'm writing about a 7-year-old lab that present today for signs associated with hypoglycemia.He has been progressive lethargic for the last week. The owner noted staggering and weakness and brought him into our clinic for evaluation yesterday.
On examination, the dog was quiet but clinically normal. His blood glucose concentration, however, was low at 26 mg/dl (reference range, 70-125 mg/dl). All other serum chemistry results (including serum sodium and potassium were normal. Radiographs of the chest and abdomen were unremarkable. The owner has been quizzed at length about possible xylitol ingestion, but there is no history of possible ingestion.
We hospitalized the dog for observation and started a 5% dextrose drip overnight. This morning, the blood glucose was still quite low (only 47 mg/dl) after being off dextrose for about an hour. I continued the glucose drip (raised it to a 10% drip), and the blood glucose concentrations ranged from 41 to 70 mg/dl throughout the day. He is eating well and alert on the IV glucose supplementation.
My rule outs are the following intoxications or medical disorders:
- Xylitol ingestion
- Atypical Addison's (the serum electrolytes and Na:K ratio were normal)
- Insulinoma (insulin-secreting pancreatic islet cell tumor)
- Portosystemic shunt
I have submitted an serum insulin level at the time when the dog's blood glucose was very low (42 mg/dl) and the results are still pending. I've also submitted a baseline cortisol concentration to help rule out Addison's disease. I have not measured his serum bile acids because I did not want to fast him just yet.
Any other thoughts, suggestions for diagnostics? Anything I am missing?
My Response:
You have the correct list of differential diagnoses and are working your way through the list properly. I'd agree with not fasting the dog — I'd just do a random bile acid measurement to first see it that's abnormal.
If this dog has an insulinoma, we have to remember that IV administration of dextrose may stimulate secretion by the pancreatic tumor. Insulin release post-hyperglycemia often results in rebound hypoglycemia, which necessitates additional dextrose administration and leads the clinician into a cyclical hyperglycemia/hypoglycemia "chase" which can be difficult to terminate.
In this cases, it an be really helpful to just use glucagon instead. Glucagon for injection (1 mg vial) is reconstituted according to the manufacturer's instructions with supplied diluent, then added to 1000 ml of 0.9% NaCl. The 1000 ng/ml solution is administered intravenously as a constant rate infusion (CRI) with the use of a syringe infusion pump. The glucagon CRI is initially given as a bolus of 50 ng/kg, then administered at a rate of 10 to 15 ng/kg/min. The dose may need to be increased up to 40 ng/kg/min as needed to maintain euglycemia.
Additional Followup:
I've put the dog on a glucagon constant rate infusion and it's been working great to maintain the blood glucose concentration in the normal range in the hospital!
The dog's resting serum cortisol concentration was normal at 3.2 µg/dl, so Addison's disease appears highly unlikely. My serum insulin and bile acid results still pending.
The owner has been internet investigating and he told me that his dog has eaten a birch limb/stick last week. I read that xylitol is derived from hardwoods such as birch — Is there any way the xylan from the birch could be metabolized to xylitol in the dog?
My Response:
You're right, the normal serum cortisol (>2.0 µg/dl) rules out Addison's disease.
As far as xylitol toxicity is concerned, I did some research myself and found that birch wood itself doesn't contain xylitol so that's unlikely to be the cause of the hypoglycemia. And this would be especially true since it was consumed a week ago, and you wouldn't expect continued hypoglycemia if the problem was due to xylitol toxicity.
Outcome:
The dog's serum insulin concentration, collected at the time of severe hypoglycemia, was extremely high (402 pmol/L; reference
range, 60-230 pmol/L). The bile acids values were normal. An abdominal ultrasound revealed a pancreatic mass with several hypoechoic areas in liver, consistent with pancreatic neoplasia with metastasis to the liver. A trial of diazoxide was performed at home, but hypoglycemia persisted.
Based on the poor prognosis and lack of response to diazoxide, the owners elected euthanasia. Multiple pancreatic and hepatic nodules were identified at necropsy; histopathology confirmed beta cell islet cell neoplasia with metastasis to the liver.
Final Diagnosis: Insulinoma (insulin-secreting carcinoma of pancreas), producing hypoglycemia.
References:
- Dunayer EK. Hypoglycemia following canine ingestion of xylitol-containing gum. Veterinary and Human Toxicology 2004;46:87-88.
- Leifer CE, Peterson ME, Matus RE. Insulin-secreting tumor: diagnosis and medical and surgical management in 55 dogs. Journal of the American Veterinary Medical Association 1986;188:60-64.
- Smith SA. Miscellaneous Endocrine Disorders. In Morgan RH, Bright, R, and Swartout MS (eds). Handbook of Small Animal Practice, Fourth Edition. W. B. Saunders, Philadelphia, PA. 2003:731-751.
- Fischer JR, Smith SA, Harkin, KR. Glucagon constant rate infusion: a novel strategy for the management of hyperinsulinemic-hypoglycemic crisis in the dog. Journal of the American Animal Hospital Association 2000; 36:27-32.
- Lennon EM, Boyle TE, Hutchins RG, et al: Use of basal serum or plasma cortisol concentrations to rule out a diagnosis of hypoadrenocorticism in dogs: 123 cases (2000-2005). Journal of the American Veterinary Medical Association 2007;231:413-16.
Źródło: endocrinevet.blogspot.com
In my second compilation of the canine and feline endocrine publications of 2010, I’m sticking with disorders of the pancreas. But now let’s now move on to islet cell tumors (eg, insulinoma) and other causes of hypoglycemia.
Listed below are 6 research papers written in 2010 that review new aspects in the diagnosis or therapy of insulin-secreting tumors of the pancreas (1, 3), pancreatic polypeptide-secreting islet cell tumor (2), glucagon-secreting islet cell tumor or glucagonoma (4), and paraneoplastic hypoglycemia (6).
2010 Papers on Canine and Feline Islet Cell Tumors of the Pancreas and Other Causes for Hypoglycemia:
1. Buishand FO, Kik M, Kirpensteijn J. Evaluation of clinico-pathological criteria and the Ki67 index as prognostic indicators in canine insulinoma. Veterinary Journal 2010;185:62-67.
2. Cruz Cardona JA, Wamsley HL, Farina LL, et al. Metastatic pancreatic polypeptide-secreting islet cell tumor in a dog. Veterinary Clinical Pathology 2010;39:371-376.
3. Moretti S, Tschuor F, Osto M, et al. Evaluation of a novel real-time continuous glucose-monitoring system for use in cats. Journal of Veterinary Internal Medicine 2010;24:120-126.
4. Oberkirchner U, Linder KE, Zadrozny L, et al. Successful treatment of canine necrolytic migratory erythema (superficial necrolytic dermatitis) due to metastatic glucagonoma with octreotide. Veterinary Dermatology 2010;21:510-516.
5. Rivera N, Ramnanan CJ, An Z, et al. Insulin-induced hypoglycemia increases hepatic sensitivity to glucagon in dogs. The Journal of Clinical Investigation 2010;120:4425-4435.
6. Rossi G, Errico G, Perez P, et al. Paraneoplastic hypoglycemia in a diabetic dog with an insulin growth factor-2-producing mammary carcinoma. Veterinary Clinical Pathology 2010;39:480-484.
Źródło: endocrinevet.blogspot.com
I
have recently switched one of my canine diabetic patients from NPH insulin to detemir. This is the first time I have used this insulin and I am looking for some help.
Rex is a 10-yr-old, male Schnauzer mix. We started him on 3 units of detemir twice daily and he is currently on 3.5 units twice daily.
We admitted Rex for a glucose curve today. His results were as follows:
8:00 am- 482 mg/dl (fasted and no insulin since 8 pm dose)
8:15 am- 3.5 units of detemir given and dog fed
9:15 am - 445 mg/dl
10:20 am- 301 mg/dl
12:30 pm- 147 mg/dl
1:25 pm- 97 mg/dl
2:30 pm- 80 mg/dl
3:30 pm- 72 mg/dl
4:40 pm- 82 mg/dl
5:10 pm- 108 mg/dl
I like the low glucose values in the middle of the day but am concerned about the severe morning hyperglycemia.
Any recommendations? Thank you for any help.
My Response:
How much does this dog weigh? The dose of detemir (Levemir insulin) we start at is generally around 0.1 mg/kg twice daily, so 7 U per day seems rather high (unless it's a big Schnauzer)
That all said, this curve doesn't look so bad. Like you, I'm not bothered by the afternoon glucoses. They still are normal and not low. Are the owners feeding the same food morning and night? Did the dog eat normally on the day of the glucose curve when hospitalized? If not, that could explain why the insulin worked so well that day; could it be that at home, the glucoses remain higher?
It seems unlikely that the blood sugar would go from 108 mg/dl at 5:10 PM to levels in the 400s 3 hours later when it's time for the shot again. Are the owners giving the insulin and then waiting before feeding?
If the dog is eating well, I like to give the insulin about 30 minutes before eating to ensure some insulin has been absorbed before feeding. We could consider that in this patient if not already being done.
Finally, is this dog feeling well? How if the thirst, appetite and attitude? We must always remember to look at the dog and talk to the owner. We can never just depend on blood glucose curves to make insulin dose adjustments,
Follow-up Information and Additional Questions:
Rex weighs 39 pounds (17.7 kg). The owners report that he is feeling great at home, has gained a little weight recently (1 pound over last 2 months). He is indeed feeling better, playing, and acting normal.
He didn't eat well while here for the curve so I would assume those middle-of-the-day glucose values would be higher at home. I can question the owners better about the timing of the feeding at home. I didn’t realize that could even be a factor!
Do you have owners feed the animal at home before coming in for the curve? Would the next step be to redo the glucose curve on a day when he has eaten that morning?
Would increasing the dose up to 4 units BID before the next curve be advisable?
My Response:
A common problem with the glucose curves is that dogs (or cats) don't eat well in the hospital, and results of a glucose curve really don’t mean much when they haven't eaten. I know it's nice to have a pretreatment glucose, but that's not as important to what else is going on throughout the day.
Given that the dog is doing well at home (which is much more important than ANY blood glucose curve!), I would not raise the dose just yet.
I would recommend repeat the glucose curve following this protocol: I would have them give the insulin injection, wait 15-30 minutes, fed exactly the food and amount that they normally do at home, and then bring the dog in to start the glucose curve shortly thereafter. If the glucose readings drop into the low-normal range as they did before, it would be helpful if you could go longer than 8 hours with your glucose monitoring.
1. Owner gives the insulin injection
2. Wait 30 minutes before feeding
3. Feed exactly the normal diet in the exact amount normally feed every other day
4. Then bring the dog to your hospital to start the glucose curve shortly thereafter
5. Measure blood glucose concentrations every 2 hours for at least 8 hours, but 12 hours is better if possible.
Finally, another way to get around some of these problems is to have the owners do home glucose monitoring. With a bit of training, most dog and cat owners can be trained how to do the measurements at home. This is particularly helpful in cats, where they almost all develop ‘stress’ hyperglycemia in the hospital.
Źródło: endocrinevet.blogspot.com
have recently switched one of my canine diabetic patients from NPH insulin to detemir. This is the first time I have used this insulin and I am looking for some help.Rex is a 10-yr-old, male Schnauzer mix. We started him on 3 units of detemir twice daily and he is currently on 3.5 units twice daily.
We admitted Rex for a glucose curve today. His results were as follows:
8:00 am- 482 mg/dl (fasted and no insulin since 8 pm dose)
8:15 am- 3.5 units of detemir given and dog fed
9:15 am - 445 mg/dl
10:20 am- 301 mg/dl
12:30 pm- 147 mg/dl
1:25 pm- 97 mg/dl
2:30 pm- 80 mg/dl
3:30 pm- 72 mg/dl
4:40 pm- 82 mg/dl
5:10 pm- 108 mg/dl
I like the low glucose values in the middle of the day but am concerned about the severe morning hyperglycemia.
Any recommendations? Thank you for any help.
My Response:
How much does this dog weigh? The dose of detemir (Levemir insulin) we start at is generally around 0.1 mg/kg twice daily, so 7 U per day seems rather high (unless it's a big Schnauzer)
That all said, this curve doesn't look so bad. Like you, I'm not bothered by the afternoon glucoses. They still are normal and not low. Are the owners feeding the same food morning and night? Did the dog eat normally on the day of the glucose curve when hospitalized? If not, that could explain why the insulin worked so well that day; could it be that at home, the glucoses remain higher?
It seems unlikely that the blood sugar would go from 108 mg/dl at 5:10 PM to levels in the 400s 3 hours later when it's time for the shot again. Are the owners giving the insulin and then waiting before feeding?
If the dog is eating well, I like to give the insulin about 30 minutes before eating to ensure some insulin has been absorbed before feeding. We could consider that in this patient if not already being done.
Finally, is this dog feeling well? How if the thirst, appetite and attitude? We must always remember to look at the dog and talk to the owner. We can never just depend on blood glucose curves to make insulin dose adjustments,
Follow-up Information and Additional Questions:
Rex weighs 39 pounds (17.7 kg). The owners report that he is feeling great at home, has gained a little weight recently (1 pound over last 2 months). He is indeed feeling better, playing, and acting normal.
He didn't eat well while here for the curve so I would assume those middle-of-the-day glucose values would be higher at home. I can question the owners better about the timing of the feeding at home. I didn’t realize that could even be a factor!
Do you have owners feed the animal at home before coming in for the curve? Would the next step be to redo the glucose curve on a day when he has eaten that morning?
Would increasing the dose up to 4 units BID before the next curve be advisable?
My Response:
A common problem with the glucose curves is that dogs (or cats) don't eat well in the hospital, and results of a glucose curve really don’t mean much when they haven't eaten. I know it's nice to have a pretreatment glucose, but that's not as important to what else is going on throughout the day.
Given that the dog is doing well at home (which is much more important than ANY blood glucose curve!), I would not raise the dose just yet.
I would recommend repeat the glucose curve following this protocol: I would have them give the insulin injection, wait 15-30 minutes, fed exactly the food and amount that they normally do at home, and then bring the dog in to start the glucose curve shortly thereafter. If the glucose readings drop into the low-normal range as they did before, it would be helpful if you could go longer than 8 hours with your glucose monitoring.
1. Owner gives the insulin injection
2. Wait 30 minutes before feeding
3. Feed exactly the normal diet in the exact amount normally feed every other day
4. Then bring the dog to your hospital to start the glucose curve shortly thereafter
5. Measure blood glucose concentrations every 2 hours for at least 8 hours, but 12 hours is better if possible.
Finally, another way to get around some of these problems is to have the owners do home glucose monitoring. With a bit of training, most dog and cat owners can be trained how to do the measurements at home. This is particularly helpful in cats, where they almost all develop ‘stress’ hyperglycemia in the hospital.
Źródło: endocrinevet.blogspot.com
I
have a 14-year-old female spayed DSH feline weighing 5.4 kg, who was diagnosed with diabetes one year ago. To date, she has been receiving 4 IU of PZI (ProZinc) twice daily, and the owners have been very good about keeping her on a diet of high protein/low carbohydrate canned food only.
The owners would like to try switching from the insulin to an oral hypoglycemic agent (glipizide or glyburide). They travel a lot and have difficulty finding someone to look after her, and even having to board her at the clinic is a problem because she is very fractious and difficult to catch and give injections too. The owners themselves can manage just fine with the insulin injections, but no one else can.
Recently, I did some blood work on her and she is doing great. She is no longer polydipsic or polyuric, her serum glucose was normal at 122 mg/dl, and her serum fructosamine was 275 µmol/l (reference range 150-350 µmol/l).
My questions are the following:
- How do I properly transition her to the glipizide or glyburide if we decide to go that route?
- Does this cat even need to continue with insulin or oral glucose products, or can I control her on diet therapy alone at this point?
- Could this cat be going into diabetes remission?
My Response:
The lack of clinical signs and normal fructosamine certainly indicates good diabetes control, and it is possible that the cat is going into remission. Clinical remission is actually not infreqent in cats with well-controlled diabetes mellitus (1).
However, remission, when it does occur, generally develops earlier than a year (generally within the first 3 months of starting insulin therapy) so it's less likely that a cat treated with insulin for a year would be in remission. In addition, when most cats are going into remission, they're generally not normal on 4 units BID — that would be an overdose in most cats in remission. The more typical scenario in a cat going into remission is that their glucose values are dropping too low even on 1 unit BID.
That all said, diabetic remission is possible at any time and it's still possible that your cat is going into remission.
Ideally, the first step in judging remission would be for you would do a complete glucose curve to see if the blood glucose concentrations remain normal through out the day. The finding of a single "normal" blood sugar really doesn't tell you very much at all.
I understand that hospitalizing this fractious cat for a glucose curve would probably not be a pleasant experience for either you or the cat; more importantly, the "stress" would likely make the results meaningless anyway. Can the owners do home glucose monitoring? If so, that would be extremely helpful. Can they, at the very least, measure urine glucose at home?
In the end, how you decide whether the diabetes is going into remission or not is to slowly taper down the insulin dosage by 0.5 U decrements (e.g., start by decreasing from 4 U, BID to 3.5 U, BID). If the blood and/or urine glucose concentration remain normal after a week, then the insulin taper can continue until the insulin can hopefully be discontinued.
The chance of an oral hypoglycemic agent (glibizide or glyburide) working is very small. I personally think it's easier to give insulin to a fractious cat than to give a pill, especially in the hospital or in a kennel.
Remember, oral hypoglycemic agents act by stimulating insulin secretion from the pancreatic islet cells (2). In a cat with borderline diabetes that is going into remission, changing from insulin therapy to one of these drugs may actually be the worst thing to do.
Use of these oral hypoglycemic drugs, by overstimulating any remaining insulin secretion, my actually lead to the final "burn out" of insulin secretion and result in permanent diabetes (2).
Reference:
1. Zini E, Hafner M, Osto M, et al. Predictors of clinical remission in cats with diabetes mellitus. Journal of Veterinary Internal Medicine 2010;24:1314-132
2. Hoenig M, Hall G, Ferguson D, et al. A feline model of experimentally induced islet amyloidosis. American Journal of Pathology 2000; 157:2143-50
Źródło: endocrinevet.blogspot.com
I know that many of you are very busy and may have trouble keeping up with the latest research studies and publications on issues concerning companion animal endocrinology. Therefore, I’ve compiled a fairly extensive list of some of the best clinical endocrine papers written last year (in 2010), and I’ll be sharing these with you over the next few weeks.
We are going to start off with papers that deal with the theme of Diabetes mellitus and its diagnosis and treatment in dogs and cats.
Listed below are 29 research papers written in 2010 that deal with a variety of diabetic topics and issues.
These range from the use of continuous glucose monitoring systems (1, 15, 22) to home glucose monitoring (5, 28); from insulin autoantibodies (4, 18) to insulin resistance (11, 25, 26); from new insulin analogues (8, 10, 24) to diabetic cataracts (12, 21); and from the causes of secondary diabetes (2, 6, 13, 14, 16) to diabetic remission (29).
2010 Papers on Canine and Feline Diabetes Mellitus:
1. Affenzeller N, Benesch T, Thalhammer JG, et al. A pilot study to evaluate a novel subcutaneous continuous glucose monitoring system in healthy Beagle dogs. Veterinary Journal 2010;184:105-110.
2. 3Blois SL, Dickie EL, Kruth SA, et al. Multiple endocrine diseases in cats: 15 cases (1997-2008). Journal of Feline Medicine and Surgery 2010;12:637-642.
3. Claus MA, Silverstein DC, Shofer FS, et al. Comparison of regular insulin infusion doses in critically ill diabetic cats: 29 cases (1999-2007). Journal of Veterinary Emergency and Critical Care 2010;20:509-517.
4. Davison LJ, Herrtage ME, Catchpole B. Autoantibodies to recombinant canine proinsulin in canine diabetic patients. Research in Veterinary Science 2010.
5. Dobromylskyj MJ, Sparkes AH. Assessing portable blood glucose meters for clinical use in cats in the United Kingdom. The Veterinary Record 2010;167:438-442.
6. Fall T, Hedhammar A, Wallberg A, et al. Diabetes mellitus in elkhounds is associated with diestrus and pregnancy. Journal of Veterinary Internal Medicine 2010;24:1322-1328.
7. Furrer D, Kaufmann K, Reusch CE, et al. Amylin reduces plasma glucagon concentration in cats. Veterinary Journal 2010;184:236-240.
8. Gilor C, Graves TK. Synthetic insulin analogs and their use in dogs and cats. The Veterinary Clinics of North America Small Animal Practice 2010;40:297-307.
9. Gilor C, Graves TK, Lascelles BD, et al. The effects of body weight, body condition score, sex, and age on serum fructosamine concentrations in clinically healthy cats. Veterinary Clinical Pathology 2010;39:322-328.
10. Gilor C, Ridge TK, Attermeier KJ, et al. Pharmacodynamics of insulin detemir and insulin glargine assessed by an isoglycemic clamp method in healthy cats. Journal of Veterinary Internal Medicine 2010;24:870-874.
11. Hess RS. Insulin resistance in dogs. The Veterinary Clinics of North America Small Animal Practice 2010;40:309-316.
12. Kador PF, Webb TR, Bras D, et al. Topical KINOSTAT ameliorates the clinical development and progression of cataracts in dogs with diabetes mellitus. Veterinary Ophthalmology 2010;13:363-368.
13. McLauchlan G, Knottenbelt C, Augusto M, et al. Retrospective evaluation of the effect of trilostane on insulin requirement and fructosamine concentration in eight diabetic dogs with hyperadrenocorticism. The Journal of Small Animal Practice 2010;51:642-648.
14. Meij BP, Auriemma E, Grinwis G, et al. Successful treatment of acromegaly in a diabetic cat with transsphenoidal hypophysectomy. Journal of Feline Medicine and Surgery 2010;12:406-410.
15. Moretti S, Tschuor F, Osto M, et al. Evaluation of a novel real-time continuous glucose-monitoring system for use in cats. Journal of Veterinary Internal Medicine 2010;24:120-126.
16. Niessen SJ. Feline acromegaly: an essential differential diagnosis for the difficult diabetic. Journal of feline medicine and surgery 2010;12:15-23.
17. Niessen SJ, Powney S, Guitian J, et al. Evaluation of a quality-of-life tool for cats with diabetes mellitus. Journal of Veterinary Internal Medicine 2010;24:1098-1105.
18. Nishii N, Takasu M, Kojima M, et al. Presence of anti-insulin natural autoantibodies in healthy cats and its interference with immunoassay for serum insulin concentrations. Domestic Animal Endocrinology 2010;38:138-145.
19. Nishii N, Yamasaki M, Takasu M, et al. Plasma leptin concentration in dogs with diabetes mellitus. The Journal of Veterinary Medical Science 2010;72:809-811.
20. O'Brien MA. Diabetic emergencies in small animals. The Veterinary Clinics of North America Small Animal Practice 2010;40:317-333.
21. Oliver JA, Clark L, Corletto F, et al. A comparison of anesthetic complications between diabetic and nondiabetic dogs undergoing phacoemulsification cataract surgery: a retrospective study. Veterinary Ophthalmology 2010;13:244-250.
22. Reineke EL, Fletcher DJ, King LG, et al. Accuracy of a continuous glucose monitoring system in dogs and cats with diabetic ketoacidosis. Journal of Veterinary Emergency and Critical Care 2010;20:303-312.
23. Rucinsky R, Cook A, Haley S, et al. AAHA diabetes management guidelines. Journal of the American Animal Hospital Association 2010;46:215-224.
24. Sako T, Mori A, Lee P, et al. Time-action profiles of insulin detemir in normal and diabetic dogs
25. Scott-Moncrieff JC. Insulin resistance in cats. The Veterinary Clinics of North America Small Animal Practice 2010;40:241-257.
26. Verkest KR, Fleeman LM, Rand JS, et al. Basal measures of insulin sensitivity and insulin secretion and simplified glucose tolerance tests in dogs. Domestic Animal Endocrinology 2010;39:194-204.
27. Zeugswetter F, Handl S, Iben C, et al. Efficacy of plasma beta-hydroxybutyrate concentration as a marker for diabetes mellitus in acutely sick cats. Journal of Feline Medicine and Surgery 2010;12:300-305.
28. Zeugswetter FK, Rebuzzi L, Karlovits S. Alternative sampling site for blood glucose testing in cats: giving the ears a rest. Journal of Feline Medicine and Surgery 2010;12:710-713.
29. Zini E, Hafner M, Osto M, et al. Predictors of clinical remission in cats with diabetes mellitus. Journal of Veterinary Internal Medicine 2010;24:1314-1321.
Źródło: endocrinevet.blogspot.com
My patient is a 4-year-F/S Shetland sheepdog who has been treated with melatonin and flax seed oil since she was 11-months-old. Her main clinical sign was a chronic decrease in appetite, which started at 8-months of age when she had her first heat cycle.
Vaginal smears and cytology at that time was consistent with early estrus. She did not have noticeable bleeding, but she is very "tidy" and licks herself a lot. No polydipsia or polyuria was noted, and her hair coat has always been completely normal. Results of her physical examination were completely normal.
Two months later, we decided to spay her in case there was any connection between going into heat and the lack of appetite. A CBC and serum chemistry panel done before surgery were both normal. Routine ovariohysterectomy was performed. Examination of the uterus showed that it was more turgid than normal, but it did not show any evidence for pyometra or mucometra.
After surgery the dog became totally anorexic and vomited multiple time. She was referred to a local internal medicine specialist for workup. Based upon results of abdominal ultrasound, endoscopic exam and intestinal/stomach biopsies, a diagnosis of helicobacter pylori infection and inflammatory bowl disease (IBD) was made. Treatment with amoxicillin, metronidazole, and a food allergy diet was instituted, which quickly cleared up the intestinal signs and anorexia.
Because of the finding of bilateral adrenomegaly on abdominal ultrasound, however, an ACTH stimulation test was also performed shortly after surgery. Serum samples for an adrenal panel were submitted to the University of Tennessee Clinical Endocrinology Service Laboratory.
Atypical Cushing's disease was diagnosed on the basis the finding of a high baseline estradiol concentration (105.1 pg/ml; reference range, 30-69. pg/ml) as well as a high ACTH-stimulated estradiol value (111.1 pg/ml; 28-69 pg/ml). The other sex steroids tested (including 17-hydroyxprogrogesteone) were all within normal limits. Based on these results, she was started melatonin and flax seed oil for the atypical Cushing's syndrome.
Now 3 years later, the owner is asking me if her dog really needs the melatonin and flax seed oil. She has declined the offer of retesting the sex steroid panel on several occasions. The owner says her dog has been normal in every way, except for mild lethargy during the morning after she gives the melatonin. The owner believes the melatonin is causing sleepiness.
My questions are:
1. Do you think this dog has atypical Cushing's disease? It doesn't appear that she ever had any clinical signs of the disease.
2. If we stop the melatonin, how would we determine the need to go back on the drug?
My Response:
I really must admit that I've heard it all now — diagnosing atypical Cushing's disease in an 11-month old dog with the primary complaints of anorexia, inflammatory bowl disease, and helicobacter!
You cannot base a diagnosis of Cushing's disease — typical or atypical — on the finding of large adrenal glands on an ultrasound exam. This dog was severely ill when the ultrasound and ACTH stimulation test were performed. One would expect a sick dog to have a "stress" response, which would include increased secretion of pituitary ACTH leading to increased cortisol section. With chronic illness and continued stress, bilateral adrenocortical hyperplasia would be an expected finding as cortisol hypersecretion continues.
Cushing's syndrome (either typical or atypical disease) is a clinical diagnosis and must be based primarily on the dog's clinical features and physical examination findings. Dogs with Cushing's syndrome do NOT have anorexia and vomiting. They have a good to increased appetite, together with polyuria, polydipsia, hair loss, potbelly, and weakness. In my opinion, it was totally inappropriate to even test the dog for atypical Cushing's disease, given the total lack of any clinical features of the disease. Plus, this disease develops in older dogs, not dogs that are less than a year of age.
Bottom line:
- In any dog with chronic nonadrenal disease, the finding of enlarged adrenal glands with abdominal ultrasonography is not an uncommon finding due to the chronic stress of illness.
- This finding of "big adrenals" can never be used to confirm a diagnosis of Cushing's syndrome — be it typical or atypical hyperadrenocorticism.
- Diagnosis must be based on a combination of the typical clinical features of Cushing's disease together with results of standard pituitary function testing (i.e., low-dose dexamethasone suppression and ACTH stimulation testing).
I agree totally with the owner here. I would stop the melatonin and flax seed oil and monitor the clinical response. Why monitor for hormones when we don't even know what the elevations mean? We see many dogs tested with the sex steroid panel that have high serum estradiol values when the other hormone concentrations are normal.
In fact, I rarely see ANY dog tested that has normal values for estradiol. I can only assume that the labor seen a high incidence of false-positive results.
In support of my clinical experience, a recent research paper published by the head dermatologist at the University of Tennessee, College of Veterinary Medicine showed that serum estradiol concentrations varied considerably in clinically normal dogs (1). They concluded in this study that the finding of high estradiol concentrations alone cannot be used to diagnose atypical Cushing's syndrome, because of the high variability of these hormone results.
References:
Frank LA, Mullins R, Rohrbach BW. Variability of estradiol concentration in normal dogs. Vet Dermatology. 2010; 21:490-493.
Źródło: endocrinevet.blogspot.com
I
'm having a problem with Rigby, a 12-year-old male Lab mix diagnosed with pituitary-dependent Cushing's disease 3 years ago. We started him on trilostane (Vetoryl) at that time and the dog has done well, with complete resolution of clinical signs of polyuria and hair loss.
The owner called today and said that Rigby has been having urinary and defecation accidents in the house for 3 weeks. He has also been pacing, and possibly circling much of the night.
It sounds to me like the dog could be suffering from canine cognitive dysfunction. Can I use selegiline for canine cognitive dysfunction when the dog is already on treatment with trilostane? I was wondering, of course, because at one point in time selegilene was commonly used to treat Cushing's disease.
My plan is to first work the dog up to rule out an urinary tract infection, but do you have any other thoughts about the pacing and circling?
My Response:
First of all, your idea to do a workup for urinary tract infection (complete urinalysis with culture) is a good one and that should be the first step in your diagnostic testing. Urinary tract infections are common in dogs with Cushing's disease, even on treatment. If you haven't recently monitored the effects of trilostane treatment with an ACTH stimulation test, that should also be done at this time.
If you believe that Rigby has canine cognitive dysfunction, you can certainly use the drug selegiline hydrochloride, also known as L-deprenyl (veterinary trade name, Anipryl) along with the trilostane that the dog's already getting.
As you know, Anipryl is approved by the FDA for use in dogs for treatment of pituitary-dependent hyperadrenocorticism, as well as canine cognitive dysfunction. This drug has fallen out of favor for treating dog's with Cushing's syndrome because it only partially controlled the disease in most dogs.
For cognitive dysfunction, some owners have reported marked improvement changes in their geriatric dog's behavior after starting Anipryl, while other dogs may not respond at all. Because of the drug's low incidence of side effects, however, it's certainly worth a try in dogs with suspected cognitive dysfunction.
I'd also recommend a good neurological exam. Remember that this dog has pituitary-dependent Cushing's disease. In most of these dogs, the cause have a pituitary ACTH-secreting tumor. With time, these pituitary tumors can grow and become large macrotumors, expanding and compressing the hypothalamus. That of course could be the cause of the dog's pacing as well. If that is suspected, a CT or MRI is recommended to confirm the presence of a large pituitary mass.
Źródło: endocrinevet.blogspot.com
I have an 12-year-old F/S lab who was diagnosed with diabetes 4 months ago. The dog had typical signs of polyuria, polydipdia and weight loss.
She was initially started on NPH insulin at 0.4 U/kg BID (8 U BID). Over the course of 2 months, we increased the NPH dose to 0.7 U/kg BID (14 U BID) but the dog continued to be symptomatic. We did a blood glucose curve and obtained the following results:
- Fed at 7:30 AM
- Glucose at 8:30 AM: 132 mg/dl
- Glucose at 10:30 AM: 103 mg/dl
- Glucose at 12:30 PM: 160 mg/dl
- Glucose at 2:30 PM: 286 mg/dl
- Glucose at 4:00 PM: 381 mg/dl
Based on that curve was concerned that the duration was too short, so we switched to insulin detemir (Levemir). I know that detemir is more potent, so we started at 0.1 U/kg BID (2 units BID). The blood glucose curve 1 week later:
- Fed at 7:30 AM
- Glucose at 8:30 AM: 580 mg/dl
- Glucose at 10:30 AM: 343 mg/dl
- Glucose at 12:30 PM: 364 mg/dl
- Glucose at 2:30 PM: 361 mg/dl
- Glucose at 4:00 PM: 401 mg/dl
We then increased detemir to 3 units BID, and checked again 8 days later:
Fed at 7:30 AM
- Glucose at 8:30 AM: 422 mg/dl
- Glucose at 10:30 AM: 234 mg/dl
- Glucose at 12:30 PM: 253 mg/dl
- Glucose at 2:30 PM: 309 mg/dl
- Glucose at 4:00 PM: 381 mg/dl
We then increased to 0.2 U/kg BID (4 units BID), and checked again in 2 weeks.
- Fed at 7:30 AM
- Glucose at 8:30 AM: 422 mg/dl
- Glucose at 10:30 AM: 283 mg/dl
- Glucose at 2:30 PM: 356 mg/dl
- Glucose at 4:00 PM: 370 mg/dl
We just did a complete urinalysis and urine culture which was negative. Results of a recent CBC and serum chemistry panel were normal, except for the high blood glucose concentration. The dog is doing well clinically at home.
I'm not sure what to make of the persistent hyperglycemia on detemir. Possible Somogyi reaction? Or does the dog just needs more insulin?
When increasing the detemir insulin dosage, should I be going up a certain percentage or unit/half-unit at a time?
My Response:
This certainly doesn't look like an overdose of insulin or Somogyi overswing to me. Most likely, this dog just needs more insulin.
However, you should double check the following points with the owner as the next step:
- That they can accurately measure and then inject the insulin reliably.
- That they are feeding the dog only in morning and evening (no other treats during the day).
- That they are measuring the amount of food being feed, calculated by a veterinarian that it's the correct amount for the dog's ideal body weight.
It doesn't appear clinically that she has any concurrent conditions that would cause insulin resistance, such as infection, inflammation, or Cushing's excess. Some dogs just require more insulin to adequately lower their blood glucose than do other dogs!
In a large dogs, I increase my detemir dose by increments of 1 unit BID. In a small-breed dogs, I increase by less; by increment of 0.5 units BID.
I then wait 1 week or so and then repeat the serial glucose curve to make any additional needed dose adjustments.
Źródło: endocrinevet.blogspot.com
She was initially started on NPH insulin at 0.4 U/kg BID (8 U BID). Over the course of 2 months, we increased the NPH dose to 0.7 U/kg BID (14 U BID) but the dog continued to be symptomatic. We did a blood glucose curve and obtained the following results:
- Fed at 7:30 AM
- Glucose at 8:30 AM: 132 mg/dl
- Glucose at 10:30 AM: 103 mg/dl
- Glucose at 12:30 PM: 160 mg/dl
- Glucose at 2:30 PM: 286 mg/dl
- Glucose at 4:00 PM: 381 mg/dl
Based on that curve was concerned that the duration was too short, so we switched to insulin detemir (Levemir). I know that detemir is more potent, so we started at 0.1 U/kg BID (2 units BID). The blood glucose curve 1 week later:
- Fed at 7:30 AM
- Glucose at 8:30 AM: 580 mg/dl
- Glucose at 10:30 AM: 343 mg/dl
- Glucose at 12:30 PM: 364 mg/dl
- Glucose at 2:30 PM: 361 mg/dl
- Glucose at 4:00 PM: 401 mg/dl
We then increased detemir to 3 units BID, and checked again 8 days later:
Fed at 7:30 AM
- Glucose at 8:30 AM: 422 mg/dl
- Glucose at 10:30 AM: 234 mg/dl
- Glucose at 12:30 PM: 253 mg/dl
- Glucose at 2:30 PM: 309 mg/dl
- Glucose at 4:00 PM: 381 mg/dl
We then increased to 0.2 U/kg BID (4 units BID), and checked again in 2 weeks.
- Fed at 7:30 AM
- Glucose at 8:30 AM: 422 mg/dl
- Glucose at 10:30 AM: 283 mg/dl
- Glucose at 2:30 PM: 356 mg/dl
- Glucose at 4:00 PM: 370 mg/dl
We just did a complete urinalysis and urine culture which was negative. Results of a recent CBC and serum chemistry panel were normal, except for the high blood glucose concentration. The dog is doing well clinically at home.
I'm not sure what to make of the persistent hyperglycemia on detemir. Possible Somogyi reaction? Or does the dog just needs more insulin?
When increasing the detemir insulin dosage, should I be going up a certain percentage or unit/half-unit at a time?
My Response:
This certainly doesn't look like an overdose of insulin or Somogyi overswing to me. Most likely, this dog just needs more insulin.
However, you should double check the following points with the owner as the next step:
- That they can accurately measure and then inject the insulin reliably.
- That they are feeding the dog only in morning and evening (no other treats during the day).
- That they are measuring the amount of food being feed, calculated by a veterinarian that it's the correct amount for the dog's ideal body weight.
It doesn't appear clinically that she has any concurrent conditions that would cause insulin resistance, such as infection, inflammation, or Cushing's excess. Some dogs just require more insulin to adequately lower their blood glucose than do other dogs!In a large dogs, I increase my detemir dose by increments of 1 unit BID. In a small-breed dogs, I increase by less; by increment of 0.5 units BID.
I then wait 1 week or so and then repeat the serial glucose curve to make any additional needed dose adjustments.
Źródło: endocrinevet.blogspot.com
I just rechecked a hypothyroid dog that I put on L-thyroxine (Soloxine) about 1 month ago. The dog's skin is very, very flaky; she is shedding a great deal and is mildly pruritic.
I came across something in one of my endocrinology books that indicates this may happen when starting thyroid supplementation, but this is the first time I've seen it in my 16 years of general practice. The skin scrape is negative, and there are no signs of any other skin pathology: there is no evidence of bacterial, yeast, or immune-mediated skin disease.
So do you think that this excessive shedding and flaking in this dog is related to initiation of the L-T4 therapy?
How frequently do you see this reaction or side effect?
What can I expect this dog's skin to do from here on? How long for this issue to resolve?
My Response:
Hypothyroid dogs occasionally develop severe shedding and flaking during the first 2 to 3 months of L-thyroxine treatment. During this time, the old telogen hairs are all being shed at the same time. With a bit of time on L-T4 replacement, the old shedded hairs are replaced with anagen hairs, and the skin cycle is restarted.
So I would expect the excessive shedding to resolve within the next 4 to 8 weeks on the L-T4 supplementation. However, you may want to treat the scaling symptomatically with a mild antiseborrheic shampoo and conditioner therapy such as Sebolux or Humilac. Adding some essential fatty acids (EFAs) to the dog's diet may also be of benefit.
If scaling persists or worsens beyond 8-weeks time, then skin biopsy for a keratinization disorder such as ichthyosis is recommended.
I can't give you an incidence for how often excessive flaking and shedding happens after initiation of L-thyroxine supplementation, but it certainly is not rare. I do see increased flaking more frequently in dogs with Cushing's disease during initial treatment with mitotane or trilostane than I do in dogs with hypothyroidism.
However, the reason I don't see this problem as often in hypothyroidism may simply be that, as a specialist, I only rarely get to treat and manage hypothyroid dogs. Although hypothyroidism can be a problem to accurately diagnose, it's an relatively easy disorder to treat.
Źródło: endocrinevet.blogspot.com
I came across something in one of my endocrinology books that indicates this may happen when starting thyroid supplementation, but this is the first time I've seen it in my 16 years of general practice. The skin scrape is negative, and there are no signs of any other skin pathology: there is no evidence of bacterial, yeast, or immune-mediated skin disease.
So do you think that this excessive shedding and flaking in this dog is related to initiation of the L-T4 therapy?
How frequently do you see this reaction or side effect?
What can I expect this dog's skin to do from here on? How long for this issue to resolve?
My Response:
Hypothyroid dogs occasionally develop severe shedding and flaking during the first 2 to 3 months of L-thyroxine treatment. During this time, the old telogen hairs are all being shed at the same time. With a bit of time on L-T4 replacement, the old shedded hairs are replaced with anagen hairs, and the skin cycle is restarted.
So I would expect the excessive shedding to resolve within the next 4 to 8 weeks on the L-T4 supplementation. However, you may want to treat the scaling symptomatically with a mild antiseborrheic shampoo and conditioner therapy such as Sebolux or Humilac. Adding some essential fatty acids (EFAs) to the dog's diet may also be of benefit.
If scaling persists or worsens beyond 8-weeks time, then skin biopsy for a keratinization disorder such as ichthyosis is recommended.
I can't give you an incidence for how often excessive flaking and shedding happens after initiation of L-thyroxine supplementation, but it certainly is not rare. I do see increased flaking more frequently in dogs with Cushing's disease during initial treatment with mitotane or trilostane than I do in dogs with hypothyroidism.
However, the reason I don't see this problem as often in hypothyroidism may simply be that, as a specialist, I only rarely get to treat and manage hypothyroid dogs. Although hypothyroidism can be a problem to accurately diagnose, it's an relatively easy disorder to treat.
Źródło: endocrinevet.blogspot.com
Molly" is a 7-year-old Laborador Retriever weighing 31 kg, who was diagnosed over a year ago as being hypothyroid based on the finding of a low-normal serum T4 concentration (0.9 µg/dl; reference range, 0.9-3.9 µg/dl). Her clinical signs included non-pruitic alopecia of the pinnae and truncal dermatitis. Based upon her clinical signs and the low serum T4 value, she was started on L-thyroxine (Soloxine) a the dosage of 0.5 mg, BID.
Over the past year, a number of post-pill serum T4 concentrations have been done, but all of her serum T4 values have remained in the low-normal range (between 0.9-1.5 µg/dl). Her dose of Soloxine was increased to 0.6 mg but there still has not been improvement in clinical signs.
This week I repeated an entire thyroid panel while the dog is on the L-T4 and send the serum to the Michigan State University Endocrine Lab (animalhealth.msu.edu). Here are the results of that thyroid panel:
TT4: 59 nmol/L (15-67 nmol)
TT3: 1.5 nmol (1.0-2.5 nmol)
FT4: 20 pmol/L (8-26 pmol)
FT3: 5.2 pmol (4.5-12 pmol)
T4AA: 11% (0-20%)
T3AA: 5% (0-10%)
TSH: 0.01 mU/L (0-37 mU/L)
Thyroglobulin AA: 2% (0-35%)
My questions: Will being on L-thyroxine cause these numbers to all be normal? Is it advisable to stop the thyroid supplementation for a few weeks and run another serum thyroid panel, as clinically it doesn't seem to be doing much? Is she really hypothyroid at all?
Thank you so much for your help!
My Response:
Yes, the goal of thyroid hormone supplementation is to completely normalize the serum thyroid panel (i.e., to raise serum total and free T4 and T3 values and suppress serum TSH concentrations). So these results indicate that the L-T4 supplementation in this dog is being well absorbed and is feeding back on the pituitary gland to lower TSH secretion.
But you are correct: if the dog isn't hypothyroidism, the clinical signs aren't going to improve. I would recommend that you stop the L-T4 supplementation and redo the thyroid panel. Unfortunately, we need the dog off all L-T4 for at least 6 weeks prior to testing to allow the hypothalamic-pituitary-thyroid axis to recover. Once you stop the thyroid medication, this dog may be mildly hypothyroid (due to iatrogenic suppression of pituitary TSH secretion) even if his thyroid gland was normal prior to the thyroid supplementation.
When you do recheck Molly after stopping the thyroid mediation, remember to also run a CBC and serum chemistry panel. This will rule out any nonthyroidal diseases, but will also help in diagnosis of hypothyroidism, especially if mild anemia, or fasting hyperlipidemia/ hypercholesterolemia is present.
PS: I don’t know what the prior post-pill test results showed serum T4 values only in the low-normal range, but the serum T4 on this panel is perfect. Have the owners been consistently giving the L-T4 without food or at time of meals?
It’s been shown that absorption of L-T4 in dogs can be better when given on an empty stomach. So if the owners were not consistent in when they administer the thyroid medication, that could explain why the previous results were so different that the current results. And it may also explain why the dog hasn’t responded to the thyroid supplementation (if she really is hypothyroid, which still needs to be determined).
References:
1. Le Traon G, Burgaud S, Horspool LJ. Pharmacokinetics of total thyroxine in dogs after administration of an oral solution of levothyroxine sodium. J Vet Pharmacol Ther. 2008;31(2):95-101.
Źródło: endocrinevet.blogspot.com
I read your recent post regarding Addison's disease and I'm writing to see if you could clear up (or add to the debate) a discussion that we are having at our hospital. I am a second-year medicine resident and our medical staff is having a debate about what is considered a normal vs. an abnormal cortisol response to ACTH stimulation and what exactly is "atypical" Addison's disease.
For example, what about dogs that have chronic gastrointestinal (GI) signs that have not yet been been diagnosed but a flat cortisol response to ACTH stimulation is found? If we perform an ACTH stimulation test on these dogs, many will have a basal cortisol level well within reference range limits (e.g., 2 to 4 µg/dl) but the post-ACTH stimulated cortisol concentration will not rise to levels 3-5 times higher than the basal cortisol concentration. Some of these dogs will have ACTH-stimulated cortisol concentrations that are below the post-ACTH reference range (e.g., in the range of only 3-6 µg/dl). Is this atypical Addison's disease?
What do you do in these cases? Look for other causes of the GI signs? And if no other cause found supplement with steroids? Should we just repeat the ACTH stimulation test down the line?
Thank you for your time!
My Response:
First of all, you must remember that the blog post on Addison's disease you are referring to was written primarily for dog owners, not veterinarians. I was trying to be clear, which is difficult when we are discussing a topic that could include typical, atypical, or secondary adrenal insufficiency.
Almost all dogs with primary hypoadrenocorticism (typical Addison's disease) and near complete destruction of the adrenal cortex will have subnormal basal and ACTH-stimulated serum cortisol concentrations (<1 μg/dl).
Dogs with secondary hypoadrenocorticism (pituitary ACTH deficiency) have low to low-normal basal cortisol values that may rise very slightly to ACTH stimulation, but the cortisol response is very blunted (post-ACTH values generally < 3 µg/dl). This has all been published (1-3), and I don't think anyone would strongly disagree with those guidelines.
The problem with "atypical" Addison's disease is that, at least most of the time, the dogs have never been worked up properly to differentiate primary from secondary hypoadrenocorticism. Most would define "atypical" Addison's simply as glucocorticoid-deficient hypoadrenocorticism, but that is really being quite simplistic and does not help guide what replacement therapy may be needed or predict prognosis.
In other words, if that "atypical" dog has primary Addison's disease with normal electrolytes, it is very possible or even likely that mineralocorticoid replacement will be needed. On the other hand, it a dog has secondary hypoadrenocorticism, mineralocorticoid replacement will never be needed, but pituitary imaging (CT or MRI scan) might be indicated to exclude a pituitary mass.
The easiest way to differentiate primary from secondary hypoadrenocorticism, of course, would be to measure plasma ACTH concentration, but that must be done before any glucocorticoids have been administered (or after 1-2 weeks off all steroids).
If the plasma ACTH value is low (generally < 20 pg/ml) in a dog with a severely blunted serum cortisol response to ACTH stimulation, that would be diagnostic for secondary hypoadrenocorticism (1-4). As you know, ACTH deficiency is rare and is most commonly associated with a pituitary tumor (3). By far the most common cause is iatrogenic secondary hypoadrenocorticism resulting from glucocorticoid administration. So it's extremely important in dogs with "atypical" Addison's disease to go back in the history and make sure that they haven't received any steroid in the last few weeks to even months.
If the plasma ACTH value is high (generally >250 pg/ml) with a severely blunted serum cortisol response to ACTH stimulation, that would be diagnostic for primary hypoadrenocorticism (1-4). If the serum electrolytes are normal, that could be called "atypical" Addison's disease. Some of these dogs will certainly go on to develop serum electrolyte changes, whereas others never seem to do so. I suspect that these latter dogs do not actually have adrenal destruction, but may have an ACTH receptor defect where circulating ACTH values are high but the adrenal gland doesn't bind the ACTH so it cannot act to stimulate cortisol secretion. Again, the best way to distinguish secondary from primary hypoadrenocorticism in these dogs is to measure plasma ACTH before any glucocorticoids are administered (or off all glucocorticoids for at least 1-2 weeks).
But let me get back to your original question about the dogs that have chronic GI signs and whose ACTH stimulation test results reveal a normal (or low) basal cortisol with a post-ACTH cortisol values that is blunted, rising to only 3-6 µg/dl. This is certainly not a "normal" response, abut it's very difficult for me to explain why these dogs would have any signs when these circulating cortisol values are within or slightly above the normal basal range. If this was a dog on mitotane or trilotane, for example, we would be very pleased with those serum cortisol results and would not be worried about hypoadrenocorticism (5-7).
In my experience, most of these dogs have a history of being treated with glucocorticoids, which could lead to secondary (iatrogenic) hypoadrenocorticism. Again, if you would measure a plasma ACTH concentration in these dogs, the values should be low-normal if they do indeed have secondary ACTH deficiency. If there is now history of glucocorticoid use, I would certainly repeat basal or ACTH-stimulated cortisol values in 2-4 weeks, but most of these dogs do not end up having primary adrenal disease.
Now that's not to say that they don't need steroid supplementation, but not for "atypical" adrenal disease.
References:
1. Peterson ME, Kintzer PP, Kass PH. Pretreatment clinical and laboratory findings in dogs with hypoadrenocorticism: 225 cases (1979-1993). J Am Vet Med Assoc 1996;208:85-91.
2. Kintzer PP, Peterson ME. Primary and secondary canine hypoadrenocorticism. Vet Clin North Am Small Anim Pract 1997;27:349-357.
3. Feldman EC, Nelson RW. Canine and Feline Endocrinology and Reproduction.Third Edition. Saunders, 2003.
4. Peterson ME, Orth DN, Halmi NS, et al. Plasma immunoreactive proopiomelanocortin peptides and cortisol in normal dogs and dogs with Addison's disease and Cushing's syndrome: basal concentrations. Endocrinology 1986; 119: 720-730.
5. Kintzer PP, Peterson ME. Mitotane (o,p'-DDD) treatment of 200 dogs with pituitary-dependent hyperadrenocorticism. J Vet Intern Med 1991;5:182-190.
6. Peterson ME, Kintzer PP. Medical treatment of pituitary-dependent hyperadrenocorticism. Mitotane. Vet Clin North Am Small Anim Pract 1997;27:255-272.
7. Ramsey IK. Trilostane in dogs. Vet Clin North Am Small Anim Pract 2010;40:269-283.
Źródło: endocrinevet.blogspot.com
Prior to veterinary school, I worked as for a few years at a major medical center as a nurse in their endocrine clinic. In older human patients with hyperthyroidism, was not that uncommon for these folks to present with perfectly normal serum T4 values but have very high serum T3 concentrations.
Do cats also develop a similar syndrome of T3 hyperthyroidism? That is, can some hyperthyroid cats maintain normal serum concentrations of T4 and free T4, but have clinical signs resulting from high circulating T3 values alone?
I've reviewed the literature, but I don't see that T3 thyrotoxicosis has ever been reported in cats. Is that because we just aren't checking serum T3 levels in hyperthyroid cats? Do you think that we are missing these cases?
My Response:
This syndrome is commonly referred to as triiodothyronine (T3) thyrotoxicosis or just T3 toxicosis. This disorder is found almost exclusively in the elderly and may be the cause of hyperthyroidism in up to 10% of older patients. T3 thyrotoxicosis is characterized by the finding of high serum T3 with normal or even low T4 levels, which can sometimes even lead to an erroneous diagnosis of hypothyroidism.
In the late 1970s and throughout most of the 1980s, we routinely measured serum T3 on all hyperthyroid cats. Although serum T3 concentrations were very high in many of these cats, we never documented a cat with isolated T3 thyrotoxicosis (1).
So over the last 35 years, I have certainly looked for this syndrome of T3 thyrotoxicosis. I have always expected to find some cats with normal T4 but high T3 levels, but to date the syndrome of T3 hyperthyroidism has yet to be documented in cats.
Today, we rarely use serum T3 concentrations as a diagnostic test for hyperthyroidism. Use of total T4 alone is diagnostic in over 90% of cats, whereas serum T3 values are high in only about two-thirds of cats (2).
That said, however, it still is possible that hyperthyroid cats could develop T3 hyperthyroidism. Certainly in circumstances where a low iodine diet is fed, you might see a situation where T3 is being secreted preferentially over T4 (3).
In states of iodine deficiency, it’s easier for the thyroid gland to make T3 compared to T4. The reason for that is simple — it takes one less iodide atom to make T3 than T4, since T3 only has 3 iodine atoms whereas T4 contains 4 iodine atoms. T4 has 1 more iodine atom than T3
T4 has 1 more iodine atom than T3
Therefore, you have a cat in which hyperthyroidism is suspected, especially if a palpable goiter was present, but total and free T4 values are normal, I would certainly recommend that you run a serum T3 concentration to rule out T3 thyrotoxicosis.
References:
Peterson ME, Kintzer PP, Cavanagh PG, et al. Feline hyperthyroidism: pretreatment clinical and laboratory evaluation of 131 cases. J Am Vet Med Assoc 1983;183:103-110.
Peterson ME, Melian C, Nichols R. Measurement of serum concentrations of free thyroxine, total thyroxine, and total triiodothyronine in cats with hyperthyroidism and cats with nonthyroidal disease. J Am Vet Med Assoc 2001;218:529-536.
Laurberg P. Mechanisms governing the relative proportions of thyroxine and 3,5,3'-triiodothyronine in thyroid secretion. Metabolism: clinical and experimental 1984;33:379-392.
Źródło: endocrinevet.blogspot.com
