ライフサイエンスコーパス: hypercalcemia

1 c hypercalcemia (also termed familial benign hypercalcemia).

2 ety of stresses including hyperlipidemia and hypercalcemia.

3 s that produce comedolysis in the absence of 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 nosis, a condition typically associated with hypercalcemia.

7 rathyroid hormone levels as a consequence of hypercalcemia.

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

9 he incidence rate of kidney stone events, or 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 n, causing high levels of 1,25D in serum and hypercalcemia.

17 Mice with lymphoma developed severe hypercalcemia.

18 d osteoclastic bone resorption and prevented hypercalcemia.

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

20 One patient had persistent hypercalcemia.

21 metabolism that results in hypercalcuria and hypercalcemia.

22 and normal mice without inducing significant 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 -1 therapy even at high doses did not induce hypercalcemia.

30 the calcium-regulating gene TRPV6 leading to hypercalcemia.

31 0% and completely blocked the development of hypercalcemia.

32 diate posttransplant period, and symptomatic hypercalcemia.

33 cluded leukopenia, hypertriglyceridemia, and hypercalcemia.

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

35 considered in the differential diagnosis of hypercalcemia.

36 d in fishes where it functions in preventing hypercalcemia.

37 alignant tumors that mediates paraneoplastic hypercalcemia.

38 e gene at levels sufficient to cause humoral hypercalcemia.

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

40 was blocked by verapamil and accentuated by hypercalcemia.

41 recombinant human interleukin-1alpha-induced hypercalcemia.

42 d heart failure without inducing significant hypercalcemia.

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

44 t peptide levels prior to the development of hypercalcemia.

45 significant and tolerated without developing hypercalcemia.

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

47 been disappointing in part to dose-limiting hypercalcemia.

48 ot cause detectable adverse effects, such as hypercalcemia.

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

50 ons to levels that have been associated with hypercalcemia.

51 ocrine tumor was the cause of the refractory hypercalcemia.

52 case of disseminated coccidioidomycosis with hypercalcemia.

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

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

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

56 28 to 35 days after injection and developed hypercalcemia (1.35 to 1.46 mmol/L) a mean of 5 days aft

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 is a common endocrinopathy characterized by hypercalcemia and elevated levels of parathyroid hormone

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

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

76 nt proportion of cancer patients suffer from hypercalcemia and have a worse prognosis.

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

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

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

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

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

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

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

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

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

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

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

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

89 ution of TRPV5 in disease phenotypes such as hypercalcemia and nephrolithiasis.

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

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

92 leukemia, a disease commonly associated with hypercalcemia and osteolysis.

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

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

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

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

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

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

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

100 lytic tumor formation and the development of hypercalcemia and tumor-associated inflammation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

127 Functional studies showed that all hypercalcemia-associated missense variants impaired hete

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

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

130 10% to 20% of all patients with cancer have hypercalcemia at some point in their disease trajectory,

131 Both hypocalcemia, and hypercalcemia at the time of admission were associated w

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

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

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

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

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

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

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

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

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

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

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

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

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

145 No lytic lesions or hypercalcemia developed in the controls.

146 Importantly, hypercalcemia did not occur before achieving target seru

147 a case of calcitriol overproduction-induced hypercalcemia due to a pancreatic neuroendocrine tumor.

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

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

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

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

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

153 vestigated the incidence of kidney stone and hypercalcemia events in a large, population-based RCT of

154 The humoral hypercalcemia factor parathyroid hormone-related protein

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

156 ate resembling familial benign hypocalciuric hypercalcemia (FBHH).

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

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

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

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

161 Hyperphosphatemia and hypercalcemia have been associated with increased corona

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

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

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

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

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

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

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

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

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

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

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

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

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

175 r, causes nephrogenic diabetes insipidus and hypercalcemia in about 20% and 10% of patients, respecti

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

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

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

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

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

181 5-dihydroxyvitamin D3 was not accompanied by hypercalcemia in rats.

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

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

184 mple annual blood test, there was no case of hypercalcemia in the vitamin D arm, compared with 1 in t

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

186 242784 completely prevented retinoid-induced hypercalcemia in thyroparathyroidectomized (TPTX) rats w

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

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

189 Additional causes of hypercalcemia include granulomatous disease such as sarc

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

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

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

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

194 Familial hypocalciuric hypercalcemia is a genetically heterogeneous disorder wi

195 Hypercalcemia is an uncommon complication of disseminate

196 Hypercalcemia is commonly caused by the increased produc

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

198 In rare cases the cause of the hypercalcemia is excessive production of calcitriol, the

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

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

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

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

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

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

205 Hypercalcemia may result if there is disseminated infect

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

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

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

209 verse events between groups, with 3 cases of hypercalcemia, none of nephrolithiasis, and 249 falls ob

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

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

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

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

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

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

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

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

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

219 Hypercalcemia of malignancy is not uncommon in patients

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

221 Humoral hypercalcemia of malignancy results from the effects of

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

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

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

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

226 immune deficiency mice and produced humoral hypercalcemia of malignancy.

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

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

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

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

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

232 Atypical presentations with hypercalcemia or eosinophilia have been reported.

233 No hypercalcemia or hypercalciuria was observed.

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

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

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

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

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

239 No excess risks of hypercalcemia or other adverse events were identified.

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

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

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

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

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

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

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

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

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

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

250 Hypercalcemia requires aggressive intravenous hydration

251 Persistent hypercalcemia requires another surgical procedure.

252 ACTH resistance, and familial hypocalciuric hypercalcemia, respectively.

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

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

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

256 Surgery to correct the hypercalcemia significantly ameliorates the ZES.

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

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

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

260 disseminated intravascular coagulopathy and hypercalcemia that characterize these cases.

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

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

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

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

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

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

267 ction mutations cause familial hypocalciuric hypercalcemia type 1 (FHH1) or autosomal-dominant hypoca

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

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

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

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

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

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

274 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 =

275 Hypercalcemia was asymptomatic and reversible.

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

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

278 d acidosis only in one mouse strain, whereas hypercalcemia was found in four strains.

279 .25 to 0.5 microgram/d, and the incidence of hypercalcemia was quite low with these doses.

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

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

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

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

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

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

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

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

288 Episodes of hypercalcemia were more frequent in the paricalcitol gro

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

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

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

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

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

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

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

296 athologically confirmed hyperparathyroidism, hypercalcemia with inappropriately elevated parathyroid

297 Biochemical evaluation showed hypercalcemia with markedly increased calcitriol levels.

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

299 In conclusion, FHH1 is a common cause of hypercalcemia, with prevalence similar to that of primar

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