Transient hyperphosphatasemia in a child with autosomal recessive vitamin D dependency.

1986 ◽  
Vol 32 (7) ◽  
pp. 1418-1419 ◽  
Author(s):  
D E Cole

Abstract The case of a 4.5-year-old girl with autosomal recessive vitamin D dependency is described. Although she had been effectively treated since one month postpartum with 1 alpha-hydroxycholecalciferol [1 alpha(OH)D3, alfacalcidol], her mean alkaline phosphatase (EC 3.1.3.1) activity in serum increased to 3680 U/L from a stable value [335 (SD 50) U/L; n = 12] within three weeks, then returned to baseline over the ensuing four months. Transient hyperphosphatasemia was diagnosed. Extensive investigation of an isolated episodic increase in alkaline phosphatase activity is as superfluous in the child with adequately treated metabolic bone disease as it is in other healthy and asymptomatic children.

2013 ◽  
Author(s):  
Adodra Annika ◽  
Kouklinos Andreas ◽  
Julies Priscilla ◽  
Shaw Mathew ◽  
Jacobs Benjamin

1985 ◽  
Vol 225 (1) ◽  
pp. 127-133 ◽  
Author(s):  
M W Smith ◽  
M E Bruns ◽  
E D M Lawson

The location of intestinal cells taken from the base of the crypt to the tip of the villus responsive to calcitriol (1,25-dihydroxycholecalciferol) and the distribution of [3H]calcitriol within the intestinal epithelium has been determined in vitamin D-deficient rats. The calcitriol responses examined were CaBP (Ca2+-binding protein) levels as measured by immunodiffusion and alkaline phosphatase levels as determined cytochemically. Calcitriol had no effect on villus structure or on enterocyte kinetics. This made it possible to compare levels of CaBP and alkaline phosphatase activity in enterocytes at different ages in rats at known times after hormone injection. Cells from both the crypt and villus synthesized CaBP in response to calcitriol. Alkaline phosphatase activity was not detectable in crypt cells, although a pool of precursor was produced in these cells in response to calcitriol. Enzyme activity was increased in all villus cells in response to calcitriol, but the quantitative description of this effect was very different from that found for calcitriol effects on CaBP synthesis. Calcitriol injected into vitamin D-deficient rats was detected, within 2h, in all cells of the crypt and villus. Most of the binding was to sites having a high affinity for the injected hormone.


PEDIATRICS ◽  
1993 ◽  
Vol 92 (6) ◽  
pp. 862-864
Author(s):  
YASUSHI NAKO ◽  
NAOBUMI FUKUSHIMA ◽  
TAKESHI TOMOMASA ◽  
KANJI NAGASHIMA ◽  
TAKAYOSHI KUROUME

Hypervitaminosis D is one of the causes of severe hypercalcemia in children. Most cases of hypervitaminosis D during childhood are due to an excessive supplementation of vitamin D by physicians or parents.1,2 To prevent metabolic bone disease of prematurity (rickets of prematurity), formulas designed for premature infants ("premature formulas"), which contain more calcium and vitamin D than standard formulas, are given to premature infants in addition to human milk.1 In some cases, separate vitamin D products are also given to these infants, although requirements for vitamin D and calcium intake in the premature infant and the formerly premature infant have not been fully estimated.1


2016 ◽  
Vol 6 (4) ◽  
pp. 568-590
Author(s):  
Alfredo Walker ◽  
Charis Kepron ◽  
Christopher M. Milroy

Fractures are commonly found in cases regarded as child abuse. The most commonly encountered fractures are to the ribs and the metaphyses. This paper examines the specificity of the classical metaphyseal lesion (CML) and rib fractures as hallmarks of child abuse. Recently, vitamin D deficiency (rickets) has been proposed as an alternative cause for the appearances typically described in CML. The literature in this area is examined. Rib fractures have also been highly associated with child abuse, particularly posterior rib fractures. As well as metabolic bone disease, resuscitation has been examined as a cause of rib fractures in young children. The current literature remains strongly supportive of rib fractures and metaphyseal fractures being indicators of child abuse.


1983 ◽  
Vol 3 (1_suppl) ◽  
pp. 24-26 ◽  
Author(s):  
Francisco Llach

It seems that CAPD may improve some patients with osteomalacia but may be similar to hemodialysis in regard to osteitis fibrosa. However, long-term prospective evaluation of the incidence of bone disease in CAPD patients is necessary before we can determine how CAPD may alter the incidence and expression of renal osteodystrophy. We need more information before we can conclude that CAPD may improve pure osteomalacia. Finally, the data available are insufficient to clarify the role of vitamin D analogues in these patients.


1986 ◽  
Vol 111 (2) ◽  
pp. 285-288 ◽  
Author(s):  
Masayoshi Yamaguchi ◽  
Teruyuki Sakashita

Abstract. The interaction of vitamin D3 and zinc on bone metabolism was investigated in the femur of weanling rats. Oral administration of vitamin D3 (1.0 μg/100 g body weight) did not cause any increase in the zinc accumulation in the femoral tissue following treatment with zinc sulphate (1.0 mg Zn/100 g). Administration of vitamin D3 or zinc produced significant increases the alkaline phosphatase activity and DNA content of the femoral diaphvsis but not of the epiphysis. The increase in alkaline phosphatase activity was enhanced additionally by simultaneous administration of vitamin D3 and zinc. Moreover, the increase in DNA content was enhanced markedly (about 4 times) by these treatments. At a dose of 0.5 μg of vitamin D3 per 100 g, DNA content was at the control level. This level was increased about 2 times by simultaneous administration of zinc (1.0 mg/100 g). The increase in alkaline phosphatase activity following simultaneous administration of vitamin D3 and zinc was significantly inhibited by treatment with cycloheximide, actinomycin D, or mitomycin C. Also, the increase in DNA content was completely inhibited by mitomycin C treatment. The present data suggest that the combination of vitamin D3 and zinc has a multiple effect on the stimulation of bone growth and mineralization in weanling rats, and that this effect is based on a stimulation of the DNA synthesis in bone cells.


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