ライフサイエンスコーパス: hypercalcemia

1 c hypercalcemia (also termed familial benign hypercalcemia).

2 and normal mice without inducing significant hypercalcemia.

3 d heart failure without inducing significant hypercalcemia.

4 l use was associated with a greater risk for hypercalcemia.

5 on of vitamin D(3) (1,25(OH)(2)D(3))-induced hypercalcemia.

6 he gut providing a mechanism for the lack of hypercalcemia.

7 nosis, a condition typically associated with hypercalcemia.

8 rathyroid hormone levels as a consequence of hypercalcemia.

9 who have excess serum PTH levels, along with hypercalcemia.

10 No patients had persistent hypercalcemia.

11 secondary effects of hyperparathyroidism and hypercalcemia.

12 th parathyroid neoplasia as well as systemic hypercalcemia.

13 of new strategies to treat related forms of hypercalcemia.

14 he effects of severe hyperparathyroidism and hypercalcemia.

15 70 of 71 patients (99%) were cured of their hypercalcemia.

16 t peptide levels prior to the development of hypercalcemia.

17 n, causing high levels of 1,25D in serum and hypercalcemia.

18 Mice with lymphoma developed severe hypercalcemia.

19 d osteoclastic bone resorption and prevented hypercalcemia.

20 n one study, there was a higher incidence of hypercalcemia.

21 One patient had persistent hypercalcemia.

22 metabolism that results in hypercalcuria and hypercalcemia.

23 ure, radiation, spinal cord compression, and hypercalcemia.

24 ssion, irradiation of or surgery on bone, or hypercalcemia.

25 ction mutations cause familial hypocalciuric hypercalcemia.

26 complications, spinal cord compression, and hypercalcemia.

27 teoclast activation associated with systemic hypercalcemia.

28 nd thus may allow reduction in PTH with less hypercalcemia.

29 0% and completely blocked the development of hypercalcemia.

30 diate posttransplant period, and symptomatic hypercalcemia.

31 cluded leukopenia, hypertriglyceridemia, and hypercalcemia.

32 of 1,25-(OH)2D3 with subsequent symptomatic hypercalcemia.

33 considered in the differential diagnosis of hypercalcemia.

34 d in fishes where it functions in preventing hypercalcemia.

35 alignant tumors that mediates paraneoplastic hypercalcemia.

36 e gene at levels sufficient to cause humoral hypercalcemia.

37 osus (SLE), generalized lymphadenopathy, and hypercalcemia.

38 was blocked by verapamil and accentuated by hypercalcemia.

39 recombinant human interleukin-1alpha-induced hypercalcemia.

40 been disappointing in part to dose-limiting hypercalcemia.

41 -1 therapy even at high doses did not induce hypercalcemia.

42 the calcium-regulating gene TRPV6 leading to hypercalcemia.

43 ot cause detectable adverse effects, such as hypercalcemia.

44 ts is the presence of lytic bone lesions and hypercalcemia.

45 ons to levels that have been associated with hypercalcemia.

46 vitamin D receptor (VDR), but are devoid of hypercalcemia.

47 case of disseminated coccidioidomycosis with hypercalcemia.

48 crine regulator of gill Ca(2+) uptake during hypercalcemia.

49 an average of 4 years, 22% will progress to hypercalcemia.

50 ety of stresses including hyperlipidemia and hypercalcemia.

51 s that produce comedolysis in the absence of hypercalcemia.

52 During dietary-induced hypo- and hypercalcemia (0.59+/-0.06 and 1.58+/-0.12 mM [Ca2+]) th

53 28 to 35 days after injection and developed hypercalcemia (1.35 to 1.46 mmol/L) a mean of 5 days aft

54 ng potent anticancer activity, caused severe hypercalcemia (18 mg/dl).

55 All patients had hypercalcemia; 20 were asymptomatic and 18 had varying s

56 aled that 41% of the patients presented with hypercalcemia, 26% presented with hypophosphatemia, and

57 r bone surgery, spinal cord compression, and hypercalcemia (a serum calcium concentration above 12 mg

58 onary calcification and ossification include hypercalcemia, a local alkaline environment, and previou

59 bservations suggest that physiological fetal hypercalcemia, acting on the CaSR, promotes human fetal

60 ary hyperparathyroidism is a common cause of hypercalcemia after kidney transplant.

61 cemia in the child is familial hypocalciuric hypercalcemia (also termed familial benign hypercalcemia

62 inistered to RANK(-/-) mice without inducing hypercalcemia, although tumor necrosis factor alpha trea

63 tics of patients with familial hypocalciuric hypercalcemia, an autosomal-dominant disease arising fro

64 lar distribution between groups; no cases of hypercalcemia and 1 case of nephrolithiasis were reporte

65 roid calcium-sensing receptor (Casr) by both hypercalcemia and a calcimimetic that decreases PTH secr

66 Because PTHrP contributes to hypercalcemia and bone metastases, switching of G-protei

67 racterized by parathyroid hormone excess and hypercalcemia and caused by hypersecreting parathyroid g

68 Kidney allograft recipients with hypercalcemia and elevated intact parathyroid hormone (i

69 thyroidectomy is normocalcemia for 6 months; hypercalcemia and elevated iPTH after this time is recur

70 predictable response of symptoms related to hypercalcemia and elevated parathyroid hormone.

71 P6 may contribute to certain defects such as hypercalcemia and growth delay in WS.

72 one concentrations, these agents can lead to hypercalcemia and have been associated with increased va

73 Operative failure is defined as hypercalcemia and high intact (1-84) parathyroid hormone

74 pplementation resulted in increased risks of hypercalcemia and hypercalciuria, which were not dose re

75 e prevention), and adverse outcomes (such as hypercalcemia and hypercalcuria), especially in understu

76 are needed to investigate whether control of hypercalcemia and hyperphosphatemia in patients undergoi

77 s receiving dialysis is often complicated by hypercalcemia and hyperphosphatemia, which may contribut

78 d active vitamin D is potentially limited by hypercalcemia and hyperphosphatemia.

79 were examined: diet-induced hypophosphatemia/hypercalcemia and hypophosphatemia secondary to mutation

80 In pathologic circumstances such as hypercalcemia and in development, parathyroid hormone-re

81 tinued in four patients due to hypercalcuria/hypercalcemia and in one for preference.

82 - mice were unexpectedly less susceptible to hypercalcemia and its toxic effects.

83 utations, which cause familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism, s

84 orm of short-limbed dwarfism associated with hypercalcemia and normal or low serum concentrations of

85 alignant cells hold promise for treating the hypercalcemia and osteolysis associated with some cancer

86 ed bone resorption, including cancer-related hypercalcemia and Paget's disease of bone, studies have

87 ed bone resorption, including cancer-related hypercalcemia and Paget's disease of bone, studies were

88 rventions which prompt further evaluation of hypercalcemia and raise physician awareness about hyperp

89 mor-induced increases in bone resorption and hypercalcemia and rapidly normalized blood ionized calci

90 biotic that has been used in humans to treat hypercalcemia and several types of cancers.

91 mice bearing CHO/MIP-1alpha tumors developed hypercalcemia and significantly more osteolytic lesions

92 on bone that result in malignancy-associated hypercalcemia and suggest that TNF may not be responsibl

93 concentrations and an increased incidence of hypercalcemia and unintended suppression of parathyroid

94 surgery to bone, spinal cord compression, or hypercalcemia), and a pilot quantitative measurement of

95 ed, 2914 (28%) had a documented diagnosis of hypercalcemia, and 880 (8%) had a diagnosis of hyperpara

96 glucose and insulin, hypo- and hyperkalemia, hypercalcemia, and alcohol and cocaine toxicity.

97 nostic tool in the differential diagnosis of hypercalcemia, and approaches to inhibit its expression

98 various complications, including fractures, hypercalcemia, and bone pain, as well as reduced perform

99 rations were markedly increased in mice with hypercalcemia, and correlated with the increase in plasm

100 experienced a DLT: grade 3 headache, grade 3 hypercalcemia, and grade 3 noncardiogenic pulmonary edem

101 ut mice, which includes hyperparathyroidism, hypercalcemia, and hypophosphatemia, may confound the ef

102 (PTHrP) expression and plasma PTHrP, marked hypercalcemia, and increased bone resorption.

103 centage of participants with hypercalciuria, hypercalcemia, and nausea by 24% (CI, 20% to 27%), 23% (

104 Hypercalciuria, hypercalcemia, and nausea were more common in women who

105 hypertension, dysrhythmias, cardiomyopathy, hypercalcemia, and renal failure.

106 rs of mineral metabolism (hyperphosphatemia, hypercalcemia, and secondary hyperparathyroidism) are po

107 erparathyroidism is the most common cause of hypercalcemia, and the treatment is primarily surgical.

108 he chief toxicity of vitamin D3 compounds is hypercalcemia, and therefore, we examined calcemic activ

109 most common cause of hospital admission for hypercalcemia, and those at greatest risk are postmenopa

110 ring the diagnosis, inadequate evaluation of hypercalcemia, and under-referral to surgeons.

111 plenomegaly, elevated lactate dehydrogenase, hypercalcemia, and unusual immunophenotype, all indicato

112 nephrocalcinosis or develop hypercalciuria, hypercalcemia, anti-KRN23 antibodies, or elevated serum

113 t-mediated bone resorption and tumor-induced hypercalcemia are potent inhibitors of the enzyme.

114 ations, bone pain, pathologic fractures, and hypercalcemia, are a major source of morbidity and morta

115 y rate, and multiple event analysis) counted hypercalcemia as an SRE.

116 omeostasis with marked hyperphosphatemia and hypercalcemia as well as elevated serum levels of parath

117 The pathogenesis of hypercalcemia associated with infection is not clear.

118 Posttransplant patients frequently have hypercalcemia-associated hyperparathyroidism, limiting t

119 DLTs included hypercalcemia at 15 mg/m(2); hypophosphatemia/hypokalemi

120 o 27-2014 in mice and found it not to induce hypercalcemia at doses of 0.05 microg i.p. three times p

121 10% to 20% of all patients with cancer have hypercalcemia at some point in their disease trajectory,

122 CKD, hyperparathyroidism, and the absence of hypercalcemia before calcitriol use and then were matche

123 (ATL), a disease frequently associated with hypercalcemia, bone destruction, and a fatal course refr

124 ntext of parathyroid hormone (PTH)-dependent hypercalcemia, but the role of Casr in the kidney is unk

125 bone formation and bone mass without causing hypercalcemia, but their effects on fractures are unknow

126 is a loss-of-function mutation that produces hypercalcemia by reducing the number of normally functio

127 ting for >1 year after the transplant, acute hypercalcemia (calcium >12.5 mg/dl) in the immediate pos

128 She was being followed up for mild hypercalcemia (calcium level, 10.8 mg/dL [2.7 mmol/L]) (

129 because the causes and clinical features of hypercalcemia can differ in these two age groups.

130 with multiple myeloma, rheumatoid arthritis, hypercalcemia, cancer cachexia, and Castleman's disease.

131 erparathyroidism is the most common cause of hypercalcemia, cancer is the most common cause requiring

132 breast-cancer cells as well as the degree of hypercalcemia caused by excessive PTHrP production by a

133 re effective than cinacalcet for controlling hypercalcemia caused by persistent hyperparathyroidism a

134 mice induces extensive osteolysis and severe hypercalcemia, daily administration of muRANK.Fc from ti

135 No lytic lesions or hypercalcemia developed in the controls.

136 Importantly, hypercalcemia did not occur before achieving target seru

137 ive drug for the treatment of posttransplant hypercalcemia due to persistent secondary hyperparathyro

138 etardation, specific neurocognitive profile, hypercalcemia during infancy, distinctive facial feature

139 -)/slc34a1(m/m)) displayed hypophosphatemia, hypercalcemia, elevated levels of alkaline phosphatase,

140 llary involvement, anemia, thrombocytopenia, hypercalcemia, elevated serum beta(2)-microglobulin and

141 itizing factors include refluxed bile acids, hypercalcemia, ethanol, hypertriglyceridemia, and acidos

142 The humoral hypercalcemia factor parathyroid hormone-related protein

143 n described in the disorders familial benign hypercalcemia (FBH), neonatal severe hyperparathyroidism

144 ate resembling familial benign hypocalciuric hypercalcemia (FBHH).

145 ercalcemic disorders, familial hypocalciuric hypercalcemia (FHH) and neonatal severe hyperparathyroid

146 the increase in osteolytic bone lesions and hypercalcemia found in ATL patients.

147 center between 2011 and 2015, and identified hypercalcemia (>10.5 mg/dL) in 10,432 patients.

148 related patients with familial hypocalciuric hypercalcemia had a missense GNA11 mutation (Leu135Gln).

149 Hyperphosphatemia and hypercalcemia have been associated with increased corona

150 3) analogs that may limit side effects (e.g. hypercalcemia) have created interest in examining this s

151 found that Tax+ mice spontaneously developed hypercalcemia, high-frequency osteolytic bone metastases

152 They have the potential for causing hypercalcemia, however, and patients often become resist

153 chemical changes included hyperphosphatemia, hypercalcemia, hyperaldosteronism, and elevated levels o

154 Severe hypercalcemia ("hypercalcemic crisis") should be managed

155 to calcium metabolism in RCTs, specifically hypercalcemia, hypercalciuria, and kidney stones, in par

156 fect of vitamin D supplementation on risk of hypercalcemia, hypercalciuria, or kidney stones was not

157 reported >/=1 of the following side effects: hypercalcemia, hypercalciuria, or kidney stones.

158 athyroid hormone (PTH), had documentation of hypercalcemia/hyperparathyroidism, or were referred to s

159 yroidism due to end-stage renal disease, but hypercalcemia, hyperphosphatemia, or both often develop

160 Idiopathic infantile hypercalcemia (IIH) is characterized by severe hypercalc

161 erall success rate in terms of resolution of hypercalcemia in 97% (215/222) of patients.

162 e patients to control the symptoms of severe hypercalcemia in a palliative setting.

163 insight into the mechanism of metastasis and hypercalcemia in advanced breast cancers.

164 of PTHrP gene expression were able to cause hypercalcemia in athymic mice.

165 fine hypercalcemia levels, common causes for hypercalcemia in children, and treatment in order to aid

166 Injection of PTH caused hypercalcemia in Fgf2+/+ but not Fgf2-/mice.

167 t excess production of PTHrP is the cause of hypercalcemia in granulomatous infections.

168 5-dihydroxyvitamin D3 was not accompanied by hypercalcemia in rats.

169 One rare cause of hypercalcemia in the child is familial hypocalciuric hyp

170 ibitor was shown to attenuate PTH-stimulated hypercalcemia in the TPTX rat model.

171 my was superior to cinacalcet in controlling hypercalcemia in these patients with kidney transplants

172 242784 completely prevented retinoid-induced hypercalcemia in thyroparathyroidectomized (TPTX) rats w

173 for bone marrow in blacks, and DPB1*0101 for hypercalcemia in whites).

174 Injection of PTH above the calvaria caused hypercalcemia in wild-type but not PGHS-2(-/-) mice.

175 Further, TSP-1 blockade attenuates hypercalcemia induced by parathyroid hormone in vivo.

176 levels of the protein significantly reduced hypercalcemia induced by PTHrP by about 50%, and signifi

177 These findings may explain why hypercalcemia inhibits Na(+) reabsorption in the proxima

178 nd initiate the proper response.Asymptomatic hypercalcemia is a common metabolic derangement that is

179 Familial hypocalciuric hypercalcemia is a genetically heterogeneous disorder wi

180 Hypercalcemia is an uncommon complication of disseminate

181 Hypercalcemia is commonly caused by the increased produc

182 In most cases, hypercalcemia is due to osteoclastic bone resorption, an

183 e medical treatment of severe or symptomatic hypercalcemia is to increase the urinary excretion of ca

184 increased PTHrP production in a patient with hypercalcemia is virtually pathognomonic of malignancy.

185 In terms of in vivo toxicity (hypercalcemia), ketone 2b is strongly calcemic in rats,

186 In this review, we define hypercalcemia levels, common causes for hypercalcemia in

187 In order to discover VDR ligands with less hypercalcemia liability, we sought to identify tissue-se

188 ale neonate presented with moderately severe hypercalcemia, markedly undermineralized bones, and mult

189 Hypercalcemia may result if there is disseminated infect

190 ated mice showed hyponatremia, hyperkalemia, hypercalcemia, metabolic acidosis, and increased serum l

191 with renal phosphate wasting and symptomatic hypercalcemia, mutations in CYP24A1 were excluded.

192 metaphyseal chondrodysplasia but less severe hypercalcemia, no receptor mutations were detected.

193 Depending on the criteria used, hypercalcemia occurred in 2.8% to 9.0% and hypercalciuri

194 Humoral hypercalcemia of malignancy (HHM) is caused by the secre

195 se associated with breast cancer and humoral hypercalcemia of malignancy (HHM) that occurs with or wi

196 imately 80% of ATLL patients develop humoral hypercalcemia of malignancy (HHM), a life-threatening co

197 us type-1 (HTLV-1) infection develop humoral hypercalcemia of malignancy (HHM).

198 ized as the major causative agent of humoral hypercalcemia of malignancy (HHM).

199 phonates, is widely used in the treatment of hypercalcemia of malignancy and osteolytic metastases.

200 g as a novel therapeutic approach in humoral hypercalcemia of malignancy and possibly multiple myelom

201 In a model of humoral hypercalcemia of malignancy in which PTHrP secreted by s

202 The potent effects of OPG in this humoral hypercalcemia of malignancy model suggest a potential th

203 Humoral hypercalcemia of malignancy results from the effects of

204 , the drug was approved for the treatment of hypercalcemia of malignancy.

205 tivity in a syngeneic tumor model of humoral hypercalcemia of malignancy.

206 rosis, Paget's disease, bone metastasis, and hypercalcemia of malignancy.

207 (PTHrP) is the agent responsible for humoral hypercalcemia of malignancy.

208 immune deficiency mice and produced humoral hypercalcemia of malignancy.

209 as the tumor product responsible for humoral hypercalcemia of malignancy.

210 vered as a tumor product that causes humoral hypercalcemia of malignancy.

211 t likely underlies the inhibitory actions of hypercalcemia on the urinary-concentrating mechanism in

212 OPG, given either at the onset of hypercalcemia or after it had occurred, blocked tumor-in

213 ped cardiac calcifications in the absence of hypercalcemia or elevation of the phosphocalcic product

214 Atypical presentations with hypercalcemia or eosinophilia have been reported.

215 No hypercalcemia or hypercalciuria was observed.

216 ontrol and 15 treatment patients due to mild hypercalcemia or hypercalcuria.

217 r metastatic to bone, even in the absence of hypercalcemia or increased circulating plasma concentrat

218 developed osteolytic bone metastasis without hypercalcemia or increased plasma PTHrP concentrations.

219 ns could be induced easily and reversibly by hypercalcemia or isoproterenol.

220 tients treated with aminobisphosphonates for hypercalcemia or metastatic bone disease often present w

221 reducing serum phosphorus but does not cause hypercalcemia or other adverse metabolic effects.

222 ion of 1 alpha,25(OH(2))D(3) without causing hypercalcemia or resistance.

223 ively infected cells may be important in the hypercalcemia, osteolytic bone lesions, neutrophilia, el

224 sphonates are drugs used in the treatment of hypercalcemia, Paget's disease, osteoporosis, and malign

225 Rates of hypercalcemia peaked at 48% at week 8 in the high PTH st

226 nor parathyroid hormone, at doses that cause hypercalcemia, produce direct effects on TZR density in

227 tal parathyroidectomy was performed at 6 wk; hypercalcemia recurred rapidly but the bone disease impr

228 nifestations including anemia, bone lesions, hypercalcemia, renal dysfunction, and compromised immune

229 diagnosis based on manifestations including hypercalcemia, renal failure, anemia, and bone lesions,

230 ients with light chain (AL) amyloidosis with hypercalcemia, renal failure, anemia, and lytic bone les

231 Hypercalcemia requires aggressive intravenous hydration

232 Persistent hypercalcemia requires another surgical procedure.

233 ACTH resistance, and familial hypocalciuric hypercalcemia, respectively.

234 In addition, these ligands did not cause hypercalcemia resulting from stimulation of the transcri

235 t on S-Ca concentrations and no incidence of hypercalcemia (S-Ca >2.6 nmol/L).

236 The use of furosemide in the management of hypercalcemia should no longer be recommended.

237 Surgery to correct the hypercalcemia significantly ameliorates the ZES.

238 re-evaluation, we observed hypocalciuria and hypercalcemia, suggesting Gitelman syndrome (GS).

239 rgery on bone, and spinal cord compression), hypercalcemia (symptoms or a serum calcium concentration

240 e normal CaR, producing NHPT and more severe hypercalcemia than typically seen with FBHH.

241 disseminated intravascular coagulopathy and hypercalcemia that characterize these cases.

242 eir expanded use and clinical development is hypercalcemia that develops as a result of the action of

243 tely elevated parathyroid hormone levels, or hypercalcemia that had lasted for more than a year and h

244 Because the precipitant was OSPS rather than hypercalcemia, these cases are best termed acute phospha

245 r disseminated intravascular coagulation and hypercalcemia, these syndromes are rare.

246 urves were constructed by inducing hypo- and hypercalcemia through alterations in dialysate calcium c

247 ic progression of breast cancer by promoting hypercalcemia, tumor growth, and osteolytic bone metasta

248 i) signaling, lead to familial hypocalciuric hypercalcemia type 2 (FHH2) and autosomal dominant hypoc

249 sis in a kindred with familial hypocalciuric hypercalcemia type 2 and in nine unrelated patients with

250 The kindred with familial hypocalciuric hypercalcemia type 2 had an in-frame deletion of a conse

251 oss of function cause familial hypocalciuric hypercalcemia type 2, and Galpha11 mutants with gain of

252 xpression showed that familial hypocalciuric hypercalcemia type 2-associated mutations decreased the

253 o proteins, result in familial hypocalciuric hypercalcemia type 3 (FHH3), an extracellular calcium ho

254 ne HR 0.31; 95% CI 0.13-0.73; p = 0.007) and hypercalcemia (valproate HR 0.25; 95% CI 0.10-0.60; p =

255 Hypercalcemia was asymptomatic and reversible.

256 Of the 7 genetically positive patients, hypercalcemia was either present at the time of diagnosi

257 ver, even when treatment was initiated after hypercalcemia was established, muRANK.Fc significantly a

258 .25 to 0.5 microgram/d, and the incidence of hypercalcemia was quite low with these doses.

259 No significant hypercalcemia was seen in a subset of participants.

260 In 37 studies, hypercalcemia was shown with increased risk shown for th

261 and bone metabolism, a murine tumor model of hypercalcemia was used.

262 Because the chief toxicity of vitamin D3 is hypercalcemia, we examined the calcemic activity of 1,25

263 H)2D3 is limited by the major side effect of hypercalcemia, we investigated the potential therapeutic

264 ere chronic kidney disease, thyroid disease, hypercalcemia, weight gain, hypertension, type 2 diabete

265 or surgery to treat bone complications, and hypercalcemia were also statistically less for the pamid

266 ry to bone, and spinal cord compression) and hypercalcemia were assessed monthly.

267 Episodes of hypercalcemia were more frequent in the paricalcitol gro

268 ologic fracture, spinal cord compression, or hypercalcemia, were taken directly from the trials.

269 Controls or ARH-77 mice, after developing hypercalcemia, were then killed and bone marrow plasma f

270 tations in the CASR have been shown to cause hypercalcemia when homozygous.

271 However, 1,25-(OH)2D3 can induce hypercalcemia, which often precludes its use.

272 related patients with familial hypocalciuric hypercalcemia who did not have mutations in the gene enc

273 We describe a patient with unexplained hypercalcemia who under went bone scintigraphy, which de

274 percalcemia (IIH) is characterized by severe hypercalcemia with failure to thrive, vomiting, dehydrat

275 athologically confirmed hyperparathyroidism, hypercalcemia with inappropriately elevated parathyroid

276 he CaSR causes fetal hyperparathyroidism and hypercalcemia, with additional effects on placental calc

277 e of furosemide in the medical management of hypercalcemia yields only case reports published before