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Biomedical subjects

L Rees

Publications and source records attributed to L Rees.

At least 73 records · Page 4Linked to original sources
PubMed1991

Human atrial natriuretic factor and renin-aldosterone in paracetamol induced fulminant hepatic failure.

It has been postulated that deficiency of a putative natriuretic factor, or resistance to such a factor, may contribute to sodium retention in fulminant hepatic failure. Levels of plasma human atrial natriuretic factor (h-ANF), plasma renin activity, and aldosterone concentration were measured in 33 patients with fulminant hepatic failure due to paracetamol overdose, and 12 healthy control subjects. Levels of h-ANF were raised only in patients with evidence of severe renal impairment (serum creatinine greater than 300 mumol/l and urine output less than 100 ml/24 hours). h-ANF values were median 4.15, range 2-9 pmol/l and 10.1, 1-25 pmol/l for the control and severe renal impairment groups respectively (p less than 0.001). In the latter plasma renin activity was raised compared to that in control subjects (median 19.8, range 1.04-41.7 and 2.86, 1.87-5.9 pmol/l/h respectively, p less than 0.02). Plasma aldosterone concentration was also raised in patients (2176, 199-6894 pmol/l compared to 368, 133-578 pmol/l in control subjects, p less than 0.01). Haemodialysis induced changes in circulating h-ANF which correlated with volume and right atrial pressure changes (p less than 0.001 and p less than 0.05 respectively). In six patients with no or mild renal failure infusion of 900 ml 5% human albumin solution caused a significant increase in plasma h-ANF (p less than 0.05) without natriuresis or diuresis, a finding compatible with the hypothesis that there may be resistance to h-ANF in this group. The present findings indicate that there is no deficiency of h-ANF in fulminant hepatic failure and that known mechanisms of h-ANF release are not impaired.

Acetaminophen↗
PubMed1990

Oxandrolone for delayed puberty in boys taking long-term steroid therapy for renal disease.

Eleven boys, mean age 15.3 years (range 13.2-17.5), with pubertal delay in association with steroid therapy for steroid-sensitive nephrotic syndrome and following renal transplantation were treated with oxandrolone 2.5 mg daily for a mean of 0.50 years (range 0.34-0.61). Mean growth velocity increased from 3.9 cm/year (range 1.1-6.3) to 6.1 cm/year (range 2.0-14.4) and was maintained at 6.1 cm/year (range 0.4-10.2) (P less than 0.05). However, there was no significant difference in growth between the treated boys and age- and puberty-matched controls. Elevation of blood cyclosporin A and creatinine levels occurred in the transplant patients. Oxandrolone may initiate a pubertal growth spurt in patients taking steroid therapy for renal disease, but should be used with extreme caution because of potential side-effects.

Adolescent↗
PubMed1990

Treatment of short stature in renal disease with recombinant human growth hormone.

Six prepubertal children with chronic renal failure (group 1), six prepubertal children with renal transplants (group 2), and six pubertal children with renal transplants (group 3) who were short (mean height SD score, -3.2, range -4.5 to -1.6) and growing poorly (mean (range) growth velocity (cm/year) over the year before treatment: group 1, 4.8 (3.5-5.8), group 2, 2.3 (0.9-4.7), and group 3, 3.2 (0.5-6.5] were treated with recombinant human growth hormone 30 units/m2/week in daily doses for a median of 0.98 years (range 0.25-0.99). Mean (range) growth velocity over the treatment period increased significantly in all groups (group 1, 10.7 (8.8-12.3), group 2, 6.1 (2.7-10.8), and group 3, 6.0 (4.6-6.8]. There was, however, no improvement in height SD score for bone age in any group. The renal function of two children deteriorated after starting treatment with growth hormone, but it was not possible to say whether the growth hormone was responsible for this. The long term effects of treatment and its influence on final height are not yet known.

Adolescent↗
PubMed1989

Plasma atrial natriuretic peptide in human fetus: response to intravascular blood transfusion.

To investigate whether atrial natriuretic peptide is present in the human fetal circulation and changes in response to fetal blood volume expansion, the concentration of plasma atrial natriuretic peptide was measured by radioimmunoassay in samples obtained by cordocentesis. Twenty-four patients referred for intravascular blood transfusion because of red cell isoimmunization at 21 to 35 weeks' gestation were studied. Plasma atrial natriuretic peptide concentrations in fetal blood (median, 8.0 pmol/L; range, 1 to 27.3) were significantly higher than those of 25 young 18- to 32-year-old adult control subjects (median, 4.5 pmol/L; range, 1 to 11.3, p less than 0.002 but similar to those found in the umbilical cord blood of 10 normal neonates immediately after delivery (median, 7.35 pmol/L; range, 2.7 to 15.5). In seven patients in whom fetal and maternal plasma atrial natriuretic peptide was measured simultaneously, all fetal concentrations were higher (p less than 0.01). The concentration of fetal atrial natriuretic peptide before and immediately after blood transfusion (n = 12) rose significantly (p less than 0.05), and the rise correlated positively with the transfusion rate (p less than 0.05). We conclude that atrial natriuretic peptide is present in plasma of the human fetus as early as 21 weeks' gestation and that its concentration increases promptly in response to vascular volume expansion. These findings suggest that atrial natriuretic peptide may play a role in fetal volume homeostasis.

Adolescent↗
PubMed1989

The neuroendocrine response to oral dextroamphetamine in normal subjects.

In 24 male subjects oral dextroamphetamine 20 mg caused a statistically significant rise in cortisol, prolactin, TSH, FSH, and LH compared to placebo. Dextroamphetamine caused a short-lived rise in growth hormone and attenuated the later rise which occurred after placebo. The findings are discussed in the light of previous reports of the neuroendocrine response to dextroamphetamine in normal subjects and in psychiatric patients.

Adolescent↗
PubMed1989

The role of dopaminergic and noradrenergic receptors in human TSH and LH release.

The present study was undertaken to evaluate the relative roles of noradrenergic (NA) and dopaminergic (DA) neurotransmission in the control of thyrotropin (TSH) and luteinizing hormone (LH) release. Oral dextroamphetamine 20 mg caused a rise in the serum levels of TSH and LH in 24 healthy male volunteer subjects. The increase in TSH secretion was augmented by prior treatment with pimozide and reduced by thymoxamine. Conversely the LH response to destroamphetamine was reduced by pimozide and possibly accentuated by thymoxamine. The results confirm an inhibitory role for DA receptors in the control of TSH release and indicate that NA receptors may exert a facilitatory role. The converse would appear to be the case with LH, with DA being facilitatory and NA possibly inhibitory.

Adult↗
PubMed1989

Chronic renal failure and growth.

Growth was assessed in 38 prepubertal children with chronic renal failure for a mean (range) of 2.3 (1-4) years. At first clinic visit their mean (range) glomerular filtration rate was 17 (7-35) ml/min/1.73 m2, their mean (range) age was 3.4 (0.2-9.1) years, and 23 (61%) were greater than two standard deviations below the mean for height. After intensive medical management of their chronic renal failure, half of the children who presented before 2 years of age showed appreciable catch up growth. Only a slow improvement in growth occurred in most children presenting over 2 years of age. At final assessment, the mean (range) glomerular filtration rate was 15 (6-42) ml/min/1.73(2) and 20 (53%) were greater than two standard deviations below the mean for height. There was no correlation between glomerular filtration rate and growth. There remained a group of children who continued to grow poorly. Many of these were of low birth weight, and had dysplastic kidneys.

Body Height↗
PubMed1988

Response of axons and glia at the site of anastomosis between the optic nerve and cellular or acellular sciatic nerve grafts.

Axonal and glial reactions at the site of optic nerve section and at the junctional zone between optic nerve and normal or acellular peripheral nerve grafts have been studied. Following optic nerve section, no axons grew into the distal optic nerve stump. Similarly, no axons invaded the acellular peripheral nerve grafts, although in both instances fibres did regenerate into the junctional zone and a few remained there at least until 30 days post lesion (dpl, the duration of the experiments). Axons regenerated into normal peripheral nerve grafts by 3-5 dpl and by 10 dpl large numbers had penetrated deeply into the grafts. The glial response to injury appeared similar in both groups of grafted animals. Astrocytes and oligodendrocytes grew out into the junctional zone over the 5-7 day period and invaded the margins of the cellular grafts by 10 dpl. They did not penetrate the acellular nerves or distal optic nerve stumps. We were unable to determine whether Schwann cells invaded the junctional zone from the normal peripheral nerve grafts. Schwann cells are both GFAP+ and Vim+, especially when reacting after injury, and Lam- when not associated with axons: it is therefore possible that Schwann cells from the cellular grafts contributed to the population of GFAP+, Vim+ cells in the junctional zone of the cellular grafts. Anti-laminin immunoreactivity persisted in the basal lamina tubes of both the normal and acellular peripheral nerve grafts. Thus, the failure of axon regeneration into acellular peripheral nerve grafts can be correlated with the absence of Schwann cells and does not appear to be related to the presence of laminin.

Anastomosis, Surgical↗
PubMed1988

Optic axons regenerate into sciatic nerve isografts only in the presence of Schwann cells.

Optic axons regenerate into normal but not acellular peripheral nerve (PN) grafts. The first axons penetrate the PN graft before 5 days and grow inside the basal lamina tubes amongst the Schwann cells. By 30 days, 4% of the surviving retinal ganglion cells (RGC) regenerate axons for at least 10 mm into the PN graft. Laminin rich basal lamina tubes persist in the acellular PN transplants but only a few axons penetrate the most proximal parts of the tubes by 5 days and none grow farther into the graft by 30 days. RGC counts demonstrate that 34% of the normal RGC population survive 30 days after anastomosing a normal PN to the transected optic nerve. After anastomosing acellular PN grafts, 25% of RGCs survive compared with 10% after optic nerve section. These findings demonstrate that laminin does not promote regeneration of axons and that Schwann cells play the primary role of offering trophic support and even a substrate for growth. RGC survival is also enhanced by PN grafts even when Schwann cells are absent. This latter result suggests that RGC survival is promoted by a trophic substance released from axons and/or Schwann cells in the PN grafts which survives the thawing/freezing procedure (used to kill the Schwann cells) and is active in the grafts in the immediate post operative period.

Animals↗
PubMed1988

Growth and endocrine function after renal transplantation.

Longitudinal height data and physical development were assessed in 45 boys and 34 girls after renal transplantation. All children received alternate day steroids and either azathioprine or cyclosporin A for immunosuppression. There was a significant increase in growth velocity after transplantation in prepubertal children. Growth velocity declined at the expected age of the normal pubertal growth spurt, however, with delay in the appearance of secondary sexual characteristics. Overnight hormone profiles in 17 adolescent subjects with short stature or maturational delay, or both, showed blunting of growth hormone and gonadotrophin pulsatility. It is likely that long term steroid treatment after renal transplantation induces the clinical and endocrine picture of delayed puberty. Failure of growth to accelerate at this time is a cause of short stature, which may have an effect on adult height.

Adolescent↗
PubMed1988

Growth and endocrine function in steroid sensitive nephrotic syndrome.

Longitudinal height data and physical development were assessed in 29 boys and 12 girls taking long term steroid treatment for steroid sensitive nephrotic syndrome. Growth in both boys and girls, assessed by changes in height standard deviation score (delta Ht SDS), worsened significantly with chronological age. There was a significant negative correlation between delta Ht SDS and duration of treatment in boys, but not in girls. There was no correlation between delta Ht SDS and relapse rate or the use of cyclophosphamide. In the boys, Ht SDS decreased significantly only after the age of 10 years and was associated with delay in the appearance of secondary sexual characteristics. Eight adolescent boys were assessed endocrinologically by an overnight hormone profile. Blunting of the pulsatility of growth hormone and gonadotrophins was seen in six. Normal profiles were seen in two subjects who were both off steroid treatment at the time of study. Abnormal endocrine function in adolescent boys treated long term for steroid sensitive nephrotic syndrome corresponded with the clinical picture of delayed onset of puberty, which accounted for severe growth retardation in a substantial proportion of subjects.

Adolescent↗
PubMed1987

The interrelationship of beta endorphin, ACTH and cortisol in depressive illness: a controlled study.

Plasma cortisol, ACTH and beta endorphin were measured before and after dexamethasone in 8 severely depressed patients and 8 age- and sex-matched controls to examine the relationship of ACTH and endogenous opioids to cortisol in depression. Despite having significantly higher plasma levels of cortisol than the controls, the depressed patients did not have correspondingly elevated plasma levels of ACTH. Beta-endorphin levels were also similar in the two groups. All three hormones suppressed to some degree after dexamethasone, but cortisol suppressed less in patients than controls. Our findings suggest that in severe depressive illness abnormalities exist in the hypothalamic-pituitary-adrenal axis peripherally as well as centrally.

Adrenocorticotropic Hormone↗
PubMed1987

Nutritional management of infants and toddlers with chronic renal failure.

Normal renal function is an essential prerequisite for normal nutrition. Renal failure results in malnutrition and growth retardation, which are particularly marked when renal failure has its onset early in life. Conversely, the careful application of nutritional therapy can ameliorate the effects of renal failure and allow improved well being and growth and possibly retard the rate of progression of renal failure. Nutritional therapy includes the provision of an adequate energy intake, appropriate intakes of water, electrolytes, vitamins and minerals and regulation of protein and phosphorus intakes. In this paper the theoretical considerations underlying these objectives are reviewed and practical ways of achieving them with least disruption to the child and his family suggested.

Child Nutritional Physiological Phenomena↗
PubMed1985

2H, 3,4He(p

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Journal Article↗