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Biomedical subjects

Z Laron

Publications and source records attributed to Z Laron.

At least 145 records · Page 8Linked to original sources
PubMed1991

Risk factors for development of diabetic nephropathy and retinopathy in Jewish IDDM patients.

Risk factors associated with diabetic microvascular complications, with special reference to ethnic origin, were looked for in 231 young Jewish insulin-dependent diabetes mellitus (IDDM) patients with duration of diabetes greater than or equal to 10 yr. Median age at diagnosis of diabetes was 9.2 yr (range 0.04-26.2 yr), and median duration of the disease was 15.3 yr (range 10.0-37.2 yr). Sixty-three percent of the patients were Ashkenazi Jews, and 37% were non-Ashkenazi Jews. HbA1 was evaluated every 3 mo in the last 10 yr of follow-up, and albumin excretion rate was tested in three 24-h urine collections. Direct and indirect ophthalmoscopy was performed every year since diagnosis of diabetes, and if retinal pathology was suspected, color photographs were taken. Microalbuminuria was detected in 31% and macroalbuminuria in 7% of the patients. Nonproliferative and proliferative retinopathy was found in 44 and 12% of the patients, respectively. On logistic regression analysis, two variables were significantly and independently associated with diabetic nephropathy--non-Ashkenazi origin and mean HbA1 values over the first 5 of 10 yr of follow-up. Variables significantly and independently related to diabetic retinopathy were non-Ashkenazi origin, mean HbA1 values over the last 10 yr of follow-up, and duration of diabetes. Because non-Ashkenazi Jews in Israel are of lower socioeconomic status than Ashkenazi Jews, we stratified our patients according to their socioeconomic parameters, median HbA1 values, and duration of diabetes. Non-Ashkenazi patients were at a higher risk to develop complications in all strata.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Congenital hereditary hypothyroidism--prenatal diagnosis and treatment.

Intrauterine diagnosis of congenital hypothyroidism was established on the basis of TSH concentration in amniotic fluid in the 22nd week of gestation for the offspring of a couple both known to have an iodide organification defect. Prenatal treatment consisted of intramniotic injections of 500 mcg Na-1-thyroxine, which was administered from the first amniocentesis until one week before delivery. Following delivery, the diagnosis was confirmed by the elevated level of TSH, 60.5 uU/ml, and a gradual decrease of fT4 to 0.8 ng/ml. Regular substitution therapy was commenced on the third day of life. The normal shape and location of the thyroid gland was demonstrated by Technetium scintiscan. At 18 months the infant revealed no significant deviation from normalcy in growth or mental capacity. This experience indicates that testing of amniotic fluid for TSH in the 22nd week of gestation can be diagnostic for congenital primary hypothyroidism. Furthermore, it is suggested that the treatment approach described is warranted in all cases in which there is a high risk of congenital primary hypothyroidism.

Amniotic Fluid↗
PubMed1990

Immunoreactive beta-endorphin, cortisol, and growth hormone plasma levels in obsessive-compulsive disorder.

Basal morning plasma levels of immunoreactive-beta-endorphin (ir-beta-EP), cortisol, and growth hormone (GH) were assessed in 13 obsessive-compulsive disorder (OCD) patients in comparison to 20 healthy controls. All subjects were drug free for at least 1 year. The mean plasma level of ir-beta-EP was significantly lower (36%) in the OCD patients when compared with the control subjects. The decrease in ir-beta-EP was not accompanied by alteration in cortisol and GH plasma levels.

Adolescent↗
PubMed1990

Pubertal development, growth and final height in girls with sexual precocity after therapy with the GnRH analogue D-TRP-6-LHRH. A report on 15 girls, followed after cessation of gonadotrophin suppressive therapy.

Since 1980 15 girls with sexual precocity who were treated with the superactive GnRH-analogue D-TRP-6-LHRH for 1-5 2/12 years were followed for 1 to 5 6/12 years after discontinuation of therapy. Reactivation of puberty became noticeable 2-4 months and growth velocity increased 4-10 months after treatment was stopped. Menarche (or re-mensis) appeared after 3-9 months in 12/15 girls and after 2 6/12 years in 1. At termination of therapy the predicted final height had improved in 6/8 patients. In the 8/15 patients who had reached their final height at the time of study, the achieved final height was practically equal to the post-treatment prediction in 3/8, above it in 4/8 and below it (but equal to the pretreatment prediction) in 1 patients only who was insufficiently treated. It was found that in patients who had started treatment at an earlier bone age, the benefit as concerned final height was greater and was better evaluated by taking into consideration their genetic growth potential.

Body Height↗
PubMed1990

Elimination characteristics of intravenously administered rIGF-I in Laron-type dwarfs.

The distribution and elimination characteristics (Ke alpha, Ke beta, t1/2) of an intravenous bolus of biosynthetic IGF-I administered to 10 patients with Laron-type dwarfism (LTD, 3 children and 7 adults) and 6 healthy volunteers (3 children and 3 adults) are reported. The mean (+/- SD) endogenous level of IGF-I in the LTD patients was 5.24 +/- 2.77 nM/l and in the controls 27.2 +/- 9.4 nM/l. In the LTD patients the mean elimination constant (Ke beta) was 0.004 +/- 0.001 min-1 and t1/2 = 2.6 +/- 0.7 h, whereas in the controls, Ke beta was 0.003 +/- 0.009 min-1 and the t1/2 = 4.4 +/- 0.5 h (p less than 0.05). The more rapid elimination of injected IGF-I in the LTD patients is assumed to be due to the absence of the GH-dependent 150 kDa IGF-I binding protein.

Adolescent↗
PubMed1990

Effect of oral clonidine, insulin-induced hypoglycemia and exercise on plasma GHRH levels in short-stature children.

Human growth hormone release is affected by a variety of pharmacological and physiological stimuli. We have studied the effect of oral clonidine, insulin hypoglycemia, and exercise on plasma hGH and GHRH levels in 31 healthy short-stature children. Thirteen underwent an oral clonidine test (0.15 mg/m2), 12 an iv. insulin test (0.1 U/kg), and 6 performed exercise (running for 10 min in a defined route). GHRH-1-44 was extracted from plasma on silica columns and determined by RIA. Although all three stimuli induced a marked increase in plasma hGH levels, only clonidine induced a significant increase in plasma GHRH levels. Maximal increment in GHRH during clonidine was 6.82 +/- 1.05 pmol/l (mean +/- SEM) as compared with 0.51 +/- 0.28 and 0.53 +/- 0.62 during hypoglycemia and exercise (p less than 0.0005 and p less than 0.005), respectively. An additional 24 subjects received TRH 0.2 mg/kg iv: 8 TRH alone, 8 TRH and insulin, and 8 TRH and clonidine. Only insulin potentiated the TRH-induced TSH response with a peak of 22.0 +/- 3.2 vs 16.0 +/- 0.8 and 15.3 +/- 1.5 mU/l (p less than 0.025) for TRH alone and TRH and clonidine, respectively. It is suggested that clonidine stimulates hGH secretion mainly through an enhancement of GHRH release, whereas stress stimuli such as hypoglycemia and exercise achieve hGH release by a different mechanism, possibly inhibition of somatostatin.

Administration, Oral↗
PubMed1990

Intravenous administration of recombinant IGF-I lowers serum GHRH and TSH.

Recombinant IGF-I was administered as an iv bolus of 75 micrograms/kg to 10 patients with Laron type dwarfism (3 children aged 9, 11 and 12 years and 7 adults aged 30.6 +/- 3.5 years) and to 8 healthy subjects (mean age 19.9 +/- 12.1 years) and determinations of IGF-I, GHRH, hGH, TSH, and glucose were made before and at 2, 5, 15, 30, 60, 90, and 120 min. The following effects were observed: a. an immediate, marked and sustained drop in blood glucose (p less than 0.001), more prolonged in the patients; b. in both groups, a dramatic rise in plasma hGH (p less than 0.01) which peaked at 60-90 min; in the patients this occurred after an initial immediate fall in plasma hGH (p less than 0.01); c. a progressive decrease of plasma GHRH and TSH (p less than 0.05, 0.02) in both patients and healthy controls. An hypothesis is put forward that acute and time-limited release of somatostatin by IGF-I is the main cause of the hormonal changes registered. As the IGF-I bolus also suppressed circulating insulin levels, the hypoglycemia is considered to be a direct effect of IGF-I.

Adult↗
PubMed1989

Persistently low immunoreactive and normally bioactive plasma LH during male puberty.

Low basal and LRH-stimulated (50 mcg/m2 i.v.) levels of plasma immunoreactive (IR) LH were repeatedly found in 8 boys aged 13 to 16 years who had been referred because of delayed onset of puberty (basal IR-LH 0.19 +/- 0.1 and peak 0.48 +/- 0.2 vs. 0.24 +/- 0.09 and 1.71 +/- 0.9 mIU/ml in matched normal controls, respectively). Upon termination of puberty (no more than 3.5 years after referral) IR-LH levels were still low in all 8. Using a rat Leydig cell bioassay system with LER-907 (NPA) as standard, LH bioactivity in these patients was compared with that in 8 matched controls (basal LH was 0.32 +/- 0.33 and 0.11 +/- 0.07, and peak levels 0.8 +/- 0.47 and 1.22 +/- 0.44 mIU/ml respectively). The ratio of basal LH bioactivity to IR-LH was higher in the patients (1.24 +/- 0.95) than in controls (0.47 +/- 0.26, P less than .05) as was that of peak bioactivity (1.89 +/- 1.2 vs. 0.83 +/- 0.35, P less than .05). In the three patients tested during sleep IR-LH levels showed no significant change. Basal plasma testosterone levels were appropriate for pubertal stage (400 +/- 80 ng/dl) and in the four patients tested following prolonged LRH stimulation (500 mcg i.v. over 3 hours) increased to 530 +/- 60 ng/dl. It is concluded that in some boys there may be consistently low plasma levels of IR-LH in association with normal LH bioactivity.

Adolescent↗
PubMed1989

Characterization of the human growth hormone receptor gene and demonstration of a partial gene deletion in two patients with Laron-type dwarfism.

Laron-type dwarfism is an autosomal recessive genetic disorder that is characterized by high levels of growth hormone and low levels of insulin-like growth factor I in the circulation. Several lines of evidence suggest that this disease is caused by a defect in the growth hormone receptor. In order to analyze the receptor gene in patients with Laron-type dwarfism and with other growth disorders, we have first determined the gene structure in normal individuals. There are nine exons that encode the receptor and several additional exons in the 5' untranslated region. The coding exons span at least 87 kilobase pairs of chromosome 5. Characterization of the growth hormone receptor gene from nine patients with Laron-type dwarfism shows that two individuals have a deletion of a large portion of the extracellular, hormone binding domain of the receptor gene. Interestingly, this deletion includes nonconsecutive exons, suggesting that an unusual rearrangement may have occurred. Thus, we provide direct evidence that Laron-type dwarfism can result from a defect in the structural gene for the growth hormone receptor.

Adult↗
PubMed1989

Serum growth hormone binding protein activity in healthy neonates, children and young adults: correlation with age, height and weight.

Serum growth hormone binding protein (GHBP) activity was estimated in healthy neonates (n = 6), children and adolescents (n = 97) and young adults (n = 19). GHBP activity was measured by incubating 125I-hGH (human growth hormone) (approximately 25,000 c.p.m.) with serum (100 microliters) in the presence and in the absence of excess unlabelled hGH, followed by separation of specifically bound 125I-hGHBP complexes from free 125I-hGH by gel filtration on Ultrogel AcA44 minicolumns. The results are expressed as the percentage specific binding relative to an adult reference serum (%RSB), after correction for endogenous hGH of the unknown serum. The between-assay coefficients of variation for two sera of %RSB activity of 51.2 and 115.4% were 6.0 and 7.0% respectively. In neonates, low values of serum GHBP were found (%RSB = 27.1 +/- 5.0 SEM) followed by a major rise during the first 6 years of life to a mean value (%RSB = 68.3 +/- 4.1 SEM) which more than doubled that of neonates. Thereafter, values rose progressively throughout childhood and puberty to reach maximum values in young adults (%RSB = 95.0 +/- 3.1 SEM). A novel observation was that serum GHBP activity correlated significantly with height standard deviation score (SDS) (males: r = 0.77, P less than 0.001; females: r = 0.56, P = 0.01) and weight SDS (P less than 0.001) for both sexes before puberty. During puberty GHBP correlated only with weight SDS in males (r = 0.60, P less than 0.01). In all age groups studied, no correlation could be found between serum GHBP and height velocity.

Adolescent↗
PubMed1989

Serum GH binding protein activities identifies the heterozygous carriers for Laron type dwarfism.

Measurement of GH-binding protein activity and IGF-I was carried out in the sera of 13 patients with Laron type dwarfism, a syndrome caused by a lack of GH receptors which leads to impairment of IGF-I generation, and those of 16 of their close relatives. GH binding protein activity was measured by incubating 125I-hGH with 100 microliters serum in the presence and in the absence of excess unlabelled hGH, followed by separation of specifically bound 125I-hGH binding protein complexes from free 125I-hGH by gel filtration. The results are expressed as percent specific binding relative to an adult reference serum. IGF-I was determined by RIA after acid extraction on octadecylsilane silica columns. All Laron type dwarfism patients had no, or only negligible GH binding protein activity, which supports the evidence that serum GH binding protein corresponds to the extracellular domain of the membranal GH receptor. Eight of the 16 relatives had serum GH binding protein activity more than 2 SD below the mean for age, a finding considered to denote heterozygocity for their molecular defect disease. The significant correlation (p less than 0.001) between serum GH binding protein activity and IGF-I levels supports this conclusion. The ability to define heterozygotes of Laron type dwarfism will be helpful in genetic counselling.

Adolescent↗
PubMed1989

Growth hormone increases plasma levels of insulin-like growth factor (IGF-I) in a teleost, the gilthead seabream (sparus aurata).

A heterologous radioimmunoassay (RIA) was applied for the determination of immunoreactive (IR)--insulin-like growth factor (IGF-I) in a teleost, the gilthead seabream (Sparus aurata). Serial dilutions of the fish plasma gave a linear curve when added to constant amounts of 125I-labelled human IGF-I(53-70) and antiserum prepared against this fragment. The RIA was used to study the effect of GH on plasma levels of IR-IGF-I in S. aurata. A single injection of human recombinant GH (1 micrograms/g) resulted in a significant increase in IR-IGF-I at 29, 48 and 72 h, when compared with saline-injected fish. This novel observation suggests that in fish, as in mammals, circulating IGF-I levels are modulated by GH.

Animals↗
PubMed1989

The use of computers in the control of diabetes in children and adolescents.

The actual and possible applications of computers in diabetes management are manifold. There are programs for medical information, storage and analysis, pertinent literature search, artificial intelligence, algorithms assisting the patient to adjust the insulin dose and education programs. One very useful microcomputer program DIACON is described in detail. This program is both an educational and therapeutic tool in that it increases both knowledge and long term compliance; it stores, displays and analyses the large amount of self blood glucose monitoring (SBGM) data, HbA1, C-peptide, nutritional data, sport activities and insulin dose. It is concluded that the use of computers in the management of diabetes has become a necessity, but despite the programs of artificial intelligence and algorithms, it is critical that the physician retains the ultimate responsibility for diagnostic and therapeutic strategies.

Adolescent↗