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Multinodular goitre with giant cell vasculitis of thyroid arteries in a woman with temporal arteritis
  1. B GRANEL,
  2. J SERRATRICE,
  3. B CHAUDIER,
  4. J REY,
  5. L SWIADER,
  6. X PACHE,
  7. C CHRISTIDES,
  8. P DISDIER,
  9. P J WEILLER
  1. Service de Médecine Interne
  2. Hôpital de la Timone
  3. 264 Rue Saint Pierre
  4. Marseille, France
  5. Service d'Anatomie Pathologique
  6. Hôpital Nord, Chemin des Bourelly
  7. 13915 Marseille, France
  8. Service de Chirurgie Endocrinienne
  9. Hôpital de la Timone
  1. Dr P Disdier, Service de Médecine Interne, Hôpital de la Timone, 264 Rue Saint-Pierre, 13385 Marseille Cedex 5, France pdisdier{at}ap-hm.fr
  1. C DE MICCO
  1. Service de Médecine Interne
  2. Hôpital de la Timone
  3. 264 Rue Saint Pierre
  4. Marseille, France
  5. Service d'Anatomie Pathologique
  6. Hôpital Nord, Chemin des Bourelly
  7. 13915 Marseille, France
  8. Service de Chirurgie Endocrinienne
  9. Hôpital de la Timone
  1. Dr P Disdier, Service de Médecine Interne, Hôpital de la Timone, 264 Rue Saint-Pierre, 13385 Marseille Cedex 5, France pdisdier{at}ap-hm.fr
  1. J F HENRY
  1. Service de Médecine Interne
  2. Hôpital de la Timone
  3. 264 Rue Saint Pierre
  4. Marseille, France
  5. Service d'Anatomie Pathologique
  6. Hôpital Nord, Chemin des Bourelly
  7. 13915 Marseille, France
  8. Service de Chirurgie Endocrinienne
  9. Hôpital de la Timone
  1. Dr P Disdier, Service de Médecine Interne, Hôpital de la Timone, 264 Rue Saint-Pierre, 13385 Marseille Cedex 5, France pdisdier{at}ap-hm.fr

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Previous studies have suggested that patients with giant cell arteritis (GCA) or polymyalgia rheumatica (PMR) may be at increased risk for thyroid dysfunctions.1 To our knowledge, histologically confirmed thyroid arteritis in a case of GCA has never been described.

A 67 year old woman, complained in September 1994 of left sided headaches, jaw claudication, and transient visual disturbance of her left eye. Biological evaluation showed an inflammatory process, and biopsy of the left temporal artery was typical of GCA. Steroids were started (1 mg/kg/day prednisolone) with initial clinical and biological improvement, but a steroid dependency was noted when the dose was reduced to under 40 mg/day. On successive clinical evaluations, we noticed an increase in the volume of the thyroid gland. Ultrasonography showed a multinodular goitre with heterogeneous nodules characterised by either cystic or solid appearance. Thyroid function tests were normal and a search for antithyroid antibodies (antimicrosomal and antithyroglobulin antibodies) was negative.

Owing to the increase in volume of the goitre and the increased number of nodules (the largest nodule measured 2.5 cm), a total thyroidectomy was performed in February 1997 (29 months after the onset of temporal arteritis). Histopathological analysis concluded that there was a multinodular goitre with benign adenomas. Analysis of the left superior thyroid artery showed an inflammatory granulomatous lesion with giant cells in the elastica externa (fig 1), whereas the right superior thyroid artery was normal. At that time, the patient was treated with prednisolone (20 mg/day) and there was a mild biological inflammatory process (erythrocyte sedimentation rate 21 mm/1st h and C reactive protein 10 mg/l). A search for antinuclear, anti-extract cell antigen, and anticardiolipin antibodies as well as lupus anticoagulant was negative. Treatment with methotrexate was added (10 mg/week), which allowed progressive tapering of the prednisolone dose.

Figure 1

Histopathological analysis of thyroid gland (haematoxylin-eosin-saffron, original magnification ×250). Giant cells and granulomatous inflammatory infiltrate near fragmented elastica tunica.

At her last medical visit in April 2000 the clinical and biological outcome was good without any sign of relapse in the GCA. Treatment with prednisone (2 mg/day), methotrexate (10 mg/week), andl-thyroxine (125 μg/day) was continued.

Associations of thyroid dysfunctions and GCA have included hypothyroidism,2 3 thyrotoxicosis,4Graves's disease,5 and de Quervain's thyroiditis.6 In the series of Bownesset al 10% of the 367 patients with PMR or GCA, or both, had antithyroid autoantibodies and 4.9% had clinical and biochemical hypothyroidism requiring replacement treatment with thyroxine, which was significantly greater than in the control group.3 To explain the association between PMR and/or GCA and autoimmune thyroid diseases, the authors suggested a common aetiological agent (perhaps infective) or a common immunological predisposition. However, a recent multicentre case-control study on 285 patients with GCA failed to show a significant relation with thyroid diseases.7

The involvement of non-classical organs in GCA with histologically proved vasculitis has been reported for coronary, renal, hepatic, and female genital tract arteries.8 As thyroid arteries are branches of the external carotid artery, the occurrence in our observation of GCA and nodular goitre with thyroid arteritis was probably not fortuitous. Moreover, GCA was seen on the same side of the head and neck (respectively left temporal artery and left superior thyroid artery). To our knowledge, only one previous observation of an inflammatory infiltrate of the thyroid gland, comprising multinucleated giant cells, has been reported and concerned subacute thyroiditis occurring simultaneously with GCA.9 As the sample was obtained by thyroid aspiration, the author could not conclude that there was GCA involvement.9

From a pathophysiological point of view we feel that, in our case, thyroid ischaemic lesions (often seen in goitres10) and/or inflammatory infiltrate induced by the vasculitis process may have played a part in the formation of the goitre. Thus a possible link between GCA and goitre must be kept in mind.

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