Thanks Ian for this very relevant albeit an old study.
This statement in the abstract is surprising:
"Two hours after the first T3 dose, the mean serum TSH for G-I and G-II decreased to 85% (P < 0.02) and 70% (P < 0.001) of their respective pretreatment values."
Really only two hours after first IV 25 mcg T3 dose, TSH is suppressed by 85% of pretreatment level !! this is a revelation for me.
Regards
Mohammad
Dr. M A Al-Jubouri, MB ChB, MSc, EurClinChem, FRCP Edin, FRCPath
Consultant Chemical Pathologist
--------------------------------------------
On Wed, 10/8/16, Ian Young <[log in to unmask]> wrote:
Subject: T3 therapy & TSH suppression
To: [log in to unmask]
Date: Wednesday, 10 August, 2016, 9:01
This seems relevant, and is in line
with the reported case:
J Clin Endocrinol Metab. 1983 Jun;56(6):1252-9.
Rapid pituitary and peripheral tissue responses to
intravenous L-triiodothyronine in hypothyroidism.
Ladenson PW, Goldenheim PD, Ridgway EC.
Abstract
Acute cardiovascular, renal, pulmonary, metabolic, and
pituitary responses to therapy of hypothyroidism with 25
micrograms iv T3 (group I G-I, n = 11) or 50 micrograms iv
T3 (group II, G-II, n = 10)/day for 1 week have been
studied. Serum T3 levels were acutely normalized in both
groups with the mean basal serum T3 levels (X +/- SE) after
7 days, 98 +/- 10 micrograms/dl and 229 +/- 19 ng/dl,
respectively. Myocardial performance, noninvasively assessed
by the pulse wave arrival time (QKd) and the
phonocardiographic systolic time interval ratio was
significantly altered after 1 day of therapy (QKd for G-I =
-10 +/- 4 msec, P less than 0.05; and for G-II = -18 +/- 14
msec, P less than 0.01). After 7 treatment days, both the
mean QKd (203 +/- 7 msec, P less than 0.001) and
phonocardiographic systolic time interval ratio (0.41 +/-
0.02, P less than 0.01) were within the normal range in
G-II. Abnormal pretreatment renal excretion of an oral water
load (G-I, 65 +/- 6%; and G-II, 57 +/- 6%) was also reversed
after 1 week (G-I, 84 +/- 5%, P less than 0.05; and G-II, 89
+/- 5%, P less than 0.01). Patients with blunted hypercapnic
(n = 6) and hypoxic (n = 4) ventilatory drives were improved
in both groups after 6 days. The mean basal metabolic rate,
serum cholesterol, and serum creatine phosphokinase were
altered by the week of therapy in a dose-response manner,
and were in the normal range in G-II. Pituitary TSH
secretion was promptly suppressed in both groups. Two hours
after the first T3 dose, the mean serum TSH for G-I and G-II
decreased to 85% (P less than 0.02) and 70% (P less than
0.001) of their respective pretreatment values. After 7 days
of therapy, the mean basal TSH levels had declined to 75% (P
less than 0.001) and 5% (P less than 0.001%) of
pretreatment, respectively. In comparison with previous
observations of responses to 100 micrograms/day iv T4 for 1
week, the 25 micrograms dose T3 was equivalent in terms of
changes in basal serum T3 and peripheral (nonpituitary)
tissue responses, but less effective than T4 in lowering
serum TSH. Based on these parameters, 50 micrograms/day iv
T3 was the most effective of the three regimens within this
time frame. The implications of these observations in the
clinical management of severe complicated myxedema are
discussed.
Best wishes
Ian Young
Professor of Medicine
Queen's University Belfast
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