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1 y Ca(2+) loss, particularly in patients with hypoparathyroidism.
2 tive that results in a very low incidence of hypoparathyroidism.
3 eatening APS-I manifestations such as AI and hypoparathyroidism.
4 a PTH replacement therapy for patients with hypoparathyroidism.
5 id hormone 1-84 (rhPTH[1-84]) in adults with hypoparathyroidism.
6 d to impaired PTH secretion, such as primary hypoparathyroidism.
7 h autosomal dominant and autosomal recessive hypoparathyroidism.
8 DR syndrome and not in one, such as isolated hypoparathyroidism.
9 nidentified gene in the etiology of X-linked hypoparathyroidism.
10 hypoplasia, conotruncal cardiac defects, and hypoparathyroidism.
11 roband of an extensive kindred with isolated hypoparathyroidism.
12 pped to 6p23-24, as a candidate for isolated hypoparathyroidism.
13 ssociated with a high incidence of permanent hypoparathyroidism.
14 ns result in autosomal dominant and sporadic hypoparathyroidism.
15 sk for the later development of hypocalcemic hypoparathyroidism.
16 tor mutation in a child with severe sporadic hypoparathyroidism.
17 oidectomy virtually eliminates postoperative hypoparathyroidism.
18 ces the incidence of permanent postoperative hypoparathyroidism.
19 spondylarthropathic changes of long-standing hypoparathyroidism.
20 ed delayed parathyroid AT to treat permanent hypoparathyroidism.
24 PS 1), which manifests in a classic triad of hypoparathyroidism, adrenal insufficiency, and candidias
27 ls from 12 families with autosomal recessive hypoparathyroidism and have investigated them for GCMB a
32 ions of 10p (one patient diagnosed as having hypoparathyroidism and three as DGS) and one patient wit
35 ociated with potential complications such as hypoparathyroidism and vocal cord paralysis in a small p
36 erized by chronic mucocutaneous candidiasis, hypoparathyroidism, and adrenal insufficiency, but patie
37 like autoimmune adrenal insufficiency (AI), hypoparathyroidism, and chronic mucocutaneous candidiasi
38 nifests as a triad of adrenal insufficiency, hypoparathyroidism, and chronic mucocutaneous infections
41 e two kindreds exhibiting X-linked recessive hypoparathyroidism are indeed related and that an identi
43 s, our results, which expand the spectrum of hypoparathyroidism-associated GCMB mutations, help eluci
44 cessive disorder characterized by autoimmune hypoparathyroidism, autoimmune adrenocortical failure, a
47 Human GATA3 haploinsufficiency leads to HDR (hypoparathyroidism, deafness and renal dysplasia) syndro
48 A3 haploinsufficiency also causes human HDR (hypoparathyroidism, deafness, and renal dysplasia) syndr
50 ions included seven cases (17%) of permanent hypoparathyroidism; five (71%) of these occurred in grou
52 study (REPLACE), we recruited patients with hypoparathyroidism (>/= 18 months duration) aged 18-85 y
53 caemic (subclinical) hyperparathyroidism and hypoparathyroidism have a low risk of progression to ove
57 parathyroid glands and exhibit a biological hypoparathyroidism, identifying Gcm2 as a master regulat
58 sease genes-including, for example, X-linked hypoparathyroidism in 3 Mb (6 cM) telomeric to Factor IX
59 d embryology and is responsible for isolated hypoparathyroidism in a subset of patients with this dis
67 stating disorder characterized by congenital hypoparathyroidism, mental retardation, facial dysmorphi
72 cal harm was 2.12 to 5.93 cases of permanent hypoparathyroidism per 100 thyroidectomies and 0.99 to 2
74 seases due to GATA-3 deficiency - such as in hypoparathyroidism, sensorineural deafness, and renal (H
75 clinical problems including cardiac defects, hypoparathyroidism, T-cell immunodeficiency and facial d
76 s, conotruncal cardiac defects, hypocalcemic hypoparathyroidism, T-cell mediated immune deficiency, a
77 ns were identified in patients with isolated hypoparathyroidism, thereby indicating that GATA3 abnorm
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