SUPPRESSION OF THE THYROTROPIN RESPONSE TO THYROTROPIN-RELEASING-HORMONE AND ITS ASSOCIATION WITH SEVERITY OF CRITICAL ILLNESS

Citation
S. Sumita et al., SUPPRESSION OF THE THYROTROPIN RESPONSE TO THYROTROPIN-RELEASING-HORMONE AND ITS ASSOCIATION WITH SEVERITY OF CRITICAL ILLNESS, Critical care medicine, 22(10), 1994, pp. 1603-1609
Citations number
23
Categorie Soggetti
Emergency Medicine & Critical Care
Journal title
ISSN journal
00903493
Volume
22
Issue
10
Year of publication
1994
Pages
1603 - 1609
Database
ISI
SICI code
0090-3493(1994)22:10<1603:SOTTRT>2.0.ZU;2-I
Abstract
Objective: To study whether the suppression of the thyrotropin (thyroi d-stimulating hormone, TSH) response to thyrotropin-releasing hormone (TRH) correlates with severity of illness and death in patients with n onthyroidal critical illness. Design: Prospective study. Setting: Inte nsive care unit (ICU) of a university hospital. Patients: Forty-one cr itically ill patients without thyroid disease with multiple organ fail ure who were admitted to the ICU. Measurements and Main Results: The T SH response to TRH was tested within 24 hrs of ICU admission. Blood sa mples were obtained just before, and at 15, 30, 60, 90, and 120 mins a fter 500-mu g injection of synthetic TRH. Triiodothyronine, free-triio dothyronine, thyroxine, free-thyroxine and TSH concentrations were mea sured in the samples obtained just before TRH injection. Acute Physiol ogy and Chronic Health Evaluation (APACHE II) scores and Sepsis scores were calculated based on the data obtained within 24 hrs of ICU admis sion. Individual variables were compared between survivors and nonsurv ivors. The APACHE II scores and Sepsis scores of nonsurvivors were sig nificantly higher than those scores of survivors. The overall occurren ce of suppressed TSH response to TRH was 88%. Peak TSH concentration o f the TSH response was significantly lower in nonsurvivors than in sur vivors. Serial measurement of the TSH response showed that nonsurvivor s experienced a decrease in peak TSH concentration from 1.55 +/- 0.78 to 0.55 +/- 0.30 mu IU/mL; in survivors, it increased from 2.10 +/- 0. 26 to 7.38 +/- 1.83 mu IU/mL. Conversely, the basal TSH concentration did not change in either survivors or nonsurvivors. The ''severity'' o f illness of nonsurvivors remained high; their mean APACHE II score va ried from 20.0 +/- 1.9 to 22.1 +/- 1.3 and the mean Sepsis score varie d from 20.0 +/- 4.3 to 25.4 +/- 4.0, while the same scores for survivo rs decreased significantly (p < .05): their APACHE II score decreased from 16.2 +/- 0.7 to 7.6 +/- 2.0 and the Sepsis score went from 14.0 /- 1.9 to 6.0 +/- 1.6. Conclusions: In critically ill patients with mu ltiple organ failure, suppression of the TSH response to TRH frequentl y occurs and correlates with severity of illness and outcome. Our data indicate that measurement of the TSH response is helpful in evaluatin g the severity of illness and prognosis for critically ill patients.