It says "to 85%" not "by 85%".
Mike
Sent from my iPad
> On 10 Aug 2016, at 10:53, Mohammad Al-Jubouri <[log in to unmask]> wrote:
>
> 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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