WordNet

holding office; "the in party"
to or toward the inside of; "come in"; "smash in the door" (同)inwards, inward
currently fashionable; "the in thing to do"; "large shoulder pads are in"
directed or bound inward; "took the in bus"; "the in basket"
childhood disease caused by deficiency of vitamin D and sunlight associated with impaired metabolism of calcium and phosphorus (同)rachitis

PrepTutorEJDIC

《具体的な場所,位置》 / …『の中に』(『で』) / …『において』,…で / 《intoの代りに移動を表す動詞と共に》…『の中へ』 / (乗り物)『に乗って』 / …『の状熊に』(『で』) / …『に従事して』,に属して / …『を身につけて』,に覆われて / 《『in』do『ing』の形で》…『するときに』,する際に(when) / 《時間》 / …『して』,…『が経過したあと』 / …『の間に』 / …『については』,…の点では / 《方法・手段・材料》…『で』 / 《人を目的語にして,性質・能力があることを示して》…の中に / …の目的で,のつもりで,として / 《比率割合》…のうちで,につき / 《過去分詞に伴って》…に[…されて] / 『中へ』(に) / 『在宅して』,帰って / (乗り物などが)『到着して』,(時期・季節が)来て / 出回って,流行して / 《俗》流行の,当世風の / 《話》特定の人々にのみ理解される
くる病
(1歳未満の)『乳児』,乳飲み子 / 《英》(普通7歳未満の)学童 / 未成年者 / 幼児の,幼児用の / 始めたばかりの,初期の
indiumの化学記号
Indiana

UpToDate Contents

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1. 小児におけるくる病の概要 overview of rickets in children
2. 遺伝性低リン血症性くる病と腫瘍誘発性骨軟化症 hereditary hypophosphatemic rickets and tumor induced osteomalacia
3. 小児における低カルシウム血症性くる病の病因および治療 etiology and treatment of calcipenic rickets in children
4. 内反膝の小児に対するアプローチ approach to the child with bow legs
5. 小児および思春期におけるビタミンD不足および欠乏 vitamin d insufficiency and deficiency in children and adolescents

English Journal

Neonatal Iron Deficiency Causes Abnormal Phosphate Metabolism by Elevating FGF23 in Normal and ADHR Mice.

Clinkenbeard EL, Farrow EG, Summers LJ, Cass TA, Roberts JL, Bayt CA, Lahm T, Albrecht M, Allen MR, Peacock M, White KE.Author information Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.AbstractFibroblast growth factor 23 (FGF23) gain of function mutations can lead to autosomal dominant hypophosphatemic rickets (ADHR) disease onset at birth, or delayed onset following puberty or pregnancy. We previously demonstrated that the combination of iron deficiency and a knock-in R176Q FGF23 mutation in mature mice induced FGF23 expression and hypophosphatemia that paralleled the late-onset ADHR phenotype. Because anemia in pregnancy and in premature infants is common, the goal of this study was to test whether iron deficiency alters phosphate handling in neonatal life. Wild-type (WT) and ADHR female breeder mice were provided control or iron-deficient diets during pregnancy and nursing. Iron-deficient breeders were also made iron replete. Iron-deficient WT and ADHR pups were hypophosphatemic, with ADHR pups having significantly lower serum phosphate (p < 0.01) and widened growth plates. Both genotypes increased bone FGF23 mRNA (>50 fold; p < 0.01). WT and ADHR pups receiving low iron had elevated intact serum FGF23; ADHR mice were affected to a greater degree (p < 0.01). Iron-deficient mice also showed increased Cyp24a1 and reduced Cyp27b1, and low serum 1,25-dihydroxyvitamin D (1,25D). Iron repletion normalized most abnormalities. Because iron deficiency can induce tissue hypoxia, oxygen deprivation was tested as a regulator of FGF23, and was shown to stimulate FGF23 mRNA in vitro and serum C-terminal FGF23 in normal rats in vivo. These studies demonstrate that FGF23 is modulated by iron status in young WT and ADHR mice and that hypoxia independently controls FGF23 expression in situations of normal iron. Therefore, disturbed iron and oxygen metabolism in neonatal life may have important effects on skeletal function and structure through FGF23 activity on phosphate regulation. © 2014 American Society for Bone and Mineral Research.
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.J Bone Miner Res.2014 Feb;29(2):361-9. doi: 10.1002/jbmr.2049.
Fibroblast growth factor 23 (FGF23) gain of function mutations can lead to autosomal dominant hypophosphatemic rickets (ADHR) disease onset at birth, or delayed onset following puberty or pregnancy. We previously demonstrated that the combination of iron deficiency and a knock-in R176Q FGF23 mutatio
PMID 23873717

Vitamin d deficiency rickets in an adolescent with severe atopic dermatitis.

Borzutzky A, Grob F, Camargo CA Jr, Martinez-Aguayo A.Author information Immunology and Rheumatology Unit, Division of Pediatrics.AbstractAtopic dermatitis (AD) affects 10% to 20% of children worldwide. Its severity may be inversely correlated with 25-hydroxyvitamin D (25OHD) levels. Although low levels of vitamin D (VD) can cause rickets in infants, VD deficiency rickets is an unusual presentation in teenagers. We report the case of a 14-year-old girl with severe AD and fish allergy since early childhood. She lived at high latitude (with less sun exposure) and, because of her atopic disorders, avoided sunlight and fish. Laboratory studies showed elevated alkaline phosphatase and parathyroid hormone levels and low serum calcium; her serum 25OHD level was <12 nmol/L. A radiograph of the wrist showed a radiolucent band in the distal metaphysis of the radius with marginal sclerosis. She was diagnosed as having hypocalcemic rickets due to VD deficiency. Treatment with VD increased her 25OHD level to 44 nmol/L, with normalization of alkaline phosphatase, parathyroid hormone, and calcium. Moreover, we observed a dramatic improvement in her AD severity with VD treatment. This case demonstrates the complex interaction between VD deficiency, AD, and food allergy. We advise a high index of suspicion of VD deficiency rickets in children of all ages with AD, particularly during accelerated growth periods and in the presence of other risk factors such as darker skin, living at high latitude, sun avoidance, and low intake of VD-rich foods. The concomitant improvement in bone-related parameters and AD severity may reflect a double benefit of VD treatment, a possibility that warrants research on VD as potential treatment for AD.
Pediatrics.Pediatrics.2014 Feb;133(2):e451-4. doi: 10.1542/peds.2013-1114. Epub 2014 Jan 27.
Atopic dermatitis (AD) affects 10% to 20% of children worldwide. Its severity may be inversely correlated with 25-hydroxyvitamin D (25OHD) levels. Although low levels of vitamin D (VD) can cause rickets in infants, VD deficiency rickets is an unusual presentation in teenagers. We report the case of
PMID 24470638

Vitamin D Supplementation and Risk of Toxicity in Pediatrics: A Review of Current Literature.

Vogiatzi MG, Jacobson-Dickman E, Deboer MD; for the Drugs, and Therapeutics Committee of The Pediatric Endocrine Society.Author information Weill Cornell Medical College (M.G.V.), New York, New York 10065; SUNY Downstate Medical Center (E.J.-D.), Brooklyn, New York 11203; and University of Virginia Health System (M.D.D.), Charlottesville, Virginia 22903.AbstractContext: Although vitamin D toxicity is rare in children, increased use of vitamin D formulations, re-examination of optimal vitamin D levels, and use of higher doses lend potential for an increased incidence of vitamin D toxicity. Evidence Acquisition: A PubMed search was conducted through May 2013 for cases of vitamin D intoxication and vitamin D trials in pediatrics. Safety data were collected and reviewed. Evidence Synthesis: A small number of pediatric studies tested vitamin D doses at or above the currently recommended upper tolerable intake. In children and adolescents, vitamin D excess was rare and usually asymptomatic. Recent cases of intoxication relate to errors in manufacturing, formulation, or prescription; involve high total intake in the range of 240 000 to 4 500 000 IU; and present with severe hypercalcemia, hypercalciuria, or nephrocalcinosis. However, mild hypercalcemia and hypervitaminosis using currently recommended doses have been reported in infants with rickets. Conclusions: Although rare, cases of vitamin D intoxication that present with dramatic life-threatening symptoms still occur in children. Moreover, recent studies in infants raise a potential need for monitoring vitamin D levels when doses at or above the currently recommended upper range are used. Further studies are needed to clarify these findings. The Drugs and Therapeutics Committee of the Pediatric Endocrine Society suggests obtaining serum 25-hydroxyvitamin D levels in infants and children who receive long-term vitamin D supplementation at or above the upper level intake that is currently recommended.
The Journal of clinical endocrinology and metabolism.J Clin Endocrinol Metab.2014 Jan 23:jc20133655. [Epub ahead of print]
Context: Although vitamin D toxicity is rare in children, increased use of vitamin D formulations, re-examination of optimal vitamin D levels, and use of higher doses lend potential for an increased incidence of vitamin D toxicity. Evidence Acquisition: A PubMed search was conducted through May 2013
PMID 24456284

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