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1 tic use of this antibody in the treatment of systemic amyloidosis.
2 but fatal hereditary form of nonneuropathic systemic amyloidosis.
3 e TTR, a condition that characterizes senile systemic amyloidosis.
4 ant D76N causes a very rare form of familial systemic amyloidosis.
5 the Ser131Cys mutation and association with systemic amyloidosis.
6 ourse or outcomes, or risk of progression to systemic amyloidosis.
7 zyme linked with a rare but fatal hereditary systemic amyloidosis.
8 amily died from renal failure as a result of systemic amyloidosis.
9 on, phase 1 trial involving 15 patients with systemic amyloidosis.
10 ndividuals older than age 65 y causes senile systemic amyloidosis.
11 new phenotype of late onset fatal hereditary systemic amyloidosis.
12 w cardiac deposition resembling human senile systemic amyloidosis.
13 thy caused by autosomal dominant, hereditary systemic amyloidosis.
14 therapeutical approach in the management of systemic amyloidosis.
15 in amyloid deposits of patients with senile systemic amyloidosis.
16 brils observed in a fatal hereditary form of systemic amyloidosis.
17 retinal vasculitis, vitreous hemorrhage, and systemic amyloidosis.
18 1 patients newly diagnosed as having primary systemic amyloidosis.
19 r conjunctivitis; some patients also develop systemic amyloidosis.
20 lin (beta2-m) which is related to hereditary systemic amyloidosis.
21 rednisone treatment in patients with primary systemic amyloidosis.
22 4, as alternative radiotracers for detecting systemic amyloidosis.
23 familial amyloid polyneuropathy, and senile systemic amyloidosis.
24 a benign course and are not associated with systemic amyloidosis.
25 f familial amyloid polyneuropathy and senile systemic amyloidosis.
26 t) TTR amyloid deposits are linked to senile systemic amyloidosis, a common disease of aging, while s
27 ECT2) to the list of proteins that can cause systemic amyloidosis, a fibrillar protein deposition dis
28 tion of immunoglobulin light chains leads to systemic amyloidosis, a lethal disease characterized by
42 se process in selected patients with primary systemic amyloidosis (AL); however, SCT for AL remains c
43 misfolded protein aggregates produced during systemic amyloidosis allow for plasma FXIIa and prekalli
45 he tissue amyloid deposits that characterize systemic amyloidosis, Alzheimer's disease and the transm
46 e of precursor protein synthesis, whereas in systemic amyloidosis, amyloid deposition occurs distant
47 n familial amyloid polyneuropathy and senile systemic amyloidosis and appears to be the causative age
48 y provide a new therapeutic approach to both systemic amyloidosis and diseases associated with local
49 asis of heart dysfunction in sporadic senile systemic amyloidosis and familial amyloid cardiomyopathy
50 ave been described for transthyretin (senile systemic amyloidosis and familial amyloid polyneuropathy
51 amyloid fibrils that putatively cause senile systemic amyloidosis and familial amyloid polyneuropathy
52 l formation and possibly the diseases senile systemic amyloidosis and familial amyloid polyneuropathy
53 posplenism may be a marker of more extensive systemic amyloidosis and has been correlated to a reduct
56 ry amyloidosis, familial amyloidosis, senile systemic amyloidosis, and localized amyloidosis were exc
57 ransthyretin (TTR) is responsible for senile systemic amyloidosis, and more than 100 mutations in the
60 ifferent forms of hereditary non-neuropathic systemic amyloidosis, caused, respectively, by Leu60Arg
61 r AL) amyloidosis is the most common form of systemic amyloidosis, characterized by the pathological
64 amyloid deposits in patients diagnosed with systemic amyloidosis could be visualized with (11)C-PIB.
65 MWCs) in serum samples from individuals with systemic amyloidosis due to aggregation and deposition o
66 ntation remains contentious in patients with systemic amyloidosis due to the risk of graft loss from
67 sociated with three amyloid diseases: senile systemic amyloidosis, familial amyloid polyneuropathy, a
68 quaternary structures associated with senile systemic amyloidosis, familial amyloid polyneuropathy, a
70 ulmonary amyloidosis associated with primary systemic amyloidosis generally presents as a diffuse int
71 hat D18G does not lead to severe early onset systemic amyloidosis, given that it is the most destabil
73 eta2-microglobulin, D76N, causing hereditary systemic amyloidosis, have become particularly relevant
74 ysozyme, which are associated with a form of systemic amyloidosis, have been investigated by a wide r
76 essive, highly penetrant, autosomal-dominant systemic amyloidosis in persons heterozygous for the cau
86 (11)C-PIB and PET could be a method to study systemic amyloidosis of type AL and ATTR affecting the h
87 tin causes the human amyloid diseases senile systemic amyloidosis or familial amyloid polyneuropathy,
88 e potential to modulate the course of senile systemic amyloidosis or familial amyloid polyneuropathy.
89 ment in patients with amyloidosis is common, systemic amyloidosis presenting with angina is rare.
90 and life-saving treatment for patients with systemic amyloidosis relies on the astute clinician reco
92 ing localized pulmonary amyloidosis, primary systemic amyloidosis, secondary amyloidosis, and familia
95 familial TTR-related amyloidosis and senile systemic amyloidosis (SSA), TTR is deposited as amyloid
96 eposition of wild-type transthyretin (senile systemic amyloidosis, SSA) or monoclonal immunoglobulin
98 ients with pulmonary amyloidosis had primary systemic amyloidosis that presented radiographically as
99 months and 4 years in whom the diagnosis of systemic amyloidosis was unsuspected before or until jus
100 ontribute to effective treatment not only of systemic amyloidosis, which is relatively rare, but also
101 in the viscera and connective tissues causes systemic amyloidosis, which is responsible for about one
102 Our purpose is to present a new case of systemic amyloidosis with a bilateral conjunctival invol
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