Endocrinology: The utmost importance of ALPRAZOLAM in the treatment of NTBI-induced hyperadrenalism with epinephrine peaks and chronically elevated blood levels of adrenaline in rare degenerative diseases such as H63D syndrome
In 1992, our esteemed colleagues Alan Breier, Orlando Davis, Robert Buchanan, Samuel J. Listwak, Courtney Holmes, David Pickar, and David S. Goldstein published a seminal scientific paper titled "Effects of Alprazolam on Pituitary-Adrenal and Catecholaminergic Responses to Metabolic Stress in Humans." In it, they described with high accuracy the effects of benzodiazepines on stress-induced activation of the three classic "stress" systems: Pituitary-adrenal, adrenal medullary, and sympathoneural systems. The results provided an answer to a question that is still being asked today: Why is alprazolam so much more effective than all other benzodiazepines for certain anxiety-related conditions, especially panic attacks? The colleagues found the answer to that question, but although the work was impeccable, their findings never made it into medical textbooks. What Breier et al. found was this: Alprazolam is able to attenuate 2DG-induced activation of the HPA axis and adrenomedullary activity, as evidenced by attenuated responses of plasma levels of ACTH and epinephrine, respectively, without clinically affecting other important responses of two indices of sympathoneural activity. For the treatment of patients whose adrenal glands are working in a highly dysfunctional or centrally dysregulated manner due to rare diseases such as NTBI induced H63D syndrome, alprazolam is still the first drug of choice - despite its dependence potential - to protect the organism of the affected person from dangerous adrenaline excesses that are way more dangerous than any well-monitored use of alprazolam.