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Biomedical subjects

K Kruse

Publications and source records attributed to K Kruse.

At least 127 records · Page 7Linked to original sources
PubMed1983

[Hydroxyproline in morning urine. A reliable parameter for bone turnover in childhood].

OH-P/Cr was measured in morning fasting urine specimens of 300 healthy subjects and of children with disorders of calcium metabolism receiving no diet. In healthy children the values were sex and age dependent reflecting the different height velocities. The OH-P excretion was not different in schoolchildren receiving a OH-P-poor diet for at least two days in comparison to subjects of the same age group with unrestricted diet. OH-P/Cr correlated well with serum alkaline phosphatase (AP) activity and decreased rapidly after a calcium load. OH-P/Cr and AP were elevated in patients with increased bone turnover (hyperparathyroidism and hypophosphatemic rickets). In contrast, the OH-P excretion was normal in children with permanent or transient isolated hyperphosphatasemia. In children with vitamin D deficiency rickets there was a further increase of OH-P/Cr in response to vitamin therapy, while the AP activity, which reflects osteoblastic activity, tended to fall. This indicates that the observed increment of the OH-P excretion in these children is due to a temporary resorption of osteoid caused by the increasing levels of vitamin D metabolites. It is concluded that the measurement of OH-P/Cr provides a useful tool of bone turnover in children, in that it makes complete 24 h-urine collections and a OH-P free diet unnecessary. In combination with other indices of calcium metabolism the determination of the OH-P ratio is considered to be a valuable measure for the diagnosis and follow-up of bone disorders.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1982

Response of kidney and bone to parathyroid hormone in children receiving anticonvulsant drugs.

The response of kidney and bone to parathyroid extract (PTE) was investigated in 8 epileptic children on long-term treatment with primidone in combination with phenytoin or other anticonvulsant drugs. The results indicate a dissociation between normal and cyclic AMP excretion and disturbed renal handling of phosphate which resembles type II pseudohypoparathyroidism suggesting an anticonvulsant drug related inhibition of cyclic AMP-induced phosphaturia. It is speculated that antiepileptic drugs may provoke renal conservation of phosphate which may explain the relative low incidence of manifest rickets or osteomalacia in site of low 25-hydroxy-vitamin D levels in epileptic patients. A normal bone response of PTE indicates that antiepileptic treatment with phenobarbital and phenytoin does not affect PTH-stimulated bone resorption in the investigated patients.

Adolescent↗
PubMed1982

Renal threshold phosphate concentration (TmPO4/GFR).

The ratio of maximum rate of renal tubular reabsorption of phosphate to glomerular filtration rate (TmPO4/GFR) was determined in 546 schoolchildren, aged between 6 and 17.9 years, using the nomogram of Walton and Bijvoet.1 TmPO4/GFR correlated with chronological age in girls and boys and in each remained significantly higher than in adults. TmPO4/GFR in the children correlated neither with fasting serum immunoreactive calcitonin and parathyroid hormone levels nor with the urinary cyclic AMP excretion. The study showed a parallel decrease in TmPO4/GFR, excretion of total hydroxyproline and serum alkaline phosphatase activities after puberty, with a significant relationship of both these indices of bone turnover to TmPO4/GFR values. This indicates that the high renal phosphate threshold of children may be an important factor for bone mineralisation by providing high extracellular inorganic phosphate concentrations during normal growth.

Adolescent↗
PubMed1981

Deficient prolactin response to parathyroid hormone in hypocalcemic and normocalcemic pseudohypoparathyroidism.

The PRL response to the infusion of 8 U/kg BW parathyroid extract (PTE) was studied in three children with pseudohypoparathyroidism type I (PHP), three patients with idiopathic hypoparathyroidism, and eight epileptic children. PTE produced a clear-but increase of serum PRL in the epileptics and patients with idiopathic hypoparathyroidism, but not in the children with PHP. Prolonged PTE administration (six doses of 4 U/kg BW over 48 h) was also without effect on the low serum PRL levels in the three patients with PHP. These patients exhibited an isolated diminished PRL reserve to other potent PRL stimuli in the presence of intact function of the remainder of the anterior pituitary. The data suggest a pituitary receptor defect in patients with PHP in addition to disturbed renal and bone responses. One patient with normocalcemic PHP, seeming to be in the early stage of the disease, demonstrated the same distinct PRL deficiency as the other two patients with manifest PHP. This suggests that the pituitary receptor defect may be an early sign and marker of PHP.

Adolescent↗
PubMed1981

Inhibitory effect of calcium on serum prolactin.

The effect of calcium (Ca) infusions on serum prolactin (Prl) was studied in normal controls and children with disorders of Ca metabolism: Three patients with secondary hyperparathyroidism (vitamin D deficiency rickets), 2 children with idiopathic hypoparathyroidism, 13 epileptic patients with anticonvulsant drug induced inhibition of calcitonin (CT) secretion and 1 patient with vitamin D resistant rickets with normal CP and low PTH secretion. Ca induced a significant decline of serum Prl in most subjects which could not be explained by the associated increase of CT or decrease of iPTH. The important role of Ca for the in vitro secretion of dopamine has been established for a long time. It is speculated that the inhibitory effect of Ca infusion or serum Prl may be due to dopamine release from nerve tracts in the hypothalamus.

Adolescent↗
PubMed1980

Parathyroid function and serum calcitonin in children receiving anticonvulsant drugs.

Serum calcitonin (CT) levels and other aspects of calcium metabolism were investigated in 40 epileptic children receiving long-term treatment with phenytoin and/or other anticonvulsant drugs, and in 38 age-matched controls. In the patients CT levels were significantly lower. Immunoreactive parathyroid hormone (iPTH) was significantly elevated exceeding the upper limit of controls in 11 patients. We also observed a highly significant correlation between iPTH and urinary cyclic AMP (cAMP) excretion but a lack of such a correlation with the renal handling of phosphate; this indicates to us a dissociation between cAMP production and phosphaturia. A significant correlation between iPTH levels and urinary hydroxyproline excretion points to a normal action of PTH on bone in the patients. The low CT levels are not due to hypocalcemia and may be directly attributed to the effects of anticonvulsant drugs. As the primary effect of CT is a direct inhibition of PTH induced calcium loss from bone, the drug-related low CT levels in association with secondary hyperparathyroidism possibly is an additional factor in anticonvulsant bone disease.

Adolescent↗
PubMed1980

Quantitative measurements of the urinary excretion of creatinine, uric acid, hypoxanthine and xanthine, uracil, cyclic AMP, and cyclic GMP in healthy newborn infants.

Serum creatinine, uric acid, and hypoxanthine and xanthine concentrations were determined in 17 mother-infant pairs at the time of delivery. Creatinine and uric acid levels were nearly similar, but hypoxanthine and xanthine were more than twice as high in the blood of the infants than in the blood of their mothers. In the same newborns the urinary excretion of creatinine, uric acid, hypoxanthine and xanthine, uracil, cAMP, and cGMP was measured on the first and fourth day of life. Creatinine, uracil, and cAMP increased, hypoxanthine and xanthine, and cGMP decreased, whereas the output of uric acid was nearly the same on both days. Correlations of the excreted substances to each other were calculated.

Cesarean Section↗
PubMed1979

Hypercalciuria in idiopathic Fanconi syndrome.

A 9 year old girl with idiopathic Fanconi syndrome and hypercalciuria is described. In order to determine whether the increased calcium excretion was directly or indirectly due to the disturbed phosphate metabolism, the behavior of the calcium excretion during therapy, the serum levels of 1,25-dihydroxyvitamin D and parathyroid hormone, and the effect of parathyroid hormone on the renal tubules were investigated. Normal serum 1,25-dihydroxyvitamin D and parathyroid hormone levels, lack of a correlation between the serum phosphate concentration and the degree of hypercalciuria, as well as unsuccessful therapy of the hypercalciuria with oral phosphate indicate that the increased calcium excretion cannot be explained by impaired renal phosphate reabsorption. The hypercalciuria in the patient was therefore regarded as being due to a primary decrease of tubular calcium reabsorption.

Calcium↗
PubMed1979

[Idiopathic hypercalciuria due to primary decrease in the renal tubular reabsorption of calcium. Hypercalciuria type 2 according to Bordier (author's transl)].

A persistent hypercalciuria and normal serum levels of calcium were measured in a 5-year-old boy suffering from recurrent macro- and microhaematuria and bilateral nephrolithiasis (stone analysis was positive for calcium-oxalate). No growth retardation or any other relevant clinical parameters concerning hypercalciuria e.g. vitamin D-intoxication or renal tubular acidosis could be observed. A slight secondary hyperparathyroidism and increased calcium excretion during fasting or calcium depleted diet indicates a primary failure of calcium reabsorption as previously described by Bordier (hypercalciuria type 2). Treatment with a combination of hydrochlorothiazide (Esidrix) and sodium chloride depleted diet resulted in a long-lasting normalization of calcium excretion and thus disappearance of symptoms in the child.

Calcium↗
PubMed1977

Serum alkaline phosphatase isoenzymes in epileptic children receving anticonvulsant drugs.

In 40 epileptic children on long-term anticonvulsant treatment, serum alkaline phosphatase (AP) isoenzymes were separated semiquantitatively using a combination of L-phenylalanine inhibition and heat inactivation. Though mean total serum AP activity was significantly increased compared to age matched controls, only 4 individual values exceeded the upper limit (mean + 2SD) of the reference sample. In epileptics the mean activity of the heat-sensitive non L-phenylalanine sensitive AP fraction (non-LPSAP) was significantly increased (P less than 0.01) and the mean Q-value (i.e. percentage ratio of heat-stable non-LPSAP/non-LPSAP) was significantly decreased (P less than 0.05), thus indicating an enhancement of the bone isoenzymes during anticonvulsant treatment. In 4 patients the isoenzyme pattern was abnormal although total serum AP activity was normal and in 3 of them the deviation indicated enhanced bone isoenzyme. The data provide evidence that in anticonvulsant treated children the bone isoenzyme, rather than hepatobiliary isoenzyme fraction, may be increased even when total serum AP activity is normal. Thus, semiquantitative separation of serum AP isoenzymes may be a helpful guide as to whether or not an eplieptic child should be given vitamin D.

Adolescent↗
PubMed1977

Serum alkaline phosphatase isoenzymes in childhood.

Using a combination of L-phenylalanine inhibition and heat inactivation, the serum alkaline phosphatase (AP) in 2 to 13 year old children without evidence of hepatobiliary, osseous, or intestinal disease was separated in three fractions; i.e. L-phenylalanine sensitive AP (LPSAP), heat-stable non-L-phenylalanine sensitive AP (heat-stable non-LPSAP) and heat sensitive non-L-phenylalanine sensitive AP (heat-sensitive non-LPSAP). The activities of total AP and the different fractions were measured using optimized test conditions. LPSAP, (mainly intestinal AP), accounts for approximately 12% of the total serum AP activity, heat-stable non-LPSAP (mainly hepatobiliary AP) for approximately 9%, and heat-sensitive non-LPSAP (mainly bone AP) for approximately 77%. To give a better differentiation between bone and liver AP, the percentage ratios of heat-stable non-LPSAP/non-LPSAP (Q value), and heat-stable non-LPSAP/total AP, were determined. Both quotients showed a significant negative correlation with total AP, which has to be taken into account in the interpretation of the results of isoenzyme determinations of serum AP activity. The above semiquantitative separation of AP isoenzymes can be readily done in a routine clinical laboratory.

Adolescent↗