Quality of life and exercise capacity in obesity and growth hormone deficiency.

OBJECTIVES: A great similarity exists between growth hormone (GH) deficiency and obesity in terms of disturbances of organ morphology and function. The aim of the study was to compare health-related quality of life (HR-QoL) as well as exercise capacity and its subjective assessment in adult patients with GH deficiency and in adult patients with obesity. METHODS: Ten (10) GH-deficient, thirty (30) obese, and thirty (30) healthy subjects participated in the study. HR-QoL comprised two parameters: QoL measured by using the Quality of Life Assessment of Growth Hormone Deficiency in Adults (QoL-AGHDA) questionnaire, and subjective evaluation of general health state by using the Visual Analogue Scale. The exercise capacity was determined in Six Minute Walking Test and it was subjectively assessed by Borg Scale for Rating Perceived Exertion and the modified Medical Research Council scale. RESULTS: Decreased HR-QoL (both parameters) was observed in both GH-deficient and obese patients, with that effect being much more pronounced in the former group. Both, GH-deficient and obese patients, revealed decreased exercise capacity, which was also subjectively assessed as decreased, especially by GH-deficient patients. Positive relationships between HR-QoL and exercise capacity or its subjective assessment, observed in healthy subjects, partially lost their significance in obese, whereas they completely disappeared in GH-deficient subjects. CONCLUSION: A decrease in HR-QoL is more pronounced in GH-deficient than in obese patients, whereas exercise capacity is unfavourably affected by both disorder to a similar extent, with the lack of clear relationship between these two parameters especially in GH-deficient patients.

Effects of growth hormone and insulin-like growth factor-I on the iron-induced lipid peroxidation in the rat liver and porcine thyroid homogenates.

OBJECTIVES: Growth hormone (GH) and its tissue mediator, insulin-like growth factor-I (IGF-I), are involved in oxidative processes, lipid peroxidation (LPO) included. Bivalent iron (Fe2+) is frequently used to experimentally induce oxidative damage to macromolecules (Fe2++H2O2+H+→Fe3++•OH+H2O). The aim of the study was to evaluate the effect of GH and/or IGF-I on the iron-induced LPO in the rat liver and porcine thyroid homogenates. METHODS: Rat liver and porcine thyroid homogenates were incubated in presence of GH (100; 10; 1.0; 0.1; 0.01; 0.001; 0.0001 µg/ml) or IGF-I (1000; 100; 10; 1.0; 0.1; 0.01; 0.001; 0.0001 µg/ml) or GH (100 µg/ml)+IGF-I, or FeSO4+H2O2 plus GH and/or IGF-I. The level of LPO was expressed as concentrations of malondialdehyde+4-hydroxyalkenals (MDA+4-HDA) per mg of protein. RESULTS: GH and/or IGF-I did not change the basal level of oxidative damage to lipids. In the rat liver homogenates, GH did not affect the iron-induced LPO, whereas IGF-I--in the lowest two concentrations--enhanced the process. In porcine thyroid homogenates, GH--in its two lowest concentrations--prevented, whereas in other concentrations, it enhanced the iron-induced LPO. IGF-I, in all used concentrations, enhanced the iron-induced LPO. CONCLUSION: GH and/or IGF-I may reveal prooxidative effects. This fact does not support their application in the treatment of disorders associated with increased oxidative damage.

The Polish version of the Quality of Life Assessment of Growth Hormone Deficiency in Adults (QoL-AGHDA) - four-stage translation and validation.

INTRODUCTION: The Quality of Life Assessment of Growth Hormone Deficiency in Adults (QoL-AGHDA) was developed simultaneously in five languages (English, Swedish, German, Italian and Spanish) to measure quality of life (QoL) in adult patients with Growth Hormone (GH) deficiency. The aim of the project was to produce a validated Polish version of the QoL-AGHDA that was conceptually equivalent to the UK-English version. MATERIAL AND METHODS: Translation and validation procedure consisted of 4 stages. Stage 1: A bilingual translation panel [7 participants, fluent in both English and Polish (Polish as their first language) with university education] translated the questionnaire. Stage 2: A lay translation panel (6 participants of an average to lower than average educational level, speaking only the target language) reviewed the wording of the draft version produced by bilingual panel to improve clarity and immediacy. Stage 3: The translated questionnaire was then field-tested with 15 adults with GH deficiency. Stage 4: Finally, the amended version underwent psychometric evaluation to check its reliability and validity (it was administered to 85 GH-deficient adults on two occasions, two weeks apart). RESULTS: The Polish QoL-AGHDA version was successfully adapted and it is characterized by a high degree of reliability and validity. The test-retest reliability coefficient for the Polish QoL-AGHDA was 0.92. The Cronbach's Alpha coefficient for the Polish QoL-AGHDA was 0.91 (N = 70) at Time 1 and 0.94 (N = 79) at Time 2. Correlation between QoL-AGHDA and Nottingham Health Profile items confirmed high convergent and divergent validity. CONCLUSIONS: The Polish QoL-AGHDA is a reliable and valid measure of QoL suitable for use in clinical studies and routine clinical practice.

Protective effects of GH and IGF-I against iron-induced lipid peroxidation in vivo.

Iron overload may enhance oxidative damage. Growth hormone (GH) and insulin-like growth factor-I (IGF-I) are involved in oxidative processes, lipid peroxidation (LPO) included. The aim of the study was to evaluate the in vivo effects of GH, IGF-I and/or iron on LPO in rat tissues. Male Wistar rats were administered iron (Fe2+; 3mg/100g b.w., i.p., on the 8th day) and/or GH (0.2IU/100g b.w.), and/or IGF-I (2microg/100g b.w.) once daily for 8 days. LPO products (malondialdehyde+4-hydroxyalkenals) were measured in rat brain, lung, small intestine, liver, kidney, testis, spleen and serum. Iron injection increased LPO only in the small intestine and that effect was completely prevented by either GH or IGF-I. In the brain, GH decreased, whereas IGF-I increased, the basal LPO. GH and IGF-I possess some ability to prevent iron-induced oxidative damage in iron sensitive tissues, but contribute to oxidative imbalance in other tissues.

The role of growth hormone and insulin-like growth factor I in oxidative processes.

Under physiological conditions, there is a balance between the production and detoxification of reactive oxygen species (ROS). In the course of several diseases, an overproduction of ROS and their increased reaction with biological macromolecules, lead to disruption of this balance and to enhanced oxidative stress. Alterations in growth hormone (GH)/insulin-like growth factor I (IGF-I) pathway (e.g., in condition of GH overproduction or deficiency) are tightly linked with enhanced oxidative stress. The results of experimental and clinical studies, in which effects of GH and IGF-I on oxidative processes were revealed, are presented in the survey.

GH replacement reduces increased lipid peroxidation in GH-deficient adults.

BACKGROUND: GH replacement improves numerous metabolic abnormalities in GH-deficient patients; increased lipid peroxidation (LPO) has been observed in GH-deficient patients; however, it is unknown if LPO is influenced by GH replacement. AIM AND METHODS: To evaluate the extent to which GH replacement might reverse the increased LPO in GH-deficient adults and to analyse if this phenomenon might be involved in the improvement of metabolic disturbances due to GH treatment. Serum concentrations of malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA), as an index of LPO, were measured at baseline, and after 12 and 24 months of GH replacement in 40 adult patients with severe GH deficiency (both in adult- and childhood-onset) and in 40 healthy volunteers, matched for sex, age and body mass index (BMI). Correlations were evaluated between LPO and lipids, IGF-I, metalloproteinase-2 and -9 (MMP-2, -9), vascular endothelial growth factor (VEGF), BMI and GH dose. RESULTS: LPO values in GH-deficient patients were several-fold higher than in controls [55.36 +/- 2.27 vs. 4.19 +/- 0.42 nmol/mg protein (mean +/- SEM), P < 0.0001] and decreased significantly over time with GH replacement to 38.61 +/- 2.15 nmol/mg protein (i.e. by approximately 30%), though still remaining markedly elevated compared with controls (P < 0.0001). The proatherogenic lipid profile parameters correlated positively with LPO in the childhood-onset subgroup before GH replacement. GH replacement restored the positive correlation between LPO and age in male patients (r = 0.57, P = 0.013; r = 0.8, P < 0.001, at 12 and 24 months of GH replacement, respectively). CONCLUSIONS: GH replacement partially reverses the grossly abnormal LPO in GH-deficient adults. It is highly probable, therefore, that oxidative mechanisms are involved in the overall improvement of metabolic changes due to GH replacement.

Significance of increased lipid peroxidation in critically ill patients.

OBJECTIVES: Increased oxidative stress and low-T3 syndrome may develop in critically ill patients. The study aimed at evaluating the level of lipid peroxidation (LPO) in critically ill patients and at estimating the relationships among LPO level, the death rate, the rate of low-T3 syndrome and patient's clinical status. METHODS: Lipid peroxidation (LPO) level was studied in seventy (70) adult, critically ill patients and 48 healthy volunteers. Critically ill patients were classified into survivors and non-survivors, or those with and without the low-T3 syndrome (normal-T3). RESULTS: LPO level was four times higher in critically ill patients than in healthy volunteers. Among non-survivors, LPO level was higher in patients with the low-T3 syndrome than in patients without this syndrome, and among survivors, the tendency was opposite. Additionally, the extent, to which LPO level increased, depended on the kind of the disease. The degree of LPO variability was higher in survivors than in non-survivors. LPO level was lower in patients with higher number of therapeutic interventions. CONCLUSION: A tremendous increase in oxidative damage to lipids in critically ill patients strongly depends on the kind of pathological process and, under certain conditions, higher LPO levels could be due to more favourable outcome.

Increased lipid peroxidation in growth hormone-deficient adult patients.

OBJECTIVES: Growth hormone (GH) deficiency in adults is associated with a higher risk of atherosclerosis and cardiovascular disease. It has recently been suggested that enhanced oxidative stress may be implicated in vascular (and probably other) disturbances, occurring in GH-deficient subjects. The aim of the study was to evaluate serum levels of lipid peroxidation (LPO) products in adult patients with severe GH deficiency during insulin tolerance test (ITT), and to estimate the relationships between LPO and GH, total cholesterol, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, and other parameters of metabolic processes. MATERIAL AND METHODS: Twelve adult patients with severe GH deficiency hospitalized in our department and 12 healthy volunteers, matched for sex, age and body mass index (BMI), were enrolled in the study. Peripheral blood was collected during ITT. The concentrations of malondialdehyde + 4-hydroxyalkenals (MDA+4-HDA), as an index of LPO, were measured in blood serum. RESULTS: Serum LPO level was approximately twice as high in GH-deficient patients as in the controls at each time point of ITT. A positive correlation was found between bone mineral density in the lumbar spine and GH concentration in GH-deficient patients. A positive correlation was found between LPO and BMI in the controls, but no such correlation was observed in GH-deficient patients. CONCLUSION: The increased LPO in GH-deficient patients may indicate enhanced oxidative stress within the vascular compartment and, possibly, in other tissues, which may contribute to the proatherogenic state and corresponding organ disturbances in GH-deficient patients, independently from conventional risk factors.

[Hypoglycemia--a new view on the problem of classification and clinical diagnostic]. / Hipoglikemia--nowe spojrzenie na problem klasyfikacji i diagnostyki klinicznej.

The commonly applied division of hypoglycemia into reactive and non-reactive one is too general and often times insufficient in clinical practice. The authors of this study presented a classification based on the clinical profile of patients with hypoglycemia. They also recommended patterns allowing proper diagnostic procedure in each classified group.