hypovolemia is corrected rapidly by administering 0.9% saline (60–70 mL/kg over the first 1–2 hr). Urine output should be assessed to determine whether the dog is becoming anuric. Fluids should be continued, at a rate appropriate to match ongoing losses, until the clinical signs and laboratory abnormalities have resolved.
Prednisolone sodium succinate (22–30 mg/kg) or dexamethasone sodium phosphate (0.2–1 mg/kg) may be used in the initial management of shock. Dexamethasone will not interfere with cortisol measurements during the ACTH stimulation test. Prednisolone or prednisone should be given at 1 mg/kg, bid, for the first few days of therapy and then at 0.25–0.5 mg/kg/day. Mineralocorticoid replacement therapy (see below) is also begun to help with electrolyte imbalances and hypovolemia. Electrolytes, renal function, and glucose should be monitored regularly to assess response to therapy.
In cases of severe, nonresponsive hyperkalemia, 10% glucose in 0.9% saline can be given for 30–60 min to increase potassium movement into the cells. Regular insulin (0.25–1 U/kg) administered IM will enhance glucose and potassium uptake, but 10% glucose (20 mL per unit of insulin) should be administered IV concurrently to avoid hypoglycemia.
For longterm maintenance therapy, the mineralocorticoid desoxycorticosterone pivalate (DOCP) is administered at 2.2 mg/kg, IM or SC, every 25–28 days. Electrolytes should be measured at 3 and 4 wk after the first few injections to determine the duration of action. Alternatively, fludrocortisone acetate is administered PO at 10–30 mcg/kg/day. Serum electrolytes should be monitored weekly until the proper dose is determined. Some dogs (especially dogs on DOCP) also require daily oral glucocorticoid therapy to adequately control clinical signs. Replacement doses of prednisone (0.2–0.4 mg/kg/day) are required in
50% of dogs. Additional glucocorticoid supplementation may be required (2–5 times maintenance) during times of illness or stress. Dogs with atypical Addison disease require only replacement doses of prednisone , although it is recommended that electrolytes be monitored every 3 mo for the first year after diagnosis. Dogs with chronic hypoadrenocorticism should be reexamined every 3–6 mo.
Treatment of horses with hypoadrenocorticism is similar—aggressive replacement of fluids, steroids, and glucose if needed in an adrenal crisis. Supportive therapy and rest are indicated in cases of chronic Addison disease.
- The Adrenal Glands
- Overview of the Adrenal Glands
- Adrenal Cortex
- Cushing Syndrome (Hyperadrenocorticism)
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Which of the following serum biochemical abnormalities is most likely to occur in a dog with primary hypothyroidism?
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