The major product secreted by the thyroid is thyroxine (T4), whereas most of the 
biologically active triiodothyronine (T3) derives from the peripheral conversion 
of T4 into T3. The deiodinase enzymes are involved in activation and 
inactivation of thyroid hormones (THs). Type 1 and type 2 deiodinase (D1 and D2) 
convert T4 into T3 whereas D3 degrades T4 and T3 into inactive metabolites and 
is thus the major physiological TH inactivator. The 
hypothalamic-pituitary-thyroid axis maintains circulating TH levels constant, 
while the deiodinases tissue-specifically regulate intracellular thyroid status 
by controlling TH action in a precise spatio-temporal fashion. Here we review 
the data related to the recent identification of a paraneoplastic syndrome 
called "consumptive hypothyroidism," which exemplifies how deiodinases alter 
substantially the concentration of TH in blood. This syndrome results from the 
aberrant uncontrolled expression of D3 that can induce a severe form of 
hypothyroidism by inactivating T4 and T3 in defined tumor tissue. This rare TH 
insufficiency generally affects patients in the first years of life, and has 
distinct features in terms of diagnosis, treatment, and prognosis with respect 
to other forms of hypothyroidism.