ライフサイエンスコーパス: hypocalcemia

1 ndently associated with occurrence of severe hypocalcemia.

2 he disorder such as chronic otitis media and hypocalcemia.

3 ataract is the most common ocular symptom of hypocalcemia.

4 alse-positive laboratory reports of critical hypocalcemia.

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

6 sly reported postburn hypoparathyroidism and hypocalcemia.

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

8 the incidence and clinical association with hypocalcemia.

9 hosphonate-treated patients developed severe hypocalcemia.

10 eduction of vision she was diagnosed to have hypocalcemia.

11 and DEXA scans were normal in patients with hypocalcemia.

12 clinic/hospital visit, or a readmission for hypocalcemia.

13 nd to compare the outcome of both methods on hypocalcemia.

14 rder with clinic and biochemical features of hypocalcemia.

15 a(2+), allowing discrimination of hyper- and hypocalcemia.

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

17 uction in calcitriol, which could exacerbate hypocalcemia.

18 espective of the surgeons' specific rates of hypocalcemia.

19 fects are likely not specifically related to hypocalcemia.

20 TH levels for the development of symptomatic hypocalcemia.

21 temporary hypocalcemia, and 0% had permanent hypocalcemia.

22 iants indeed showed ADH1 symptoms, including hypocalcemia (60% in the UKB and 78% in AOU).

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

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

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

26 eased PGs, and (iv) minimizing postoperative hypocalcemia after total thyroidectomy.

27 Hypocalcemia also reduces overall milk production and ca

28 thyroidectomy, 47 patients (24.4%) developed hypocalcemia and 18 (9.4%) were symptomatic.

29 yperparathyroidism-treating drugs can induce hypocalcemia and arrhythmias.

30 ivery of EDTA may cause side effects such as hypocalcemia and bone resorption.

31 Severe hypocalcemia and elevated acute-phase response developed

32 Hypocalcemia and gastrointestinal adverse events were si

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

34 and increased risk of complications such as hypocalcemia and hemodynamic instability, limiting their

35 rphosphatemia, especially when combined with hypocalcemia and hyperparathyroidism, leads to an increa

36 pe was the combination of hyperphosphatemia, hypocalcemia and hyperparathyroidism, which led to a mea

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

38 Hypocalcemia and hyperphosphatemia caused by parathyroid

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

40 etention required diuretic therapy, and mild hypocalcemia and hyperphosphatemia occurred in the setti

41 aracterized by parathyroid hormone-resistant hypocalcemia and hyperphosphatemia.

42 steosclerotic bone dysplasia with associated hypocalcemia and ocular abnormalities.

43 These perturbations lead to hypocalcemia and reduced bone mineral density, which was

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

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

46 Severe hypocalcemia and suboptimal hypocalcemia management afte

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

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

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

50 1,25(OH)(2)D(3) up-regulates VDR expression, hypocalcemia and vitamin D deficiency result in drastica

51 s associated with risks related to temporary hypocalcemia and vocal quality dysfunction.

52 safe and effective in reducing postoperative hypocalcemia and voice dysfunction rates in patients und

53 Evidence of hypocalcemia and voice dysfunction.

54 roid condition and no preoperative corrected hypocalcemia and voice or vocal quality dysfunction were

55 n proposed to have a physiological effect on hypocalcemia and voice quality.

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

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

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

59 onic ingestion of CA can cause urolithiasis, hypocalcemia, and duodenal cancer, emphasizing the need

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

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

62 Both hypocalcemia, and hypercalcemia at the time of admission

63 ications, such as anemia, hyperphosphatemia, hypocalcemia, and hypertension, often require pharmacolo

64 Hypomagnesemia, hypocalcemia, and hypokalemia were not found.

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

66 postoperative outcomes including RLN injury, hypocalcemia, and neck hematoma.

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

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

69 IONM was not associated with postoperative hypocalcemia (AOR, 0.99; 95% CI, 0.99-1.00) or neck hema

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

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

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

73 rosis (MS), can also occur in the context of hypocalcemia as a rare intriguing clinical scenario.

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

75 embrane targeting, and/or signaling, whereas hypocalcemia-associated missense variants increased expr

76 a higher incidence of transient symptomatic hypocalcemia at 2 weeks (38.0% vs. 19.3%, P<0.001).

77 The absolute reduction in the rate of hypocalcemia at 24 hours was 24% (95% CI, 11.9%-35.2%) a

78 Symptoms of hypocalcemia can be due to increased neuromuscular excit

79 Severe post-thyroidectomy hypocalcemia can be life-threatening; data on this speci

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

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

82 96 patients (4.2%) in the placebo group had hypocalcemia compared with no patients in the dexamethas

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

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

85 ategies required to monitor and treat severe hypocalcemia, denosumab should be administered after car

86 ge; in this subset, 59.1% experienced severe hypocalcemia despite being discharged with calcium and v

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

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

89 r a primary hospital or emergency department hypocalcemia diagnosis (emergent care).

90 somal dominant hypomagnesemia with secondary hypocalcemia disorder.

91 Patients with hypocalcemia due to CaR mutations also show disproportio

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

93 Our work indicates that hypocalcemia due to GoF in CASR with ADH1-associated sym

94 calcium drop, and 6 (5%) developed clinical hypocalcemia during (177)Lu-PSMA therapy.

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

96 ever, patients with two-session RFA had less hypocalcemia, especially those with high ALP.

97 Patients who experienced severe hypocalcemia had higher rates of nerve injury and unexpe

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

99 M6 in familial hypomagnesemia with secondary hypocalcemia (HSH).

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

101 iated with prevention of metabolic acidosis, hypocalcemia, hyperkalemia, and cardiac electrical distu

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

103 Biochemical tests revealed hypocalcemia, hyperphosphatemia and hypomagnesemia with

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

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

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

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

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

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

110 y higher incidence of severe and very severe hypocalcemia in female dialysis-dependent patients aged

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

112 The diagnosis of milk fever or hypocalcemia in lactating cows has a significant economi

113 Monitoring subclinical hypocalcemia in milk samples can expedite treatment and

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

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

116 Cinacalcet resulted in hypocalcemia in seven patients.

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

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

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

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

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

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

123 table and potentially important mechanism of hypocalcemia-induced bradycardia and asystole, potential

124 However, very rarely, case reports revealed hypocalcemia-induced optic neuritis as well as our case.

125 Hypocalcemia is a derangement in serum calcium level due

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

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

128 Postoperative hypocalcemia is one of the most common complications fol

129 Further evaluation of (177)Lu-PSMA-induced hypocalcemia is required to better understand mechanisms

130 Hypocalcemia is the most common complication after thyro

131 Severe hypocalcemia and suboptimal hypocalcemia management after thyroidectomy are common.

132 Conclusion: Hypocalcemia may occur in response to (177)Lu-PSMA-I&T,

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

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

135 significantly higher in those who developed hypocalcemia (median, 3,249 cm(3) [interquartile range,

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

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

138 When classifying patients into categories of hypocalcemia, normocalcemia, or hypercalcemia, unadjuste

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

140 Severe hypocalcemia occurred in 5.8% (n = 428) of 7366 thyroide

141 Hypocalcemia occurred more frequently with denosumab.

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

143 Severe hypocalcemia occurs after subtotal or total parathyroide

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

145 4.3% male patients), of whom 229 (10.9%) had hypocalcemia on admission.

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

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

148 sed odds of RLN injury, but no difference in hypocalcemia or neck hematoma.

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

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

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

152 Severe hypocalcemia patients had higher rates of recurrent lary

153 report a 43-year-old woman with a history of hypocalcemia presenting with optic neuritis, characteriz

154 The aim of the study was to determine severe hypocalcemia rate following thyroidectomy and factors as

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

156 he exact pathology and optimal management of hypocalcemia-related optic neuritis.

157 A severe hypocalcemic event was defined as hypocalcemia requiring intravenous calcium, emergent cli

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

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

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

161 lenging to identify asymptomatic subclinical hypocalcemia (SCH) in transition dairy cows.

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

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

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

165 Very severe hypocalcemia (serum calcium below 6.5 mg/dL [1.63 mmol/L

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

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

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

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

170 patient with acquired severe hypomagnesemia, hypocalcemia, tubulointerstitial nephropathy, and rapidl

171 Autosomal-dominant hypocalcemia type 1 (ADH1) is a rare genetic form of hyp

172 calcemia type 1 (FHH1) or autosomal-dominant hypocalcemia type 1 (ADH1), respectively, but the popula

173 receptor (CaSR) result in autosomal dominant hypocalcemia type 1 (ADH1), which may cause symptomatic

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

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

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

177 al disorder designated as autosomal dominant hypocalcemia type 2.

178 fore identified as having autosomal dominant hypocalcemia type 2.

179 reduced serum PTH levels in mice without the hypocalcemia typical of CaSR drugs.

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

181 Rate of severe hypocalcemia varied by diagnosis and procedure (0.5% for

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

183 The rate of symptomatic hypocalcemia was 19% lower in the dexamethasone group th

184 week weighted cumulative incidence of severe hypocalcemia was 41.1% with denosumab vs 2.0% with oral

185 tate-specific antigen response in those with hypocalcemia was 78% (SD, 24%).

186 weighted cumulative incidence of very severe hypocalcemia was also increased with denosumab (10.9%) v

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

188 After multivariate adjustment, severe hypocalcemia was associated with multiple factors includ

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

190 Severe hypocalcemia was defined as total albumin-corrected seru

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

192 This pronounced bradycardic effect of hypocalcemia was mediated primarily by I(CaL) attenuatio

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

194 Permanent hypocalcemia was more frequent after total or subtotal t

195 albumin requirements and the development of hypocalcemia was reduced.

196 Multivariate analysis showed that hypocalcemia was related to serum ALP.

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

198 ho presented during infancy with symptomatic hypocalcemia were found to have a homozygous serine (S)

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

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

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

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

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

204 higher frequency of postoperative transient hypocalcemia with autotransplantation (IRR=1.90, 95% CI:

205 hosphatemia with hyperparathyroidism, and of hypocalcemia with hyperparathyroidism were also associat

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

207 a type 1 (ADH1), which may cause symptomatic hypocalcemia with low parathyroid hormone concentrations

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

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

210 ptic neuritis could have an association with hypocalcemia, with or without elevated intracranial pres