Background and aim. Gestational diabetes mellitus (GDM) and type 2 diabetes mellitus (DM2) are suggested to be caused by the same metabolic disorder. Defects in gut hormone-dependent regulation of β-cell function (entero-insular axis) have been proposed to contribute to the pathogenesis of DM2. The aim of study was to evaluate whether an impaired secretion of glucagon-like peptide-1 (GLP-1) and/or glucose-dependent insulinotropic polypeptide (GIP) could play a role in the development of carbohydrate disorders during pregnancy. Subjects and methods. The study group (GDM) consisted of 13 gestational women with diabetes mellitus in whom GDM was diagnosed according to the World Health Organization criteria (75-g oral glucose tolerance test (OGTT)). The control group consisted of 13 pregnant women with normal glucose tolerance (NGT), matched according to age and duration of pregnancy. For all patients, plasma glucose, insulin, GLP-1 and GIP concentrations were evaluated after an OGTT, i.e. at 0, 30, 60, 90 and 120 min after glucose load. Results. Fasting plasma glucose concentrations were similar in both groups, but the 0–120 min area under the curve (AUC) for glucose was significantly greater in the GDM group than in the NGT group (p < 0.0005). Fasting insulin concentration was higher (p < 0.05) and the 2-h insulin response (AUC_total) was significantly greater (p = 0.01) in the GDM group than in the NGT group. Insulin resistance was significantly higher in GDM compared with control women (homeostasis model assessment, p = 0.003). Fasting GLP-1 concentrations were higher in the GDM group (p = 0.05), but no differences were observed in GLP-1 response (AUC) between the studied groups. Fasting and stimulated GIP response did not differ between groups at any time of the study (p > 0.05). Positive correlations were observed between fasting GLP-1 and insulin concentration (r = 0.56, p < 0.004) and between fasting GLP-1 and insulin resistance (r = 0.43, p < 0.029). Conclusion. An impaired secretion of GLP-1 and GIP does not seem to play a major role in the pathogenesis of GDM.

Growth hormone (GH) has been used in the treatment of short stature in children with GH deficiency (GHD) for 60 years, and for about 30 years also in the treatment of adults with GHD, in whom such treatment is carried out due to metabolic indications. In Poland, GH treatment is reimbursed only in children with GHD, while so far it has not been refunded in adults with GHD. There are two groups of adults (or adolescents after growth completion) with GHD, who require GH therapy: patients with GHD that occurred in childhood (childhood-onset GHD — CO-GHD) and patients with GHD acquired in adulthood (adulthood-onset GHD — AO-GHD). This review presents a brief outline of the history of GH treatment in humans, the latest data on the causes and symptoms of GHD in adults, and the complications of untreated GHD. Current recommendations regarding diagnosis, treatment and monitoring of GH therapy in adults are also discussed. Moreover, the review paper presents the objectives, assumptions, and plans of implementation of the “National Treatment Program for Severe Growth Hormone Deficiency in Adults and Adolescents after Completion of the Growth Promoting Therapy”, as well as the expected health and economic effects of introduction of GH treatment in adults with GHD in Poland. Growth hormone (GH) has been used in the treatment of short stature in children with GH deficiency (GHD) for 60 years, and for about 30 years also in the treatment of adults with GHD, in whom such treatment is carried out due to metabolic indications. In Poland, GH treatment is reimbursed only in children with GHD, while so far it has not been refunded in adults with GHD. There are two groups of adults (or adolescents after growth completion) with GHD, who require GH therapy: patients with GHD that occurred in childhood (childhood-onset GHD — CO-GHD) and patients with GHD acquired in adulthood (adulthood-onset GHD — AO-GHD). This review presents a brief outline of the history of GH treatment in humans, the latest data on the causes and symptoms of GHD in adults, and the complications of untreated GHD. Current recommendations regarding diagnosis, treatment and monitoring of GH therapy in adults are also discussed. Moreover, the review paper presents the objectives, assumptions, and plans of implementation of the “National Treatment Program for Severe Growth Hormone Deficiency in Adults and Adolescents after Completion of the Growth Promoting Therapy”, as well as the expected health and economic effects of introduction of GH treatment in adults with GHD in Poland.

Mathematical models have been applied in prediction of growth hormone treatment effectiveness in children since the end of 1990s. Usually they were multiple linear regression models; however, there are also examples derived by empirical non-linear methods. Proposed solution consists in application of machine learning technique – artificial neural networks – to analyse this problem. This new methodology, contrary to previous ones, allows detection of both linear and non-linear dependencies without assuming their charactera priori. The aims of this work included: development of models predicting separately growth during 1st year of treatment and final height as well as identification of important predictors and in-depth analysis of their influence on treatment’s effectiveness. The models were derived on the basis of clinical data of 272 patients treated for at least 1 year, 133 of whom have already attained final height. Starting from models containing 17 and 20 potential predictors, respectively for 1st year and final height model, we were able to reduce their number to 9 and 10. Basing on the final models, IGF-I concentration and earlier growth were indicated as belonging to most important predictors of response to GH therapy, while results of GH secretion tests were automatically excluded as insignificant. Moreover, majority of the dependencies were observed to be non-linear, thus using neural networks seems to be reasonable approach despite it being more complex than previously applied methods.

Introduction Vitamin D3 [25(OH)D] deficiency is a significant problem in Polish children. In many regions of the world, 25(OH)D concentrations show seasonal variation and differences between boys and girls, due to seasonal differences in insolation, as well as different sociological and...

In a considerable proportion of patients with childhood-onset growth hormone (GH) deficiency (GHD), a normalisation of GH secretion at the attainment of final height (FH) is observed. The aim of the present study was to assess the incidence of, and to find out the predictors of, persistent and transient GHD, available in the pre-treatment period, in patients with childhood-onset isolated, non-acquired GHD.The analysis comprised 150 short children (117 boys), with childhood-onset isolated, non-acquired GHD who completed GH therapy and attained FH. Before treatment and at FH (in retesting), auxological parameters were measured, GH peak in stimulation tests and IGF-I concentration were assessed, and pituitary height (PHt) was measured before treatment.The incidence of persistent GHD was 12.0%. The patients with persistent GHD had before treatment significantly lower GH and IGF-I secretion, as well as significantly better increase of height SDS (DHSDS) during GH therapy than those with transient GHD. A negative correlation was observed between DHSDS and IGF-I concentration, but not between DHSDS and GH peak. There was no significant difference in the incidence of pituitary hypoplasia between the patients with persistent and transient GHD.The incidence of persistent GHD in patients with childhood-onset, isolated, non-acquired GHD is relatively low. Despite the fact that the predictors of persistent and transient GHD may be identified in childhood, a diagnosis of GHD should be verified in retesting after the attainment of FH in each case.

Background: The diagnosis of growth hormone (GH) deficiency (GHD) in short children seems unquestionable when both GH peak in stimulating tests (GHST) and IGF-I concentration are decreased. However, the discrepancies between the results of GHST and IGF-I secretion are observed. It seems purposeful to determine the significance of GHST and IGF-I assessment in diagnosing GHD. The relationship between GH secretion and thyroid function, as well as GH influence on the peripheral thyroxine (T₄) to triiodothyronine (T₃) deiodination, mediated by IGF-I, were identified. Thus, clear differences in thyroid function between GH-deficient and non-GH-deficient subjects should exist. Methods: Analysis comprised 800 children (541 boys), age 11.6 ± 3.1 years (mean ± SD), with short stature, in whom two (2) standard GHST (with clonidine and with glucagon) were performed and IGF-I, free T₄ (FT₄), free T₃ (FT₃) and TSH serum concentrations were assessed. The patients were qualified to the following groups: GHD - decreased GH peak in GHST and IGF-I SDS (n = 81), ISS - normal GH peak and IGF-I SDS (n = 347), low GH - normal IGF-I SDS, and decreased GH peak (n = 212), low IGF - decreased IGF-I SDS, and normal GH peak (n = 160). The relationships among the results of particular tests were evaluated. Results: In the groups with decreased IGF-I concentrations (GHD Group and low IGF Group), the more severe deficit of height was observed, together with higher TSH and FT₄ but lower FT₃ levels than in groups with normal IGF-I concentrations (ISS Group and low GH Group), independently of the results of GHST. TSH, FT₄ and FT₃ concentrations were - respectively - similar in two groups with decreased IGF-I secretion, as well as in two groups with normal IGF-I levels. Significant correlations were found between patients' height SDS and IGF-I SDS, between FT₃ and IGF-I SDS (positive), and between FT₄ and IGF-I SDS (negative), with no correlation between GH peak and any of the parameters analyzed. Conclusion: The assessment of thyroid function in children with short stature provides the evidence that measurement of IGF-I concentration may be a procedure reliable at least to the some degree in diagnosing GHD as the results of GHST.