OBJECTIVES: Non-thyroidal illness syndrome (NTIS) is a form of hypothyroidism that occurs during illness. NTIS is characterized by low thyroid hormones (TH) level in the serum and tissues, with normal serum TSH levels that are considered "inappropriately" normal. The mechanisms responsible for a lack of increase in serum TSH during NTIS are unknown. However, a decreased expression of hypothalamic TRH has been documented in deceased humans with NTIS. It has been suggested that pro-inflammatory cytokines are responsible for the inhibition of TRH release. If a similar TSH response occurs in severely ill patients with primary hypothyroidism has not been reported.
DESIGN: Seven severely ill patients with unknown or poorly treated primary hypothyroidism are presented. Serum TSH and TH were measured at admission and during TH replacement.
SETTING: Tertiary university hospital.
RESULTS: Besides suffering severe illness, patient's serum TSH was high and decreased once TH replacement was given. Levothyroxine administration was enough to down regulate TSH secretion. Serum reverse T3 (rT3) was normal or high and showed further elevation with stepwise increase in levothyroxine doses.
CONCLUSIONS: The thyroid axis inhibitory feedback system is fully preserved in primary hypothyroidism during severe illness. In NTIS, serum TSH levels remain within normal limits because the supply of TH to TRH neurons is sustained normally. Pro-inflammatory cytokines does not play a major role inhibiting TRH release during NTIS associated to primary hypothyroidism. D3 activity increases in humans with severe illness, a mechanism behind the increased requirements in TH replacement to achieve normal serum TH.