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Biomedical subjects

K W Kastrup

Publications and source records attributed to K W Kastrup.

50 records · Page 3Linked to original sources
PubMed1978

Somatomedin in newborns and the relationship to human chorionic somatotropin and fetal growth.

The significance of somatomedin A (SM) and human chorionic somatomammotropin (HCS) in fetal growth was examined. SM, determined by chick embryo assay, was studied during the last trimester of pregnancy, in maternal serum and cord blood at term and in a group of normal newborns in the first week of life. Furthermore a group newborns of diabetic mothers was studied in the first or second day of life. HCS was measured in maternal serum and in cord blood at term. In amniotic fluid inhibitory factors caused a low SM activity as measured by the bioassay. The following results were obtained: 1) Normal values of SM in the last trimester with a decline at term were found in 3 normal primigravidae. 2) The mean levels of SM in 22 mothers and their offspring were decreased. The difference between the two values was significant, but a positive correlation was found between the maternally related pairs of SM values. Moreover, a positive correlation was found between maternal SM, birth weight and length. HCS was not correlated to above-mentioned parameters, but there was positive correlation between placental weight and birth weight. 3) In 6 newborns during the first 5 days SM rose from very low values to normal values found in infants in their first year. 4) The mean value of SM in ten newborns of diabetic mothers was not significantly different from the mean value of control group. The results do not exclude the possibility of a transplacental transport of SM and the positive correlation between SM levels and birth weight found in this investigation supports the concept that SM plays an important role in fetal growth.

Amniotic Fluid↗
PubMed1975

Case report: plasma adrenalin in a child with ketotic hypoglycemia and calcifications of the suprarenal glands.

Urinary excretion of adrenalin has been reported to be reduced during insulin-induced hypoglycemia in a significant proportion of children having ketotic hypoglycemia. By employing a sensitive double-isotope derivative technique, plasma adrenalin and plasma noradrenalin were determined in a boy 6 years 9 months old who had had ketotic hypoglycemia with intermittent hypoglycemic symptoms from the age of 10 months. Bilateral calcifications of the suprarenal glands were present. The adrenocortical function was normal. The plasma adrenalin response to hypoglycemia were practically absent, being only 4% of the value obtained in healthy children. The results were related to previous findings of a low plasma adrenalin response in patients with ketotic hypoglycemia without adrenal calcifications and support the assumption that ketotic hypoglycemia is associated with hypoadrenalinemia.

Adrenal Gland Diseases↗
PubMed1975

Increased immunoreactive plasma and urinary growth hormone in growth retardation with defective generation of somatomedin a (Laron's Syndrome).

In a boy 4 years old with clinical hypopituitary dwarfism, high plasma and urinary levels of immunoreactive growth hormone were found. Somatomedin A levels in serum were low and failed to respond after short-term treatment with human growth hormone. The parents were first cousins. In the arginine and insulin tolerance tests the initially high immunoreactive growth hormone levels were later followed by a decrease to high normal values. Insulinopenic response was present during the arginine and glucose tolerance tests. As a growth hormone molecule defect is not found in these patients and no growth or other metabolic response to exogenous HGH can be demonstrated, it is concluded that a defective somatomedin generation may be present, probably in conjunction with a generalized receptor defect and deficient feedback system with abnormal release of HGH. The lack of somatomedin A is responsible for the severe growth retardation and the disturbance in carbohydrate metabolism is probably caused by sustained high growth hormone levels.

Carbohydrate Metabolism, Inborn Errors↗
PubMed1974

Long-term infusion of growth hormone release inhibiting hormone in acromegaly: effects on pituitary and pancreatic hormones.

Growth hormone release inhibiting hormone (GH-RIH) was infused at a rate of 1.3 mug/min for 28 hours into four patients with acromegaly, two of whom also had clinical diabetes mellitus. Growth hormone and glucagon were suppressed throughout the infusion though delayed secretion of insulin occurred in association with both meals and an oral glucose load. Glucose tolerance was improved in one diabetic patient who was taking chlorpropamide while the other required much less insulin than usual. Secretion of endogenous thyroid-stimulating hormone was lowered in one euthyroid patient on carbimazole. Luteinizing hormone, follicle-stimulating hormone, ACTH, and prolactin were not affected. Serum somatomedin levels were reduced in one patient. There was a rapid rebound of all the suppressed hormones when the infusions stopped. Longer-acting analogues of GH-RIH will be needed before long-term therapy of acromegaly or diabetes mellitus becomes possible, but such preparations should be available soon for clinical trial.

Acromegaly↗
PubMedDate not supplied

Final height and craniofacial development after surgical resection of craniopharyngioma.

Seventeen patients (twelve males and five females) with craniopharyngioma were studied by retrospective review (stature, bone age, and hormone therapy) and by follow-up assessment in all seventeen survivors (stature and craniofacial development). Roentgencephalometric films in the lateral and frontal projections were analyzed. Individual and mean facial diagrams were produced based on 221 reference points in the individual patients and compared to normative data. The posterior cranial base was significantly reduced in length and the cranial base angle was significantly increased. In the facial regions great variations in size and prognathy of the jaws were recorded; on average the patients' maxilla and especially the mandible were short and retrognathic in relation to the anterior cranial base when compared to average adults. Average size and shape of the calvaria, cranial base, and facial regions in the adult male craniopharyngioma group corresponded closely to the average male at the stage of maximum growth in body height, i.e., around 14 years of age. It was concluded that size and morphology of the sphenoid and basioccipital bones were severely affected, possibly as a result of the interfering growth of a craniopharyngioma in childhood. The retrusion of the facial regions might be present as a result of the flattening of the posterior cranial base, but the relatively short and retruded mandible could also be caused by growth hormone deficiency before diagnosis/operation and in periods of sub-optimal therapy. The close resemblance of craniofacial morphology between adult males with craniopharyngioma and normal boys at the time of peak height velocity might reflect the fact that imitation of the natural, optimal balance between growth hormone and sex steroid in puberty is difficult to obtain in therapy.

Adolescent↗