Retrospective analysis of the effects of low-dose, high frequency human growth hormone on serum lipids and prostate specific antigen (original) (raw)
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Dicle Medical Journal / Dicle tıp Dergisi, 2011
Bu çalışma karpal tünel sendromlu (KTS) erkek hastalarda endokrin hormon ve lipid düzeyleriyle klinik özellikler arasındaki ilişkiyi belirlemek amacıyla düzenlendi. Gereç ve yöntem: Çalışmaya 15 erkek KTS hastası ve 16 sağlıklı kontrol dahil edildi. Serum serbest T3, serbest T4, tiroid stimüle edici hormon (TSH), serbest testosteron, dehidroepiandrosteron sülfat, trigliserid ve total kolesterol düzeyleri analiz edildi. Klinik değerlendirmede semptom şiddeti ve el fonksiyonları Boston Karpal Tünel Anketi ile belirlendi. Bulgular: Karpal tünel sendromu hastalarında serum serbest T3, serbest T4, TSH, serbest testosteron, dehidroepiandrosteron sülfat, trigliserid ve total kolesterol değerleri kontrollerle benzer düzeylerdeydi (p> 0.05). KTS hastalarında klinik özellikler ile laboratuar parametreleri arasında da istatistiksel olarak anlamlı bir korelasyon yoktu (p> 0.05). Sonuç: Karpal tünel sendromu olan erkek hastalarda serum serbest T3, serbest T4, TSH, serbest testosteron, dehidroepiandrosteron sülfat, trigliserid ve total kolesterol düzeyleri normal aralıkta görülmektedir. Kadın ve erkek hastalarda total kolesterol ve trigliserid gibi lipid düzeyleri ve endokrin faktörler ile KTS arasındaki ilişkiyi araştıracak yeni çalışmaların yapılması gerekmektedir.
Growth hormone secretion in response to glucagon stimulation test in healthy middle-aged men
Arquivos Brasileiros de Endocrinologia & Metabologia, 2009
To investigate the growth hormone (GH) response to glucagon stimulation test (GST) in a population of healthy men over 50 years old in comparison to insulin tolerance test (ITT), analysis of the spontaneous 24-hour GH profile and insulin-like growth factor 1 (IGF-I). Me thods: 27 healthy men aged between 51 and 65 years were tested. Results: Using non-parametric correlation analysis, a positive correlation between GH peak after GST and mean IGF-I (r = 0.528; p = 0.005) was found, as well with GH peak in 24-hour profile (r = 0.494; p = 0.009). No correlation was found comparing GH peak after ITT with the same parameters. Ten subjects presented GH peak of less than 3.0 μg/L after GST, none confirmed in ITT. Conclusions: GH peak response to GST was lower than ITT, but it showed a positive correlation with mean IGF-I and also with GH peak in 24-hour profile. However, GST should not be used to differentiate organic growth hormone deficiency (GDH) from the expected decline on GH secretion due to aging. Arq Bras Endocrinol Metab. 2009;53(7):853-8.
Growth Hormone & IGF Research, 2013
Objective: A peak GH less than 3 μg/L to insulin tolerance test (ITT) is commonly used as a threshold indicating severe adult GH deficiency (GHD). This cut-off is based on results obtained by polyclonal radioimmunoassays preferably under standard conditions at hospital. Our aim was to evaluate the validity of this cut-off limit using two currently used immunometric GH assays and to compare GH responses in the ITT and the GH releasing hormone + arginine (GHRH + ARG) test in healthy adults at our outpatient endocrine unit. Design: ITT was performed on 73 subjects and the GHRH + ARG test on those 28 who showed insufficient response to the ITT. Methods: GH was measured by an immunofluorometric and immunochemiluminometric assay. Results: GH peak above 3 μg/L was observed in 56% of the healthy volunteers with adequate hypoglycemia in the ITT. Among the 28 subjects with a peak GH below 3 μg/L, only two overweight men had a GH peak response below the commonly used cut-off limit of 9.1 μg/L in the GHRH + ARG test. Conclusions: Lean healthy adults could erroneously be classified as GH deficient by the ITT while their results in the GHRH + ARG test were normal. The GH results are highly dependent on the immunoassay used, but false positive results in the ITT are often obtained even if lower cutoff limits determined on the basis on the calibration of the GH assay are used. Confounding factors seemed to blunt the GH response to the ITT more than to the GHRH + ARG test at our outpatient clinic.
Effects of Increasing Age, Dosage, and Duration of PTH Treatment on BMD Increase—A Meta-analysis
Calcified Tissue International, 2012
We studied the effects of increasing age, dosage, and duration of parathyroid hormone (PTH) treatment on changes in bone mineral density (BMD). Randomized placebo controlled trials on PTH treatment in men or women were retrieved from PubMed (1951 to present), Web of Science (1945 to present), or Embase (1974. The search date was November 16, 2010. All studies comparing PTH treatment to either placebo or antiresorptive drugs-for example, bisphosphonates or hormone replacement therapy-were included. A total of 214 studies were identified in the initial search, and 15 of these trials were included. By metaregression analysis, we found that the increase in spine BMD (Z-score) after PTH treatment was blunted by increasing age (R 2 = 0.27; 2p = 0.01, slope -0.023 Z-scores per year, 11 studies). By increasing PTH dosage (lg/d), spine BMD increased significantly (2p = 0.002) with a slope of ?0.011 Z-scores/ lg/d of teriparatide. Furthermore, the duration of treatment was positively correlated to spine BMD (P \ 0.001) with a slope of ?0.043 Z-score for each extra month of treatment. We evaluated the BMD effect in hips and found no age dependency (R 2 = 0.04; P = 0.66; 8 studies). However, for the spine, we found a significant relation to daily dosage (P = 0.011), Z-score coefficient 0.0051 ± 0.0020 (2p \ 0.01). The treatment duration also correlated positively by a Z-score coefficient of 0.0170 ± 0.0053, 2p \ 0.01 per extra month of treatment. PTH treatment alone seems to be able to improve BMD significantly. However, the BMD increase was significantly lower with increasing age in the spine. No age dependency was observed in the hips. In general the effect of treatment was improved with increasing dosage and duration of treatment from 6 to 36 months.
2009
To investigate the growth hormone (GH) response to glucagon stimulation test (GST) in a population of healthy men over 50 years old in comparison to insulin tolerance test (ITT), analysis of the spontaneous 24-hour GH profile and insulin-like growth factor 1 (IGF-I). Me thods: 27 healthy men aged between 51 and 65 years were tested. Results: Using non-parametric correlation analysis, a positive correlation between GH peak after GST and mean IGF-I (r = 0.528; p = 0.005) was found, as well with GH peak in 24-hour profile (r = 0.494; p = 0.009). No correlation was found comparing GH peak after ITT with the same parameters. Ten subjects presented GH peak of less than 3.0 μg/L after GST, none confirmed in ITT. Conclusions: GH peak response to GST was lower than ITT, but it showed a positive correlation with mean IGF-I and also with GH peak in 24-hour profile. However, GST should not be used to differentiate organic growth hormone deficiency (GDH) from the expected decline on GH secretion due to aging. Arq Bras Endocrinol Metab. 2009;53(7):853-8.
Growth Hormone & IGF Research, 2008
To evaluate the long-term evolution of cardiovascular parameters, lipid metabolism, body composition and bone mass in untreated and treated adult growth hormone deficient patients (AGHD) comparing the differences between the two groups and within each group. Seventy-one AGHD-patients were enrolled; 48 received growth hormone (GH) therapy: treated group (TG) and 23 received no GH therapy: control group (CG). In the TG, 22 were childhood-onset (CO) GH-deficient patients, 18-44 years (12 males) and 26 were adult-onset (AO) GH-deficient patients, 27-66 years (10 males). In the CG, 10 patients were AGHD-CO, 20-43 years (8 males) and 13 were AGHD-AO, 25-70 years (8 males). For patients in the TG, GH was administered at a starting dose of 0.1mg/day, adjusted to maintain IGF-I levels between 0 and 2 SDS for gender and age. At baseline and during the 4th year of replacement therapy or follow-up, the following parameters were evaluated: body mass index, waist circumference, blood glucose, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, total cholesterol/HDL-cholesterol ratio, systolic and diastolic blood pressure, 2-D echocardiogram with mitral Doppler, bone mineral density (total body, lumbar spine, and femoral neck), bone mineral content (BMC) and body composition. In the TG, there was a decrease in diastolic blood pressure (-4.0+/-1.8 mmHg, p<0.035) and an increase in blood glucose levels (0.58+/-0.19 mmol/L, p<0.025), bone mineral content (0.2+/-0.0 kg, p<0.015) and bone mineral density of lumbar spine (0.3+/-0.1 SDS, p<0.015) and femoral neck (0.4+/-0.1 SDS, p<0.001). All other variables did not show significant changes in any of the two groups. At year 4, changes (delta) differed between patients in the TG and those in the CG with regard to cholesterol levels (TG: -0.27+/-0.16 mmol/L, CG: 0.34+/-0.23 mmol/L, p<0.045), blood glucose (TG: 0.58+/-0.19 mmol/L, CG: -0.12+/-0.19 mmol/L, p<0.025) and BMC (TG: 0.2+/-0.0 g, CG: 0.0+/-0.0 g, p<0.015). An assessment of the changes in variables over time, with and without therapy, considering CO and AO separately, revealed a significant difference in total cholesterol levels during year 4 in CO patients CO (TG: -0.28+/-0.25 mmol/L and CG: 0.84+/-0.25 mmol/L, p<0.015). No differences related to the time of onset of GHD were found in changes in the remaining variables studied. There were no differences related to gender, GHD etiology or the presence of other pituitary hormone deficiencies in the evolution of the parameters analyzed. Our 4-year study in GH deficient adults showed significant beneficial effects on some cardiovascular risk parameters and BMC in treated patients. However, there are still unsettled issues regarding long-term benefits and these patients should be carefully monitored.
Metabolism, 1996
The role of growth hormone (GH) and thyroid hormone in the regulation of lipid and lipoprotein metabolism is not fully established. Furthermore, the possible linkage between the well-known GH-induced increase in peripheral thyroxine (T4) to triiodothyronine (T3) generation and the effects of GH on lipid and lipoprotein metabolism has not been elucidated. In this double-blind placebo-controlled study, we compared the effects of GH and T3 administration alone and in combination on lipid and lipoprotein metabolism in a group of healthy young adults. The dose of T3 was selected to mimic the T3 increase seen during exogenous GH exposure. Eight normal male subjects (aged 21 to 27 years; body mass index, 21.11 to 27.17 kg/m 2) were randomly studied during four 10-day treatment periods with (1) daily subcutaneous placebo injections and placebo injections and placebo tablets, (2) daily subcutaneous GH injections (0.1 IU/kg • d) and placebo tablets, (3) daily T3 administration (40 leg on even dates or 20 ~g on uneven dates) plus placebo injections, and (4) daily GH injections plus T3 administration. GH administration increased free T 3 (FT3) to the same level as during T3 administration. GH caused decreased levels of total cholesterol (TC) and low-density lipoprotein (LDL) cholesterol and increased levels of triglycerides (TG) and lipoprotein(a) (Lp(a)), but no changes in high-density lipoprotein (HDL) cholesterol and apolipoprotein B (apo B), T3 administration caused no alteration in these parameters, except for decreased levels of TC comparable to those seen after GH administration. Combined GH and T3 administration caused changes identical to those seen after GH administration, in addition to decreased apo B levels and a further decrease of TC levels. We conclude that GH and iodothyronines in the physiologic range exert distinct but disparate effects on lipids and lipoproteins, and do not support the hypothesis that the effects observed during GH administration are exclusively secondary to changes in peripheral T3 levels.
Growth Hormone & IGF Research, 1999
Hypopituitary adults receiving conventional hormone replacement therapy are reported to have increased cardiovascular mortality. Previous studies indicate that these patients have several abnormalities in lipoprotein metabolism, including reduced low density lipoprotein (LDL) uptake and impaired metabolism of triglyceride-rich lipoproteins. The effects of 24 months of 0.21 IU/kg per week recombinant growth hormone (rh-GH) on the lipoprotein profiles of 22 GH-deficient adults were studied. Samples were collected after a 12-h fast at baseline and 24 months. Total cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol, LDL cholesterol, apolipoprotein (apo) A, apo B and apo [a] were determined by routine laboratory methods. LDL particle size was determined by non-denaturing gradient gel electrophoresis. Visceral adiposity was determined by dual energy X-ray absorptiometry (DEXA). Insulin sensitivity was measured in a subset of 17 subjects using a two-stage hyperinsulinaemic-euglycaemic clamp.