Biomedical subjects

B Rikken

Publications and source records attributed to B Rikken.

22 records · Page 2Linked to original sources

PubMed1992

Shape of the craniofacial complex in children with Turner syndrome.

The shape of the craniofacial complex was established in 69 children with Turner syndrome aged between 3.5 and 16.6 years. The children had not been treated with growth hormone (GH) or anabolic steroids. On a standardized lateral roentgenencephalogram 13 linear and 7 angular variables were measured. Data of all variables were available from normal Dutch children for comparison. The main abnormalities were located in the cranial base and in the mandible and consisted of a short posterior cranial base, all increased cranial base angle and a short, retrognathic and posteriorly rotated mandible. The maxilla was smaller than normal and also slightly posteriorly rotated. The abnormalities were already present in young children with Turner syndrome. Indications were found that in Turner syndrome interstitially as well as appositionally growing cartilage is affected. The changes in the maxilla can be explained in various ways. They may be due to defective growth of the nasal cartilage or to a disorder in the intramembranous ossification of the maxilla or they may be adaptive to the changes in the cranial base and the mandible. From this study it can be concluded that patients with Turner syndrome exhibit several craniofacial abnormalities, probably due to a cartilage disorder.

Adolescent↗

PubMed1992

[Growth hormone deficiency: diagnosis and treatment].

Growth hormone (GH) and thyroxine are the major growth promoting hormones in postnatal life. The pulsatile pattern of GH-release by the anterior pituitary is regulated by the interaction of stimulating and inhibiting hormones and influenced by physiological and pharmacological factors. GH promotes longitudinal bone growth mainly through activation of insulin-like growth factor I (IGF-I), but there may also be a direct effect. The most important clinical feature of growth hormone deficiency (GHD) is a low growth velocity resulting in short stature. In addition to retardation of bone maturation many GH-deficient children exhibit a number of typical, clinical characteristics. The diagnosis GHD can be confirmed by performing GH-stimulation tests and IGF-I measurements. However, the maximal GH-response to provocative stimuli is a poor indicator of the spontaneous GH-secretion. Classifications and etiology of GHD are given. Since 1958 GH-deficient children are treated with human GH with initially disappointing results regarding attained final height. Early diagnosis and treatment and optimization of GH-dose, mode of administration and injection frequency might improve final height. In The Netherlands the currently used GH-dose is 12-14 IU/m2/week in 6 or 7 daily doses administered subcutaneously. Ongoing retrospective and prospective studies serve to determine optimal treatment schedules. Up to now, important adverse effect of GH-therapy with the current GH-doses in GH-deficient children are not known. The beneficial effects of long-term GH-treatment of GHD adults is at present subject to ongoing investigation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1991

Growth and pubertal development during and after treatment with a slow-release gonadotropin-releasing hormone agonist in central precocious puberty.

The auxological data of 25 patients (21 girls, 4 boys) with central precocious puberty (CPP), treated for 4 years with a slow-release gonadotropin-releasing hormone agonist [Decapeptyl-controlled release (D-CR) 3.75] every 4 weeks intramuscularly, and of 6 patients (3 girls, 3 boys), treated for 5 years, are presented. After 3 years of D-CR a stabilization of height velocity (HV) at about 4 cm/year was observed. Bone maturation (ratio of change in bone age to change in chronological age; delta BA/delta CA) slowed down to a mean delta BA/delta CA ratio of 0.5 +/- 0.2 (mean +/- SD) measured over 48 months. As a result, predicted adult height (PAH) improved from 156.3 +/- 7.4 to 162.2 +/- 6.8 cm in girls (p less than 0.001) and from 174.4 +/- 18.6 to 184.3 +/- 17.1 cm in boys after 4 years. In the 5th year an ongoing improvement of PAH was observed. 20 additional girls discontinued D-CR for at least 12 months after treatment with D-CR for 2 years or more. In 11 girls menses started after 10.6 +/- 3.1 months; 9 girls had no menarche after 12-16 months. HV increased in the first and second 6 months to a level of about 6.0 cm/year, decreased in the third 6 months after cessation to the level before discontinuing D-CR and decreased further afterwards. Bone maturation (delta BA/delta CA) increased progressively in the first 18 months after discontinuation, with a stabilization at about 1.3. PAH did not change in the first 12 months after discontinuation of D-CR, but showed a decrease afterwards.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Height↗

PubMedDate not supplied

A nationwide cohort study on Creutzfeldt-Jakob disease among human growth hormone recipients.

OBJECTIVE: In 1991, a Dutch patient who had been treated from 1963 to 1969 with human-derived growth hormone died of Creutzfeldt-Jakob disease (CJD). This study was performed to investigate whether among other Dutch human growth hormone recipients there were clinically suspected cases of iatrogenic CJD. METHODS: In a retrospective cohort study, all patients (n = 564) treated with human-derived growth hormone before May 1985 and recorded in the Dutch National Growth Registry were followed up until January 1995 for a clinical diagnosis of CJD. For this purpose, all human growth hormone recipients were linked to a database of the Foundation for Health Care Information comprising hospital discharges with a clinical diagnosis of iatrogenic CJD. Linkage of the two databases was performed on the basis of date of birth and gender. Subsequently, verification of patient's name and initials of the positively matched pairs took place. RESULTS: Linkage provided 37 positively matched pairs concerning 29 individual patients. After verification, no name from the hospital discharge records corresponded to the names of the human growth hormone recipients. CONCLUSIONS The follow-up of 564 Dutch human growth hormone recipients, who had been treated with human growth hormone until 1985 did not establish any clinically suspected case of iatrogenic CJD. Future cases, however, can still emerge due to the potentially long incubation period of prion diseases.

Adult↗