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Biomedical subjects

M A Preece

Publications and source records attributed to M A Preece.

At least 181 records · Page 10Linked to original sources
PubMed1984

Body proportions in precocious puberty.

Sitting height (SH) and sub-ischial leg length (SLL) were measured in 10 boys and 16 girls with precocious puberty; the patients were aged from 1.5 to 13.4 years at the time. Standard deviation scores (SDS) calculated for chronological age and bone age showed higher scores for SH than for SLL in all but two patients, both girls: the differences between the SDS for SH and SLL were more marked in the boys. The findings indicate that growth of the trunk is usually greater than growth of the legs in precocious puberty, particularly in boys.

Age Determination by Skeleton↗
PubMed1984

Hypoplastic optic nerves and pituitary dysfunction. A spectrum of anatomical and endocrine abnormalities.

Fourteen children with optic nerve hypoplasia associated with either mid-brain abnormalities or pituitary dysfunction, or both, are described. All patients were either partially sighted or blind. One case is reported in detail. The importance of hypoglycaemia in the neonatal period and later in childhood is emphasised in relation to diagnosis and developmental delay. Pituitary dysfunction is variable and may be progressive. Forty percent of the patients had a septum pellucidum and its presence or absence cannot be used as a radiological marker for the condition. Long term endocrine follow up of these patients is required.

Adolescent↗
PubMed1984

Patterns of growth in the hepatic glycogenoses.

Longitudinal growth data from 31 patients with hepatic glycogen storage disease (type I (8 patients), type Ib (three patients), type III (13 patients), and type IX (phosphorylase kinase deficiency) (7 patients) ) have been reviewed. All patients were below the mean for height at presentation; the mean height standard deviation scores were -2.13 (type I), -2.0 (type Ib), -2.4 (type III), and -1.6 (type IX). Untreated, most patients with type I and Ib grew slowly with no catch up growth but three patients with mild disease grew normally. Most children with type III disease grew at a normal velocity throughout childhood. Puberty was delayed and final height normal. Some of the children with type III and all of those with type IX had catch up growth throughout childhood. Intensive treatment of patients with severe forms of type I and Ib disease resulted in catch up growth, but this was not complete if the treatment was started late.

Body Weight↗
PubMed1984

The 3-M syndrome.

Five patients from four families, including two male sibs, are reported with clinical and radiological features of the 3-M syndrome.

Abnormalities, Multiple↗
PubMed1983

Normal somatic growth in children receiving low-dose prophylactic co-trimoxazole.

Co-trimoxazole is an effective antibacterial agent for the prophylaxis of urinary tract infection. Because experimental evidence raises the possibility that high-dose cotrimoxazole might interfere with normal somatic growth, the longitudinal growth and growth velocities were analysed in 114 girls receiving long-term, low-dose prophylactic cotrimoxazole. They were aged 2-12 years at the start of prophylaxis which was given in a daily dose of approximately 10 mg sulphamethoxazole (SMX) and 2 mg trimethoprim (TMP)/kg body weight for at least 6 months and for up to 6 years. There was no significant variation from normal in height or weight attained or in growth velocity overall in 114 girls, 51 of whom had vesico-ureteric reflux (VUR). No difference was found in growth velocity when periods of 6 months on or off prophylactic therapy were compared in 53 girls. Growth did not vary between cohorts of girls receiving co-trimoxazole prophylaxis for 2, 3 or 4 years and growth proceeded normally in the 51 girls with VU reflux. We have not found evidence that long-term, low-dose cotrimoxazole prophylaxis has any adverse effect upon somatic growth in girls with a previous urinary infection with or without vesico-ureteric reflux and who are otherwise healthy.

Body Height↗
PubMed1983

Prolonged oestrogen treatment inhibits growth hormone-induced growth in hypopituitary dwarf mice.

This paper presents an investigation into the effects of prolonged oestrogen treatment (20 days) on basal growth and on growth stimulated by GH in hypopituitary dwarf mice. Body weight and tail length were measured during the treatment period and uptake of 35SO4(2-) into costal cartilage in vivo at the end of the treatment period. This study confirmed that treatment with human GH promotes a dose-dependent increase in body weight, tail length and uptake of 35SO4(2-) in vivo; there was a highly significant correlation between these responses. Treatment with oestrogen alone had no significant effect on any of the parameters measured. All groups receiving combined oestrogen and human GH treatment showed a significant increase in body weight and tail length compared with animals receiving the same dose of oestrogen alone. However, the increase in body weight and tail length was significantly less in animals given the highest dose of oestrogen plus human GH than that observed in animals treated with the same dose of human GH alone. Treatment with oestrogen had no significant effect on the uptake of 35SO4(2-) stimulated by human GH. Possible mechanisms for the growth-inhibiting effects of oestrogens are discussed.

Animals↗
PubMed1983

Increased thymidine incorporation into fetal rat cartilage in vitro in the presence of human somatomedin, epidermal growth factor and other growth factors.

The incorporation of [3H]thymidine by rat costal cartilage in vitro was studied at different fetal and postnatal ages and the effect of partially purified human somatomedin, mouse epidermal growth factor, platelet secretion products, insulin and growth hormone on thymidine uptake by fetal cartilage was examined. Thymidine uptake in plasma-free medium was many times greater in late fetal life than after birth. The incorporation of [3H]thymidine into costal cartilage from 21-day fetuses was significantly (P less than 0.05) increased above control values in the presence of 10 micrograms somatomedin/1, and when cartilage was incubated in medium containing somatomedin and diluted human plasma there was a synergistic action. Epidermal growth factor at a concentration of 1 ng/l was a potent stimulator of thymidine uptake. Secretion products from human platelets after their aggregation by thrombin stimulated [3H]thymidine uptake at a concentration of 2% (v/v), but were inhibitory at high concentrations. High concentrations of platelet secretion products stimulated the incorporation of [35S]sulphate by cartilage. A pharmacological concentration of 10 mu. insulin/ml stimulated [3H]thymidine uptake, but not concentrations of 1 or 100 mu./ml. Growth hormone had no effect. The results showed that fetal cartilage had a greater endogenous mitogenic activity than postnatal cartilage. While somatomedins may be important in the regulation of fetal body growth, other protein growth factors also stimulate fetal skeletal tissues.

Aging↗
PubMed1982

Growth and endocrine changes in the hepatic glycogenoses.

The biochemical and endocrine responses of 13 patients with hepatic glycogen storage disease (HGSD) (type I-six patients, type Ib-two, type III-three, type IX-two patients) to an oral glucose load have been investigated. Longitudinal growth data was available in all patients. The height velocity standard deviation score (HVSDS) was positively correlated with the plasma somatomedin and inversely correlated with the glucose-insulin ratio, plasma cortisol and plasma growth hormone concentrations. There was no correlation between plasma glucagon and HVSDS with treatment was accompanied by a rise in plasma somatomedin and a fall in growth hormone and cortisol. In two patients the glucose-insulin ratio decreased. Growth retardation in HGSD can be explained as part of the adaptation to the inability to maintain normal glucose homeostasis.

Adolescent↗
PubMed1982

Diagnosis and treatment of children with growth hormone deficiency.

Growth hormone deficiency embraces a heterogeneous group of disorders with multiple aetiologies. The biggest single division is between those children whose growth hormone deficiency is due to a structural lesion and those where it is not. In both cases other pituitary hormones may, or may not, be affected, although when a structural lesion is present multiple pituitary hormone deficiency is the rule rather than the exception. In the absence of structural lesions the pathogenesis of the condition in still largely obscure, although some mechanisms, such as cranial irradiation, are now well recognized. Birth trauma is also now a strong candidate as a predisposing factor. The prevalence of growth hormone deficiency is still uncertain, but is probably about 1 in 4000 live births. The clinical features of growth hormone deficiency are usually fairly clear, with short stature, low growth velocity, excess subcutaneous fat and delayed skeletal maturation being the principal clinical features. Laboratory investigation still largely depends upon the assessment of pituitary growth hormone secretion in response to a variety of provocation tests and is still in many ways unsatisfactory. Treatment consists of parenteral growth hormone replacement using material of human cadaveric origin. Non-primate growth hormones are of no value. Other endocrine abnormalities, when present, are treated appropriately, and with early diagnosis and optimal therapy the height prognosis is reasonably good. The principal aims for the future must be to ensure supplies of therapeutic growth hormone, improve some of the diagnostic procedures and ensure early ascertainment.

Adolescent↗
PubMed1981

Indices of serum androgens in normal puberty: correlations of two indices with chronological age, bone age and pubertal development in boys and girls.

Two indices of free serum androgenic activity, the normalized androgen ration (NAR) and the free androgen index (FAI) were determined in 218 normal children aged 8-17.9 years. Before the onset of puberty and between chronological age 8 and 11.9 years, NAR and FAI were similar in both sexes, the NAR being less than 0.8 and FAI less than 0.1. In boys mean NAR value increased from 0.87 to 1.39 between 12.5 and 17.5 years, and mean FAI from 0.14 to 1.85 between 12.5 and 17.5 years. In girls mean NAR increased from 0.79 to 0.85 between 12.5 and 15.5 years, and mean FAI from 0.11 to 0.23, between 12.5 and 15.5 years. Both indices did not change significantly between 15.5 and 17.5 years in girls. A rapid increase in NAR and FAI occurred in boys from a mean testicular volume of 4.1 to greater than 20 ml and from genital stage G2+ to 5+. In girls a gradual increase in NAR and FAI occurred from breast stage B2+ to 5+ . Although the androgen indices increased in both sexes between pubic hair stages PH2+ and 6+, the values in girls were always less than in boys at corresponding stages suggesting an increased androgen sensitivity of the female pubic hair follicle during adolescence. The peak rise in NAR and FAI in boys between 13 and 15 years correlated closely with the timing of the pubertal growth spurt in this sex. A similar rise was not seen in girls at the time of their peak growth velocity between 11 and 13 years and suggested that androgens play only a minor or complementary part in the female growth spurt.

Adolescent↗
PubMed1981

Growth hormone treatment in children with craniopharyngioma: final growth status.

Twenty-seven out of thirty craniopharyngioma patients treated with human growth hormone (hGH) for 2 years or more (average 4.5 years) reached final adult heights above the population third centile, though none was above the fiftieth centile. However, only twelve of twenty-eight patients had final heights above the lower limits to be expected from their parents' heights. All patient eventually had long legs relative to sitting height (final mean subischial leg length SDS = + 0.2, final mean sitting height SDS = -3.0). Twenty-nine patients were TSH-deficient, twenty-two were ACTH-deficient, thirteen were deficient in ADH and all had total (85%) or partial (15%) gonadotrophin deficiency. Following the administration of testosterone or hCG the boys had, on average, only half the normal adolescent growth spurt. This may have been due to the lateness of starting androgens in these patients and we recommend, when considering height, that testosterone or hCG should be started when a bone age of 13.0 "years' is reached or when a lower bone age has remained unchanged for a year. The girls showed adolescent height spurt; the average increase after oestrogen treatment commended was 1.7 cm.

Adolescent↗