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At least 19 recordsLinked to original sources
PubMed1977

Transitory growth hormone deficiency successfully treated with human growth hormone.

This study was carried out in order to determine whether children with a transitory type of growth hormone deficiency showed an accelerated growth in height velocity on treatment with human growth hormone (HGH). Following careful diagnostic routine procedures 13 extremely short children were diagnosed as having isolated growth hormone deficiency, and were successfully treated with HGH. A true isolated growth hormone deficiency was present in 5 of the children, whereas 8 showed a normal increase in serum growth hormone on repeated growth hormone stimulation tests after their development of puberty and termination of HGH treatment. Three boys with bone ages of 5.5, 8.0 and 9.5 years showed an undisputable effect following HGH administration. They showed an initial growth at the start of treatment, and a second growth spurt during development of puberty. Two of the boys reached final statures of 14 cm taller than the predicted heights. The other patients, including the children with true isolated growth hormone deficiency showed an initial spurt of growth at the start of the HGH treatment immediately followed by a pubertal growth spurt. The mean accleration of height velocity for the children with true isolated growth hormone deficiency was from 3.4 cm during the year before treatment to 7.0 cm during the first year on treatment, as compared to 2.8 and 7.4 cm, respectively, for the children with transitory growth hormone deficiency. A girl with severe anorexia nervosa who had a transitory growth hormone deficiency, showed an accelerated high velocity from 1.1 cm to 7.6 cm during the first year following treatment with HGH.

Adolescent↗
PubMed1978

Re-evaluation of exercise as a screening test for ruling out human growth hormone deficiency.

Human growth hormone (HGH) response to exercise was studied in 27 normal children and 152 children with a chief complaint of short stature and in 9 patients with HGH deficiency. Of the 152 children 107 could be ruled out of HGH deficiency since HGH level increased to more than 5 ng/ml during exercise, and of the remaining 45 children of non-responders to exercise, 22 were ruled out of HGH deficiency since bone age to chronological age ratio was more than 0.9 and/or height increment for the past 3 years was more than 15 cm. Seventeen patients were hospitalized for further examinations, which resulted in finding normal HGH secretion in response to insulin-induced hypoglycemia, arginine infusion and/or propranolol-glucagon test in 12 children and also in finding no HGH deficiency in children higher than -2.0 S.D., but 5 HGH-deficient children in those lower than -2.0 S.D. Exercise can be used as a screening test for ruling out HGH deficiency when HGH secretion in response to exericse is evaluated by height, bone age and height increment of the patients.

Adolescent↗
PubMed1978

Collaborative study of the effects of human growth hormone in growth hormone deficiency. V. Treatment with growth hormone administered once a week.

Twenty-two GH-deficient patients received 6 IU GH weekly for 6 months. They increased their growth rate from 1.0 +/- 0.2 to 2.9 +/- 0.3 (SE) cm/6 months (P less than 0.01). However, their rate of growth was significantly less (P less than 0.05) than the rate [4.1 +/- 0.5 (SE) cm/6 months] observed earlier when they had received 2 IU GH three times a week. Seven patients received weekly GH for 18 months and they also grew significantly less (P less than 0.01) than when they had received GH divided over the week. These results suggest that once a week GH does not provide the most effective therapy for GH deficiency.

Drug Administration Schedule↗
PubMed1978

Glucagon response to arginine in growth hormone deficient children before and after treatment with growth hormone and in children with non-endocrine short stature.

In order to assess the role of growth hormone in the modulation of alpha cell function, the plasma pancreatic glucagon response to intravenous arginine (0.5 g/kg) was determined in thirty-two children with non-endocrine short stature and in eighteen growth hormone deficient children. 60 min after arginine infusion, the growth hormone deficient children had significantly higher (P less than 0.05) plasma glucagon values than the children with non-endocrine short stature. Following short-term growth hormone therapy (2 iu qd or bid for 5 days) in eleven of these growth hormone deficient children, plasma pancreatic glucagon response to arginine was diminished, and there was a significantly (P less than 0.02) more rapid return to basal values than in the untreated group. The same trends persisted after long-term growth hormone therapy (2 iu three times per week for 12-30 months) in ten children but were not statistically significant. We conclude that growth hormone may play a role in modulating plasma pancreatic glucagon response. The persistent glucagon response to arginine noted in growth hormone deficient children might reflect a greater gluconeogenic stress imposed upon these children during fasting or decreased catabolism of glucagon in the growth hormone deficient state.

Adolescent↗
PubMed1977

Collaborative study of the effects of human growth hormone in growth hormone deficiency: IV. Treatment with low doses of human growth hormone based on body weight.

In order to define the minimum effective dose of human growth hormone (GH) in growth hormone deficient children, GH was administered to three groups of patients based on their body weight. Five children who received 0.01 International Unit (IU) GH/kg three times a week (tiw) failed to respond with a significant increase in their rate of growth. A dose of 0.03 IU GH/kg tiw increased the growth rate of 12 patients from 3.5 +/- 0.4 (SE) cm/year to 6.4 +/- 0.4 (SE) cm/year (P less than 0.001) during the first 12 months of therapy. Eight children (67%) larger than or equal to 6.0 cm/year. A similar increase growth rate from 3.6 +/- 0.4 (SE) cm/year to 7.3 +/- 0.4 (SE) cm/year (P less than 0.001) was observed over the first 12 months of therapy in 16 growth hormone deficient children who were given 0.06 IU GH/kg tiw. Thirteen children (81%) grew larger than or equal to 6.0 cm/year. During a second year of treatment, children receiving either 0.03 or 0.06 UI GH/kg tiw again showed a significant increase in their rate of growth. However, the response was significantly less than that observed during the first year of treatment. Comparison of these results with those available in the literature suggests that the most efficient, although not necessarily the optimal, initial dose of GH in children with growth hormone deficiency is 0.06 IU GH/kg administered three times a week.

Adolescent↗
PubMed1979

[Psychosomal dwarfism with reversible growth hormone deficiency (author's transl)].

The diagnosis of psychosocial dwarfism in a 9 year-old boy with severe growth retardation (-6 1/2 standard deviations) was deduced from the typical history. The bone age was severely retarded and in the first days after admission a deficiency of growth hormone and other pituitary hormones was established. The change in environment per se led to a spontaneous reversal of the growth hormone deficiency within a short time. A rapid catch up growth was observed over the subsequent 2 1/2 years, as well as a normalisation of the psychological retardation.

Age Determination by Skeleton↗
PubMed1979

Serum cholesterol and triglycerides in children with growth hormone deficiency.

To test the hypothesis that hyperlipidemia is characteristic of growth hormone deficiency in childhood, we have measured serum cholesterol and triglyceride concentrations in 24 euthyroid children with growth hormone deficiency. Although modest elevations of cholesterol and/or triglyceride above the 95th percentile for age, race, and sex were present in 46% of the children studied, the mean (+/- 1 SD) cholesterol of 173 +/- 36 mg/dl and the mean triglyceride of 80 +/- 42 mg/dl were not significantly different from published normal mean values. Administration of human growth hormone for 4 mo to 15 of these subjects did not alter these mean cholesterol and triglyceride values, but did result in a marked improvement in the growth rate. Some individuals (n = 6) with a subnormal growth response to therapy and/or a low serum thyroxine and high serum cholesterol were treated for an additional 4 mo with growth hormone and thyroid hormone together. There was a statistically significant decrement in serum cholesterol in this group. We conclude that modest hyperlipidemia does exist in some children with growth hormone deficiency. Subclinical hypothyroidism may play a role in the hypercholesterolemia of some children, as may growth hormone deficiency itself. Any association of growth hormone and lipid metabolism remains to be clarified.

Adolescent↗
PubMed1977

Effects of immunologically induced growth hormone deficiency on myelinogenesis in developing rat cerebrum.

Chronic deficiency of growth hormone was produced in rats by injecting highly specific antibodies against rat somatotropin during the first week of postnatal life. Antisera were prepared by immunizing adult rhesus monkeys with purified rat growth hormone. The rate of body and brain growth was significantly decreased when compared with controls injected with nonimmune serum, and 50-day-old animals showed a profound and apparently specific endocrine deficiency of pituitary growth hormone as measured by bioassay. Defective cerebral maturation was evidenced by a 70 to 80 percent decrease of myelin lipids, a 65 percent reduction of deoxyribonucleic acid, and a small but significant decline in ribonucleic acid. An abnormal accumulation of undifferentiated glia was seen in the subependymal zone in association with decreased amounts of stainable myelin in subcortical white matter. The data suggest that pituitary growth hormone and/or its secondarily induced trophic factor, somatomedin B, influences the maturation of neural cells by regulating the replication of glia and the subsequent differentiation of oligodendrocytes to form myelin.

Age Factors↗
PubMed1979

Long-term response to human growth hormone in 36 children with idiopathic growth hormone deficiency.

The results of long term treatment with human growth hormone (Crescormon, 12.4 IU/m2/week) in 36 patients with idiopathic growth hormone deficiency are given. Birth trauma--in particular assisted breech delivery (30%)--is the major aetiological cause. Twelve patients had isolated growth hormone deficiency (IGHD), 24 had multiple pituitary hormone deficiencies (MPHD) of which 19 were treated with additional thyroid hormones. The results were judged by the criteria of height velocity, total height gain and change of height prediction (TW2, age based). It is concluded that the growth hormone dose chosen in many cases is insufficient to maintain high growth rates after the first year of treatment, when "catch-up" no loner takes place. The tendency of patients supplemented with thyroid hormone to grow better--without additional bone-age advancement--calls for careful search for hypothyroidism and suggests the use of thyroxin in cases of doubt.

Body Height↗
PubMed1979

[Growth hormone deficiency during the course of histiocytoses. A report on a case of Hand-Schuller-Christian disease (author's transl)].

Hand-Schuller-Christian disease frequently products histiocytic localization in the part of the posterior hypothalamus which is responsible for diabetes insipidus. Retarded growth is also relatively frequent and has multiple etiologies. An isolated deficiency in growth hormone (GH) which may be due to localization of the disease in the anterior hypothalamus is much rarer. In the case reported the possibility of this localization was only suspected because of the presence of a hyperprolactinemia. Retarded growth was obviously present but it was difficult to relate this to a GH defian 7 ng/ml. Follow-up examinations did however provide definite proof of a hormonal deficiency. This confirms the notion of partial growth hormone deficiency and the difficulty of providing proof during the usual stimulation tests in some cases.

Adolescent↗
PubMed1977

Results of intermittent treatment of growth hormone deficiency with human grwoth hormone.

The growth in stature of two groups of growth hormone deficient children has been compared. The frist group received intermittent treatment with human Growth Hormone (hGH), 1 year on, 1 year off, subsequent years on; the second group received continous treatment. This latter group had a significantly better mean growth response. The reduction in treatment velocity in years subsequent to the first was not prevented by the year off treatment, the mean velocity of the intermittent group in their 3rd year being the same as that of the continous group in their second. We conclude that intermittent hGH therapy is of less values than continous treatment and should be avoided, at least pending further evidence.

Age Determination by Skeleton↗
PubMed1978

Growth hormone modulation of arginine-induced glucagon release: studies of isolated growth hormone deficiency and acromegaly.

Plasma glucagon and insulin responses to L-arginine were compared in normal controls and patients with isolated growth hormone deficiency and acromegaly. Patients with isolated growth hormone deficiency were characterized by high plasma glucagon response and low plasma insulin response, whereas acromegalic patients showed exaggerated plasma glucagon response and almost normal insulin response. These results suggest that growth hormone is probably required for optimum function of the islets, and since hyperglucagonaemia was observed in both growth hormone deficiency and acromegaly, metabolic disturbances stemming from the respective primary diseases may affect glucagon secretion.

Acromegaly↗
PubMed1975

A note on the bone age at which patients with true isolated growth hormone deficiency enter puberty.

Nineteen boys with true isolated growth hormone deficiency developed the first stages of puberty at an average bone age of 12.0"years" (Tanner Whitehouse Method 2, RUS score). The average chronological age was 15.0 years. Seven similar girls entered puberty at 10.9"years" in bone age and 13.7 years in chronological age. The means and ranges of bone age at beginning of puberty of these patients are very close to those of normal children.

Adolescent↗
PubMed1978

A follow-up study of vascular disease in growth-hormone-deficient dwarfs with diabetes.

Thirty-one growth-hormone-deficient dwarfs were re-examined after a period of 10 to 12 years. These subjects had initially shown glucose intolerance, insulinopenia and hyperlipidemia comparable to those of diabetic patients matched for age and sex, but vascular complications were not present in dwarfs. After 10 years glucose tolerance became progessively more abnormal in dwarfs than could be accounted for by expected deterioration with age, and hyperglycemia after mixed meals remained greater than in control subjects. Serum lipid and serum lipoprotein concentrations were abnormal in over one third of the dwarfs. Despite the metabolic similarity to the diabetic patients, clinical complications of diabetes were absent in dwarfs: retinopathy did not occur, and the prevalence of hypertension and arteriosclerosis was considerably lower in dwarfs than in the diabetic subjects in both study periods. The follow-up data support the hypothesis that growth hormone has at least a supportive role in the pathogenesis of vascular disease in the diabetic state.

Adult↗
PubMed1978

Insulin binding and insulin sensitivity in isolated growth hormone deficiency.

125I-insulin binding to monocytes was examined in five children and one adult with isolated growth hormone deficiency before and after three to 12 weeks of growth hormone treatment, and in eight controls. Before treatment, mean plasma glucose was 15 mg per deciliter below controls, and plasma insulin was reduced by 40 per cent. Insulin binding to monocytes was 70 per cent greater than controls (P less than 0.005). Insulin-mediated glucose uptake (determined in the adult patient) was 25 per cent greater than mean control levels. After treatment, plasma glucose rose to control levels, plasma insulin increased to 75 per cent above controls (P less than 0.01), and insulin binding fell to 50 per cent below controls (P less than 0.01). Insulin-mediated glucose uptake fell to 30 per cent below the mean control rate. Insulin binding increases in growth hormone deficiency and falls after treatment. These changes may contribute to alterations in insulin sensitivity accompanying altered growth hormone availability.

Adult↗
PubMed1978

Exercise tolerance test. Single-sample screening technique to rule out growth-hormone deficiency.

Parent-directed vigorous exercise was evaluated as a screening test for adequacy of pituitary growth-hormone release in 57 short-statured children. This method obviated the need for pharmacologic provocative testing in all but the four children with growth-hormone deficiency. In 92% of the euendocrine children, the immediate postexercise venous sample demonstrated an adequate growth-hormone level. Vigorous physical exercise after an 8- to 12- hour fast with a single postexercise serum growth-hormone sample is a reliable, safe, and cost-effective screening test for growth-hormone deficiency.

Adolescent↗
PubMed1977

Growth-hormone deficiency in congenital rubella.

Two boys with congenital rubella and concomitant growth-hormone deficiency responded to human-growth-hormone replacement and have already (over a period of 18 mo) achieved a significant increase in height. The association of these two diagnoses requires recognition so that treatable endocrine disorders, which are becoming recognized more often in congenital rubella, are always positively excluded when affected children with inexplicable short stature are seen.

Anthropometry↗