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Clinical and Biochemical Responses to Nadolol and Clonidine in Hyperthyroidism
Author(s) -
Herman V. S.,
Joffe B. I.,
Kalk W. J.,
Panz V.,
Wing J.,
Seftel H. C.
Publication year - 1989
Publication title -
the journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.92
H-Index - 116
eISSN - 1552-4604
pISSN - 0091-2700
DOI - 10.1002/j.1552-4604.1989.tb03288.x
Subject(s) - nadolol , clonidine , medicine , endocrinology , epinephrine , blood pressure , heart rate , norepinephrine , propranolol , dopamine
Some features of hyperthyroidism mimic sympathetic nervous system overactivity. We have compared the clinical (scored on the Wayne Therapeutic Index), hemodynamic (blood pressure and heart rate) and biochemical (plasma epinephrine, norepinephrine, glucose, free fatty acids, insulin, growth hormone and free thyroxine index) effects of clonidine (α 2 ‐agonist, which reduces plasma catecholamine levels) with those of nadolol (non‐selective beta adrenergic receptor antagonist) in ten female hyperthyroid patients. Each patient received nadolol for 1 week followed by clonidine for 1 week in a single‐blind manner. All measurements were made before treatment and then repeated at the end of the nadolol and clonidine treatment periods. Thyroid function remained unaltered during the study. Both agents caused significant clinical improvement— the mean Wayne Index score was 18 pretreatment, 2 on nadolol and 6 on clonidine (P < .003 for each). Heart rate was reduced by both drugs, but blood pressure was unchanged. Side effects occurred in eight out of ten patients while on clonidine. Nadolol increased plasma concentrations of epinephrine from 47 ± 18 pg/mL to 87 ± 24 pg/mL, and norepinephrine from 241 ± 154 pg/mL to 338 ± 224 pg/mL (P < .001 for each). In contrast, clonidine depressed norepinephrine levels from 241 ± 154 pg/mL to 110 ± 49 pg/mL (P < .001) without lowering plasma epinephrine significantly. Plasma free fatty acids tended to fall on both agents compared to pretreatment levels. The blood glucose, insulin and growth hormone concentrations were unaffected by either drug. We conclude that, despite the similar clinical effects of nadolol and clonidine, these drugs have contrasting effects on plasma catecholamine concentrations. Beta‐adrenergic receptor antagonists remain the drugs of choice for the symptomatic relief of hyperthyroidism, because of the high incidence of side effects caused by clonidine. However, clonidine could be considered for patients with conditions in which beta‐adrenergic antagonists are contraindicated.