Lower Free T3 Levels Linked to Poorer Outcomes in Chronic Obstructive Pulmonary Disease Patients with Acute Hypercapnic Respiratory Failure.
J Crit Care Med (Targu Mures)
; 10(1): 56-63, 2024 Jan.
Article
em En
| MEDLINE
| ID: mdl-39108803
ABSTRACT
Aim of the Study Non-thyroidal illness syndrome (NTIS) is often observed in critically ill patients. This study aimed to examine thyroid hormone changes in patients with chronic obstructive pulmonary disease (COPD) experiencing acute hypercapnic respiratory failure (AHRF) and to evaluate the impact of these alterations on clinical outcomes. Materials and Methods:
This retrospective investigation involved 80 COPD patients (age 71.5±9.5 years; 57.5% male) admitted to the intensive care unit (ICU) due to AHRF. NTIS was identified when free triiodothyronine (fT3) levels were below the lower limit, and thyroid-stimulating hormone (TSH) and free thyroxine (fT4) levels were within the normal range or below the lower limits.Results:
NTIS was detected in 63.7% of the patients. Decreased fT3 levels were found in 36.3% of the patients, reduced T4 levels in 33.8%, and diminished TSH levels in 15%. Patients with low fT3 levels exhibited elevated C-reactive protein levels, white blood cell counts, and APACHE II scores, necessitated vasopressor infusion more frequently during their ICU stay, and had increased mortality. The in-hospital mortality rate was 28.8%. Logistic regression analysis revealed that fT3 level (odds ratio [OR]., 0.271; 95% confidence interval [CI]., 0.085-0.865; p=0.027), APACHE II score (OR, 1.155; 95% CI, 1.041-1.282; p=0.007), and vasopressor use (OR, 5.426; 95% CI, 1.439-20.468; p=0.013) were crucial predictors of in-hospital mortality.Conclusions:
A high prevalence of NTIS is observed in COPD patients with AHRF, with low fT3 levels frequently observed. The presence of lower levels of fT3 is associated with a greater severity of the disease and a significant prognostic indicator.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article