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Biomedical subjects

D Hartwell

Publications and source records attributed to D Hartwell.

24 records · Page 2Linked to original sources

Serum bone Gla-protein as a marker of bone growth in children and adolescents: correlation with age, height, serum insulin-like growth factor I, and serum testosterone.

Serum bone Gla-protein (BGP) was determined by RIA in 450 normal children (229 girls and 221 boys, aged 6-19 yr). Serum BGP concentrations changed in relation to age and sex with a pattern that resembles the height velocity curves for children. The increase in serum BGP occurred at the expected age of the growth spurt in both sexes, and the peak values occurred at the age of 12 yr in girls [mean, 49.2 +/- 5.6 (+/- SE) micrograms/L] and 14 yr in boys (64.0 +/- 6.3 micrograms/L). In the boys aged 10-14 yr and in the girls aged 9-12 yr, serum BGP correlated significantly with serum insulin-like growth factor I (IGF-I), serum testosterone, age and height. When the interrelationship was analyzed by means of partial correlation, with age held constant, serum BGP still correlated significantly with the other parameters, but when height was fixed there was only a correlation with serum IGF-I. In children with untreated central precocious puberty, the mean serum BGP concentration was significantly higher than in age-matched normal children [mean, 61.4 +/- 31.7 (+/- SD) vs. 29.0 +/- 10.3 micrograms/L; P less than 0.001]. Serum BGP values decreased significantly in these patients during 1 yr of treatment with a LHRH analog (buserelin) and cyproterone acetate. We conclude that serum BGP is a sensitive marker of bone growth in normal children and in children with increased growth velocity. Repeated measurements may provide useful information in the diagnosis and treatment of children with disturbances in bone turnover.

Adolescent↗

Comparisons between two receptor assays for 1,25-dihydroxyvitamin D.

We present a competitive protein binding assay (CPBA) for 1,25(OH)2D employing 1,25(OH)2D receptor from calf thymus, which was compared with a CPBA-employing receptor from rachitic chick intestine. The thymus receptor assay was more sensitive, specific and precise than the intestinal receptor assay. The thymus receptor assay measured both 1,25(OH)2D2 and 1,25(OH)2D3 with equal affinity, whereas 1,25(OH)2D2 was 1.1 times less potent than 1,25(OH)2D3 in the displacement from the chick intestinal receptor. Mean serum values of 1,25(OH)2D in normal subjects, post-menopausal women, pregnant women, and patients with chronic renal failure measured by the two assay systems did not differ. Furthermore, both assays showed that 1,25(OH)2D was unchanged in post-menopausal women after treatment with vitamin D2 or vitamin D3, 4000 IU/day for 8 weeks. We conclude that the high sensitivity of the thymus receptor and the equal affinity for the D2 and D3 analogue make the thymus receptor assay a reliable alternative to the chick intestinal receptor assay.

Adult↗

Is the effect of phototherapy in psoriasis partly due to an impact on vitamin D metabolism?

To elucidate the effect of phototherapy on vitamin D metabolism in psoriatics, the serum concentrations of the major vitamin D metabolites (25-hydroxy-vitamin D (25(OH)D), 1,25-dihydroxy-vitamin D (1,25(OH)2D), and 24,25-dihydroxy-vitamin D (24,25(OH)2D)) were studied in 10 patients with disseminated psoriasis, both before and after phototherapy. Some 3-4 weeks of Goeckerman therapy induced significantly increased serum levels of 25(OH)D (mean: 24.6 ng/ml versus 54.4 ng/ml; (p less than 0.001] and 24,25(OH)2D (mean: 2.01 ng/ml versus 3.49 ng/ml; (p less than 0.001)). After phototherapy the mean serum level of 1,25(OH)2D increased nearly to the level found in healthy controls (mean: 23.8 vs. 32.2 pg/ml). However, this increase was not significant. It is shown that conventional phototherapy does have an impact on vitamin D metabolism in psoriatics. Since previous investigations have indicated an abnormal vitamin D metabolism in patients with psoriasis, it is possible that the beneficial effect of phototherapy in this disease might be due partly to an impact on vitamin D metabolism.

Adult↗

Bone metabolism and bone status in osteoporotic patients.

We have studied bone turnover and bone status in 29 patients with hip fractures and compared them with normal subjects and patients with arthritis of the hip. Markers for bone formation, bone Gla protein, alkaline phosphatase and whole body retention of 99mTc-diphosphonate, and fasting urinary hydroxyproline, a marker for bone resorption, were all significantly higher in the hip fracture group than in the control group. The serum concentrations of 1,25-dihydroxyvitamin D were similar in the three groups, whereas the serum 25-hydroxyvitamin D concentration in the control group was higher than in the patient groups. The bone mineral content (BMC) measured in the distal forearm and the spine was lower than normal in the hip fracture group. We conclude that patients with hip fractures have an increased bone turnover with no signs of bimodality and low BMC values at all locations.

Aged↗

Effect of vitamin D2 and vitamin D3 on the serum concentrations of 1,25(OH)2D2, and 1,25(OH)2D3 in normal subjects.

Serum concentrations of vitamin D2 and vitamin D3 metabolites were measured in 19 normal subjects before and during treatment with either vitamin D2 or vitamin D3, 4000 IU per day for 8 weeks. Vitamin D2 treatment increased the serum concentration of 1,25(OH)2D2, but a corresponding decrease in 1,25(OH)2D3 resulted in an unchanged serum concentration of total 1,25(OH)2D. During treatment with vitamin D3, the serum concentration of 1,25(OH)2D metabolites was unchanged. We conclude that the production of 1,25(OH)2D is tightly regulated and that 1 alpha-hydroxylase does not discriminate between D2 and D3 metabolites in normal subjects.

Adult↗

Long-term bone loss in insulin-dependent diabetic patients with microvascular complications.

Insulin-dependent diabetic patients have an approximately 10% decreased bone mineral content (BMC) when they are studied a few years after clinical onset of diabetes. After that time, patients without diabetic microvascular complications have no, or only very little, further bone loss. The aim of the present study was to investigate if any substantial long-term bone loss occurs in diabetic patients with microvascular complications. We studied 19 insulin-dependent diabetic patients with neither physiologic nor pathologic conditions known to interfere with bone metabolism, other than diabetes. BMC was determined twice, with an interval of 11 years. At initial examination, no patient had diabetic microangiopathy, but at final examination 7 patients had developed diabetic microvascular complications while 12 patients had not. As compared with gender- and age-matched controls, both subgroups had significantly decreased BMC at the initial examination. During the study period, the patients with complications showed further bone loss, whereas the subgroup without complications had unchanged decreased BMC. At final examination, BMC was significantly lower in patients with microvascular complications than in patients without them. The biochemistry of bone metabolism showed a significantly increased fasting urinary excretion of calcium and hydroxyproline in patients with complications, but not in the group without complications, and there was a negative correlation between plasma BGP (osteocalcin) and hemoglobin A1C for all patients. These findings indicate that, in addition to a decreased BMC (before or shortly after clinical onset of diabetes), patients who develop microvascular complications also develop ongoing bone loss. This loss may be caused by an increased bone resorption, but decreased bone formation during periods of poor diabetic control may be involved as well.

Adult↗