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The effects of levothyroxine replacement or suppressive therapy on health status, mood, and cognition.
Samuels, MH, Kolobova, I, Smeraglio, A, Peters, D, Janowsky, JS, Schuff, KG
The Journal of clinical endocrinology and metabolism. 2014;(3):843-51
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Abstract
CONTEXT TSH-suppressive doses of levothyroxine (L-T4) have adverse effects on bone and cardiac function, but it is unclear whether central nervous system function is also affected. OBJECTIVE The aim of the study was to determine whether women receiving TSH-suppressive L-T4 doses have decrements in health status, mood, or cognitive function. DESIGN AND SETTING A cross-sectional comparison was made among three groups of women in an academic medical center research clinic. PATIENTS Twenty-four women receiving chronic TSH-suppressive L-T4 doses, 35 women receiving chronic replacement L-T4 doses, and 20 untreated control women participated in the study. INTERVENTIONS Subjects underwent testing at a single outpatient visit. MAIN OUTCOME MEASURES We measured health status (SF-36), mood (Profile of Mood States, Symptom Checklist 90-R, Affective Lability Scale), and cognitive function (declarative memory [Paragraph Recall], working memory [N-back, Subject Ordered Pointing], motor learning [Pursuit Rotor, Motor Sequence Learning Test], and executive function [Letter Cancellation Test, Trail Making Test, Iowa Gambling Test]). RESULTS Women receiving TSH-suppressive or replacement L-T4 doses had decrements in health status and mood compared to healthy controls. These decrements were more pronounced in women receiving replacement, rather than suppressive, L-T4 doses. Memory and executive function were not affected in either treated group, compared to healthy controls. CONCLUSIONS Women receiving TSH-suppressive doses of L-T4 do not have central nervous system dysfunction due to exogenous subclinical thyrotoxicosis, but TSH-suppressed and L-T4-replaced women have slight decrements in health status and mood that may be related to self-knowledge of the presence of a thyroid condition or other uncharacterized factors. These mood alterations do not impair cognitive function.
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Assessment of hydration by means of bioelectrical impedance and arm muscle area during growth hormone (GH) replacement therapy: A prospective study of 130 GH-deficient patients.
Badre-Esfahani, S, Nellemann, B, Danielsen, D, Fisker, S, Christiansen, JS, Jørgensen, JO
Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society. 2007;(3):227-33
Abstract
OBJECTIVE Growth hormone (GH)-deficiency is associated with a reduced extracellular volume (ECV), whereas GH replacement may cause fluid retention. We have tested a simple method to assess hydration in GH-deficient patients (GHD) based on concomitant measurements of body resistance by bioelectrical impedance analysis (BIA), and arm muscle area (AMA). DESIGN We prospectively followed 130 patients (54 females, 76 males) with adult-onset GHD before and during 1-5 years GH replacement therapy. METHODS Concomitant measurements of body resistance and AMA were done on four occasions: before treatment, after one month and one year of treatment, and at the most recent visit. Based on normative data obtained in 142 women and 84 men an inverse relationship was documented between body resistance and AMA. Assuming that linear height and the concentration of electrolytes remain constant, body resistance at a given AMA will reflect specific hydration. RESULTS In the patients a gender-specific inverse correlation between body resistance and AMA existed, which was different from the control group and changed during GH replacement. A deviation between predicted (based on normative data) and measured body resistance at a given AMA was recorded in the patients before and during therapy compatible with relative dehydration in the untreated state followed by an increase in hydration during therapy. CONCLUSIONS Concomitant measurements of BIA and AMA in GHD patients may provide a non-invasive and simple means to estimate hydration before and during GH replacement.
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Changes in prothrombin and activated partial thromboplastin time during replacement therapy with human recombinant growth hormone in growth hormone deficient adults.
Miljic, D, Miljic, P, Doknic, M, Pekic, S, Djurovic, M, Colovic, M, Popovic, V
Hormones (Athens, Greece). 2006;(3):187-91
Abstract
BACKGROUND In rodents, Growth Hormone (GH) has been shown to stimulate coagulation parameters, including Prothrombin Time (PT), activated Partial Thromboplastin Time (aPTT) and vitamin K dependent coagulation factors. However, there are no reports on the influence of GH replacement therapy on global coagulation tests in Growth Hormone Deficiency (GHD). OBJECTIVE The aim of this study was to investigate the effects of GH administration on basic coagulation parameters: PT, aPTT and fibrinogen concentrations in adult GHD patients before and during one year of GH replacement. DESIGN Twenty-one adult patients with severe GHD (mean age +/- SE: 38.6 +/- 2.8 years) were included in this hospital based, prospective, interventional study. All patients were treated with rhGH for 12 months (GH dose: 0.4 mg/day for male and 0.6 mg/day for female patients). IGF-1 concentrations were determined using RIA-INEP kits. Basic coagulation tests, i.e. aPTT and fibrinogen concentrations, were measured before and after 3, 6 and 12 months of treatment with rhGH. Control values were obtained from fourteen "healthy" subjects matched by age, sex and body mass index (BMI). RESULTS At baseline, we observed no significant differences in PT, aPTT and fibrinogen values between GHD and healthy subjects. IGF-1 concentrations increased significantly within 3 months of GH therapy (8.2 +/- 1.5 vs. 24.2 +/- 2.9 nmol/l, p <0.05) and remained stable thereafter. A significant increase in PT values, which was more pronounced in female subjects, was noted after 6 and 12 months of treatment with GH. aPTT values increased significantly after 12 months of treatment only in male patients (28.8 +/- 4.6 vs. 39.7 +/- 2.1 s.; p <0.05). No significant changes in fibrinogen concentrations were found during the study. CONCLUSIONS Twelve months of GH replacement therapy led to a significant increase in PT and aPTT values in adult GHD patients, while fibrinogen concentrations did not change. Changes in PT were more pronounced in female GHD patients, while an increase in aPTT values was observed only in male patients with GHD. The clinical significance of these changes needs further evaluation.
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Weight-related dosing, timing and monitoring hydrocortisone replacement therapy in patients with adrenal insufficiency.
Mah, PM, Jenkins, RC, Rostami-Hodjegan, A, Newell-Price, J, Doane, A, Ibbotson, V, Tucker, GT, Ross, RJ
Clinical endocrinology. 2004;(3):367-75
Abstract
OBJECTIVE The objective of this study was to examine the variables determining hydrocortisone (HC) disposition in patients with adrenal insufficiency and to develop practical protocols for individualized prescribing and monitoring of HC treatment. DESIGN AND PATIENTS Serum cortisol profiles were measured in 20 cortisol-insufficient patients (09.00 h cortisol < 50 nmol/l) given oral HC as either a fixed or 'body surface area-adjusted' dose in the fasted or fed state. Endogenous cortisol levels were measured in healthy subjects. Pharmacokinetic analysis was performed using P-Pharm software, and computer simulations were used to assess the likely population distribution of the data. RESULTS Body weight was the most important predictor of HC clearance. A fixed 10-mg HC dose overexposed patients to cortisol by 6.3%, whereas weight-adjusted dosing decreased interpatient variability in maximum cortisol concentration from 31 to 7%, decreased area under the curve (AUC) from 50 to 22% (P < 0.05), and reduced overexposure to < 5%. Food taken before HC delayed its absorption. Serum cortisol measured 4 h after HC predicted cortisol AUC (r(2) = 0.78; P < 0.001). CONCLUSIONS We recommend weight-adjusted HC dosing, thrice daily before food, monitored with a single serum cortisol measurement using a nomogram. This regimen was prospectively examined in 40 cortisol-insufficient patients, 85% of whom opted to remain on the new thrice-daily treatment regimen.
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Insulin resistance and lipids in hypertensive women on hormone replacement therapy.
Kawecka-Jaszcz, K, Czarnecka, D, Dembińska-Kieć, A, Olszanecka, A, Zdzienicka, A
Blood pressure. 2002;(1):28-34
Abstract
Hypertension, hyperinsulinaemia and dyslipidaemia are strong and independent risk factors for cardiovascular diseases. Their increasing frequency in postmenopausal women suggests that oestrogen deficiency may be a contributing factor. It is well known that oestrogen replacement therapy in postmenopausal women improves carbohydrate and lipid metabolism, but the effect of combined hormone replacement therapy (HRT) remains unclear. The purpose of the present study was to evaluate the effect of HRT on blood pressure, carbohydrate metabolism and lipid profile in postmenopausal women with primary arterial hypertension. The study population consisted of 76 postmenopausal women (mean age 51.1 +/- 6.8 years). Forty hypertensive women received HRT (17-beta-oestradiol, norethisterone acetate, TTS, Estracomb Novartis), whereas 36 women remained without hormonal therapy. One-year combined transdermal HRT did not affect significantly blood pressure and blood pressure variability. HRT was shown to improve lipid profile with a significant decrease in total cholesterol as early as at 3 months. It does not influence carbohydrate metabolism parameters studied by glycaemia and insulinaemia in a standard oral glucose tolerance test. In conclusion, combined percutaneous HRT may reduce the lipid-depended cardiovascular risk in postmenopausal women with arterial hypertension.
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The increased insulin sensitivity in growth hormone-deficient adults is reduced by growth hormone replacement therapy.
Riedl, M, Ludvik, B, Pacini, G, Clodi, M, Kotzmann, H, Wagner, O, Kautzky-Willer, A, Prager, R, Luger, A
European journal of clinical investigation. 2000;(9):771-8
Abstract
BACKGROUND Growth hormone deficiency is associated with increased morbidity and mortality from cardiovascular diseases, which might be related to changes in glucose and lipid metabolism. DESIGN To assess the influence of long-term growth hormone replacement therapy (GHRT) on glucose metabolism we examined eight growth hormone-deficient (GHD) adults (seven female/one male; age, 46 +/- 3 years; body mass index, 31 +/- 2 kg m-2) over a period of 18 months in comparison to an adequate control group consisting of eight obese subjects matched for age, sex, and body mass index. We performed frequently sampled intravenous glucose tolerance tests (FSIGT) with minimal model analysis before the study, and after 12 and 18 months. RESULTS Following GHRT, insulin-like growth factor-1 (IGF-1) increased significantly from a basal level of 75.9 +/- 18.9 to 200.8 +/- 31.0 microg L-1 after 12 months of therapy and remained stable, thereafter. GHRT did not affect fasting blood glucose, basal insulin, cholesterol, blood pressure and body weight. However, at 12 months, HbA1c (6.0 +/- 0.1 vs. 5.6 +/- 0.1% at basal, P < 0.05) and triglyceride (2.3 +/- 0.4 vs. 1.4 +/- 0.3 mmol L-1) significantly increased but returned to pretreatment values at 18 months. Insulin sensitivity was higher in GHD (8.2 +/- 3.1) compared to controls (3. 6 +/- 0.53 x 10-4 min-1/(microU mL-1), P = 0.06) and decreased significantly after 18 months of GHRT to 5.1 +/- 2.6, P < 0.05. Basal insulin secretion was similar to that in the control group and increased significantly after 12 and 18 months, total insulin secretion only after 12 months. SG (glucose effectiveness)was lower in GHD patients (0.0095 +/- 0.001 min-1) compared to controls (0.020 +/- 0.003 min-1, P < 0.05) and increased significantly after 12 and 18 months of GHRT (0.016 +/- 0.002, and 0.015 +/- 0.001 min-1, P < 0. 05), respectively. Hepatic insulin extraction rate was similar in both groups and remained unchanged following GHRT. CONCLUSION We conclude that long-term GHRT induces a significant decrease of the increased insulin sensitivity in GHD patients to levels observed in body mass index-matched control subjects. This is accompanied by an increase in basal and total insulin secretion as well as in glucose effectiveness as a possible compensatory mechanism.