Subacute thyroiditis is an acute inflammatory disorder of the thyroid gland most likely due to viral infection.1
No association between subacute thyroiditis and renal cell carcinoma has been reported to date.
Among neoplastic diseases, renal cell carcinoma is recognized for its unpredictable various paraneoplastic syndromes.2,3
The biologic basis for these unusual features of renal cell carcinoma might be the mediation of effects by cytokines, such as interleukin-6 (IL-6), or growth factors produced by the tumour and immune mechanisms.4,5
IL-6 has been shown to be involved in the pathophysiology of paraneoplastic syndromes, in particular the elevation of C-reactive protein and haptoglobin levels but also paraneoplastic cholestasis (Stauffer syndrome), paraneoplastic thrombocytosis, neutrophilia and monocytosis.6
All of these paraneoplastic syndromes spontaneously regress after surgical remove of the neoplastic tissue.
Variations in serum IL-6 levels have also been reported in cases of thyroid dysfunction: increased levels have been found in patients with thyroidal destructive processes such as subacute thyroiditis and some forms of amiodarone-induced thyrotoxicosis, and after percutaneous ethanol injection into “hot” thyroid nodules.7,8,9
In the past, high levels of IL-6 during the course of subacute thyroiditis was thought to be the result of cytokine release from the damaged thyrocyte. However, Yamada and colleagues10
showed that IL-6 levels do not fall along with other parameters of disease activity during treatment with corticosteroids. An alternative explanation may be that elevated IL-6 levels during the course of subacute thyroiditis are the cause, not the result, of the destructive process.
We did not measure the preoperative level of IL-6 in our patient, but his fever, the elevated C-reactive protein level and erythrocyte sedimentation rate, and the paraneoplastic cholestasis were clinical clues of high circulating IL-6 levels. We suggest that the destructive process in the thyroid that presented clinically as subacute thyroiditis may have been triggered by high levels of IL-6.
Resolution of the patient's thyroiditis and its pathologic parameters was much faster than that in the average case of subacute thyroiditis. In addition, the common pathophysiologic influence of IL-6 in thyroiditis and renal cell carcinoma suggests that the subacute thyroiditis manifested as a paraneoplastic syndrome of the renal cell carcinoma.