ライフサイエンスコーパス: rickets

1 hypothyroidism, panhypopituitarism and renal rickets).

2 3) cause autosomal dominant hypophosphatemic rickets.

3 emia is the most prevalent inherited form of rickets.

4 calcemia, secondary hyperparathyroidism, and rickets.

5 d enamel defects as well as hypophosphatemic rickets.

6 D supplementation and presence of suspected rickets.

7 ceiving medical therapy for hypophosphatemic rickets.

8 haracteristic for dentin in hypophosphatemic rickets.

9 , or disorders of vitamin D action can cause rickets.

10 support for the view that the CML is due to rickets.

11 ch normalized serum calcium and improved his rickets.

12 wed the distal femoral histologic slices for rickets.

13 ecta (IO), and eight had vitamin D-resistant rickets.

14 sult in increased FGF23 and hypophosphatemic rickets.

15 in D deficient mothers' infants are prone to rickets.

16 sent in human patients with hypophosphatemic rickets.

17 atus of adult patients with hypophosphatemic rickets.

18 ties in two mouse models of hypophosphatemic rickets.

19 ull mouse, a mouse model of hypophosphatemic rickets.

20 isease: autosomal-recessive hypophosphatemic rickets.

21 D, calcium, and phosphorus metabolism cause rickets.

22 autosomal dominant form of hypophosphatemic rickets.

23 ely diagnosed with X-linked hypophosphatemic rickets, a disorder caused by renal wasting of phosphate

24 X-linked hypophosphatemic rickets, a dominantly inherited disease, is caused by mu

25 associated with clinical conditions such as rickets, abdominal distention, hair depigmentation, and

26 nockout mice develop severe hypocalcemia and rickets, accompanied by disruption of active intestinal

27 Autosomal dominant hypophosphatemic rickets (ADHR) is an inherited disorder of isolated rena

28 Autosomal dominant hypophosphatemic rickets (ADHR) is unique among the disorders involving F

29 disorder autosomal dominant hypophosphatemic rickets (ADHR) was previously mapped to the region of ch

30 mouse homologue of X-linked hypophosphatemic rickets, administration of 1,25(OH)(2)D(3) further incre

31 Recent reports of rickets among African American children drew attention t

32 Vitamin D deficiency not only causes rickets among children but also precipitates and exacerb

33 Reports from 2000 and 2001 of rickets among children living in North Carolina, Texas,

34 AAP guidelines emphasize the higher risk of rickets among these children.

35 We reviewed reports of nutritional rickets among US children <18 y of age that were publish

36 in the alphaKLOTHO (KL) gene presented with rickets and a complex endocrine profile, including parad

37 extremities and between patients with OI or rickets and a group of 17 healthy, matched children.

38 e II in humans, including the development of rickets and alopecia.

39 dicated a reemergence of vitamin D-deficient rickets and an alarming prevalence of vitamin D insuffic

40 tion of adults with genetic hypophosphatemic rickets and compared their periodontal status with simil

41 In premature infants, clinical rickets and fractures are common.

42 autosomal recessive disease characterized by rickets and impaired growth due to failure of renal synt

43 s the role of vitamin D in the prevention of rickets and its importance in the overall health and wel

44 Rickets and osteomalacia are seen by day 35; however, as

45 ciated with CasR deficiency, indicating that rickets and osteomalacia in CasR-deficient mice are not

46 recessive hypophosphatemic rickets, manifest rickets and osteomalacia with isolated renal phosphate-w

47 d mineralization of the bone protein matrix (rickets and osteomalacia).

48 of alkaline phosphatase (TNSALP), results in rickets and osteomalacia.

49 a (XLH) is the most common heritable form of rickets and osteomalacia.

50 al tubular toxicity led to hypophosphataemic rickets and/or renal tubular acidosis in six children, a

51 hyperphosphatemia syndrome, hypophosphatemic rickets, and hypophosphatasia), and bone resorption (Gor

52 rickets, autosomal-dominant hypophosphatemic rickets, and oncogenic osteomalacia demonstrate that ele

53 hypocalcemia, secondary hyperparathyroidism, rickets, and osteomalacia, accompanied by 90% reduction

54 onstrated hypocalcemia, hyperparathyroidism, rickets, and osteomalacia.

55 neonate is at risk to develop hypocalcemia, rickets, and possibly extraskeletal disorders (e.g., typ

56 inappropriately alkaline urine, poor growth, rickets, and renal calcification.

57 omolog of X-linked dominant hypophosphatemic rickets, and transgenic mice that overexpress a mutant F

58 1-null mice, which are the hypophosphatemic rickets animal model, postnatally developed severe perio

59 ), also known as pseudo-vitamin D-deficiency rickets, appears to result from deficiency of renal vita

60 suggests that patients with hypophosphatemic rickets are more prone to periodontal bone loss than the

61 f how excess FGF23 leads to hypophosphatemic rickets are not clear.

62 Reports of clinical rickets are particularly evident in minority infants and

63 The primary objective was the healing of rickets, as assessed by means of radiographic scales.

64 Healing of rickets at 6 months in 9 patients was accompanied by imp

65 of phosphaturia in X-linked hypophosphatemic rickets, autosomal-dominant hypophosphatemic rickets, an

66 presence or absence of vitamin D deficiency rickets, bone mineral content, and serum parathyroid hor

67 th oral phosphate and vitamin D improves the rickets, but has significant morbidity and does not sign

68 RK1/2 phosphorylation in vitro, but leads to rickets by decreasing VEGF protein stability.

69 Hypophosphatemia causes rickets by impairing hypertrophic chondrocyte apoptosis.

70 ght possibly to suggest vitamin D deficiency rickets: calcium 5.1mg/dL, (8.8-10.8); phosphorus 4.1mg/

71 Rickets can be secondary to disorders of the gut, pancre

72 our finding of a disproportionate number of rickets cases among young, breast-fed, black children, w

73 metabolism and symptoms of hypophosphatemic rickets, circling behavior, hyperactivity, head shaking,

74 An adolescent with hypophosphatemic rickets developed cardiac calcifications in the absence

75 Children suspected of having rickets during the first year of life had a RR of 3.0 (1

76 conventional therapy of vitamin D deficiency rickets even without evidence of alopecia.

77 isorder hypophosphatemic vitamin D-resistant rickets exist, the Hyp and Gy mice.

78 ed that autosomal recessive hypophosphatemic rickets family carried a mutation affecting the DMP1 sta

79 ompared with control subjects, patients with rickets had similar bone area but reduced bone density (

80 as again become an epidemic in children, and rickets has become a global health issue.

81 ons (APL) and hereditary vitamin D-resistant rickets have a similar congenital hair loss disorder cau

82 Rickets, historically referred to as "the English diseas

83 ave been linked to human vitamin D-resistant rickets (hVDRR) and result in high serum 1,25(OH)(2)D(3)

84 Hereditary vitamin D-resistant rickets (HVDRR) is caused by heterogeneous inactivating

85 ally apparent hereditary vitamin D-resistant rickets (HVDRR) usually results from a loss of function

86 in a case of hereditary vitamin D resistant rickets (HVDRR) without alopecia and successful manageme

87 hereditary 1,25-dihydroxyvitamin D resistant rickets (HVDRR).

88 ing a form of hereditary vitamin D-resistant rickets (HVDRR).

89 X-linked hypophosphatemic rickets (HYP) is a dominant disorder characterized by re

90 e responsible for X-linked hypophosphataemic rickets (HYP).

91 We identified 166 cases of rickets in 22 published studies.

92 increasing number of reports of nutritional rickets in certain populations of American infants, and

93 Vitamin D deficiency causes rickets in children and will precipitate and exacerbate

94 (XLH) is the most frequent form of inherited rickets in humans caused by mutations in the phosphate-r

95 r of skin cancer; and the high prevalence of rickets in immigrant groups in more temperate regions.

96 entrations higher than 50 nmol/L and prevent rickets in infants and young children.

97 aminoaciduria and glycosuria, together with rickets in some patients.

98 istinct from other forms of hypophosphatemic rickets in that affected individuals present with hyperc

99 The epidemic scourge of rickets in the 19th century was caused by vitamin D defi

100 re no radiographic or pathologic features of rickets in the cohort.

101 is a common cause of rickets, other types of rickets, including hereditary forms, must be considered

102 The child at risk of rickets is now white, breastfed, protected from the sun

103 thogenesis of rare forms of hypophosphatemic rickets is rapidly reshaping our understanding of disord

104 mice prevents rachitic changes suggests that rickets is secondary to hypocalcemia, hypophosphatemia,

105 Rickets is seen in association with vitamin D deficiency

106 trophic chondrocyte layer, characteristic of rickets, is secondary to impaired apoptosis of these cel

107 In patients with hypophosphatemic rickets, it seems that the dose of phosphate and in part

108 radiographic and/or histological evidence of rickets, limb deformities, muscle weakness, and bone pai

109 sorder, autosomal recessive hypophosphatemic rickets, manifest rickets and osteomalacia with isolated

110 hogenesis of FGF23-mediated hypophosphatemic rickets, more work will need to be done before CYP24A1 i

111 accompanied by renal dysfunction, childhood rickets, neurological crisis, and hepatocellular carcino

112 are concentrations at which osteomalacia and rickets occur).

113 Rickets, once thought vanquished, is reappearing.

114 ons above the concentrations associated with rickets or osteomalacia influence calcium absorption.

115 hate accumulates extracellularly, leading to rickets or osteomalacia.

116 but failed to correct the hypophosphatemia, rickets, or osteomalacia.

117 emia, hypophosphatemia, hyperparathyroidism, rickets, osteomalacia, and alopecia--the last a conseque

118 X-linked hypophosphatemia, characterized by rickets, osteomalacia, and hypomineralized dentin format

119 d in phenotypic changes, including dwarfism, rickets, osteomalacia, hypophosphatemia, increased serum

120 0.2, and 5.4 +/- 0.1 mg/dl), and severity of rickets/osteomalacia (bone mineral density: -36, -36, an

121 5(OH)2 vitamin D levels, hypercalciuria, and rickets/osteomalacia.

122 the human disease X-linked hypophosphatemic rickets/osteomalacia.

123 pophosphatemia, renal phosphate wasting, and rickets/osteomalacia.

124 d production of 1,25-dihydroxyvitamin D, and rickets/osteomalacia.

125 ed with multiple medical outcomes, including rickets, osteoporosis, multiple sclerosis and cancer.

126 gh vitamin D deficiency is a common cause of rickets, other types of rickets, including hereditary fo

127 e (function), and the presence or absence of rickets (outcome).

128 e, a fresh understanding of risk factors for rickets persuades pediatricians to recognize and treat t

129 ls, as well as observations in patients with rickets, provide evidence of this pathway's importance i

130 In this disorder, rickets results from hyperphosphaturia and inappropriate

131 The receptor for bursicon is encoded by the rickets (rk) gene and belongs to the G protein-coupled r

132 hat activates the G protein-coupled receptor rickets (rk).

133 r1-deficient mice developed hypophosphatemic rickets secondary to renal dysfunction.

134 ese observations establish that the Bursicon/Rickets signaling pathway is necessary for both wing exp

135 l of 10 adult patients with hypophosphatemic rickets (two males and eight females) were evaluated.

136 for autosomal recessive vitamin D-dependent rickets type 1 (VDDR1).

137 ause autosomal recessive vitamin D-dependent rickets type 1, and it has recently been reported that h

138 Vitamin D-dependent rickets type I (VDDR-I), also known as pseudo-vitamin D-

139 eficiency, also known as vitamin D-dependent rickets type I, an autosomal recessive disease character

140 types characteristic of vitamin D-dependency rickets type I.

141 e that closely resembles vitamin D-dependent rickets type II in humans, including the development of

142 reds with VDR mutations (vitamin D-dependent rickets type II, VDDR II) have demonstrated hypocalcemia

143 At the turn of the last century, rickets (vitamin D deficiency) was one of the most commo

144 Rickets was curable through administration of 1,25(OH)(2

145 , with its resulting skeletal abnormalities (rickets), was likely to be fatal in early life.

146 ociation with hereditary vitamin D resistant rickets, we now characterize this alopecia as clinically

147 Approximately 83% of children with rickets were described as African American or black, and

148 aining 1,25(OH)(2)D(3) but rapidly developed rickets when phosphorus and 1,25(OH)(2)D(3) were restric

149 nock-out (KO) mice manifest hypophosphatemic rickets, which highlights the crucial roles of this mole

150 ression of FGF23 results in hypophosphatemic rickets, which is characterized by renal phosphate wasti

151 1) Vitamin D deficiency is more than rickets, which is the final stage of the deficient state

152 The patient exhibited vitamin D resistant rickets, which was confirmed by an absent response of he

153 Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is a rare disorder of

154 c (NPT2c), cause hereditary hypophosphatemic rickets with hypercalciuria (HHRH), a disorder character

155 treatment of patients with hypophosphatemic rickets with phosphate and vitamin D preparations.

156 N), and X-linked recessive hypophosphataemic rickets (XLRH)) have been mapped to Xp11.22.