[Growth hormone administration in the treatment of growth retardation in juvenile SLE--case history]. / Leczenie hormonem wzrostu zaburzen wzrastania w przebiegu mlodzienczego tocznia ukladowego--opis przypadku.

INTRODUCTION: A chronic autoimmune inflammatory process and a long-term steroid therapy seems to underlie growth inhibition in children suffering from juvenile systemic lupus erythematosus (JSLE). The study objective was to assess the effect of one-year GH therapy on the growth rate in a 17-year-old girl with JSLE diagnosed when she was 11. CASE DESCRIPTION: Growth rate slowdown was observed when the girl was eleven (up to the age of 10 the growth was harmonious--50 centile). Since then, the mean gain in body height was approximately 1 cm/year. At the age of 16 (prior to the start of GH therapy), she was 148 cm high (below 3 centile), telarche II degrees, pubarche I degrees. The skeletal age corresponded to approximately 11 years according to the method of Greulich-Pyle. The girl underwent hormonal examinations in the Endocrinology Outpatient Department, including stimulatory tests of pituitary GH reserve, and based on the findings she was qualified for GH therapy, at a weekly dose of 30 IU. Within the 6-month-therapy, the patient grew by 7.5 cm, with the final outcome of 161 cm. The period of treatment was free of JSLE exacerbations or glucose tolerance disturbances. The only side effects included enhanced thirst and transitory oedema of the lower extremities observed in the first week of therapy. At the same time the patient's general feeling improved. CONCLUSIONS: During a one-year GH therapy, the girl achieved catch-up growth, which was accompanied by body weight reduction and no significant side effects.

[Serum levels of matrix metaloproteinase 2 (MMP-2), matrix metaloproteinase 9 (MMP-9) and tissue inhibitor of metaloproteinase 2 (TIMP-2) in children and adolescents with growth hormone deficiency]. / Ocena stezenia metaloproteinazy macierzy pozakomorkowej 2 (MMP-2), metaloproteinazy macierzy pozakomorkowej 9 (MMP-9) i tkankowego inhibitora metaloproteinazy 2 (TIMP-2) u dzieci i mlodziezy z niedoborem hormonu wzrostu.

INTRODUCTION: Matrix metaloproteinases (MMPs) have been implicated in various pathological processes including inflammatory response, atherosclerosis and cardiovascular disease. Growth hormone deficiency (GHD) is associated with prematury atherosclerosis and cardiovascular disease. Circulating levels of matrix metaloproteinases and their tissue inhibitors (TIMPs) so far have not been assessed in children and adolescents with GHD. MATERIAL AND METHODS: Serum levels of matrix metaloproteinase 2 (MMP-2), matrix metaloproteinase 9 (MMP-9) and tissue inhibitor of metaloproteinase 2 (TIMP-2) were measured in 44 (11 girls and 33 boys) children and adolescents with newly diagnosed GHD [age (mean+/-SD) 12.5+/-2.7 years, height 1.3+/-0.1 m, body surface area (BSA) 1.1+/-0.2 m(2) and body mass index (BMI) 17.4+/-2.2 kg/m(2)] and in 32 (11 girls and 21 boys) healthy children and adolescents (age 12.4+/-2.9 years, height 1.6+/-0.2 m, BSA 1.4+/-0.3 m(2) and BMI 18.7+/-2.6 kg/m(2)). Human MMP-2, MMP-9 and TIMP-2 measurements were carried out with the use of ELISA kits. RESULTS: Patients with GHD had significantly higher concentrations of MMP-2 (287.2+/-60.5 vs. 235.8+/-41.3 ng/ml, p<0.0001) and TIMP-2 (81.4+/-14.9 vs. 62.7+/-15.9 ng/ml, p<0.0001) levels than the control healthy group. There was no difference in MMP-9 levels (338.5+/-197.9 vs. 276.3+/-121.7 ng/ml, p=0.12) between patients with GHD and controls. CONCLUSIONS: Children and adolescents with GHD have elevated serum concentrations of MMPs-2 and TIMP-2.

[Effect of human growth hormone treatment on the eyes of patients with somatotropic pituitary insufficiency and in girls with Turner's syndrome]. / Ocena wplywu terapii ludzkim hormonem wzrostu na narzad wzroku pacjentów z somatotropinowa niedoczynnoscia przysadki i pacjentek z zespolem Turnera.

INTRODUCTION: The increased use of human growth hormone (hGH) in numbers of children rise questions concerning the safety of GH replacement therapy (GHRT). Adverse effects of hGH treatment (pseudotumor cerebri, papilloedema, retinal changes mimicking diabetic retinopathy, neovascularization) have been reported in some papers. PURPOSE: The aim of this study was to evaluate the influence of hGH therapy on the organ of vision. MATERIAL AND METHODS: 10 girls with Turner's syndrome aged 12-16 years (mean 13.8+/-1.69) and 20 patients with somatotropic pituitary insufficiency aged 7-18 years (mean 12.98+/-2.81) were studied. The mean duration of GHRT in patients with Turner's syndrome was 3.05+/-1.42 years (from 1 year to 5 year), in patients with somatotropic pituitary insufficiency was 2.45+/-2.32 years (from 8 months to 10 years). All patients underwent ophthalmic examination, including contrast sensitivity, direct and indirect ophthalmoscopy and fluorescein angiography. RESULTS: All parts of ophthalmological examination were normal. There were no abnormalities in fluorescein angiography. Contrast sensitivity was correct in all eyes. CONCLUSIONS: There was no harmful effect of GHRT on the retina and optic nerve in young patients. The follow-up and ophthalmologic evaluation is advisable.

Cardiac mass and function, carotid artery intima media thickness, homocysteine and lipoprotein levels in children and adolescents with growth hormone deficiency.

INTRODUCTION: Early atheromatic changes have been found in the carotid and the femoral arteries of young adults with growth hormone (GH) deficiency (GHD). It has been shown that adults with GHD have increased cardiovascular risk factors. The aim of this study was to compare atherosclerotic risk factors in children with GHD and a normal population. PATIENTS AND METHODS: Twenty-five patients (10 girls, 15 boys) with GHD qualified for GH replacement treatment were included in the study. The control group consisted of 22 healthy children (11 girls, 11 boys) with no family history of atherosclerosis and cardiovascular disease. Cardiac mass and function was evaluated by one-dimensional, two-dimensional echocardiography and the Doppler method. Common carotid intima-media thickness was measured with a linear probe (7.5 MHz). Lipid metabolism parameters (total cholesterol, HDL- and LDL-cholesterol, triglycerides), lipoprotein A (Lp(a)) and homocysteine levels were measured. RESULTS: Cardiac dimensions and systolic parameters were within normal values in both groups. The mean index of left ventricular mass (68.37 +/- 18.64 g/m2) in patients with GHD did not differ significantly compared to controls (68.48 +/- 15.56 g/m2). No significant differences between the study and control group were observed when comparing systolic and ejection fraction values. Significantly higher mean values of IVRT parameter were found (70.8 +/- 14.2 ms vs 64.09 +/- 8.54% ms; p < 0.05). Other parameters characterizing systolic function were not significantly different. The mean concentration of total (178.28 +/- 31.1 mg/dl) and LDL-cholesterol (106 +/- 28.68 mg/dl) was significantly higher in patients with GHD than in controls (157.59 +/- 22.39 mg/dl, 84.54 +/- 22.01 mg/dl; p <0.05). Lp(a) (40.34 +/- 12.45 mg/dl vs 11.02 +/- 4.82 mg/dl; p <0.05) and apolipoprotein B (ApoB) (71.12 +/- 18 mg/dl vs 56.72 +/- 11.46 mg/dl; p < 0.05) were significantly higher in patients with GHD. Carotid artery intima-media thickness (IMT) values were significantly higher in patients with GHD compared to healthy children (IMT-L 0.53 +/- 0.058 mm vs 0.41 +/- 0.045 mm; IMT-R 0.54 +/- 0.048 vs 0.42 +/- 0.42 mm, respectively). CONCLUSIONS: No significant differences in parameters of cardiac systolic function and left ventricular mass were found between patients with GHD and healthy children. However, significantly higher Isovolumetric relaxation time (IVRT) values in the group of patients may suggest impaired diastolic function. Significantly elevated IMT values in the common carotid artery were observed in patients with GHD in comparison with healthy children, which may prove the onset of atheromatosis.