[Renal osteodystrophy - a multifactorial disorder].
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Biomedical subjects
Publications and source records attributed to K Ijaiya.
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Metoclopramide (MCP), a derivative of procainamide was compared with exercise, arginine, insulin and thyrotropin releasing hormone (TRH) as a prolactin (PRL) releaser in children. The peak response of plasma PRL after oral administration of MCP was greater than that after strenuous exercise and after i.v. administration of pharmacodynamic agents. Normal PRL and TSH responses were observed after TRH administration in all subjects. Variable PRL responses were seen after exercise and after i.v. administration of arginine and insulin, despite significant growth hormone (GH) release following the administration of these agents. MCP produced no increase in plasma TSH. Metoclopramide may be useful for dynamic testing of PRL release in children. It can be taken orally and is free of side-effects.
The growth hormone (GH) and prolactin (PRL) responses to metoclopramide (MCP) were compared to those with arginine and insulin-induced hypoglycaemia in eight children. While a significant rise in GH release after stimulation with arginine and insulin occurred in all subjects (P less than 0.05), no significant increase after MCP ingestion was observed. Metoclopramide, a dopamine antagonist, stimulated PRL release in all children, while arginine and insulin-induced hypoglycaemia stimulation tests showed variable PRL responses. A statistically significant increase in cortisol secretion 5 h following MCP was observed (trend test, Cox & Stuart, 1955) (P less than 0.05), but the plasma concentration at this time was still within the normal range. Metoclopramide stimulation is not a suitable test for growth hormone deficiency in children.
Basal prolactin concentrations in forty-eight children with acute or chronic renal disease have been compared with those in thirty-four healthy control subjects. Elevated basal prolactin levels and an abnormal prolactin response to intravenous thyrotropin-releasing hormone were found in children with chronic renal failure on maintenance intermittent haemodialysis. No significant change in plasma prolactin concentrations and osmolality was observed before and after haemodialysis, despite a fall in plasma creatinine concentrations. The elevated prolactin levels fell to normal in three patients after successful renal transplantation. It is suggested that the kidney has an important role to play in prolactin metabolism.
Plasma growth hormone (GH) concentrations after insulin and arginine stimulation were estimated in 11 dialyzed and 6 non-dialyzed children with chronic renal failure. Twenty healthy children served as controls. Plasma GH peak concentration and estimation of the total area under the plasma GH concentration-time curve by the trapezoidal rule were used to evaluate results. Elevated basal GH levels and an exaggerated response to the stimuli were seen in several of the patients. The causes of the abnormal GH secretion and the role of high GH levels in carbohydrate intolerance are discussed. No consistent pattern was seen in GH secretion during haemodialysis without glucose in the dialysate. In children undergoing haemodialysis with a fluid containing glucose, plasma GH fell considerably.
Eight children (aged between 8 1/2 and 15 1/2 years) with chronic renal failure receiving intermittent haemodialysis, and 2 children with renal transplants were studied. The response of TSH and prolactin (PRL), and basal T4 and T3 values was measured. Basal TSH was normal, and rose only slightly after TRH stimulation. Plasma T4 and T3 were below normal levels in 6 children. Mean basal PRL was raised and could not be stimulated by TRH. This study demonstrates the involvement of the hypothalamus and pituitary in chronic renal disease. The cause of the abnormal secretion of TSH and PRL in chronic renal failure is discussed in the light of clinical importance.
LH and FSH response to intravenous injection of GnRH was evaluated in a group of patients with chronic renal failure on intermittent haemodialysis and in two children with successful renal transplant. Basal plasma LH was elevated in children with chronic renal failure as compared to control, and significantly increased following GnRH injection in most of the children. Basal plasma FSH was higher than in the control group, and slightly increased after GnRH. These data suggest an abnormal response to GnRH in chronic renal failure and an involvement of hypothalamus and pituitary in chronic renal disease. The role of abnormal gonadotrophin secretion in growth retardation and pubertal delay of these children is still not well understood.
The DIDMOAD syndrome is a combination of diabetes mellitus, diabetes insipidus, optic atrophy and labyrinthine deafness. The inheritance is autosomalrecessive. Diagnostic and therapeutic possibilities are discussed on the basis of a further case of this pathogenetically not yet clarified disease pattern. Early detection of this syndrome in juvenile diabetics is important for long-term prognosis and genetic family advice.
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The case of a 9-year-old girl treated elsewhere for anemia due to iron deficit is described. The first diagnosis of Crohn's disease made by us and for which the girl received treatment had to be revised, because an intestinal tuberculosis was later accepted to be the correct diagnosis. The authors emphasize the importance of safe diagnostic distinctions between Crohn's disease and intestinal tuberculosis. Diagnostic and therapeutic procedures are discussed.
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Report on a girl aged 12 years and 2 months and a boy aged almost 14. The first always had normal T4- with always raised T3, belongs, therefore, to the entity T3-hyperthyreosis described by Hollander in 1968. The boy had clear clinical signs of hyperthyreosis, but was untreated for 14 months, because a nuclear medical institute had found T4 to be normal and did not investigate T3. One suspects that proper treatment would have been given, if T3 would have been examined early. Discussion of the entity: T3 hyperthyreosis and of the circumstances under which T3 may be found to be raised even in the absence of the disease.
Isolated Triiodothyronine (T3) hyperthyroidism in childhood is rate. The incidence among hyperthyroid children is about 10%. The authors present a case history of a 12 2/12 year old girl with T3-thyrotoxicosis. Cause, diagnosis and therapy are thoroughly discussed. The importance to estimating serum T3 concentration for establishing the diagnosis of T3 hyperthyroidism is emphasized.
The fetal alcohol syndrome was observed in four girls aged 1 2/12 to 9 2/12 years, two of whom were sisters. Three of the children are older than all others previously described as having this syndrome. The signs consist of a decrease of body length and weight beginning at birth, microcephalus, marked decrease of intelligence and narrowing of the palpebral fissure. Frequently congenital cardiac defects are found and sometimes anomalies of the genitalia and other malformations. Experience so far indicates a causal relationship between considerable alcohol abuse of mothers during pregnancy and intra-uterine fetal damage. The prognosis is poor; in severe cases of chronic alcoholism interruption of pregnancy should be seriously considered.
Report on 3 cases of primary lymphedema in childhood. Lymphangiography, introduced by Kinmonth into radiodiagnosis, is essential. Aplasia, hypoplasia and hyperplasia of the lymphatic system can thus be differentiated. Conservative treatment is discussed.
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