ライフサイエンスコーパス: hyperparathyroidism

1 production of parathyroid hormone (secondary hyperparathyroidism).

2 localization study for patients with primary hyperparathyroidism.

3 ach does not independently predict recurrent hyperparathyroidism.

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

5 diseases such as osteoporosis and secondary hyperparathyroidism.

6 venous sampling (SVS) in persistent primary hyperparathyroidism.

7 going parathyroidectomy for sporadic primary hyperparathyroidism.

8 e to sestamibi scintigraphy in patients with hyperparathyroidism.

9 ach to the majority of patients with primary hyperparathyroidism.

10 ated with inflammation, fluid retention, and hyperparathyroidism.

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

12 tions, with a particular emphasis on primary hyperparathyroidism.

13 i arm underwent operative treatment of their hyperparathyroidism.

14 ven in individuals with asymptomatic primary hyperparathyroidism.

15 nacalcet in renal transplant recipients with hyperparathyroidism.

16 roidectomy in patients with sporadic primary hyperparathyroidism.

17 for kidney transplant patients with tertiary hyperparathyroidism.

18 ffective for the treatment of posttransplant hyperparathyroidism.

19 , particularly in patients who had secondary hyperparathyroidism.

20 failure pattern after parathyroidectomy for hyperparathyroidism.

21 modialysis with moderate to severe secondary hyperparathyroidism.

22 al approaches for many patients with primary hyperparathyroidism.

23 e majority of patients with sporadic primary hyperparathyroidism.

24 is recommended for all children with primary hyperparathyroidism.

25 tive patients undergoing surgery for primary hyperparathyroidism.

26 pocalcemia, hyperphosphatemia, and secondary hyperparathyroidism.

27 ill result in operative failure or recurrent hyperparathyroidism.

28 which to regulate PTH synthesis in secondary hyperparathyroidism.

29 tion of parathyroid lesions in patients with hyperparathyroidism.

30 lation of parathyroid TGF-alpha in secondary hyperparathyroidism.

31 parathyroid glands in patients with primary hyperparathyroidism.

32 ally invasive approaches to the treatment of hyperparathyroidism.

33 a subset of kindreds with familial isolated hyperparathyroidism.

34 parathyroid lesions in patients with primary hyperparathyroidism.

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

36 ent of patients with persistent or recurrent hyperparathyroidism.

37 arian and nonagenarian patients with primary hyperparathyroidism.

38 nt hypercalcemia due to persistent secondary hyperparathyroidism.

39 g recommended targets and adequately control hyperparathyroidism.

40 t deficiencies and the sequelae of secondary hyperparathyroidism.

41 ctively reduce PTH secretion in all forms of hyperparathyroidism.

42 r treatment of certain patients with primary hyperparathyroidism.

43 nt of psoriasis, osteoporosis, and secondary hyperparathyroidism.

44 changes often seen in patients with primary hyperparathyroidism.

45 ents were evaluated and explored for primary hyperparathyroidism.

46 he 2002 NIH workshop on asymptomatic primary hyperparathyroidism.

47 um calcium and PTH concentrations in primary hyperparathyroidism.

48 omas or hyperplasia in patients with primary hyperparathyroidism.

49 parathyroid function and the development of hyperparathyroidism.

50 ients with kidney transplants and persistent hyperparathyroidism.

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

52 ditional notions of renal osteodystrophy and hyperparathyroidism.

53 fore reoperation for persistent or recurrent hyperparathyroidism.

54 ermanent recurrent laryngeal nerve injury or hyperparathyroidism.

55 cipients of renal transplants with secondary hyperparathyroidism.

56 s and proteinuria in patients with secondary hyperparathyroidism.

57 n renal transplant recipients with secondary hyperparathyroidism.

58 additional tool in the evaluation of primary hyperparathyroidism.

59 h a decreased surgical cure rate for primary hyperparathyroidism.

60 There was no evidence of hyperparathyroidism.

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

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

63 regarding the care of patients with primary hyperparathyroidism (1 degrees HPTH) has evolved in para

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

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

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

67 ents with ESRD commonly experience secondary hyperparathyroidism, a condition primarily managed with

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

69 592 (22%) out of 2666 patients with classic hyperparathyroidism (abnormal calcium and PTH) were refe

70 cinoma is an extremely rare cause of primary hyperparathyroidism, accounting for fewer than 1% of cas

71 ntrolling hypercalcemia caused by persistent hyperparathyroidism after kidney transplant.

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

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

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

75 ium and vitamin D deficiencies and secondary hyperparathyroidism also contribute.

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 The most common etiologies are primary hyperparathyroidism and cancer.

81 H may be affected by the degree of secondary hyperparathyroidism and concurrent treatment with vitami

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

83 diet (Nx-Phos) to induce advanced secondary hyperparathyroidism and divided into the following group

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

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

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

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

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

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

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

91 Secondary hyperparathyroidism and loose stools were more frequent

92 Hyperparathyroidism and low vitamin D status have been i

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

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

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

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

97 een associated with progression of secondary hyperparathyroidism and renal osteodystrophy.

98 D metabolism, and the treatment of secondary hyperparathyroidism and renal osteodystrophy.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 Secondary hyperparathyroidism as the result of chronic kidney dise

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

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

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

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

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

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

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

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

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

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

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

129 Primary hyperparathyroidism can be cured by removal of the parat

130 Primary hyperparathyroidism can be cured by surgical removal of

131 Secondary hyperparathyroidism classically appears during the cours

132 Secondary hyperparathyroidism commonly complicates CKD and associa

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

134 Secondary hyperparathyroidism contributes to extraskeletal calcifi

135 Secondary hyperparathyroidism contributes to extraskeletal complic

136 Secondary hyperparathyroidism contributes to post-transplant CKD m

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 Primary hyperparathyroidism (HPT) in multiple endocrine neoplasi

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

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

158 patients undergoing reoperative surgery for hyperparathyroidism (HPT).

159 procedure of choice in patients with primary hyperparathyroidism (HPT).

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

161 Persistence of hyperparathyroidism, hypovitaminosis D, and immunosuppre

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

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

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

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

166 previously unreported mechanism of secondary hyperparathyroidism in CKD.

167 athyroid hormone may contribute to secondary hyperparathyroidism in CKD.

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

169 r than 30 months, the incidence of recurrent hyperparathyroidism in patients followed for longer than

170 therapeutic option for controlling secondary hyperparathyroidism in patients with chronic kidney dise

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

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

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

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

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

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

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

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

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

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

181 Tertiary hyperparathyroidism is a common cause of hypercalcemia a

182 Primary hyperparathyroidism is a common endocrine disorder of ca

183 Primary hyperparathyroidism is a common endocrine disorder often

184 Primary hyperparathyroidism is a frequent and potentially debili

185 Secondary hyperparathyroidism is a frequent complication of chroni

186 Postkidney transplant hyperparathyroidism is a significant problem.

187 Primary hyperparathyroidism is an endocrine disorder characteriz

188 Hyperparathyroidism is an independent, potentially remed

189 Remedial surgery for primary hyperparathyroidism is challenging and requires meticulo

190 Management of secondary hyperparathyroidism is challenging with traditional ther

191 Secondary hyperparathyroidism is characterized by increased serum

192 Persistent hyperparathyroidism is common after kidney transplantati

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

194 Hyperparathyroidism is due to increased activity of the

195 Primary hyperparathyroidism is generally discovered when asympto

196 Hyperparathyroidism is present in up to 50% of transplan

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

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

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

200 Primary hyperparathyroidism is the most common cause of hypercal

201 Although primary hyperparathyroidism is the most common cause of hypercal

202 Primary hyperparathyroidism is the third most common endocrine d

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

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

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

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

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

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

209 cinomas and benign and malignant tumors from Hyperparathyroidism-Jaw Tumor Syndrome patients, and (3)

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

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

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

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

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

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

216 3 patients with moderate-to-severe secondary hyperparathyroidism (median level of intact parathyroid

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

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

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

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

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

222 Secondary hyperparathyroidism often occurs in chronic kidney disea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

239 Primary hyperparathyroidism (PHPT) is a common endocrine disease

240 Symptomatic primary hyperparathyroidism (PHPT) is associated with increased

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

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

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

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

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

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

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

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

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

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

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

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

253 in children with renal failure and secondary hyperparathyroidism require further studies to evaluate

254 (VDR) gene leads to hypocalcemia, secondary hyperparathyroidism, rickets, and osteomalacia, accompan

255 consecutive remedial operations for primary hyperparathyroidism selectively used minimally invasive

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

257 All patients with primary hyperparathyroidism should undergo localization studies

258 atemia, calcitriol deficiency, and secondary hyperparathyroidism (SHPT) are common complications of c

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

260 uring parathyroidectomy for sporadic primary hyperparathyroidism (SPHPT).

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

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

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

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

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

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

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

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

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

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

271 physiologic imaging in patients with primary hyperparathyroidism undergoing parathyroidectomy.

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

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

274 1 consecutive surgical patients with primary hyperparathyroidism underwent both (123)I/(99m)Tc-sestam

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

276 ms were more common in patients with primary hyperparathyroidism versus thyroid controls, but were no

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

278 Increasing severity of hyperparathyroidism was associated with increased cortic

279 Secondary hyperparathyroidism was manifested in 28% of patients at

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

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

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

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

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

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

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

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

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

289 Secondary hyperparathyroidism, which is defined by a high concentr

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

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