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Concurrent hypothyroidism and hyperadrenocorticism in canines.


Hypothyroidism is reported to be present concurrent to hyperadrenocorticism (Peterson et al., 1982). This might be due to chronic hypercortisolism (iatrogenic or naturally occurring) which suppresses pituitary secretion of thyroid stimulating hormone (TSH) (Torres et al., 1991). Ferguson and Peterson (1992) suggested that concurrent hypothyroidism was due to excess cortisol altering thyroid hormone binding to plasma proteins or enhanced metabolism of thyroid hormones. Serum total thyroxine ([T.sub.4]) and triiodothyronine ([T.sub.3]) concentrations are decreased in approximately 70 percent of dogs with hyperadrenocorticism (Peterson, 1984). In addition, more than 60 percent of dogs with low serum total [T.sub.4] concentrations also had low free [T.sub.4] concentrations (Ferguson and Peterson, 1992).

History and Clinical findings

A Non descript dog (Case I) and two German shepherds dogs (Case II and III) were presented with history of alopecia for more than six months. Polyuria and polydipsia were present in all dogs. Case I and Case II showed mild obesity with pendulous abdomen. On physical examination, all dogs showed truncal alopecia, thinning of skin, telengectasis and comedones. Case III had hyperpigmentation throught the body. Skin scraping of case III revealed Demodex canis.

Haematology revealed normal hemogram with haemoglobin ranging from 11 to 12.6 g/dl, Packed Cell Volume (PCV) from 28.7 to 37.4 per cent and Red Blood cells (RBC) 4.22 to 5.99 x [10.sup.6] cumm. Leukogram was found to be in high normal range. White Blood cells (WBC) ranged from 11 to 16.8 x [10.sup.3] cumm, neutrophils 63 to 82 per cent, lymphocytes 13 to 34 per cent, monocytes 2-3 per cent and eosinophils 1-2 per cent. Serum biochemistry revealed elevated levels of alkaline phosphatase (320-456 IU/L), alanine aminotransaminase (222-289 IU/L), triglycerides (89154 mg/dl), cholesterol (185-339 mg/dl) and glucose (126-208 mg/dl).

Ultrasound of adrenal glands was performed as per standard procedure (Hoffman, 2003). The left and right adrenal glands were hypoechoic and homogenous. The thickness of left and right adrenal gland ranged from 8.2-12 mm and 8-9.9 mm respectively. Both glands were enlarged. Barthez et al. (1995) reported that in Pituitary dependent Hyperadrenocorticism (PDH) dogs bilaterally enlarged adrenal glands were frequent finding which was due to constant stimulation by ACTH. He further stated that a thickness of more than 7.5 mm for left adrenal gland was considered to provide best sensitivity and specificity as a diagnostic test for PDH.

Cortisol and total [T.sub.4] levels were estimated. Hyperadrenocorticism was diagnosed with urine cortisol and creatinine ratio (UCCR) and low dose dexamathasone suppression test (LDDST) using canine specific cortisol ELISA kit. The UCCR of three dogs ranged from 18.4 to 229 x [10.sup.-6]. Stolp et al. (1983) suggested that in hyperadrenocorticoid dogs urine cortisol creatinine ratio was more than 10 x [10.sup.-6]. The mean serum cortisol at basal and 4 and 8 hour post dexamethasone injection values for three cases were 6.54 pg/dl, 1.6 [micro]g/dl and 5.5 [micro]g/dl respectively. LDDST results showing failure to suppress at 4 and 8 hours after administration are diagnostic of hyperadrenocorticism. In some dogs with PDH cortisol is temporarily suppressed at 4 hours and elevated at 8 hours. Suppression was defined as a serum cortisol concentration of < 1.5 [micro]g/dl 4 hours after dexamethasone administration or serum cortisol concentration < 50 percent of baseline concentration 4 or 8 hours after dexamethasone administration (Liss, 2012). Total [T.sub.4] estimated using chemiluminiscent method was found to be low (< 0.5 [micro]g/dl).


Mitotane, Ketoconazole and Trilostane are three treatments commonly used in management of PDH in dogs (Boari and Aste, 2003). The most serious adverse effect associated with mitotane administration is development of total or near total adrenocortical destruction with concomitant glucocorticoid, mineralocorticoid deficiency, hyperkaliaemia and hyponatraemia (Addison's disease). Ketoconazole, an imidazole derivative is an orally active broad spectrum antimycotic drug that at high doses, interferes with steroid biosynthesis. Ketoconazole is effective in only 50% percent cases and has side effects involving gastrointestinal system. Trilostane is a synthetic orally active steroid analogue. It can act as a competitive inhibitor of the 3-beta-hydroxysteroid dehydrogenase enzyme system and it thereby inhibits the synthesis of several steroids, including cortisol and aldosterone (Ruckstuhl et al., 2002). Trilostane is currently not available in India. Hence, treating hyperadrenocorticism was not considered because of the above stated reasons.

The treatment of choice for hypothyroidism is L-thyroxine preparation (0.02 mg/kg orally twice daily to start) (Boari and Aste, 2003) and then the dose and the frequency should be adjusted based on the result of therapeutic monitoring. All the dogs were treated with levothyroxin (Tablet Eltroxin) at the dose rate of 22 [micro]g/kg twice daily. Hair growth was seen after 2 months of treatment. The progress was monitored regularly. Two dogs collapsed due to complication of hyperadrenocorticism (Nichols, 1997). One dog is showing progress.


Barthez, P.Y., Nyland, T.G. and Feldman, E.C. (1995). Ultrasonographic evaluation of the adrenal glands in dogs. J. Am. Vet. Med. Assoc. 207: 1180-83.

Boari, A and G. Aste, (2003). Diagnosis and Management of Geriatric Canine Endocrine Disorders. Vet. Res. Commun. 27: 543-54.

Ferguson, D.C. and M.E. Peterson. (1992). Serum free and total iodothyronine concentrationsin dogs with hyperadrenocorticism. Am. J. Vet. Res. 53: 1636-40.

Hoffmann, K.L. (2003). Ultrasonographical examination in canine hyperadrenocorticism. Aust. Vet. J. 81: 27-30.

Liss, D. (2012). Testing the endocrine system for adrenal disorders and diabetes mellitus: It is all about signaling hormones. Vet. Tech. 33: 1-4.

Nichols, R. (1997). Complications and concurrent disease associated with canine hyperadrenocorticism. Vet. Cl. North. Am. Small. Anim. Pract. 27: 309-20.

Peterson, M.E. (1984). Hyperadrenocorticism. Vet. Cl. North. Am. Small. Anim. Pract. 14: 731-49.

Peterson, M.E., S.R. Gilbertson and W.D. Drucker. (1982). Plasma cortisol response to exogenous ACTH in 22 dogs with hyperadrenocorticism caused by adrenocortical neoplasia. J. Am. Vet. Med. Assoc. 180: 542-44.

Stolp, R., A. Rijnberk and J.C. Meijer, (1983). Urinary corticoids in the diagnosis of canine hyperadrenocorticism. Res. Vet. Sci. 34: 141-44.

Torres, S.M.F., P.J. McKeever and S.D. Johnston, (1991). Effect of oral administration of prednisolone on thyroid function in dogs. Am. J. Vet. Res. 52: 416-21.

Ruckstuhl, N.S., C.S. Nett and C.E. Reusch (2002). Results of clinical examinations, laboratory tests, andultrasonography in dogs with pituitary dependent hyperadrenocorticism treated with trilostane. American J. Vet. Res. 63: 506-12.

M. Sandhya Bhavani (1), P.S. Thirunavukkarasu (2), S. Kavitha (3) and A.P. Nambi (4)

Department of Veterinary Clinical Medicine, Ethics and Jurisprudence, Madras Veterinary College

Tamil Nadu Veterinary and Animal Sciences University

Chennai--600007 (Tamil Nadu)

(1.) Post Graduate Scholar and Corresponding author E-mail:

(2.) Professor and Head

(3.) Associate Professor

(4.) Professor and Head
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Title Annotation:Clinical Article
Author:Bhavani, M. Sandhya; Thirunavukkarasu, P.S.; Kavitha, S.; Nambi, A.P.
Publication:Intas Polivet
Article Type:Report
Geographic Code:9INDI
Date:Jul 1, 2013
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