Graves’ Disease and the Manifestations of Thyrotoxicosis
DeGroot LJ.
ncbi.nlm.nih.gov/books/NBK2...
ADRENAL CORTEX
There are no obvious signs or symptoms of altered adrenal cortical function in thyrotoxicosis, but distinct changes have been detected. In thyrotoxicosis the adrenal cortex is often hyperplastic. Administered adrenal steroids disappear from the plasma at an accelerated rate [265]. Their metabolism by reduction of the steroid nucleus is accelerated, and conjugation of the reduced steroids is proportionally increased. Since plasma corticoid levels are normal and their rate of metabolism is increased, total daily metabolism and excretion of 17-ketosteroids and 17 hydroxy-corticoids are usually increased [385,403].
Along with the accelerated plasma cortisol clearance of thyrotoxicosis, the pathways of metabolism are also altered. For example, thyrotoxicosis is associated with a relatively increased excretion of 11-oxycorticoid metabolites [267]. The 11-oxy compounds are biologically inactive. Because of the negative feedback control from the pituitary, this preferential channeling of steroids into the 11-oxy derivatives could be partly responsible for increased steroid production. There is increased production of steroids by the adrenal gland in order to maintain a normal concentration of active steroids in the peripheral blood and in the tissues [405]. Secretion of adrenocorticotropic hormone (ACTH) by the pituitary is reported to be increased [406]. There are increases in secretory episodes during the day, but the fall to zero secretion after midnight is retained.
A reduced response to exogenous ACTH [407] indicates that adrenal reserve is reduced. In fact, it has been hypothesized that in severe thyrotoxicosis and in thyroid storm there may be an element of adrenal insufficiency. This contention has not been proved. There is no reason to believe that T4 opposes the peripheral action of adrenal steroids.
An increase in the 5-alpha metabolite of testosterone (androsterone) and a relative decrease in the 5-beta metabolite (etiocholanolone) are seen in the urine of thyrotoxic patients [408], but no comparable change in adrenal corticoid metabolism has been observed. These interesting biochemical alterations could have physiologic significance, for the ketosteroid 5-alpha metabolites, such as androsterone, are biologically active. In hypothyroidism the reverse change occurs, that is, an increase in the biologically inactive 5-beta metabolites such as etiocholanolone. Because administration of large amounts of androsterone depresses the level of serum lipids, Hellman and co-workers [408] have hypothesized that this change in steroid metabolism may be a way in which T4 (or its lack) affects lipid metabolism and produces a depression or elevation in serum cholesterol concentration.
DEATH IN THYROTOXICOSIS
Given current therapeutic resources, death from thyrotoxi cosis or from its treatment should be rare. Thyroid storm, when it occurs, can be a lethal event. In a study from Scottish hospitals, 20 of 33 hyperthyroid patients who died had congestive heart failure, 6 bronchial pneumonia, and 6 embolism in various sites. Nineteen had atrial fibrillation. Eight were considered to have thyroid storm [443]. One might suspect that several causes of death might be identified in any particular case, and that rarely if ever would pure thyrotoxicosis be the only assignable cause. In two recent deaths of which we are aware, in patients with fulminant thyrotoxicosis, the immediate cause was sudden cardiovascular collapse, with shock and arrhythmias including ventricular fibrillation, which was resistant to all usual resuscitative efforts.
Depressed Cortisol and adrenal cortex
Adrenal Glandular vs Adrenal Cortex
Take hydrocortisone and adrenal cortex together?
Starting Adrenal Cortex, jittery feeling
Adrenal cortex and Ndt dose times
