Thyroid and cortisol hormone response to sepsis

Sepsis is dysregulated host response to infection that results in life-threatening organ dysfunction. Virtually every body system can be affected by this syndrome to greater or lesser extents.

Endocrine alterations are well characterised in sepsis with variations in circulating blood levels and/or receptor resistance.

In response to any psychological or physical stressor, there is widespread neurohormonal activation to adapt body with the stressor. Production and secretion of stress hormones increase to modulate behaviour Many studies have been performed investigating specific hormonal perturbations such as critical illness-induced corticosteroid insufficiency ,all of which are associated with worse outcomes and poor of body inflammation. However, the endocrine system as a whole has been largely overlooked as a fundamental contributor to the integrated host response to sepsis thyroid axis is affected during sepsis with decreased pituitary release of thyroid stimulating hormone (TSH) and inhibition of the peripheral conversion of thyroxine (T4) by 5-deiodinase to the much more metabolically active triiodothyronine (T3). High cortisol levels also inhibit this enzymatic conversion.

Inclusion Criteria:

• The study will include Adults (≥18 years), both genders
• septic patients admitted to critical care unit

Exclusion Criteria:

• thyroid disease
• hypopituitarism
• Addison disease
• Cushing syndrome)

include Adults (≥18 years), both genders, admitted to critical care unit with sepsis

Exclusion patient with Previous diagnosis of endocrinal changes (thyroid dysfunction , hypopituitarism, Addison disease, Cushing syndrome)