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1 zation (hyperphosphataemic familial tumoural calcinosis).
2 e of nephrocalcinosis and dystrophic cardiac calcinosis.
3 elop nephrocalcinosis and dystrophic cardiac calcinosis.
4 s performed to assess for acroosteolysis and calcinosis.
5 ating as well as decreasing the incidence of calcinosis.
6 lantation has also led to improvement of the calcinosis.
7 erosis and systemic lupus erythematosus with calcinosis.
8 nd 2 additional patients (4%) had persistent calcinosis.
9 s spectrum that includes an association with calcinosis.
10 leles was protective, for the development of calcinosis.
11 e MRI changes can precede the development of calcinosis.
12 frequently complicated by the development of calcinosis.
14 of SSc, including synovitis, tenosynovitis, calcinosis, acroosteolysis, and distal vascularization a
17 quency of US features, sensitivity of US for calcinosis and acroosteolysis, and respective confidence
20 chanism may underlie the development of both calcinosis and fingertip ulcers in patients with DM.
22 0, which appears to have an association with calcinosis and p155 with lipodystrophy), cytokine polymo
23 es such as arthroplasty, excision of painful calcinosis, and digital sympathectomy have been employed
26 JDM or for developing complications such as calcinosis, and the clinical findings of persistent nail
27 Other extramuscular manifestations, such as calcinosis, are particularly difficult to treat, and stu
29 Many agents have been used for treatment of calcinosis but none has been accepted as a standard ther
31 a 12-year history of SLE who presented with calcinosis cutis at the time of SLE diagnosis developed
37 cularly CA, as potential therapies to target calcinosis cutis: these should now be investigated in hu
40 ulting in hyperphosphatemic familial tumoral calcinosis due to impaired glycosylation of the phosphat
41 Additional outcome measures were onset of calcinosis, effect of treatment on height, and complicat
43 using a pharmaceutical dissolution model of calcinosis (hydroxyapatite (HAp) tablet), prior to evalu
44 mperfecta), mineralization (familial tumoral calcinosis/hyperostosis hyperphosphatemia syndrome, hypo
46 sease duration were strongly associated with calcinosis in all multivariate models, independent of th
47 genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and
48 scuss the most recently published data about calcinosis in connective-tissue diseases with emphasis o
56 Autoantibodies to NXP-2 were associated with calcinosis (odds ratio, 15.52; 95% CI, 2.01-119.90), whe
58 tissues, as exemplified by familial tumoral calcinosis, pseudoxanthoma elasticum, generalized arteri
59 iffer by altering collagen or through medial calcinosis, raise the blood pressure, increase shearing
60 th diffuse and limited scleroderma or CREST (calcinosis, Raynaud phenomenon, esophageal dysmotility,
63 ars, digital-tip ulcers, telangiectasia, and calcinosis than those with ssSSc, in part related to inc
66 h anti-p140 antibodies, the association with calcinosis was significant compared with the rest of the
67 persistent weakness, muscle dysfunction, and calcinosis were most frequent (23-30%) at the last evalu
68 20% of adults with dermatomyositis (DM) have calcinosis, which can lead to significant morbidity.
69 r-old girl who presented with severe tumoral calcinosis with dural and carotid artery calcifications.