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Yes, I read somewhere (I think here on SM or a link from here) that about 15-20% of dogs have inverted results, which is why the test is done in pairs (pre and post).
that's really interesting. Is it possible it was just a fluke and that the gallbladder contracted and released bile? I think I've heard that that is possible and that sometimes just the smell of food can trigger it. I think I'd almost want to retest one more time just to see. I'd be curious if anyone has any additional info on Pre-meal results only being high
 

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Michele,
The reason you do paired testing is because a certain percent are reversed. There is no reason to retest because you get reversed number (pre higher than post). Dr. Center presented this information when she spoke at our Nationals a few years ago.
 

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My Baby Nicco

I am new on here and was told by someone that I could possibly receive some advice and help on here. I have a 2 year old maltese baby that has been diagnosed with PSS or portal systemic shunt. I have been to my vet and a specialist and so far have spent over $1800 on treatments and visits. My poor Nicco has to have surgery to save his life but the surgery will be $2500 to $3900 and they want half before surgery and the rest following the procedure. I would be able to pay it out but not all at once like they want. I Just don't have that type of money right now. My daughter and her baby moved in with us and my son is still in college. Any help on a vet that you know that would let me make payments would literally be a lifesaver. We love him so much and it is killing us to watch him. He will eventually die without this surgery.

Thank you so much for any help and advice on this. I am truly scared. I live in Texas between Galveston and Houston.

Again thank you and God bless!
Shelly Whitley
 

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You might try organizing a benefit or something that will help to raise funds for LS and your little dog. Even the Yorkie aid for shunts is unable to handle all the incoming liver shunt yorkies who need help these days.
Also, ask your vet if they have any ideas how to raise money. Check the rescue groups near you for ideas. A car wash! A bake off! If you have kids check with their schools on helping to raise funds. It would be a great human interest story for kids.
 

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Does the vet doing surgery accept CareCredit? That is an option. The cheapest place to get shunt surgery in the U.S. is probably still the University of TN vet school in Knoxville, TN.
Cornell is managing a lot of Maltese with diet and medication. If this is an option for your dog it would be worthwhile looking into.
 

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Liver Shunts and Cholestrol

When my 3 yr old seemed quite sickly over a year ago, we had tests and scans done. I was so upset, thinking it was shunts, knowing that the op is very dangerous. However, we were relieved to be told that although he may have a small liver shunt, it wasn't the problem and the liver hadn't begun to shrink. The specialist told us that although his Cholestrol levels were very high, this was normal for Maltese dogs and he gave me a download of information on a study carried out re this.
Our little boy's problem turned out to be an underactive Thyroid. He is now on medication for the rest of his life, but he is so much better. He has tests every 3 months to ensure he is on the right levels of meds and we have cut out a lot of foods that contain fat. He has lean skinless chicken or turkey and dry kibble mixed together, plus low fat chicken treats.
He will never be the most agile or energetic dog, but we love him in spite of this. He is now 4 years old and absolutely adores going out to the park or the fields and being let off the lead to mooch around, sniffing and peeing everywhere! He gets 'selective hearing' issues, and is not so obedient as when he is at home.
 

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Any living being health problems can either be genetic, acquired, or a combination of the two. In the case of liver problems in our dogs usually the cause is genetic.
 

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I'm very confused here, I'm new to SM. I also want to get a maltese, I was wondering what tests I should ask the breeder to run before purchasing the dog? And what tests should I run after I get the dog?
 

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That is between you and your breeder.
I would ask her/him if he is aware any genetic issues w/liver, neurological, etc., in his line---a history? "Is this the first pairing of these 2 dogs" is an important question to ask. Ask the breeder if they keep a data base of issues from their breeding.
Most Bile Acid Tests (BAT) are given at 16 weeks or there about so will you want to take possession of the dog before then? If so, then you would have to specifically order the test from your own vet. I would prefer my own vet to do the testing---personal preference only. Also, just so you know this test is not part of the regular blood draw.
I would also get names from your breeder of people who have bought from her and call them to ask about particular issues. Ask other people who have experience w/your breeder.
A good breeder will admit where the issues are---some don't, and you become a detective of sorts. If a breeder doesn't appreciate your curiosity, then keep looking, but do be sensitive in how you formulate your questions!
 

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OMG! Your pups are so cute! The tiny one caught my eyes b/c my Maltese is around 12 lbs (but ALL Love). Is yours consider a "toy"? Thanks!

P.S: My oscar is having a **** of a time with re-occurence Urinary Tract Infections. This is his 4th?? And has been in so many antibiotics. I am searching for a holistic way to treat it from now on. His little liver can't take all these drugs. I read that "Cuban Oregano" also known as Mexican Mint has properties that Fight Bacteria in the U.Track. Confrimed by researches and I holistic vet had mentioned it to me over the radio a while back but when she said Oragano Herb, I said what? I regret not taking her advice!
 

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Hello: I have some personal experience with the Adrenal Glands (not sure if it is the same thing) but the Neurosurgeon has explained to me that Adrenal Glands, if out of balance is (or will be) the cause of Liver Cushing Decease and others. I download a report from the Universary of TN. We just had Oscar tested yesterday. The blood work will be sent to the U. of TN and tell us which hormone is out of wack. If you need some information on the Adrenal Panel, feel free to contact me. Clinical signs that hormones out of balance: Humping (although fixed), excessive water intake, especially at night, reoccurance Urinary track infections, weak back legs, panting for no apperant reason and the urine is very clear or clinical term: "has no gravity". Sure enough, we had his adrenal gland ultrasound and the left one is larger than his right one. too large for this breed! Now we are just waiting to determine which monthly treatment he'll receive. The Neurosurgeon has explained to us that the Adrenal Panel is responsible for liver issues, like tumors and kidney failure. If you want the 2 page report from the U of TN. Please email me and I will send it to you. I am not sure I can post such a long report?? Thanks! Please: Get Pet Ins. Most small breeds are having problems due to cross breeding *unless you got yours from a Very Reputable Breeder!!!!
 

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This is our personal story and experiences with the Adrenal Glands, which regulate many parts of your Dog's chemistry and health. It is a Bit long and when you get to the U. of TN Report, there is a lot of medical terminology. I hope this helps.

STEROID PROFILES IN THE DIAGNOSIS OF CANINE ADRENAL DISORDERS
Jack W. Oliver, DVM, Ph.D
Knoxville, TN
Hello: My name is Teresa and the reason for this information is to help educate Maltese & All pet owners about the Adrenal Panel-Testing. It is very important to know that if your pet is not showing ANY Clinical signs of Adrenal issues, then this information is not for you. I am NO Doctor or pretend to know it all! To the contrary, I was Lost when my Maltese, our only “child” got sick.
I have simply spent 100’s of hours doing research. Since I have already done the work, why not share it? If I can help one pet and their owner, my hours spent up at night will be well Worth it!
We were forced to learn quick after we made over 50 visits to 3 different animal hospital in search for answers (met with 8 Doctors) and 9 months of pure ****; I’ve decided to share with you some of my research. My 6 year old Maltese Was Healthy, until……
What are Adrenal Clinical Signs? The following are clinical signs from our pet: I’m sure there are many other symptoms that I am not aware of! Only a good vet or specialist can decide your specific case:

1. Re-occurrence bladder infections (UTI). Which our baby had four of them
2. I noticed his water intake would increase, especially late at Night! Of course, he’d urinate on his pads about 2-3x over night.
3. His urine would be “diluted” or what the professionals call “low gravity urine”. His pee-pee pads looked like it was just plain water.
4. 4. He humps his stuff animal everyday after having his dinner and would “get it on, if you know what I mean”. (Yes! He was Neutered at 7-8 months old).
5. Once in a while, he would pant for no apparent reason.
6. Anal Glands getting full/packed up within weeks of extracting them by the vets. And/or infected—greenish color.

I am going to warn you right now: If you want to save your dog from this ailment, you better have 1 of 3 things: a cushy savings account, a credit card with a good line of credit OR GOOD Pet Insurance! After years of my husband bugging me for pet insurance and a $10,000 Plus in bills, I finally got it (too late now). That’s another thing too. When you purchase Pet Insurance, READ THE FINE PRINTS! VIP as of few months ago, has a limit of $1,500 (might as well don’t have any ins). AND they treat a condition ONLY for the calendar year! Why? The following year, when your policy “renews” that condition now becomes a “Pre-Existent”. Guess what? They do not cover Pre-Existence Conditions: How Clever! I would have Never known about this, if I didn’t take the time to read their fine prints. I chose PetPlan. They are rated #1 in customer service. Look them up. Good reviews for a pet insurance company. I do NOT work for them or make any commissions (although I wish to help us with our vet bills). We are simply impressed with their policies/coverage. We haven’t put any claims yet and pray we will never have to, but many people have and got their checks. I chose the gold plan which covers up to $20,000 per calendar year. My monthly payments are $33. Ok! Back to the subject (Sorry).

*****After meeting with one of the Best Animal Neurosurgeon in the Country, we have learned the above conditions are “clinical signs” of the Adrenal Glands! The glands regulate hormones. Too much or too little of one or more hormones can cause health problems, such as reoccurrence urinary track infection and/or anal glands getting full within weeks of being drained. They can also get infected.

until one day I noticed a drop of blood on his pee-pee pads. He ended up having a stone in his bladder. Had surgery to remove it but 6 weeks post op, he couldn’t hold his urine. This incompetent vet, which I am convinced he Learned a big lesson with our horrible experience and therefore, have decided not to name (I promised to the specialist)Maltese having 3 surgeries (one was to correct a botched one by an incompetent vet)

INTRODUCTION
Diagnosis of adrenal disease in domestic animals usually is dependent on the manipulation of the hypothalamo-pituitary-adrenal axis (HPA) and the measurement of cortisol (i.e., ACTH stim test; low dose dexamethasone suppression (LDDS) test; urine cortisol/creatinine ratio test; or the combined dexamethasone suppression/ACTH stimulation test). More recently, other steroid measurements have been utilized to evaluate the HPA, including steroid hormone profiles1,2, and 17-hydroxyprogesterone,3-5 which have revealed that suspected adrenal disease conditions may be caused by steroids other than cortisol (or in addition to cortisol).3 Determination of pituitary-dependent hyperadrenocorticism (PDH), or adrenal-dependent hyperadrenocorticism (ADH), is now usually made by evaluation of the 4-hour timepoint of the LDDS test6, by endogenous ACTH measurement,7 or by ultrasound visualization of the adrenal glands.7,8 Hyperadrenocorticism (HAC) is defined as an overproduction of steroid hormones by the adrenal cortex.4 Cushing’s syndrome refers to all causes of hyperadrenocorticism with excess production of cortisol,6 while atypical Cushing’s disease refers to hyperadrenocorticism caused by increased levels of intermediate adrenal steroids that frequently are referred to as “sex steroids”.9

WHY? This explains why this test is being done: STEROID HORMONE PROFILES/GENERAL
****Steroid hormone profiling in veterinary medicine was begun at The University of Tennessee Clinical Endocrinology Service, with the premise being that multiple steroid hormone analyses would increase the diagnostic accuracy of adrenal function tests.1 Measurement of multiple steroids in Pomeranians2 led to the recognition of a syndrome called “Alopecia-X”11 by dermatologists. Others have reported on adrenal syndromes in dogs called “atypical Cushing’s disease”,3,9 or “adrenal hyperplasia-like syndrome”,9,10-13 that used steroid profiling. Cortisol is known to have negative control effect on the HPA axis, but it’s now also understood that other steroids can have this effect as well.9,14,15 Steroid profiling in dogs and cats has led to the realization that HAC can be due to primary adrenal tumors that secrete other steroids besides cortisol.16-21 Steroid profiling in ferrets led to the realization that HAC in this species is primarily due to increased levels in blood of estradiol, 17-hydroxyprogesterone and/or androstenedione,9,22 and measurement of these steroids has helped define medical control of ferret adrenal disease.23-27 Steroid profiles have also helped to better understand the condition of SARDS in dogs, where steroids other than cortisol frequently are involved.28 Steroid profiling is also helping to understand drug effects on adrenal secretory activity (mitotane, trilostane, melatonin).29-31

STEROID HORMONE PROFILES/SPECIFIC
Steroid hormone profiles are indicated when other routine tests of adrenal function are negative (ACTH stim; LDDS; combined dexamethasone suppresson/ACTH stim) and the dog still exhibits signs of Cushing’s syndrome, indicating the likelihood of atypical Cushing’s disease being present.3,9 The issue of non-adrenal illness has been raised as a possible consideration in atypical Cushing’s disease cases.21 Results of studies in dogs with chronic illness, but without clinical evidence of HAC, have shown that 17-hydroxyprogesterone (17OHP) concentration may be increased.21 However, results of other studies of adrenal function testing in dogs with non-adrenal illness have demonstrated only minor effects on test results.32,33 Also, in studies that have measured only 17OHP as a means of detecting HAC, the sensitivity and specificity of using post-ACTH 17OHP concentration as a diagnostic test for HAC were low, and post-ACTH 17OHP analysis was not recommended as a screening test for HAC.4 These studies provide evidence that measurement of a singular adrenal intermediate steroid (such as 17OHP) may give equivocal results, but when profiles of steroid intermediates are used, the sensitivity and specificity of the test procedure is much improved.29 It has been emphasized that adrenal function testing should be performed in dogs with clinical and/or biochemical evidence of HAC, and not in dogs with non-adrenal related disease.6
Steroids that may be involved with atypical Cushing’s disease are androstenedione, estradiol, 17-hydroxyprogesterone, progesterone and aldosterone.9 Other steroids that aren’t commonly measured may be involved as well, such as corticosterone21 and deoxycortisone.16 Estradiol is unique because treatment of excess estradiol can be difficult, the hormone can be secreted by tissues other than the gonads or adrenals35-38 and because secretion is independent of ACTH stimulation or dexamethasone suppression testing, as currently done. For dogs with atypical Cushing’s disease (PDH etiology), expect hepatomegaly, hepatopathy and bilateral adrenomegaly to be present along with increased endogenous ACTH level and the usual clinical signs, bloodwork and often haircoat problems. Steroid profiling in dogs and cats has led to the realization that HAC can be due to primary adrenal tumors that secrete other steroids besides cortisol.16-21 Steroid profiling in ferrets led to the realization that HAC in this species is primarily due to increased levels in blood of estradiol, 17-hydroxyprogesterone and/or androstenedione,9,22 and measurement of these steroids has helped define medical control of ferret adrenal disease.23-27 Steroid profiles have also helped to better understand the condition of SARDS in dogs, where steroids other than cortisol frequently are involved.28 Steroid profiling is also helping to understand drug effects on adrenal secretory activity (mitotane, trilostane, melatonin).29-31
Treatment Implications
Primary adrenal tumors. Adrenal steroid profiles reveal that adrenal tumors in dogs, cats and ferrets have a variety of secretory patterns, with serum cortisol levels often being normal.l9,17,18-22,29,39 Similar findings have been reported in humans with adrenoadenomas.42 In ferrets, mice, rats, guinea pigs and hamsters, sex steroid-producing adrenocortical tumors occur following gonadectomy, in association with the significant increase in serum gonadotropin levels that develop.43-47 The elevated luteinizing hormone (LH) level that occurs following gonadectomy leads to neoplastic transformation and expression of LH hormone receptors on sex steroid-producing adrenocortical cells in ferrets46,47 and rodents.48 Also, in humans, there is evidence of stimulatory effects of LH on adrenocortical cell growth and function,49 and LH receptor protein has been identified in the zona reticularis layer of the adrenal gland by immunohistochemical staining.50 In spayed female dogs, plasma gonadotropin levels post-gonadectomy rise to levels ten times what they were pre-gonadectomy, providing evidence of the strong and continuous LH stimulus that possibly plays a role in adrenocortical tumor development.51,52 Evidence is accumulating in human studies that some cortisol and other steroid-producing adrenal tumors or hyperplasias are under the control of ectopic or aberrant hormone receptors (e.g., gastrointestinal peptide, beta-adrenergic, vasopressin, serotonin and angiotensin II), and that these receptors may provide alternative mechanisms for pharmacologic control of adrenal tumors.53,54 Control of the secretory activity of adrenal tumors with beta-adrenergic and LH receptors has now been demonstrated by use of beta-receptor antagonists (propranolol)53 and gonadotropin antagonists such as leuprolide and deslorelin.23,24 Surgical removal of adrenal tumors is usually indicated, but age and health considerations impact this decision. If surgery is not an option, then mitotane is usually the next consideration. Adrenal profiles are indicated to determine the functionality of adrenal tumors in light of the multiple hormone secretion patterns that are seen.
Mitotane. Adrenal hormone profiles reveal that most intermediate hormones are decreased by mitotane the same as for cortisol, but that estradiol may remain unaffected. In cases that continue to have elevated estradiol levels, varying clinical signs of Cushing’s disease will be present.29
Trilostane. Enzyme inhibition by trilostane occurs for 3-beta hydroxysteroid dehydrogenase, but also for 11-beta hydroxylase.30 Thus, 11-deoxycortisol levels build-up in dogs treated with trilostane. It is also apparent that other intermediate steroid levels increase (androstenedione, 17-hydroxyprogesterone, estradiol and progesterone) in dogs treated with trilostane,29 which could be due to the 11-beta hydroxylase inhibition, and possibly 21-hydroxylase enzyme inhibition.29 The reason why only 11-deoxycortisol levels were increased in the above study30 may be due to the length of trilostane exposure (3-7 weeks), compared to dogs that are exposed to trilostane for extended periods. Steroid profiling in dogs and cats has led to the realization that HAC can be due to primary adrenal tumors that secrete other steroids besides cortisol.16-21 Steroid profiling in ferrets led to the realization that HAC in this species is primarily due to increased levels in blood of estradiol, 17-hydroxyprogesterone and/or androstenedione,9,22 and measurement of these steroids has helped define medical control of ferret adrenal disease.23-27 Steroid profiles have also helped to better understand the condition of SARDS in dogs, where steroids other than cortisol frequently are involved.28 Steroid profiling is also helping to understand drug effects on adrenal secretory activity (mitotane, trilostane, melatonin).29-31
For dogs with atypical Cushing’s disease (ADH etiology), expect hepatomegaly, hepatopathy and unilateral adrenomegaly to be present (and maybe atrophy of contra-lateral gland) along with decreased endogenous ACTH level and the usual clinical signs, bloodwork and often haircoat problems. For primary hyperaldosteronism conditions, due to primary adrenal tumor or bilateral adrenal hyperplasia, expect hypertension in association with hypernatremia and muscular weakness (cervical ventroflexion, hindlimb weakness) due to hypokalemia.39 Retinal hemorrhage and blindness40 and renal disease41 can occur in cats. For hyperadrenocorticoid cases that also have low aldosterone levels, this pattern can be indicative of a primary adrenal tumor, and ultrasound is indicated to confirm a tumor’s presence or absence.29

****Trilostane reportedly offers effective control of Cushing’s syndrome,30 but the long-term effects of the elevated intermediate steroids remain ill-defined. Some dogs do have return of clinical signs of Cushing’s syndrome while on trilostane.29 Because trilostane seems to pre-dispose dogs to increased adrenal toxicity with mitotane, an acute switch from trilostane to mitotane treatment should not be done.29
Aromatase enzyme inhibitors (anastrozole, exemestane, melatonin). The aromatase enzyme occurs in gonadal and adrenal tissues (and other tissues such as fat and skin cells), and converts androstenedione to testosterone or estrone, both of which are then converted to estradiol. Neither estrone nor testosterone have been observed to be increased in dogs with adrenal disease, but estradiol frequently is increased, and causes many of the clinical signs associated with Cushing’s disease.29 Aromatase enzyme-inhibiting drugs will decrease estradiol levels, but currently are infrequently used (except melatonin) in animals due to cost considerations.
Anti-gonadotropin drugs (melatonin, leuprolide acetate, deslorelin acetate, androgens). Adrenal tissues in different species (e.g., ferrets, rodents, humans) are known to have luteinizing hormone (LH) receptors present.44-50 In ferret studies, anti-gonadotropin drugs are effective in lowering sex steroid levels.23-24,27 Sex steroid levels are also decreased in dogs with adrenal disease that are treated with melatonin,31 but it is not known if LH receptors are present in canine adrenal tissues. Androgenic drugs have anti-gonadotropin effects via negative feedback effects on the hypothalamo-pituitary tissues.
Melatonin. Results of in vitro cell culture (human H295R adrenocortical carcinoma cells) studies in our lab55 revealed that both 21-hydroxylase and aromatase enzymes were inhibited by melatonin. Also, in dogs with adrenal disease that are treated with melatonin, and repeat adrenal steroid panels are done, cortisol levels are consistently reduced, and estradiol levels are variably reduced.29 Inhibition of the 21-hydroxylase enzyme would lower cortisol levels, and inhibition of the aromatase enzyme would lower estradiol levels. Estradiol levels were decreased in a prior study of dogs treated with melatonin.31 Results of in vitro studies with human MCF-7 breast cancer cells also revealed that melatonin inhibited aromatase enzyme, which resulted in reduced estradiol levels.56 Melatonin treatment for cases of mild adrenal disease in dogs may be effective, and particularly in cases where sex steroids are increased.
Melatonin plus phytoestrogens. Melatonin has the above listed effects, and phytoestrogens (isoflavones, lignans, genistein) are known to inhibit 3-beta hydroxysteroid dehydrogenase.57,58 Lignans and genistein are also known to decrease the activity of aromatase enzyme in MCF-7 cells in vitro.58 So, combinations of melatonin and phytoestrogens may have efficacy in treating hyperestrinism conditions.

Hyperestrinism in Dogs
Hyperestrinism in dogs may be a new and emerging disease entity. In sample submissions to the Clinical Endorinology Service (2005) at The University of Tennessee, 40% of adrenal panels had elevated estradiol levels present (>70 pg/ml).29 In hyperestrinism cases, estradiol is the estrogen that is increased, ACTH stim and LDDS tests are usually normal for cortisol, thyroid function is normal or controlled, liver problems are frequent and typical (very elevated alkaline phosphatase, hepatomegaly, steroid hepatopathy, hyperechoic liver by ultrasound), PU/PD is frequent, panting may be present, haircoat problems often are present, skin biopsy results suggest an endocrinopathy, there is no change in estradiol level in response to ACTH stim or LDDS tests as currently conducted, resistance to mitotane may occur and increase often occurs in response to trilostane. Effective treatment options for hyperestrinism in dogs is limited at the present time, and drugs that could be expected to be efficacious (aromatase inhibitors – excluding melatonin) often are limiting due to cost. Melatonin and phytoestrogen treatment may be effective for the above listed reasons. Mitotane will likely be effective if the source of estradiol is the adrenal tissues. Trilostane treatment frequently results in increased estradiol levels,29 and this may be a reason why less than effective treatment with the drug sometimes occurs.


CONCLUSIONS
Steroid hormone profiles in dogs are indicated when hyperadrenocorticism is suspected due to typical clinical and/or biochemical signs of disease, but the usual tests of adrenal function have been normal. The profiles are effective in ruling out presence of atypical Cushing’s disease, cases of hyperestrinism and for delineating the secretory profile of adrenal tumors (functionality), which often are associated with elevated levels of steroids other than cortisol.

KEY WORDS
Hormone, Tumor, Endocrine, Atypical, Hyperadrenocorticism

REFERENCES

1Lothrop CD, et al. AJVR 1984; 45:2304.2Schmeitzel LP, et al. JAVMA 1990; 197:1333.3Ristic JME, et al. J Vet Intern Med 2002; 16:433.4Chapman PS, et al. Vet Rec 2003; 153:771.5Benitah N, et al. JAVMA 2005; 227:1095.6Feldman EC et al., In Feldman E, Nelson R eds. Canine and Feline Endocrinology and Reproduction, 3rd Ed. St. Louis: WB Saunders, 2004; 252.7Gould SM, et al. J Sm Anim Pract 2001; 42:113.8Saunders MH, Proc of the 24th ACVIM Forum, 2006; 523.9Oliver JW, Proc of the 20th ACVIM Forum, 2002; 541.10Schmeitzel LP, et al. Kirk’s Current Therapy XII, Small Animal Practice, J Bonagura and R Kirk, eds. Philadelphia: WB Saundsrs, 1995; 600.11Schmeitzel LP, Proc of the 15th AAVD/ACVD, 1999; 131.12Kintzer P, Proc of the 17th ACVIM Forum, 1999; 435.13Rosychuk R, Proc of the AVMA Annual Meeting, 1999.14Selman PJ, et al. Eur J Endocrinol 1994; 131:422.15Selman PJ, et al. Steroids 1996; 61:133.16Reine N, J Vet Intern Med 1999; 13:386.17Syme HM, et al. JAVMA 2001; 219:1725.18Hill KE, et al. JAVMA 2005; 226:556.19Boord M, et al. JAVMA 1999; 214:666.20Rossmeisl JH, et al. JAAHA 2000; 36:512.21Behrend EN, et al. JAVMA 2005; 227:1762. 22Rosenthal KL, et al. JAVMA 1996; 209:1097.23Wagner RA, et al. JAVMA 2001; 218:1272.24Wagner RA, et al. AJVR 2005; 66:910.25Ramer JC, et al. JAVMA 2006; 229:1743.26Johnson-Delaney CA, Exot Mammal Med Surg 2005; 3:7.27Murray J, Exot Mammal Med Surg 2005; 3:1.28Carter R, et al. Proc of the Am Coll of Vet Ophthal, 2003.29Oliver JW, Clin Endo Serv Univ TN; unpublished data.30Seiber-Ruckstuhl NS, et al. Dom Anim Endocrinol 2006; 31:63.31Ashley PF, et al. JAVMA 1999; 215:1111.32Kaplan AJ, et al. JAVMA 1995; 207:445.33Gieger TL, et al. J Vet Intern Med 2003; 17:154.34Behrand EN, et al. JAVMA 2005; 226:1662.35Bulun SE, et al. Semin Reprod Med 1999; 17:349.36Bulun SE, et al. J Ster Biochem Molec Biol 2003; 86:219. 37Simpson E, et al. Endocrine-Related Cancer 1999; 6:131.38Ackerman GE, et al. J Clin Endocrinol Metab 1981; 53:412.39DeClue AE, et al. J Vet Intern Med 2005; 19:355.40Ash RA, et al. J Feline Med Surg 2005; 7:173.41Javadi S, et al. Dom Anim Endocrinol 2005; 28:85.42Glaz E, et al. J Ster Biochem Mol Biol 1993; 45:57.43Russfield AB, Meth Achiev Exp Pathol 1975; 7:132. 44Bielinska M, et al. Endocrinology 2003; 144:4123.45Bielinska M, et al. Endocrinology 2005; 146:3975.46Bielinska M, et al. Vet Pathol 2006; 43:97.47Shoemaker NJ, et al. Molec Cellular Endocrinol 2002; 197:117.48Apaja PM, et al. Endocrinology 2005; 146:3224.49Breuschlein F, et al. Horm Metab Res 2004; 36:392.50Pabon JE, et al. J Clin Endocrinol Metab 1996; 81:2397.51Olson PN, et al. AJVR 1992; 53:762.52Reichler IM, et al. Theriogenology 2005; 63:2164.53Lacroix A, et al. Endocrine Reviews 2001; 22:75.54Lacroix A, et al. Trends Endocrinol Metab 2004; 15:375.55Fecteau KA, et al. Clin Endo Serv Univ TN; unpublished data.56Cos S, et al. J Pineal Res 2005; 38:136.57Wong Z, et al. J Ster Biochem Molec Biol 1999; 71:191.58Brooks JD, et al. J Ster Biochem Molec Biol 2005; 94:461. Proc. 25th ACVIM, 471-473, Seattle, WA 2007
 

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Sorry I'm new to all this. My little guy Tucker is 13 weeks old. I have only had him for a week and he started vomiting a few days after I got him, refused to eat or drink and ended up at the vet with dehydration and hypoglycemia and almost didn't make it through the night. I had bloodwork done and they found elevated liver enzymes. My breeder told me that none of her dogs have had liver problems and she doesn't think this is what he has. The vet said that because he is so tiny (about 2 lbs) it isn't safe to do the bile testing because he has to fast for 12 hrs and that if it was a liver shunt he would probable be too tiny to do well with the surgery. She said the prognosis for him isn't good. I am to feed him every two hours (which he refuses) and keep him well hydrated. He eats well first thing in the am but after that refuses. I've been trying to use a syringe to feed him his wet food watered down slightly but he resists that too. I feel like I am being mean! He is on a pill for his liver, lactulose, neoease and Amoxicillan. I am wondering what I can do to ensure him the best outcome possible. I am so worried. It's such a tough call because I've only had him a week and I love him so much. I am a single mom so money is a concern as well. The breeder seems completely unconcerned and feels he is just adjusting to his new home and will straighten out with time. I go back to the vet on Friday to see if the bloodwork has improved at all. Any information or ideas would be greatly appreciated! Thanks
 

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Sorry I'm new to all this. My little guy Tucker is 13 weeks old. I have only had him for a week and he started vomiting a few days after I got him, refused to eat or drink and ended up at the vet with dehydration and hypoglycemia and almost didn't make it through the night. I had bloodwork done and they found elevated liver enzymes. My breeder told me that none of her dogs have had liver problems and she doesn't think this is what he has. The vet said that because he is so tiny (about 2 lbs) it isn't safe to do the bile testing because he has to fast for 12 hrs and that if it was a liver shunt he would probable be too tiny to do well with the surgery. She said the prognosis for him isn't good. I am to feed him every two hours (which he refuses) and keep him well hydrated. He eats well first thing in the am but after that refuses. I've been trying to use a syringe to feed him his wet food watered down slightly but he resists that too. I feel like I am being mean! He is on a pill for his liver, lactulose, neoease and Amoxicillan. I am wondering what I can do to ensure him the best outcome possible. I am so worried. It's such a tough call because I've only had him a week and I love him so much. I am a single mom so money is a concern as well. The breeder seems completely unconcerned and feels he is just adjusting to his new home and will straighten out with time. I go back to the vet on Friday to see if the bloodwork has improved at all. Any information or ideas would be greatly appreciated! Thanks
The 12 hour fasting rule is outdated. These dogs do not need to be fasted that long. Your vet may not be up on the latest information about the test but you can bring this handout with you to help them understand the newer protocol: http://www.ytca.org/health_biletestproced.doc-1.pdf This was written by Dr. Sharon Center, the leading expert on Liver Shunt and Bile Acid testing in dogs.

I am sorry your breeder is not more concerned. I hope that you are able to find the best course of treatment for your little one and I kinda hope the breeder is right that he just has had issues adjusting. It would not be unusual for a puppy just separated from his litter-mates and mom to struggle with the stress.
 

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Nicole, the Amoxicillan also can cause tummy issues so a probiotic should be added & 1/4-1/2 tablet of pepcid AC. The most important things are keeping his blood sugar up and him well hydrated, even if you need to syringe liquid into him.
I agree w/Carina that 12 hrs. is no longer mandated. She always is right on the button w/info & advice.
Please let us know how he is doing. If your vet doesn't like the info. from Dr. Center I would look around for a vet who specializes in small breed dogs. I had a small dog w/liver shunt who was operated & lived a long (if sometimes difficult w/seizures) life. He was diagnosed w/in the lst 6 months.
 

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Thanks for the input. I also was wondering about diet. The vet gave me some Medi Cal Recovery canned dog food. Tucker doesn't really like it, I have to water it down and feed him with a syringe. I had asked the vet if I should be making his food. She kind of brushed me off and said not now because he needs to get bigger and gain weight. I would assume that feeding him something that will help his liver work the best it can would be benificial and then he will want to eat and gain weight.....am I wrong in thinking this? He never pooped at all yesterday when he was eating the medi cal so this am I gave him some food I made with chicken and brown rice and boiled egg and veggies and he ate about a tsp witih very little encouragement. It seems promising. He also had a soft bm about 2 hours after. (sorry if this is TMI) I just want to make sure I am doing what is best for him. Thanks
 

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Nicole, there are some already prepared canned foods for liver issues (for example Hill's LD, Royal Canine Hepatic (which I have used)) and others that I have used in the US. RC also has an hepatic kibble. There are also lots that can be home cooked, but for now I would stick w/one that you know is balanced. There are a few members here that make their own liver diets. My Kitzel also used Sam-E when his enzymes went up due to too many meds w/his surgery or the anesthesia. With the hepatic food and the Sam-E for a month his came back down in the normal range.
You can also add pumpkin (not pumpkin pie mix) but the veggie, to his food for a while to firm up the bms.
 

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Nicole, can you share the blood results with us? I'd be curious to know what the ALT/AST levels are. And I'd also be curious why the vet has prescribed lactulose ... which will cause your puppy to have a very soft stool. Lactulose is something that generally is not prescribed except in the case of a definitely diagnosed liver shunt.
 
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