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The thyroid gland is the body’s metabolic thermostat controlling body temperature, energy use, growth rate and affecting the operation of all bodily processes and organs.
Thyroid hormone production is centrally regulated: Thyroxine (T4) from the thyroid gland is peripherally converted in the liver and kidney cells into T3 and reverse T3 (rT3). T3 is the active hormone and is five times as potent as T4, but rT3 is almost biologically inactive.
Reverse T3 (rT3) is primarily produced from monodeiodiation of thyroxine in the peripheral tissue rather than by direct secretion by the thyroid gland. Physical, mental and environmental stresses can inhibit the deiodinating enzyme, causing less T4 to be converted to T3, thus decreasing the amount of active thyroid hormone available to the cells. More T4 is then shunted towards rT3 causing an elevation in rT3. Reverse T3 has no thyroid action except it binds to T3 receptors blocking the action of active T3.
Reverse T3 has the same molecular structure as T3 however its three dimensional arrangement (stereochemistry) of atoms is a mirror image of T3 and thus fits into the receptor upside down thus preventing the active T3 binding to the receptor and activating the appropriate thyroid response. Unfortunately blood tests for T3 measure both normal T3 and reverse T3 levels as it is unable to distinguish between the two. Thus T3 levels may appear normal however a significant proportion of this may be due to the presence of the inactive reverse T3 isomer giving a false impression of true thyroid function. To overcome this diagnostic problem we can specifically measures reverse T3 alone to rule out reverse T3 dominance. In normal patients T3 dominates and reverse T3 usually makes up less than 10% of total T3 levels.
Measuring rT3 levels is useful when ‘sick euthyroid’ conditions are suspected. When a patient produces excessive levels of rT3 they will usually present with hypothyroid symptoms.
