ライフサイエンスコーパス: hyperparathyroidism

1 production of parathyroid hormone (secondary hyperparathyroidism).

2 and effective method for treating secondary hyperparathyroidism.

3 s and proteinuria in patients with secondary hyperparathyroidism.

4 n renal transplant recipients with secondary hyperparathyroidism.

5 additional tool in the evaluation of primary hyperparathyroidism.

6 h a decreased surgical cure rate for primary hyperparathyroidism.

7 There was no evidence of hyperparathyroidism.

8 ach does not independently predict recurrent hyperparathyroidism.

9 nd WT mice, indicating a secondary cause for hyperparathyroidism.

10 rative localization in patients with primary hyperparathyroidism.

11 venous sampling (SVS) in persistent primary hyperparathyroidism.

12 going parathyroidectomy for sporadic primary hyperparathyroidism.

13 e to sestamibi scintigraphy in patients with hyperparathyroidism.

14 ach to the majority of patients with primary hyperparathyroidism.

15 ated with inflammation, fluid retention, and hyperparathyroidism.

16 operated on 1-2 times previously because of hyperparathyroidism.

17 tions, with a particular emphasis on primary hyperparathyroidism.

18 i arm underwent operative treatment of their hyperparathyroidism.

19 ven in individuals with asymptomatic primary hyperparathyroidism.

20 nacalcet in renal transplant recipients with hyperparathyroidism.

21 roidectomy in patients with sporadic primary hyperparathyroidism.

22 for kidney transplant patients with tertiary hyperparathyroidism.

23 ffective for the treatment of posttransplant hyperparathyroidism.

24 , particularly in patients who had secondary hyperparathyroidism.

25 d cell proliferation causing hyperplasia and hyperparathyroidism.

26 failure pattern after parathyroidectomy for hyperparathyroidism.

27 reatment for patients suffering from primary hyperparathyroidism.

28 localization study for patients with primary hyperparathyroidism.

29 al approaches for many patients with primary hyperparathyroidism.

30 e majority of patients with sporadic primary hyperparathyroidism.

31 is recommended for all children with primary hyperparathyroidism.

32 tive patients undergoing surgery for primary hyperparathyroidism.

33 pocalcemia, hyperphosphatemia, and secondary hyperparathyroidism.

34 ill result in operative failure or recurrent hyperparathyroidism.

35 which to regulate PTH synthesis in secondary hyperparathyroidism.

36 tion of parathyroid lesions in patients with hyperparathyroidism.

37 lation of parathyroid TGF-alpha in secondary hyperparathyroidism.

38 parathyroid glands in patients with primary hyperparathyroidism.

39 ally invasive approaches to the treatment of hyperparathyroidism.

40 a subset of kindreds with familial isolated hyperparathyroidism.

41 parathyroid lesions in patients with primary hyperparathyroidism.

42 oid TGF-alpha self-upregulation in secondary hyperparathyroidism.

43 ent of patients with persistent or recurrent hyperparathyroidism.

44 arian and nonagenarian patients with primary hyperparathyroidism.

45 nt hypercalcemia due to persistent secondary hyperparathyroidism.

46 g recommended targets and adequately control hyperparathyroidism.

47 t deficiencies and the sequelae of secondary hyperparathyroidism.

48 ctively reduce PTH secretion in all forms of hyperparathyroidism.

49 r treatment of certain patients with primary hyperparathyroidism.

50 nt of psoriasis, osteoporosis, and secondary hyperparathyroidism.

51 changes often seen in patients with primary hyperparathyroidism.

52 ents were evaluated and explored for primary hyperparathyroidism.

53 he 2002 NIH workshop on asymptomatic primary hyperparathyroidism.

54 ion may represent therapeutic strategies for hyperparathyroidism.

55 diseases such as osteoporosis and secondary hyperparathyroidism.

56 modialysis with moderate to severe secondary hyperparathyroidism.

57 parathyroid function and the development of hyperparathyroidism.

58 ients with kidney transplants and persistent hyperparathyroidism.

59 a frequent but not universal complication of hyperparathyroidism.

60 to clarify the role of persistent (tertiary) hyperparathyroidism.

61 ditional notions of renal osteodystrophy and hyperparathyroidism.

62 fore reoperation for persistent or recurrent hyperparathyroidism.

63 ermanent recurrent laryngeal nerve injury or hyperparathyroidism.

64 cipients of renal transplants with secondary hyperparathyroidism.

65 The primary endpoint was the frequency of hyperparathyroidism 1-year posttransplant.

66 of limited neck exploration (LE) for primary hyperparathyroidism (1 degrees HPT).

67 binders on the skeletal lesions of secondary hyperparathyroidism (2 degrees HPT).

68 rgoing initial parathyroidectomy for primary hyperparathyroidism (2002-2014).

69 s were reviewed in 143 patients with primary hyperparathyroidism (35 men, 108 women; median ages, 58

70 Primary hyperparathyroidism, a disorder in which there is a tend

71 592 (22%) out of 2666 patients with classic hyperparathyroidism (abnormal calcium and PTH) were refe

72 ntrolling hypercalcemia caused by persistent hyperparathyroidism after kidney transplant.

73 cet in the treatment of persistent secondary hyperparathyroidism after kidney transplantation.

74 yroid hormone and the frequency of secondary hyperparathyroidism after kidney transplantation.

75 nrolled in a prospective study of leptin and hyperparathyroidism, all of whom were enrolled based on

76 reduce complications (such as for anemia and hyperparathyroidism), although outcome research to suppo

77 horus and attenuate progression of secondary hyperparathyroidism among patients with CKD who have nor

78 osities and marrow fibrosis are hallmarks of hyperparathyroidism and are present in bones of transgen

79 a fall in [Ca2+]o and [Mg2+]o with secondary hyperparathyroidism and bone resorption.

80 nized to be present in patients with primary hyperparathyroidism and critical for bone reconstruction

81 ed hematopoietic environment associated with hyperparathyroidism and erythropoietin may tie to a comm

82 d with beneficial effects in mouse models of hyperparathyroidism and heart failure without inducing s

83 t patients with normocalcaemic (subclinical) hyperparathyroidism and hypoparathyroidism have a low ri

84 range, 58-82 years) with biochemical primary hyperparathyroidism and inconclusive results at US and (

85 horylation for the pathogenesis of secondary hyperparathyroidism and indicate that mTORC1 is a signif

86 stamibi performs well in complicated primary hyperparathyroidism and is recommended as first-line ima

87 In CKD, uremic toxins, hyperparathyroidism and Klotho deficiency lead to chroni

88 Secondary hyperparathyroidism and loose stools were more frequent

89 Hyperparathyroidism and low vitamin D status have been i

90 ol is effective in decreasing posttransplant hyperparathyroidism and may have beneficial effects on r

91 y was performed on 110 patients with primary hyperparathyroidism and no prior neck surgery.

92 etic resonance (MR) imaging in patients with hyperparathyroidism and nonlocalized disease who have ne

93 Failure to diagnose primary hyperparathyroidism and refer patients to surgeons leads

94 was attended by the development of secondary hyperparathyroidism and severe osteomalacia.

95 effect of DBP on calcemic (osteoporosis and hyperparathyroidism) and cardiometabolic diseases (hyper

96 hosphatemia, vitamin D deficiency, secondary hyperparathyroidism, and anemia.

97 tients now present with asymptomatic primary hyperparathyroidism, and consensus guidelines have been

98 nd is seen in phosphate nephropathy, primary hyperparathyroidism, and distal renal tubular acidosis.

99 e, not requiring intervention), 22 (45%) had hyperparathyroidism, and eight (16%) had low amounts of

100 cidosis, hyperphosphatemia, hypoalbuminemia, hyperparathyroidism, and hypertension among 30,528 adult

101 ated with anemia, acidosis, hypoalbuminemia, hyperparathyroidism, and hypertension but only weakly as

102 ous or malignant thyroid nodules, coexisting hyperparathyroidism, and in patients with large goiters

103 , with prevalence similar to that of primary hyperparathyroidism, and is associated with altered dise

104 , altered calcium homeostasis, and secondary hyperparathyroidism, and may contribute to cardiovascula

105 ality are increased in patients with primary hyperparathyroidism, and might be predicted by parathyro

106 raditional symptoms in patients with primary hyperparathyroidism, and open the door to the continued

107 iency, with mineral abnormalities, secondary hyperparathyroidism, and osteomalacia.

108 ompletely avoided osteomalacia and secondary hyperparathyroidism, and simultaneously increased trabec

109 important role in the evaluation of primary hyperparathyroidism, and surgical referral may be predic

110 selected on the basis of stages 3 to 4 CKD, hyperparathyroidism, and the absence of hypercalcemia be

111 om were enrolled based on their diagnosis of hyperparathyroidism, and their candidacy for surgical in

112 inary concentrating ability, hypothyroidism, hyperparathyroidism, and weight gain.

113 s of mineral metabolism, including secondary hyperparathyroidism, are thought to contribute to extras

114 alcium absorption that resulted in secondary hyperparathyroidism as evidenced by increased serum 1,25

115 Secondary hyperparathyroidism as the result of chronic kidney dise

116 et al. demonstrate that in murine secondary hyperparathyroidism associated with CKD or Ca deficiency

117 kely to become a major therapy for secondary hyperparathyroidism associated with renal failure and fo

118 of kidney transplant patients with tertiary hyperparathyroidism at a single institution over a 7-yea

119 of medical and surgical therapy for primary hyperparathyroidism; based on measurements of quality of

120 ly to attenuate the progression of secondary hyperparathyroidism but also possibly to reduce the risk

121 time daily) significantly improved secondary hyperparathyroidism but did not alter measures of LV str

122 utive patients underwent surgery for primary hyperparathyroidism by a single surgeon between 1990 and

123 ral paricalcitol on posttransplant secondary hyperparathyroidism by conducting an open label randomiz

124 The treatment of secondary hyperparathyroidism by correction of serum calcium and p

125 At dosages sufficient to correct secondary hyperparathyroidism, calcitriol and paricalcitol were pr

126 e consistent finding of a high prevalence of hyperparathyroidism, calcium concentrations should be ch

127 Primary hyperparathyroidism can be cured by removal of the parat

128 Primary hyperparathyroidism can be cured by surgical removal of

129 Secondary hyperparathyroidism classically appears during the cours

130 Secondary hyperparathyroidism commonly complicates CKD and associa

131 nt, 29% of paricalcitol-treated subjects had hyperparathyroidism compared with 63% of untreated patie

132 Secondary hyperparathyroidism contributes to extraskeletal calcifi

133 Secondary hyperparathyroidism contributes to extraskeletal complic

134 Secondary hyperparathyroidism contributes to post-transplant CKD m

135 calcemia and raise physician awareness about hyperparathyroidism could improve outcomes and produce l

136 thyroid hormone levels were lower and severe hyperparathyroidism decreased significantly.

137 A significant proportion of patients with hyperparathyroidism do not undergo appropriate evaluatio

138 nts undergoing parathyroidectomy for primary hyperparathyroidism due to parathyroid hyperplasia betwe

139 signs include early onset diabetes, gout and hyperparathyroidism, elevated liver enzymes, and congeni

140 In secondary hyperparathyroidism, enhanced expression of TGF-alpha in

141 rming imaging before any surgery for primary hyperparathyroidism, even in the case of conventional bi

142 nonsyndromal form, termed familial isolated hyperparathyroidism (FIHP), or as part of a syndrome, su

143 imetic agents for the treatment of secondary hyperparathyroidism focused on the development of ring c

144 r sestamibi scintigraphy for any etiology of hyperparathyroidism from 2006 through 2010.

145 The surgical success rate for hyperparathyroidism from high-volume centers exceeds 95%

146 re pronounced in participants with secondary hyperparathyroidism (group-by-time interaction: P = 0.00

147 In summary, treatment of hyperparathyroidism halts late-stage progression of rode

148 Another variant of primary hyperparathyroidism has been described in which the seru

149 PTH concentrations in primary and secondary hyperparathyroidism have been associated with bone disea

150 ical guidelines for the treatment of primary hyperparathyroidism have been established by the 2002 NI

151 order (CKD-MBD) is associated with secondary hyperparathyroidism (HPT) and serum elevations in the ph

152 patients after curative surgery for primary hyperparathyroidism (HPT) have an elevated parathyroid h

153 Primary hyperparathyroidism (HPT) in multiple endocrine neoplasi

154 ts with end-stage renal disease will develop hyperparathyroidism (HPT).

155 ecursor of the classic hypercalcemic primary hyperparathyroidism (HPT).

156 of benign clonal expansion characteristic of hyperparathyroidism (HPT).

157 patients undergoing reoperative surgery for hyperparathyroidism (HPT).

158 Persistence of hyperparathyroidism, hypovitaminosis D, and immunosuppre

159 percalciuria was diagnosed in 15.6%, primary hyperparathyroidism in 1.6%, and normocalcemic hyperpara

160 DR 4-1 also effectively suppressed secondary hyperparathyroidism in 1alpha-hydroxylase knockout mice.

161 perparathyroidism in 1.6%, and normocalcemic hyperparathyroidism in 3.1% of the breast cancer populat

162 for understanding the aetiology of secondary hyperparathyroidism in chronic kidney disease (CKD).

163 ing evaluated for the treatment of secondary hyperparathyroidism in chronic kidney disease patients r

164 previously unreported mechanism of secondary hyperparathyroidism in CKD.

165 athyroid hormone may contribute to secondary hyperparathyroidism in CKD.

166 and is involved in the etiology of secondary hyperparathyroidism in CKD.

167 here is a significant incidence of secondary hyperparathyroidism in short-limb GBP patients, even tho

168 percalcemia, and 880 (8%) had a diagnosis of hyperparathyroidism in the medical record.

169 ce in 1418 nondialysis patients with CKD and hyperparathyroidism in the Veterans' Affairs Consumer He

170 y were, however, virtually absent in primary hyperparathyroidism, in which the transition between bon

171 iRNAs that were dysregulated in experimental hyperparathyroidism, including miR-29, miR-21, miR-148,

172 views the diagnosis and treatment of primary hyperparathyroidism, including recent literature on the

173 changes and presentation of sporadic primary hyperparathyroidism, including the assessment of neuroco

174 the regulation of these miRNAs in secondary hyperparathyroidism indicates their importance for parat

175 ed in the parathyroid of rats with secondary hyperparathyroidism induced by either chronic hypocalcem

176 tients receiving hemodialysis with secondary hyperparathyroidism (intact parathyroid hormone >/=300 p

177 Tertiary hyperparathyroidism is a common cause of hypercalcemia a

178 Primary hyperparathyroidism is a common endocrine disorder of ca

179 Primary hyperparathyroidism is a common endocrine disorder often

180 Primary hyperparathyroidism is a frequent and potentially debili

181 Secondary hyperparathyroidism is a frequent complication of chroni

182 Postkidney transplant hyperparathyroidism is a significant problem.

183 Primary hyperparathyroidism is an endocrine disorder characteriz

184 Hyperparathyroidism is an independent, potentially remed

185 Remedial surgery for primary hyperparathyroidism is challenging and requires meticulo

186 Secondary hyperparathyroidism is characterized by increased serum

187 Persistent hyperparathyroidism is common after kidney transplantati

188 Almost always, primary hyperparathyroidism is due to a benign overgrowth of par

189 Hyperparathyroidism is due to increased activity of the

190 Primary hyperparathyroidism is generally discovered when asympto

191 Hyperparathyroidism is present in up to 50% of transplan

192 Primary hyperparathyroidism is rare and due to an adenoma in up

193 Hyperparathyroidism is reported in 10% to 66% of renal t

194 Although the cause of primary hyperparathyroidism is still poorly understood, surgical

195 Primary hyperparathyroidism is the most common cause of hypercal

196 Although primary hyperparathyroidism is the most common cause of hypercal

197 Primary hyperparathyroidism is the third most common endocrine d

198 tcomes in patients with asymptomatic primary hyperparathyroidism is unproven, but data suggest that s

199 reatment for adults with symptomatic primary hyperparathyroidism, is recommended for all children wit

200 e human CDC73/HRPT2 gene are associated with hyperparathyroidism-jaw tumor (HPT-JT) syndrome, an auto

201 r gene, which is mutated in the germ line of hyperparathyroidism-jaw tumor patients.

202 the HRPT2 gene, mutations of which cause the hyperparathyroidism-jaw tumor syndrome (OMIM145001).

203 Parafibromin, the product of the HRPT2 (hyperparathyroidism-jaw tumor syndrome 2) tumor suppress

204 a gene recently implicated in the hereditary hyperparathyroidism-jaw tumor syndrome, parathyroid canc

205 ch as multiple endocrine neoplasia type 1 or hyperparathyroidism-jaw tumor syndrome.

206 The hyperparathyroidism-jaw tumour (HPT-JT) syndrome is an a

207 d hereditary parathyroid carcinomas, and the hyperparathyroidism-jaw tumour (HPT-JT) syndrome, which

208 nts frequently have hypercalcemia-associated hyperparathyroidism, limiting the role of vitamin D anal

209 Surgical amelioration of secondary hyperparathyroidism may outweigh the risk of parathyroid

210 3 patients with moderate-to-severe secondary hyperparathyroidism (median level of intact parathyroid

211 plant recipients treated with cinacalcet for hyperparathyroidism met inclusion criteria.

212 RNA) in parathyroid glands from experimental hyperparathyroidism models and patients receiving dialys

213 gery within the previous 24 months, familial hyperparathyroidism, multiglandular disease, and renal f

214 The phenomenon of normocalcemic hyperparathyroidism (NCHPT) remains largely unknown and

215 ypercalcaemia (FHH), neonatal severe primary hyperparathyroidism (NSHPT) or autosomal dominant hypoca

216 Secondary hyperparathyroidism occurred in 6.3% of the cohort and 1

217 Secondary hyperparathyroidism often occurs in chronic kidney disea

218 ed study of the endocrine effects of primary hyperparathyroidism on brain function.

219 The influence of persisting hyperparathyroidism on long-term clinical outcomes in RT

220 rther studies should determine if persistent hyperparathyroidism or its treatment influences long-ter

221 of parathyroid hormone (primary or tertiary hyperparathyroidism) or from an extrinsic abnormal chang

222 schemia - diabetes, end-stage renal failure, hyperparathyroidism, or even symptoms of left upper limb

223 ne (PTH), had documentation of hypercalcemia/hyperparathyroidism, or were referred to surgeons.

224 roid hormone (PTH) are seen in patients with hyperparathyroidism, or with infusion of PTH in rodents.

225 tionate short stature in children as well as hyperparathyroidism, osteomalacia, enthesopathies, osteo

226 After transplantation, persistent hyperparathyroidism (parathyroid hormone > 130 ng/L) and

227 In rat and human secondary hyperparathyroidism, parathyroid AP2 expression strongly

228 and calcium levels, recurrent or persistent hyperparathyroidism, parathyroid reoperations, morbidity

229 D deficiency is a common cause of secondary hyperparathyroidism, particularly in elderly people.

230 neral density (BMD) in patients with primary hyperparathyroidism (pHPT) and compare those results to

231 Parathyroid adenomas (PAs) causing primary hyperparathyroidism (PHPT) are histologically heterogene

232 mally invasive parathyroidectomy for primary hyperparathyroidism (pHPT) depends on the successful pre

233 Primary hyperparathyroidism (pHPT) is a common clinical entity,

234 Importance: Primary hyperparathyroidism (pHPT) is a common clinical problem

235 Primary hyperparathyroidism (PHPT) is a common endocrine disease

236 Primary hyperparathyroidism (PHPT) is a common endocrine disorde

237 Primary hyperparathyroidism (PHPT) is a common endocrinopathy ch

238 Symptomatic primary hyperparathyroidism (PHPT) is associated with increased

239 dical treatments on fracture risk in primary hyperparathyroidism (PHPT) is unknown.

240 changes are common in patients with primary hyperparathyroidism (pHPT), but the associations of seru

241 During parathyroidectomy for primary hyperparathyroidism (PHPT), discovering a minimally "enl

242 d parathyroid exploration (OPTX) for primary hyperparathyroidism (pHPT).

243 in older patients with asymptomatic primary hyperparathyroidism (PHPT).

244 land is the definitive treatment for primary hyperparathyroidism (pHPT).

245 asive parathyroidectomy (MIP) due to primary hyperparathyroidism (primary HPTH).

246 The prevalence of posttransplant, persistent hyperparathyroidism (PTH >65 pg/mL) was 89.5%, 86.8%, 83

247 ondary to hypocalcemia, hypophosphatemia, or hyperparathyroidism, rather than impaired VDR action.

248 parathyroid cell proliferation in secondary hyperparathyroidism rats and in vitro in uremic rat para

249 Twenty-nine subjects with secondary hyperparathyroidism received oral paricalcitol 1 mug/d f

250 hether a significant number of patients with hyperparathyroidism remain undiagnosed and untreated.

251 and high PTH strata, and rates of persistent hyperparathyroidism remained higher than 40% when define

252 consecutive remedial operations for primary hyperparathyroidism selectively used minimally invasive

253 In secondary hyperparathyroidism (SH), VDR content is reduced as hype

254 All patients with primary hyperparathyroidism should undergo localization studies

255 roid hyperplasia for patients with secondary hyperparathyroidism (SHPT) and to compare the outcome of

256 rence of 2 surgical strategies for secondary hyperparathyroidism (SHPT) within 36 months of follow-up

257 uring parathyroidectomy for sporadic primary hyperparathyroidism (SPHPT).

258 ified 159 patients with persistent/recurrent hyperparathyroidism subsequently cured with additional s

259 ECT/CT) in a patient with advanced secondary hyperparathyroidism successfully treated with surgery.

260 ng tests are not common, symptomatic primary hyperparathyroidism tends to predominate.

261 , MRAs attenuate the appearance of secondary hyperparathyroidism that accompanies excretory Ca2+ loss

262 n plasma-ionized [Ca2+]o and [Mg2+]o lead to hyperparathyroidism that accounts for bone wasting.

263 ediated gut-bone crosstalk in mice models of hyperparathyroidism that may help predict its clinical c

264 modialysis with moderate to severe secondary hyperparathyroidism, the use of etelcalcetide was not in

265 f what was necessary to return patients with hyperparathyroidism to a eucalcemic state, namely, excis

266 ed 3883 hemodialysis patients with secondary hyperparathyroidism to receive cinacalcet or placebo for

267 eans of left pancreatectomy 31 years before, hyperparathyroidism treated with subtotal parathyroidect

268 mplex is a product of the HRPT-2 (hereditary hyperparathyroidism type 2) tumor suppressor gene, which

269 physiologic imaging in patients with primary hyperparathyroidism undergoing parathyroidectomy.

270 Consecutive patients with primary hyperparathyroidism undergoing preoperative 4D-CTs and s

271 Between 1999 and 2007, 1407 patients with hyperparathyroidism underwent bilateral neck exploration

272 1 consecutive surgical patients with primary hyperparathyroidism underwent both (123)I/(99m)Tc-sestam

273 Patients with secondary hyperparathyroidism underwent ultrasound guided RFA of p

274 Methods: Patients who had hyperparathyroidism, underwent dual-time-point (18)F-FCH

275 modialysis with moderate to severe secondary hyperparathyroidism, use of etelcalcetide compared with

276 ductions in pretransplant and posttransplant hyperparathyroidism, vitamin D deficiency, and fracture

277 Increasing severity of hyperparathyroidism was associated with increased cortic

278 Secondary hyperparathyroidism was manifested in 28% of patients at

279 tive predictive value of BIJ PTH for primary hyperparathyroidism were 80% and 71%, respectively.

280 ients referred for reoperation of persistent hyperparathyroidism were included and investigated with

281 tal of 114 consecutive patients with primary hyperparathyroidism were included from January 8, 2008,

282 atients with a clinical diagnosis of primary hyperparathyroidism were included in the study.

283 of diabetes history, and posttransplantation hyperparathyroidism were not related to Charcot neuroart

284 iod, 1368 parathyroid operations for primary hyperparathyroidism were performed at our institution.

285 initial neck surgery for nonfamilial primary hyperparathyroidism were selected for analysis.

286 e control of pathogenic PTH function such as hyperparathyroidism, where control of excess hormonal ac

287 are vitamin D insufficient develop secondary hyperparathyroidism, which is associated with increased

288 Secondary hyperparathyroidism, which is defined by a high concentr

289 itamin D deficiency contributes to secondary hyperparathyroidism, which occurs early in chronic kidne

290 retrospective study of patients with primary hyperparathyroidism who underwent a combined imaging pro

291 Records of 462 patients with primary hyperparathyroidism who underwent preoperative imaging w

292 records were reviewed for 102 patients with hyperparathyroidism who underwent triple-phase 4D CT and

293 n patients with moderate-to-severe secondary hyperparathyroidism who were undergoing dialysis.

294 Study in primary and uraemic secondary hyperparathyroidism will indicate whether the efficacy o

295 fashion the brains of patients with primary hyperparathyroidism with functional imaging studies, sho

296 h for the treatment of patients with primary hyperparathyroidism with image-localized, presumed singl

297 ents underwent parathyroidectomy for primary hyperparathyroidism with ioPTH monitoring.

298 We examined the association of secondary hyperparathyroidism with risk of preeclampsia.

299 ave investigated treatment of posttransplant hyperparathyroidism with the calcimimetic agent cinacalc

300 We hypothesized that many patients with hyperparathyroidism would be untreated due to not consid