The objective of this study was to assess health-related quality of life (HRQoL) in patients with advanced non-small cell lung cancer (NSCLC). In Serbia, there is the lack of available data on HRQoL in lung cancer patients. The special attention in our study has been paid on relationships between socio-economic factors and HRQoL. This cross-sectional study was undertaken in group of 100 NSCLC patients with advanced stage diseases. HRQoL was measured using three standard instruments: 36-item Short Form Health Survey, EORTC QLQ-C30 and its Lung Cancer module (EORTC QLQ-LC13). Unexpected, highly educated patients reported significantly worse social functioning (P=0.044), and higher degree of financial difficulties (P=0.047), in comparison with less-educated. Also unusual, unemployed patients had significantly better HRQoL in all domains and significantly lower symptom distress. Significantly better overall HRQoL (P=0.043), social (P=0.024), emotional (P=0.001) and mental functioning (P=0.011) were observed in patients treated with chemotherapy in comparison with newly diagnosed ones. In addition, the most prominent side effects of chemotherapy were nausea and vomiting, and all QoL domains correlated significantly with them. Patients who undergo active treatment improve their HRQoL but chemotherapy-induced emesis adversely affects many HRQoL domains. Additionally, HRQoL is highly dependent on patient's socio-economic characteristic.
lung cancer, anxiety, depression, quality of life, chemotherapy, chemotherapy-induced nausea and vomiting.
Patients treated with cranial radiation are at risk of GH deficiency (GHD). We evaluated somatotroph responsiveness to maximal provocative tests exploring the GH releasable pool in relation to the impact of radiation damage to the hypothalamic-pituitary unit. The GH-releasing effect of GHRH plus GH secretagogue [GH-releasing peptide (GHRP)-6] (GHRH+GHRP-6) was studied in 22 adult patients (age, 23.2 +/- 1.4 yr; 8 female and 14 male; mean body mass index, 22.6 +/- 0.7 kg/m(2)) who received cranial radiation for primary brain tumor distant from hypothalamic-pituitary region 7.6 +/- 0.7 yr before GH testing. Two stimulatory tests for GH secretion were employed: insulin tolerance test (ITT, 0.15 IU/kg regular insulin i.v. bolus); and GHRH+GHRP-6 test: GHRH (Geref Serono, Madrid, Spain; l microg/kg) plus GHRP-6 (CLINALFA, Laufelingen, Switzerland; 1 microg/kg) as i.v. bolus. Serum GH was measured (Delphia; Perkin Elmer, Wallac, Turku, Finland) at -30, -15, 0, 15, 30, 45, 60, 90, and 120 min. Anterior pituitary function was normal in all except in 1 female with hyperprolactinemia. Twelve out of 22 irradiated patients were GH-deficient (GHD) with both tests. Eleven out of 22 (50%) irradiated patients were severely GHD, according to the ITT (GH < 3 microg/liter; mean GH peak, 1.5 +/- 0.5 microg/liter). In 9 irradiated patients, in whom ITT was performed as well, mean peak GH after the GHRH+GHRP-6 test was 6.2 +/- 0.8 microg/liter, which is considered as severe GHD, according to our own cut-off for the test (peak GH < 10 microg/liter). GH responses to both tests were highly concordant, but the differential in the GH peak concentrations between GHD and non-GHD irradiated patients was significantly larger for the GHRH+GHRP-6 test than that for the ITT. The 2 discordant responses, i.e. poor response to the ITT and good response to the GHRH+GHRP-6 test, were found in 1 hyperprolactinemic female patient and in 1 other female. One irradiated patient was diagnosed as GHD only with the combined test, because ITT was contraindicated because of epilepsy. PRL and cortisol responses to ITT were normal in all irradiated patients and did not depend on the GH status. IGF-I levels were not informative or discriminative between the GHD and non-GHD irradiated adult patients. In conclusion, the use of GH secretagogues plus GHRH is an easy, reliable and accurate way of assessing GH secretion in cranially irradiated patients. Impairment of the GH releasable pool in the irradiated patients, with a maximal provocative test, reflects alterations in the hypothalamic-pituitary unit caused by radiotherapy.
The aim of this survey was to estimate the incidence of primary CNS tumors among children aged 0-14 in Belgrade during the period 1991-2004. Incidence rates were age-adjusted according to the world standard population. The average age-adjusted incidence rates were 3.4/100,000 for boys, 2.4/100,000 for girls, and 2.9/100,000 for both genders. There was a nonsignificant tendency toward increased CNS tumor incidence (y = 2.547 + 0.052 x, p = .549). The age-specific incidence rates were 3.0/100,000 (0-4 years), 2.2/100,000 (5-9 years), and 3.8/100,000 (10-14 years). Among the population aged between 0 and 14, the cumulative probability of acquiring primary CNS tumors was 1 per 1961 for boys and 1 per 2778 for girls. Astrocytoma was the most common pathohistological type of primary CNS tumors accounting for 41.5% of cases.
Golubicic I, Nikitovic M, Mitrovic N, Dieguez C, Casanueva FF. Growth hormone secretagogues in pathological states: diagnostic implications. Acta Paediatr 1997; Suppl423:97-101. Stockholm.The identification and cloning of the receptor for synthetic growth hormone (GH) secretagogues, even before the endogenous ligand has been identified or its precise physiological role established, suggests that there is a novel target of action for this class of drug. In an attempt to select patients who will benefit from GH treatment, GH secretagogues are being evaluated for their usefulness in diagnosing GH deficiency. The effects of GH-releasing peptides (GHRPs) on GH release as a function of age and metabolic status, and in different neuroendocrine pathologies, are described, as are the different mechanisms of action, potency and reproducibility of the response to GHRPs compared with GH-releasing hormone (GHRH). GHRPs offer the advantage over GHRH in natural models of deranged GH secretion in that, in various metabolic states (e.g. obesity, anorexia nervosa and non-insulin-dependent diabetes mellitus), the GH response to GHRH is more impaired than it is to GHRPs. However, in some neuroendocrine pathologies, the reverse is true. Thus, both secretagogues provide separate information on the physiological status of somatotrophs. Growth hormone-releasing peptide-6, growth hormone-releasing hormone, hexarelin, metabolic derangements, neuroendocrine pathologies V Popovic, Institute of Endocrinology, University Clinical Centre, Belgrade, Yugoslavia ISSN 0803-5326Neuroendocrine control of the pulsatile pattern of growth hormone (GH) secretion is complex. The multicomponent nature of the neuronal network and the complex transcriptional machinery that regulates GH gene expression have been characterized (1). In addition to the specific hypothalamic regulatory' hormones -GHreleasing hormone (GHRH) and somatdstatinother substances can influence GH secretion, namely pituitary cyclic AMP, oestrogens, glucocorticoids, GH-releasing peptides (GHRPs) and their nonpeptide pharmacological analogues. Metabolic states, such as obesity and malnutrition, and even metabolites, such as glucose, amino acids and free fatty acids, also participate in the control of GH secretion (2-4).In an attempt to improve our understanding of the complicated regulation of GH secretion in humans, and its relevance to clinical practice, we have studied the effects of GHW-6 and hexarelin, which is an analogue of GHRP-6 containing a 2-methyl substitution of D-tryptophan. Such small synthetic hexapeptides have no sequence homology with GHRH and are characterized by their high potency and selectivity in the reIease of GH in different clinical conditions (metabolic and neuroendocrine) associated with altered or impaired GH secretion. The well-known GHRP-6 (5, 6) acts through a specific receptor. This has recently been cloned and supports the existence of a second route of GH regulation, although the endogenous ligand for this receptor has not yet been identified. The GHRP-6 ...
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