Cesko-Slovenska Pediatrie最新文献

The number of skin diseases in childhood (atopic dermatitis, toxoallergic exanthematous eruption, dermatomycoses, bacterial and viral skin infections) is increasing. External pharmacological treatment remains despite medical and allergological treatment still an important method in the majority of child dermatoses. The authors emphasize that the prerequisite of success of this treatment is assessment of the correct diagnosis and extensive medical and pharmacological knowledge.

A boy with organically conditioned central precocious puberty and growth hormone deficiency (congenital cyst in the area of the third ventricle) is treated concurrently with an analog of gonadoliberine D-Trp-6-LHRH (Triptorelin) and growth hormone. Treatment was started at the calendar age od 9.4 years and bone age of 10.8 years. At the end of the first year of treatment the progression of bone age within one calendar year declined from 1.9 to 1.4 and after 18 months of treatment to 1.3. The growth rate increased from the initial value of 7.9 cm/year to 12.1 cm/year after 12 months of treatment, and subsequently reached a stable level of 10.2 cm/year. The growth prognosis increased markedly from the initial value of 168 cm to 174 cm at the end of the first year; a further improvement to 176 cm was recorded after 18 months of treatment.

Clinical observations and experimental studies indicate that administration of growth hormone (GH) affects thyroid parameters either via inhibited TSH secretion or via activation of the peripheral conversion of T4 to T3. For a period of six months after the onset of GH treatment basic thyroid parameters (TSH and total T3 and T4) were followed up in two groups of children: in 10 euthyroid girls with Turner's syndrome (TS) (age 6.2-11.3 years), hitherto not treated with GH and in six children (2 boys) with isolated idiopathic growth hormone deficiency (IGHD) (age 9.5-14.1 years). In the latter group GH treatment, 0.37 to 0.47 IU/kg/week for a period of 0.8 to 4.3 years preceded. This treatment was discontinued for 30 days before the investigation was started. During this treatment the condition was assessed as euthyroid without administration of L-thyroxine. Both groups of children were treated with GH administered by daily injection, girls with TS had a dose of 1 IU/kg/week, children with IGHD 0.42 IU/kg/week. In these girls with TS in the course of six months no change of the investigated parameters was recorded. In children with IGHD after three months' treatment a drop of T4 from (mean +/- SD) of 119 +/- 11 to 84 +/- 21 nmol/l (p = 0.01) occurred and a rise of the T3/T4 (x 100) index from 1.77 +/- 0.24 to 2.73 +/- 0.69 (p = 0.01) and of TSH from 1.1 +/- 0.7 to 2.2 +/- 0.6 mU/l (p = 0.005). The T3 level did not change. Within 6 months of treatment these changes receded completely and the levels returned to baseline values.(ABSTRACT TRUNCATED AT 250 WORDS)

Within the framework of an international prospective multicentre study 93 girls with gonadotropin-dependent precocious puberty were treated with Decapeptyl-Depot LHRH agonist (75 micrograms/kg, once a month by the i.m. route). This treatment led to prompt, immediate and long-term suppression of the pituitary-ovarian axis with subsequent regression of premature onset of secondary sex signs, to the arrest of premature menstruation, to normalization of the pathologically accelerated growth and inhibition of the accelerated bone maturation. This improved the mean expected growth during the first four years of treatment from 159 to 165 cm (p < or = 0.01). Concurrently in the majority complete normalization of the severely impaired mental condition of the affected girls due to the premature onset of puberty occurred (mean onset of puberty -4.5 years). Selective suppression of the pubertally increased gonadotropin secretion was even after prolonged treatment fully reversible after termination of treatment with a subsequent onset of normal puberty and cyclic ovarian activity. Undesirable side-effects and antibodies against Decapeptyl were not detected, the local tolerance of the injected microcapsules was satisfactory. GnRH agonists in depot form are becoming, due to their superior suppressive action incl. that on bone maturation, the drug of choice in long-term treatment of central precocious puberty as they are the first which mitigate or can prevent, if treatment is started in time, a final small stature which frequently is the greatest handicap for a life-time (frequently associated with adverse bodily disproportions).

A group of five girls with central precocious puberty (CPP) (four girls with idiopathic CPP and one girl with organically conditioned CPP) were treated for a mean period of 17 months (12-20 months) with an agonist of gonadoliberine (aGnRH) D-Trp-6-LHRH(Triptorelin), 60-100 micrograms/kg by the i.m. route, every four weeks. The calendar age (CA) of the girls was at the onset of aGnRH treatment 7.3 +/- 0.7 years, the bone age (BA) 9.6 +/- 1.0 years. Previously Cyproterone acetate treatment administered for an average period of 26 months (4-56 months) was gradually discontinued in the course of 12 weeks. After 12 months aGnRH treatment the growth rate slowed down from 8.1 #/- 2.1 to 6.2 +/- 1.7 cm/year (NS). The bone age increment per calendar year declined at the end of the first year of treatment from 1.7 +/- 0.8 to 0.94 +/- 0.4 (NS). Prediction of the adult height did not change in the course of one year (before aGnRH therapy 158.6 +/- 5.3 after one year's treatment 159.0 +/- 5.3 cm). In all girls premature maturing was arrested already during the original Cyproterone acetate treatment. With the exception of a single patient during aGnRH therapy progression was not recorded. In this girl with the idiopathic form of CPP the authors observed during regular Triptorelin administration, starting from the fourth month, clinical and biochemical manifestations of secondary therapeutic failure after termination of hitherto administered Cyproterone acetate treatment-"escape from treatment". Clinical and hormonal indicators improved after addition of Cyproterone acetate. This patient lacks typical symptoms suggesting McCune-Albright's syndrome.