ライフサイエンスコーパス: rickets

1 hypothyroidism, panhypopituitarism and renal rickets).

2 normalization of serum calcium and rescue of rickets.

3 3) cause autosomal dominant hypophosphatemic rickets.

4 emia is the most prevalent inherited form of rickets.

5 calcemia, secondary hyperparathyroidism, and rickets.

6 D supplementation and presence of suspected rickets.

7 ceiving medical therapy for hypophosphatemic rickets.

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

9 ch normalized serum calcium and improved his rickets.

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

11 oni syndrome, short stature, osteopenia, and rickets.

12 tal markers of vitamin D deficiency, such as rickets.

13 ng them at great risk of vitamin D-deficient rickets.

14 tion has not been confirmed in children with rickets.

15 or 23 (FGF23) in hereditary hypophosphatemic rickets.

16 osphatemia (XLH), a form of hypophosphatemic rickets.

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

18 ties in two mouse models of hypophosphatemic rickets.

19 autosomal dominant form of hypophosphatemic rickets.

20 d enamel defects as well as hypophosphatemic rickets.

21 haracteristic for dentin in hypophosphatemic rickets.

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

23 wed the distal femoral histologic slices for rickets.

24 sult in increased FGF23 and hypophosphatemic rickets.

25 sent in human patients with hypophosphatemic rickets.

26 atus of adult patients with hypophosphatemic rickets.

27 ull mouse, a mouse model of hypophosphatemic rickets.

28 isease: autosomal-recessive hypophosphatemic rickets.

29 D, calcium, and phosphorus metabolism cause rickets.

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

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

32 ical analyses presented evidence of residual rickets, a healed trauma, dental pathological conditions

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

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

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

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

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

38 the association of serum 25(OH)D with having rickets adjusted for calcium intake in a reanalysis of a

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

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

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

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

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

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

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

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

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

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

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

50 zed or insufficiently treated dRTA can cause rickets and failure to thrive in children, osteomalacia

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

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

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

54 iency is common in many societies and causes rickets and non-skeletal disorders in children.

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

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

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

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

59 linked hypophosphataemic rickets, fluorosis, rickets and osteomalacia).

60 In addition to rickets and osteomalacia, patients with XLH have a heavy

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

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

63 le, increased serum phosphorus, and improved rickets and prevented early declines in growth in childr

64 MAPK inhibition improved growth and rickets and, notably, almost normalized the growth plate

65 at the diagnosis of XLH is based on signs of rickets and/or osteomalacia in association with hypophos

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

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

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

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

70 onstrated hypocalcemia, hyperparathyroidism, rickets, and osteomalacia.

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

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

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

74 1-null mice, which are the hypophosphatemic rickets animal model, postnatally developed severe perio

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

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

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

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

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

80 hat at 200 mg/d, the adjusted odds of having rickets at 47.5 nmol/L was 0.80, whereas it was 0.2 at 6

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

82 /L (0.1-0.4 mg/dL); radiographic evidence of rickets (at least five participants were required to hav

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

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

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

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

87 Hypophosphatemia causes rickets by impairing hypertrophic chondrocyte apoptosis.

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

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

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

91 onstatistically significant fewer 'suspected rickets' cases in the vitamin D group (8.00%) than the p

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

93 130 to 300 mg/d, the adjusted odds of having rickets decreased dramatically with increasing 25(OH)D s

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

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

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

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

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

99 hypophosphatemia (XLH), a form of inherited rickets featuring elevated fibroblast growth factor 23 (

100 hate homeostasis (X-linked hypophosphataemic rickets, fluorosis, rickets and osteomalacia).

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

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

103 itamin D requirements to prevent nutritional rickets has been thwarted by inconsistent case definitio

104 of FGF23 excess that cause hypophosphatemic rickets, has also driven major paradigm shifts in our un

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

106 Rickets, historically referred to as "the English diseas

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

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

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

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

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

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

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

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

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

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

117 t FGF23, improves phosphate homoeostasis and rickets in children aged 5-12 years with X-linked hypoph

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

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

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

121 lementation can prevent and cure nutritional rickets in infants and children.

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

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

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

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

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

127 the pathogenesis of hypophosphatemia-driven rickets in their offspring.

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

129 Nutritional rickets is believed to result from the interaction of in

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

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

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

133 Rickets is seen in association with vitamin D deficiency

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

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

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

137 growth factor 23 (FGF23), hypophosphataemia, rickets, lower extremity bowing, and growth impairment.

138 associated with severe complications such as rickets, lower limb deformities, pain, poor mineralizati

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

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

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

142 are concentrations at which osteomalacia and rickets occur).

143 equent cause of hypophosphataemia-associated rickets of genetic origin and is associated with high le

144 Rickets, once thought vanquished, is reappearing.

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

146 can prevent FGF23-mediated hypophosphatemic rickets or osteomalacia.

147 hate accumulates extracellularly, leading to rickets or osteomalacia.

148 lism, use of vitamin D supplements, signs of rickets, or intention to move from Ulaanbaatar within 4

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

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

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

152 ncy is associated with bone diseases such as rickets, osteomalacia, and osteoporosis.

153 wasting with consecutive hypophosphataemia, rickets, osteomalacia, disproportionate short stature, o

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

155 0.2, and 5.4 +/- 0.1 mg/dl), and severity of rickets/osteomalacia (bone mineral density: -36, -36, an

156 resented in childhood or even adulthood with rickets/osteomalacia and/or osteopenia/osteoporosis, hyp

157 5(OH)2 vitamin D levels, hypercalciuria, and rickets/osteomalacia.

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

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

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

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

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

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

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

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

166 In this disorder, rickets results from hyperphosphaturia and inappropriate

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

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

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

170 and infant clinical diagnosis for "suspected rickets." Secondary outcomes included biomarkers of bone

171 The primary endpoint was change in rickets severity at week 40, assessed by the Radiographi

172 Changes in rickets severity from baseline to weeks 40 and 64 (asses

173 64 (assessed radiographically using Thacher Rickets Severity Score and an adaptation of the Radiogra

174 Total Thacher Rickets Severity Score decreased by a least squares mean

175 participants were required to have a Thacher Rickets Severity Score of >=1.5 at the knee); and a conf

176 ey eligibility criteria were a total Thacher rickets severity score of at least 2.0, fasting serum ph

177 greater clinical improvements were shown in rickets severity, growth, and biochemistries among child

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

179 nal phosphate wasting and hypophosphataemia, rickets, skeletal deformities, and growth impairment.

180 (FGF) 23 causes hereditary hypophosphatemic rickets, such as X-linked hypophosphatemia (XLH) and tum

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

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

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

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

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

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

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

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

189 vitamin D requirement to prevent nutritional rickets varies inversely with calcium intake and vice ve

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

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

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

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

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

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

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

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

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

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

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

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

202 c (NPT2c), cause hereditary hypophosphatemic rickets with hypercalciuria (HHRH).

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

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