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Therapeutic management of goiter in calves.


Iodine is an indispensable component of hormones produced by thyroid gland and is essential for mammalian life. Iodine deficiency may go unobserved for prolonged periods before thyroid gland enlargement (goiter) occurs. Goiter may be manifested as retarded maturation and growth of skin and its appendages, the skeleton and/or central nervous system (Hopkins and Thorburn, 1972). Thyroid hormones have been evaluated as potential regulators (Suguna et al., 2013). Ramakrishna et al. (1992) reported that goitre as an emerging mineral disorder in animal grazed on iodine deficient endemic areas. The condition is described as 'neonatal animal hypothyroidism' with colloidal goiter, alopecia, unthriftiness, thyroid thrill and a high rate of mortality, associated with decreased serum [T.sub.3], [T.sub.4] levels and increased TSH activity (Singh et al., 2003). The present paper describes the clinicopathological studies of goiter in cow calves with its therapeutic management.

Materials and Methods

Eight to ten months old, 9 non-descript male calves were presented with complaint of swelling on either side of neck with a gradual increase in size. Further anamnesis revealed cabbage feeding. These calves were also not offered iodized salts in the feed. Clinically, all animals were dull, weak and had stunted growth as compared to other healthy animals along with prominent enlargement of thyroid glands (Fig. 1). The consistency of enlarge glands was hard on palpation. On the basis of history, clinical signs and anatomical position of enlargement these cases were tentatively diagnosed as goiter.

Firstly all 9 animals were divided in to three equal groups and treated with 3 different treatments for 20 days. The animals of group I were treated by supplementation of iodized salts 200 gms per day in feed whereas in group II, the animals were treated with tincture iodine @ 5ml intraruminally once in a day. The animals of group III were given hormonal treatment with Thyroxine sodium tablets (Thyrox-25 (a)). Ten tablets per day of thyroxine sodium of 25 mcg were given orally.


After different treatments, animals of group I showed non significant clinical improvement whereas mild changes were seen in group II after treatment on 15th day. The animals of group III showed a very positive response and faster recovery on 15th day. The complete recovery within 20 days was observed in group III (Fig.2). The clinical improvement was faster in thyroxine sodium treated group as compared to other group of animals. The response to treatment further confirmed the diagnosis. So, the results in present study indicated beneficial effect of thyroxine sodium for management of cases for enhancement of recovery of the goiter affected animals.


Similar finding was also observed by the Vijlder (2003) who also described that disorders in the synthesis, storage and secretion of thyroid hormones provide molecular basis of abnormalities in thyroid growth or thyroid dishormonogenesis which results in congenital hypothyroidism. The major pathogenic mechanisms responsible for development of thyroid hyperplasia include iodine deficient diets (Paulikova et al., 2002). Dietary substances that interfere with thyroid metabolism can aggravate the effect of iodine deficiency and they are termed goitrogens. Cruciferous vegetables, including cabbage, kale, cauliflower, broccoli, turnips and rapeseed, contain glucosinolates; their metabolites compete with iodine for thyroidal uptake (Zimmermann, 2009). Singh et al. (2003) reported successful treatment of congenital goiter in goats with colloidal iodine @ 0.1mg/kg b. wt. for 100 days. However, in this case treatment with iodine did not show significant improvement. This might be attributed to the fact that there could be some defect in uptake of iodine by thyroid gland. In many instances the animal which survives initial danger period after birth may recover except for partial persistence of goiter (Radostitis et al., 2003). Thyroid hormones also modulate zinc transport activity of intestinal and renal brush border membrane (Dake et al., 2013). It is therefore advised to begin thyroxine therapy as soon as possible to increase chances of treatment.


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Ramakrishna, C., Prasad, M.C., Ram kumar and Sharma, A.K. (1992). Prevalence of Goitre/ hypothroidsim in goats in and around Bareiilly. Indian Vet. Med. J. 16: 37-40.

Singh, J.L., Sharma, M.C., K. Mahesh, Varshney, V.P., Ahmad, A.H. and Prasad, S. (2003). Clinicobiochemical profile and therapeutic management of congenital goiter in kids. Indian J. Vet. Med. 23:82-87.

Sugnuna, K., Sarath, T., Mehrotra, S., Arunmozhi, N., Agarwal, A. K. and Umashankar. (2013). Serum Tri-Iodothyronine and Thyroxin Profile in Insulin Treated Preganant Goats. 90: 123-24.

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Deepak Kumar Kashyap, Devesh Kumar Giri (1) and Govina Dewangan

Teaching Veterinary Clinical Complex Arawali Veterinary College Rajasthan University of Veterinary and Animal Sciences (RAJUVAS) Bajor Sikar--332403 (Rajasthan)

(1.) Corresponding author. E-mail: a--Brand of Macleods Pharmaceuticals Ltd., Mumbai
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Title Annotation:Clinical Article
Author:Kashyap, Deepak Kumar; Giri, Devesh Kumar; Dewangan, Govina
Publication:Intas Polivet
Article Type:Report
Date:Jan 1, 2015
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