Department of Pathology, Faculty of Veterinary Medicine, Akdeniz University, Burdur, Turkey Immunohistochemical Observations on TSH Secreting Cells in Pituitary Glands o Goat Kids with Congenital Goitre O. Ozmen 1 and M. Haligur Address of authors: Department of Pathology, Faculty of Veterinary Medicine, Akdeniz University, 15100, Burdur, Turkey; 1 Corresponding author: Tel.: +90 248 234 4500; fax: +90 248 234 4505; E-mail: oozmen@akdeniz.edu.tr With 6 figures and 1 table Received for publication August 31, 2004 Summary Pituitary glandsof normal-termed stillborn goat kids with congenital goitre and normal-termed stillborn goat kids with- out congenital goitre were examined macroscopically, histo- pathologically and immunohistochemically. Thyroid glands of these animals were also examined grossly and microscopically. The pituitary glands of kids with goitre were larger than those of normalkids, and on histopathological examination there was hyperplasia of the acidophil cells in the ventral part of the glands.However,it was impossible to distinguish thyroid sti- mulating hormone (TSH)-secreting cells from other acidophil cells in sections stained with haematoxylin and eosin (HE). Red granules were observed in the cytoplasm of these hyper- plasticcells in periodic acid-Schiff (PAS)-stained sections. Sections were also immunostained with an antibody against TSH using thestreptavidin–biotinperoxidasetechnique. Immunohistochemistry revealed TSH-secreting cells to have increased in number in the pituitary glands of kids with con- genitalgoitrebecauseof the extensiveproliferation when compared with those of normal kids.The present study indi- cated that the presence of multiple fetuses (twins or triplets) may be a predisposing factor for congenital goitre. Introduction The thyroid gland of animalsis a bilobed structurethat overlaysthe trachea ata point justbelow the larynx. The functionalunit of the thyroid gland is the thyroid follicle, a sphericalstructurecomposedof an outer monolayerof cuboidalcells and the colloid, the thyroglobulin–hormone complex, which is the storage reservoir of thyroid hormone. The colloid stored in the lumen is a clear, viscous fluid. The size of the follicles and the length of their cells vary according to the functional stage of the gland. The cells may vary from an inactive squamous cell to the highly active, tall columnar cell.Interspersed between the follicles are thyroid C cells, the source ofcalcitonin,the hormone associated with calcium metabolism. A third type of hormonal tissue, the parathyroid, is embedded within the thyroid or located in its close proximity (Dellmann and Brown, 1981; Kaneko, 1997). Thyroid stimulating hormone (TSH) is secreted from the adenohypophysis and stimulates thyroid glands (Jones et al., 1997). TSH concentration in blood starts increasing from birth to 4 or 8 h. This increase is strongly inhibited by delaying the first milk intake. Therefore,it appearsthat mechanisms involved in this surge are more complex than stimulation of the hypothalamic–pituitary axis by neonatalcooling alone (Cabello and Wrutniak, 1990).TSH-secreting cells or thyro- tropes,predominate in the ventral region of the pars distalis (Dellmann and Brown, 1981). Non-neoplastic and non-inflam- matory enlargement of the thyroid gland, commonly known as goitre,may develop in all domesticmammals,birds and reptiles(Rickettset al., 1985;Falconer,1987;Rotkiewicz et al., 1988;Osameand Ichijo, 1994;Topper et al., 1994; Schilleret al., 1995;Kaneko, 1997;Corradini et al., 2000; Simon et al., 2000; Garner et al., 2002; Fyfe et al., 2003). The major pathogenicmechanisms responsiblefor the development of thyroid hyperplasia include iodine-deficient diets,goitrogenic compounds that interfere with thyroxino- genesis,excessdietaryiodine and geneticallydetermined defects in the enzymes responsible for biosynthesis of thyroidal hormones. All mentioned mechanisms result in an inadequate thyroxine (T 4 ) synthesis and decreased blood concentration of thyroxine and triiodothyronine (T 3 ). This is detected by the hypothalamus and pituitary gland,stimulating an increase in TSH, which resultsin hypertrophy and hyperplasia of follicularcellsof the thyroid (Capen, 1995,2002;Kaneko, 1997). Simple goitre is a compensatory increase in thyroid glandu- lar mass(hyperplasia and hypertrophy) so that the gland maximizes iodine uptake and is able to synthesize and release a normalamount of T 4 . At this time,the patient is physiolog- ically normal,but the gland can become quite large. Ulti- mately,in iodine deficiency,the goitrousgland fails to synthesize sufficient T 4 and hypothyroidism occurs (Kaneko, 1997). Animals born to dams on iodine-deficient diets are more likely to develop severe thyroid hyperplasia and have clinical evidenceof hypothyroidism. Offspring of iodine-deficient mothers may be stillborn or aborted late in pregnancy. Of the animals born alive, some are weak and partly hairless with subcutaneus oedema of head and neck (Bestetti, 1975;Bath et al., 1979; Ricketts et al., 1985; Capen, 1995, 2002; Kaneko, 1997; Wither, 1997). There are two general types of goitres: (1) non-toxic goitres, which produce either normal amounts of hormone (simple goitre) or below-normal amountsof hor- mone(hypothyroid), and (2) toxic goitres,which produce excessamountsof hormone (hypertrophy). Furthermore, a defector deficiency atany trophic step can also result in thyroid disease (Kaneko, 1997). The occurrence of goitre in animals is well known.Several studieshave demonstrated thyroidal changesand serum U.S. Copyright Clearance Center Code Statement: 0931–184X/2005/5209–0454 $15.00/0 www.blackwell-synergy.com J. Vet. Med. A 52, 454–459 (2005) 2005 The Authors Journal compilation 2005 Blackwell Verlag, Berlin ISSN 0931–184X