The metabolic responses to spinal cord injury (SCI) involve every organ and tissue of the body and yet, surprisingly, little is known about the underlying mechanisms. Many factors are known to affect levels of circulating thyroid hormones such as activity level, nutritional status, systemic illness, drugs, age and trauma. Even healthy person requisited to the bedrest, the normal circadian variation in T3 and T4 may be disappeared. So any condition of traumatic stress will be associated with changes in serum thyroid hormone levels that have been referred to as several syndromes. During chronic disease processes, the state of stress results in hypermetabolism, increased energy expenditure, hyperglycemia and muscle loss. It is anticipated that appropriate metabolic support could improve the outcome in these patients, but considerable controversy remains regarding the indicated therapeutic approach. In patients with SCI, regression or loss of existing functions can be monitored in patients in frequently developed situations due to metabolic problems such as heterotopic ossification, urinary tract infections, deep vein thrombosis, pressure ulcers, neuropathic pain, psychological problems and thyroid dysfunction. In this report we present a chronic SCI patient admitted to the clinic with the chief complaint of loss of the functional status who was diagnosed as a thyroid dysfunction.
Key words: Spinal cord injury, Thyroid dysfunction, Metabolic changes
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