ライフサイエンスコーパス: hypocalcemia

1 l to 8.0 mg/dL and had symptoms and signs of hypocalcemia.

2 al dominant hypocalcemia type 1, may lead to hypocalcemia.

3 uction in calcitriol, which could exacerbate hypocalcemia.

4 espective of the surgeons' specific rates of hypocalcemia.

5 TH levels for the development of symptomatic hypocalcemia.

6 temporary hypocalcemia, and 0% had permanent hypocalcemia.

7 rder with clinic and biochemical features of hypocalcemia.

8 he disorder such as chronic otitis media and hypocalcemia.

9 alse-positive laboratory reports of critical hypocalcemia.

10 h, and metabolic derangement, in particular, hypocalcemia.

11 sly reported postburn hypoparathyroidism and hypocalcemia.

12 After hypoxia, however, hypocalcemia acts synergistically with hyperoxic reoxyge

13 ceptor from patients with autosomal dominant hypocalcemia (ADH) repressed the transcription of miR-9

14 eviously in subjects with autosomal dominant hypocalcemia (ADH), five appear at the junction of TM he

15 Hypocalcemia also reduces overall milk production and ca

16 Severe hypocalcemia and elevated acute-phase response developed

17 Hypocalcemia and gastrointestinal adverse events were si

18 ith failure to thrive, short stature, severe hypocalcemia and gross motor delay.

19 We report a patient with PTH-resistant hypocalcemia and hyperphosphatemia but without evidence

20 Hypocalcemia and hyperphosphatemia caused by parathyroid

21 eudohypoparathyroidism type Ib (PHP-Ib) have hypocalcemia and hyperphosphatemia due to renal parathyr

22 aracterized by parathyroid hormone-resistant hypocalcemia and hyperphosphatemia.

23 steosclerotic bone dysplasia with associated hypocalcemia and ocular abnormalities.

24 receptor (VDR)-knockout mice develop severe hypocalcemia and rickets, accompanied by disruption of a

25 f TRPM6 causes hypomagnesemia with secondary hypocalcemia and show that individuals carrying mutation

26 postoperatively for hematoma, evaluated for hypocalcemia and symptoms of hypocalcemia, and followed

27 fore, stimulation of the parathyroid by both hypocalcemia and uremia is dependent upon intact dicer f

28 of the parathyroid to both acute and chronic hypocalcemia and uremia, the major stimuli for PTH secre

29 1,25(OH)(2)D(3) up-regulates VDR expression, hypocalcemia and vitamin D deficiency result in drastica

30 Hypersensitivity was not due to hypocalcemia and was actually accelerated by increased d

31 thyroids autotransplanted, 47% had temporary hypocalcemia, and 0% had permanent hypocalcemia.

32 rdiac defects, thymic hypoplasia or aplasia, hypocalcemia, and characteristic facial features.

33 were GI hemorrhage (n = 1) and pancreatitis, hypocalcemia, and elevated lipase (n = 1; all in same pa

34 , evaluated for hypocalcemia and symptoms of hypocalcemia, and followed up to assess for cure defined

35 Hypomagnesemia, hypocalcemia, and hypokalemia were not found.

36 hypoalbuminemia, hyponatremia, hypokalemia, hypocalcemia, and hypomagnesemia; 14 patients (52%) had

37 many renal diseases, including Mg2+ wasting, hypocalcemia, and polycystic kidney diseases.

38 scular disease, delayed fracture healing, or hypocalcemia, and there were no cases of osteonecrosis o

39 n, which causes a form of autosomal dominant hypocalcemia, appears to increase the affinity of the re

40 Post-surgical hypoparathyroidism and hypocalcemia are known to occur after nearly 50% of all

41 cemia needs to be verified, as many cases of hypocalcemia are the artifact of hypoalbuminemia.

42 mal facies, thymic hypoplasia, cleft palate, hypocalcemia, associated with chromosome 22 microdeletio

43 The resulting hypoparathyroidism and hypocalcemia can range from asymptomatic to life-threate

44 ion on proteinuria could not be explained by hypocalcemia, changes in parathyroid hormone, or fibrobl

45 rathyroid hormone (PTH) in response to acute hypocalcemia compared with the >5-fold increase in contr

46 Conclusions and Relevance: Hypocalcemia correlates with the extent of bleeding in p

47 his diet increased FGF23 except in rats with hypocalcemia despite high PTH levels.

48 increased parathyroid hormone in response to hypocalcemia; despite lower calcium levels, parathyroid

49 somal dominant hypomagnesemia with secondary hypocalcemia disorder.

50 Patients with hypocalcemia due to CaR mutations also show disproportio

51 idence; the case reported could suggest that hypocalcemia due to DGS could be the common biochemical

52 There was no evidence of hypocalcemia, ectopic calcification, or definite drug-re

53 Familial hypomagnesemia with secondary hypocalcemia (HSH) (MIM 307600) was studied in three inb

54 emale sex, QT-prolonging drugs, hypokalemia, hypocalcemia, hyperglycemia, high creatinine, history of

55 rickets type II, VDDR II) have demonstrated hypocalcemia, hyperparathyroidism, rickets, and osteomal

56 Biochemical tests revealed hypocalcemia, hyperphosphatemia and hypomagnesemia with

57 Hypoparathyroidism is characterized by hypocalcemia, hyperphosphatemia, and absent or markedly

58 antly reduced Galphas mRNA levels and showed hypocalcemia, hyperphosphatemia, and elevated PTH levels

59 eased Gsalpha mRNA levels, and to associated hypocalcemia, hyperphosphatemia, and secondary hyperpara

60 n of the vitamin D receptor (VDR) results in hypocalcemia, hypophosphatemia, hyperparathyroidism, ric

61 hanges suggests that rickets is secondary to hypocalcemia, hypophosphatemia, or hyperparathyroidism,

62 esulting in laboratory reports of "critical" hypocalcemia (ie, calcium level < 6 mg/dL [1.5 mmol/L])

63 erited in the same mode as the PTH-resistant hypocalcemia in kindreds with PHP-Ia and/or pseudo-pseud

64 ansient asymptomatic sick sinus syndrome and hypocalcemia in one patient at 17 mg/m2.

65 There is debate about the proper therapy of hypocalcemia in sepsis because calcium administration ma

66 Cinacalcet resulted in hypocalcemia in seven patients.

67 tive intolerance in the cinacalcet group and hypocalcemia in the parathyroidectomy group.

68 isk factors for developing postthyroidectomy hypocalcemia include hyperthyroidism, vitamin D deficien

69 Chronic hypocalcemia increased serum PTH >4-fold less in PT-Dice

70 The risk of permanent hypocalcemia increased when total or subtotal thyroidect

71 al cells in vitro, whereas in vivo, systemic hypocalcemia increases PTHrP production, an effect that

72 ured at baseline and seven more times during hypocalcemia induced during cardiopulmonary bypass in 22

73 he syndrome of hypomagnesemia with secondary hypocalcemia is caused by defective TRPM6.

74 tion of serum phosphate is thought to induce hypocalcemia is discussed, and the treatment of hyperpho

75 Postoperative hypocalcemia is one of the most common complications fol

76 stprandial calciuria with episodic, relative hypocalcemia may represent a previously unreported mecha

77 recent literature on predictive factors for hypocalcemia, measurement of serum calcium and parathyro

78 Hypocalcemia needs to be verified, as many cases of hypo

79 er rat calcitonin (rCT), at doses that cause hypocalcemia, nor parathyroid hormone, at doses that cau

80 in-associated grade 3 or 4 hypomagnesemia or hypocalcemia occurred in 13 (30%) and hearing loss in tw

81 Hypocalcemia occurred more frequently with denosumab.

82 ase reactions occurred with zoledronic acid; hypocalcemia occurred more frequently with denosumab.

83 Severe hypocalcemia occurs after subtotal or total parathyroide

84 Familial hypomagnesemia with secondary hypocalcemia (OMIM 602014) is an autosomal recessive dis

85 4.3% male patients), of whom 229 (10.9%) had hypocalcemia on admission.

86 patients suffered complications from ionized hypocalcemia or elevated serum total calcium.

87 No patient had characteristic symptoms of hypocalcemia or injuries attributed to the inappropriate

88 yperparathyroidism induced by either chronic hypocalcemia or uremia, which was measured by increased

89 es that include conotruncal cardiac defects, hypocalcemia, palatal and facial anomalies and developme

90 Gadodiamide administration causes spurious hypocalcemia, particularly at doses of 0.2 mmol/kg or hi

91 Taken together, these results suggest that hypocalcemia reduces the circulating concentrations of F

92 No patients in either group had permanent hypocalcemia requiring long-term supplementation.

93 case of severe hyperphosphatemia and tetanic hypocalcemia resulting from the inadvertent oral ingesti

94 in D-deficient neonate is at risk to develop hypocalcemia, rickets, and possibly extraskeletal disord

95 ptor mice were growth retarded and developed hypocalcemia, secondary hyperparathyroidism, and rickets

96 f the vitamin D receptor (VDR) gene leads to hypocalcemia, secondary hyperparathyroidism, rickets, an

97 rb whale dentin in vitro and the significant hypocalcemia seen in the knockout mice.

98 ptor (hCaR), which causes autosomal dominant hypocalcemia, showed enhanced signaling activity and inc

99 tion, muscle weakness, skeletal deformities, hypocalcemia, tetany, and seizures.

100 nation for the rapidity of the shock and the hypocalcemia that is so characteristic of the disease.

101 were detected in two unrelated patients with hypocalcemia; they were therefore identified as having a

102 in of function that cause autosomal dominant hypocalcemia type 1, may lead to hypocalcemia.

103 alcemia type 2 (FHH2) and autosomal dominant hypocalcemia type 2 (ADH2), respectively, whereas somati

104 m concentrations, whereas autosomal dominant hypocalcemia type 2-associated mutations increased cell

105 al disorder designated as autosomal dominant hypocalcemia type 2.

106 fore identified as having autosomal dominant hypocalcemia type 2.

107 which could exacerbate calcium deficiency or hypocalcemia unless calcium itself modulates FGF23 in th

108 well as environmental stresses like hypoxia, hypocalcemia, viral infection, and tissue injury.

109 in both calcium and vitamin D, the resulting hypocalcemia was associated with low FGF23 despite high

110 calcium level was measured on admission, and hypocalcemia was defined as a serum calcium level of les

111 increase in serum PTH during citrate-induced hypocalcemia was lower in the TPN recipients, consistent

112 Transient hypocalcemia was more common in DUN (30% vs 8%; P < 0.00

113 Permanent hypocalcemia was more frequent after total or subtotal t

114 albumin requirements and the development of hypocalcemia was reduced.

115 The incidence of postoperative transient hypocalcemia was significantly higher in the hyper group

116 Hyperphosphatemia and hypocalcemia were present in only 12 and 6% of patients,

117 Transient symptoms of hypocalcemia were seen at 30 mCi/kg.

118 uld be considered in a patient with profound hypocalcemia which is refractory to conventional therapy

119 d individuals show severe hypomagnesemia and hypocalcemia, which lead to seizures and tetany.

120 is analysis in eight unrelated patients with hypocalcemia who did not have CASR mutations.

121 hymus with associated deficiency of T cells, hypocalcemia with hypoplasia or aplasia of the parathyro

122 ht regulation frequently occur, and treating hypocalcemia with parenteral calcium administration rema

123 xhibited dose-dependent hypophosphatemia and hypocalcemia, with markedly elevated FGF23 (38 to 456 fo