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Feline hyperthyroidism

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Feline hyperthyroidism is an endocrine disorder in which the thyroid gland produces too much thyroid hormone. Hyperthyroidism is the most common endocrinopathy of cats. The complete pathogenesis is not fully understood.

Background[edit]

In 1979 the first clinical report of a cat with hyperthyroidism was reported.[1] More studies and greater awareness would follow and today hyperthyroidism is a common condition in small animal practice. Whether that is due to increased prevalence or better testing is not entirely agreed upon.[2]

A study in 1987 transplanted thyroid tissue from affected cats into nude mice. The mice were administered levothyroxine, which suppresses thyroid-stimulating hormone. The thyroid cells remained in the hyperthyroid state. This study helped provide evidence for thyroid dysfunction as the cause rather than thyroid stimulation.[2]

Causes[edit]

The majority of cases of hyperthyroidism in cats are the result of benign tumours. The most commonly identified abnormalities of the thyroid gland in hyperthyroid cases are follicular cell adenoma and multinodular adenomatous hyperplasia. 1% to 3% of feline hyperthyroid cases are caused by malignant tumours. These are not always able to be distinguished from benign tumours.[2]

What triggers these adenomas is still unknown. Mutations in the thyrotropin receptor genes may be responsible for the unregulated growth of the cells.[3] Diet and environmental factors, as well as genetic factors, may play a role.[4] According to epidemiologic studies, the feeding of commercial cat food is a risk factor for the development of the disease, which is attributed to the high content of thyroid-enlarging (strumigenic) substances such as soy isoflavones or phthalates.[5][3] Cats fed canned food are 2.5 to 5 times more likely to develop hyperthyroidism.[6] In addition, environmental factors such as the use of certain litters may also play a role in the development of the disease.[7][8] Polybrominated diphenyl ethers (PBDEs), which are used as flame retardants in textiles (they are now banned in the EU and some US states), could also be involved in the pathogenesis due to their endocrine effects: The chronically increased TSH production could lead to hypertrophy of the thyroid follicles.[6] It is believed that the cause of hyperthyroidism is multifactorial. Studies have identified different mutations as causing thyroid cell autonomy.[2]

Iodine[edit]

Excessive iodine administration has been hypothesised as causing thyrotoxicosis in cats, as it does in humans; however, cats have been shown in multiple long terms studies to be able to regulate their levels of thyroid hormone within safe ranges when administered iodine. Iodide intake and it's effects are unknown.[2]

Soy isoflavones[edit]

Soy is often used in commercial cat food diets as a vegetable protein. In one study more than half of commercial cat foods surveyed contained soy isoflavones. Genistein and daidzein, both of which occur in soybeans, inhibit the enzymes thyroid peroxidase and thyroxine 5-deiodinase. This causes decreased thyroxine and triiodothyronine concentrations. In response to decreased triiodothyronine levels the body will produce more thyroid-stimulating hormone to normalise triiodothyronine levels, this has been shown to result in increased thyroxine levels. In addition these effects are heightened when a cat is suffering from iodine deficiency. However, further research is needed to confirm a link between soy isoflavones and hyperthyroidism.[2]

Goitrogens[edit]

Goitrogens are chemicals that disrupt thyroid hormone production. Chemicals such as bisphenol A and polybrominated diphenyl ethers have been shown to exist in indoor cats at heightened levels and are hypothesised to be a potential cause of hyperthyroidism. Bisphenol A is common in canned cat foods, although no association between it and hyperthyroidism has currently been demonstrated. Polybrominated diphenyl ethers (PBDEs) are often used as fire retardants and are known to be a goitrogen; however, levels of these chemicals have been shown to be the same in euthyroid cats as hyperthyroid cats. No association has been proven in a study for the association between PBDEs and hyperthyroidism.[2]

Signs and symptoms[edit]

Hyperthyroidism is a disease that slowly progresses and symptoms are very subtle at first. It can take up to two years from onset of symptoms for a diagnosis of hyperthyroidism to be made.[2]

The most common symptom is weight loss, occurring in 98% of hyperthyroid cases. Other symptoms that occur more than 50% of the time, include: polyphagia (81%), without obesity; restlessness (76%); tachycardia (66%); polydipsia and polyuria (60%); emesis; and cardiac murmur (53%).[2]

Less common symptoms include: diarrhoea (33%), increased volume of faeces (31%), anorexia (26%), polypnoea (25%), myasthenia (25%), muscle tremors (18%), congestive heart failure (12%), excessive nail growth (12%), and dyspnoea (11%).[2]

Hypertension is seen in 5-20% of hyperthyroid cats, but a clear cause-and-effect relationship has not been established.[6]

Hyperthyroidism may also be the cause of life-threatening arterial thromboembolism. In 1.7% of cats with thromboembolism, hyperthyroidism was not previously known. This results in sudden hind limb paralysis and severe pain.[9]

Cachexia is a possible symptom in hyperthyroid cats but due to improved screening and diagnostics it is less common for a cat to become cachectic before starting treatment.[2]

Risk factors[edit]

Multiple case control studies have looked at diet and hyperthyroidism. These studies have found associations between commercial diets and hyperthyroidism. Other risk factors identified include non-Siamese related breeds, lack of outdoor access, flea medication, pesticides, certain cat litters, female sex, sleeping on the floor, organic fertiliser, human baby food, carpet cleaners, natural gas, lack of deworming, and a fish diet.[10] These mixed results suggest a multifactoral cause with diet being having an important role.[2]

Age of onset[edit]

The age of onset has been reported to be between 4–22 years with an average of 13 years, with some individual cases occurring in cats below the age of 4 years. More than 95% of cases occur in cats 8 years and older.[2]

Diagnosis[edit]

Testing for hyperthyroidism is routine for elderly cats and standard blood tests that can be performed in clinic allow for measurement of serum thyroxine levels. With this advancement diagnosis is often made before clinical signs are well noticeable and severe.[2]

Laboratory tests[edit]

The blood count often shows an increase in white blood cells (leukocytosis) and a decrease in eosinophil granulocytes (eosinopenia) and lymphocytes (lymphopenia) as a result of the stress response to high thyroxine levels. Red blood cell count and hemoglobin content are in the upper normal range. There is usually a slight to moderate increase in the activity of various enzymes (ALAT, ASAT, LDH, AP) in the serum. The fructosamine level is reduced due to the increased protein metabolism and is usually below 200 μmol/l.[3]

Blood urea and creatinine levels may be elevated as a result of the renal dysfunction often associated with hyperthyroidism.[4][11] However, the coexistence of hyperthyroidism and chronic kidney disease may be masked to some extent because thyroxine increases metabolism and cardiac output, improving blood flow to the kidneys. This increases the glomerular filtration rate, which favors the excretion of toxic metabolites. Paradoxically, therefore, renal insufficiency may become clinically manifest after treatment of hyperthyroidism. According to Egner and Carr,[12] these laboratory changes, together with positive palpatory findings, are evidence of the disease.

Special thyroid function tests must be carried out for further diagnosis.

The initial step should be to determine the serum concentration of thyroxine (T4). However, in veterinary medicine, the total thyroxine concentration is typically determined, rather than that of free (non-protein-bound) thyroxine (fT4). Nevertheless, the latter is more sensitive.[13] The normal range for T4 in cats is between 1.1 and 4.5 μg/dL, for fT4 between 1.0 and 2.8 ng/dL when determined by equilibrium dialysis.[14] In approximately 20% of animals, the T4 level is normal despite the presence of disease, which may be due to fluctuations in the hormone level during the course of the day or a reduction in the T4 level as a result of other secondary diseases. The measurement of fT4 has a sensitivity of 95%, but 20 to 30% of thyroid-healthy cats also have elevated fT4 levels. Therefore, if fT4 levels are elevated, total T4 must also be measured, which should be in the upper reference range in animals with hyperthyroidism.[15] Furthermore, various medications, including glucocorticoids, non-steroidal anti-inflammatory drugs (NSAIDs), phenobarbital, and trimethoprim-sulfonamide combinations, can influence T4 levels.[3] In the event of a clinical suspicion, it is advisable to repeat the determination at a later date.

Another method is the thyroid suppression test. In this procedure, a synthetic triiodothyronine (T3, typically Liothyronine) is administered to the cat over two days. A cat with a healthy thyroid gland will respond to this treatment by reducing the secretion of TSH (negative feedback), which will result in a decline in the T4 concentration. However, as the hyperthyroidism has already led to a permanently low TSH level, the administration of T3 in sick cats does not result in a reduction in TSH and T4.[4]

Another diagnostic procedure is the TRH stimulation test. In this test, the cat is administered thyrotropin-releasing hormone (TRH), which leads to a significant increase in the T4 concentration in healthy cats. In diseased animals, on the other hand, there is no or at most a slight increase.[16] However, this test sometimes has considerable side effects in cats (salivation, vomiting, palpitations, defecation), which is why it is rarely used. The TSH test, which determines the serum content of thyrotropin, a hormone that regulates the thyroid gland, is now also available for cats.[14] As in humans, early forms of hyperthyroidism can be detected based on low or unmeasurable TSH levels. However, the TSH stimulation test, which functions in a similar manner to the TRH function test, is no longer conducted as TSH is no longer available on the market.

Imaging procedures[edit]

Thyroid sonography, a diagnostic technique that has been utilized in human medicine for decades, has only recently been employed in veterinary medicine, primarily for research purposes. The primary reasons for this are the high equipment requirements and the associated high equipment costs. High-resolution linear transducers with at least 7.5 MHz, preferably 10 to 13 MHz, with a small contact surface are utilized.[17] Sonography can be employed to diagnose thyroid enlargement in all hyperthyroid cats, whereas the diagnostic reliability of palpation is only 84%, even among experienced veterinarians.[18] Thyroid scintigraphy is a valuable diagnostic procedure, yet it is only available in a limited number of veterinary clinics. In this procedure, a cat is administered a radionuclide (e.g., the iodine isotope 131I or the technetium isotope 99mTc), and its accumulation in the adenomas is then visualized. The principal advantage of this method is that the precise location of the tumors in the thyroid gland can be determined, which is advantageous with regard to surgical therapy. On rare occasions, additional thyroid tissue may colonize outside the thyroid gland (ectopia, particularly in the mediastinum) and become diseased as a result of disorders during organogenesis. Such displaced thyroid tissue can only be detected by scintigraphy.[19]

To date, Magnetic Resonance Imaging (MRI) and Computer Tomography (CT) have not been employed for thyroid diagnostics in cats. Furthermore, such equipment is only accessible at large veterinary clinics.

Therapy[edit]

Currently, three therapy options are available for hyperthyroidism in cats: the use of thyrostatic drugs, surgical removal of the diseased thyroid tissue, and radioiodine therapy. Regardless of the procedure selected, subsequent treatment of concomitant and secondary diseases (e.g., kidney damage, high blood pressure, heart disease) is typically necessary.[12] In order to ascertain the potential adverse effects of reduced thyroid hormone levels on renal function, a 30-day course of medication is recommended prior to the implementation of more radical measures such as thyroidectomy or radioiodine therapy.[6]

Thyreostatics[edit]

Therapy with thyrostatic agents is relatively straightforward and is therefore the most commonly used. Thyrostatic drugs inhibit the formation of thyroid hormones, but, in contrast to other methods, do not eliminate the pathologically altered tissue. Nevertheless, these drugs can usually be used in long-term therapy without any problems or can also be used to stabilize patients before a surgical procedure. In veterinary medicine, thiamazole (syn. methimazole, trade names Felimazole, Felidale and Thiamatab) or carbimazole (trade name Vidalta) are employed. Carbimazole is rapidly converted into methimazole when administered orally.[20] According to the manufacturer, side effects (including vomiting, lethargy, itching, liver disease, and blood count changes) occur in approximately 20% of cats, particularly with long-term treatment. However, these typically resolve once the drug is discontinued. Additionally, thiamazole cannot be used in cats with concomitant liver disease, diabetes, or blood clotting disorders.

Iopanoic acid may also be employed in the event of intolerance to thiamazole. It inhibits the conversion of T4 to T3 and has a negligible incidence of side effects.[12]

Thyroidectomy[edit]

Although surgical removal (thyroidectomy) is an effective treatment, it is also associated with a high risk of complications, particularly in cats with severe hyperthyroidism, due to the inherent risks associated with anesthesia. Prior to the surgical procedure, it is common practice to administer thyrostatic drugs. There are several techniques for the removal of the thyroid gland, with the objective of preserving the epithelial cells to the greatest extent possible. Additionally, there is a potential risk of injury to crucial cervical nerves (recurrent laryngeal nerve, vagosympathetic trunk) during surgery. A total thyroidectomy results in a deficiency of thyroid hormones, which must be compensated for by lifelong administration.[21] In the event of unilateral removal, a transient hypothyroidism frequently develops postoperatively, although this is typically not a cause for concern.[4] Furthermore, there is a risk of recurrence with surgical removal, particularly in the presence of ectopic thyroid tissue.[22]

Radioiodine therapy[edit]

Radioiodine therapy is the treatment of choice due to its efficacy and tolerability. A single treatment is typically sufficient, eliminating the need for long-term drug treatment (which can be problematic in some cats) and the risks associated with surgical removal.[23] However, it is associated with significant radiation protection requirements and is currently only available at two veterinary facilities in Germany. In addition to the limited availability, the associated costs and the need for hospitalization represent a disadvantage. In close consultation with the responsible supervisory authorities, it has been possible to reduce the required duration of hospitalization from approximately three weeks to a few days.[24] The necessary duration of hospitalization is determined by dosimetry and is seven to ten days.[5]

Thermal or chemical destruction of the thyroid gland[edit]

Destruction of the thyroid tissue using a radiosurgical device under ultrasound control (thermal ablation) or by injection of 96% ethanol (chemical ablation) is practically no longer relevant. Both forms of treatment have increased side effects such as laryngeal paralysis or Horner's syndrome.[5]

References[edit]

  1. ^ M. E. Peterson et al.: Spontaneous hyperthyroidism in the cat. In: Proc. Am. College Vet. Intern. Med. 1979, p. 108.
  2. ^ a b c d e f g h i j k l m n Scott-Moncrieff, J. Catherine (2015). "Feline Hyperthyroidism". In Feldman, Edward C.; Nelson, Richard W.; Reusch, Claudia; Scott-Moncrieff, J. Catharine (eds.). Canine and feline endocrinology (Fourth ed.). St. Louis, Missouri: Elsevier Saunders. pp. 137–190. ISBN 978-1-4557-4456-5.
  3. ^ a b c d Eva Höfel, Thomas Rieker: Hyperthyreose – Aktuelles zur Pathogenese und Diagnose. In: Fachpraxis. No. 63, 2013, p. 6–11.
  4. ^ a b c d M. E. Peterson: Hyperthreodism. In: Stephen J. Ettinger, Edward C. Feldman: Textbook of veterinary internal medicine. 5th edition. Volume 2, Saunders, 2000, ISBN 0-7216-7256-6, pp. 1400-1419.
  5. ^ a b c Andrea Monika Mathes, Reto Neiger: Hyperthyreose der Katze. In: Kleintierpraxis. 55, 2010, p. 685–698.
  6. ^ a b c d Thomas Graves: Aktuelle Aspekte der Hyperthyreose bei der Katze. In: Vet. Focus. 19.3, 2009, p. 2–5.
  7. ^ R. W. Nelson, C. G. Couto (Ed.): Feline Hyperthyreose. In: Innere Medizin der Kleintiere. 1st edition. Urban & Fischer, München/ Jena 2006, ISBN 0-323-01724-X, p. 758–772.
  8. ^ P. H. Kass et al.: Evaluation of environmental, nutritional, and host factors in cats with hyperthyroidism. In: J. Vet. Int. Med. 13(4), 1999, p. 323–329. ISSN 0891-6640
  9. ^ Kieran Borgeat et al.: Arterial thromboembolism in 250 cats in general practice: 2004-2012. In: Journal of veterinary internal medicine. Volume 28, No. 1, 2014 Jan-Feb, p. 102–108, doi:10.1111/jvim.12249, PMID 24237457, PMC 4895537 (free full text).
  10. ^ Edinboro, Charlotte H; Scott-Moncrieff, J Catharine; Glickman, Larry T (2010). "Feline Hyperthyroidism: Potential Relationship with Iodine Supplement Requirements of Commercial Cat Foods". Journal of Feline Medicine and Surgery. 12 (9): 672–679. doi:10.1016/j.jfms.2010.07.011. ISSN 1098-612X.
  11. ^ J. D. Broussard et al.: Changes in clinical and laboratory findings in cats with hyperthyreodism from 1983 to 1993. In: J. Am. Vet. Med. Assoc. 206(3), 1995, p. 302–305. PMID 7751233.
  12. ^ a b c Beate Egner, Anthony P. Carr: Hyperthyreose bei der Katze – Welche Rolle spielen ACE-Hemmer? In: kleintier konkret. 11, 2008, p. 11–14.
  13. ^ M. E. Peterson: Measurement of serum concentrations of free thyroxine, total thyroxine, and total triiodothyronine in cats with hyperthyroidism and cats with nonthyroidal disease. In: J. Am. Vet. Med. Assoc. 218(4), 2001, p. 529–536. PMID 11229503.
  14. ^ a b R. Hämmerling: Die feline Hyperthyreose. In: Der praktische Tierarzt. 86(5), 2005, p. 320–324. ISSN 0032-681X
  15. ^ Stephanie Nather et al.: Hyperthyreose der Katze. In: Kompendium Kleintier 2017, p. 52–57.
  16. ^ M. E. Peterson et al.: Use of the thyrotropin releasing hormone stimulation test to diagnose mild hyperthyreodism in cats. In: J. Vet. Intern. Med. No. 4, 1999, p. 279–286. ISSN 0891-6640
  17. ^ C. Poulsen Nautrup et al.: Schilddrüse und Nebenschilddrüsen. In: C. Poulsen Nautrup, R. Tobias (Ed.): Atlas und Lehrbuch der Ultraschalldiagnostik bei Hund und Katze. 2nd edition. Published by Schlütersche publishing company, Hannover 1998, ISBN 3-87706-663-1, p. 113–116.
  18. ^ W. Kraft et al.: Symptome bei Hyperthyreose der Katze: eine retrospektive Studie. In: Kleintierpraxis. 44(10), 1999, p. 719–732. ISSN 0023-2076
  19. ^ M. E. Peterson, D. V. Becker: Radionuclide thyroid imaging in 135 cats with hyperthyroidism. In: Vet. Radiol. 25(1), 1984, p. 23–27. ISSN 0196-3627
  20. ^ M. E. Peterson, D. P. Aucoin: Comparison of disposition of carbimazole and methimazole in clinically normal cats. In: Res. Vet. Sci. 54(3), 1993, p. 351–355. PMID 8337482.
  21. ^ C. D. Welches et al.: Occurrence of Problems after Three Techniques of Bilateral Thyroidectomy in Cats. In: Vet. Surgery. 18(5), 1989, p. 392–396. PMID 2815557.
  22. ^ E. C. Naan et al.: Results of thyroidectomy in 101 cats with hyperthyroidism. In: Vet. Surg. 35(3), 2006, p. 287–293. PMID 16635010
  23. ^ M. E. Peterson: Radioiodine treatment of hyperthyroidism. In: Clin. Tech. Small Anim. Pract. 21(1), 2006, p. 34–39. PMID 16584029.
  24. ^ M. Puille et al.: Radiojodtherapie bei Katzen: Strahlenschutz der Kontaktpersonen. In: Tierärztl Prax. 33 (K), 2005, p. 291–295. ISSN 1434-1239

External links[edit]

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