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1 with IgG3-IgG2a complexes in BALB/c (type II cryoglobulinemia).
2 bacterial endocarditis causing his type III cryoglobulinemia.
3 portant etiologically in the pathogenesis of cryoglobulinemia.
4 ion for therapeutically challenging cases of cryoglobulinemia.
5 herapeutic options remain limited for type I cryoglobulinemia.
6 eutical formulations and in vivo in cases of cryoglobulinemia.
7 olutions of antibodies and the mechanisms of cryoglobulinemia.
8 at greater risk of developing CKD, MPGN, and cryoglobulinemia.
9 th the renal injury and systemic features of cryoglobulinemia.
10 Risks were also increased for cryoglobulinemia.
11 patitis occurring in the setting of systemic cryoglobulinemia.
12 utic strategy for preventing renal injury in cryoglobulinemia.
13 disease, IgM-mediated neuropathies and mixed cryoglobulinemia.
14 ignificant association between cirrhosis and cryoglobulinemia.
15 show clinical or physical signs of syndromic cryoglobulinemia.
16 tients had PCT, vitiligo, lichen planus, and cryoglobulinemia.
17 ry that resembles important aspects of human cryoglobulinemia.
18 itis syndrome, Sjogren's syndrome, and mixed cryoglobulinemia.
19 s (HCV) infection is associated with type II cryoglobulinemia.
20 , for an overall prevalence of 3.0% in mixed cryoglobulinemia.
21 tion does not appear to have a role in mixed cryoglobulinemia.
22 patient was also found to have type II mixed cryoglobulinemia.
23 omerulonephritis, with or without associated cryoglobulinemia.
24 pheresis for the presumed essential type III cryoglobulinemia.
25 argest cohort of patients with type II mixed cryoglobulinemia.1 Steroids and rituximab appear to be t
27 al lymphopoietin transgenic mice, a model of cryoglobulinemia and associated membranoproliferative gl
31 fficulty of identifying infectious causes of cryoglobulinemia and emphasizes that an initial, highly
33 coinfection with HGV in patients with mixed cryoglobulinemia and HCV infection in the United States.
34 ases, and type II/III, which is called mixed cryoglobulinemia and is seen in hepatitis C virus infect
40 ransgenic (TSLPtg) mice, which develop mixed cryoglobulinemia and severe cryoglobulinemia-associated
42 observed infrequently in patients with mixed cryoglobulinemia and were caused by nonspecific binding
44 14 patients with HCV infection and type III cryoglobulinemia, and in 5 (13.5%) of 37 patients with H
45 found in patients with HCV infection without cryoglobulinemia, and in that population, the maximum an
47 bulinemia, none of 29 patients with type III cryoglobulinemia, and none of 6 patients with EMC were p
48 kin lymphoma, Waldenstrom macroglobulinemia, cryoglobulinemia, and thyroiditis were all <.0038, the B
49 patients with HCV infection with and without cryoglobulinemia, anti-CCP was not observed in patients
50 cal benefit in systemic lupus erythematosus, cryoglobulinemia, antineutrophil cytoplasmic antibodies+
51 iate logistic regression analysis identified cryoglobulinemia as an independent prognostic factor of
52 s with type II and 29 patients with type III cryoglobulinemia associated with HCV infection, 6 patien
53 ch develop mixed cryoglobulinemia and severe cryoglobulinemia-associated membranoproliferative glomer
54 us-prone MRL-Fas(lpr) mice can induce GN and cryoglobulinemia, but the features that confer nephritog
55 patic manifestations of HCV infection: mixed cryoglobulinemia, chronic kidney or end-stage renal dise
56 scosity, peripheral neuropathy, amyloidosis, cryoglobulinemia, cold-agglutinin disease, or evidence o
57 scosity, peripheral neuropathy, amyloidosis, cryoglobulinemia, cold-agglutinin disease, or transforme
58 sisted of the IgG3 cryoglobulin only (type I cryoglobulinemia) compared with IgG3-IgG2a complexes in
60 systemic vasculitis associated with type II cryoglobulinemia (cryoglobulinemic vasculitis), a prolif
61 of clinical syndromes, including "essential" cryoglobulinemia (elicited by the hepatitis viruses) and
62 V infection, 6 patients with essential mixed cryoglobulinemia (EMC; all with type II), 50 hospital co
63 patic manifestations include sicca syndrome, cryoglobulinemia, glomerulonephritis, and porphyria cuta
64 role for hepatitis G virus (HGV) in type II cryoglobulinemia has not been defined, although prevalen
66 sk of MPGN (HR, 2.23; 95% CI, 1.84-2.71) and cryoglobulinemia (HR, 16.91; 95% CI, 12.00-23.81) respec
71 obulinemia, sera from 29 patients with mixed cryoglobulinemia (including 13 with rheumatic symptoms a
75 itive anti-nuclear autoantibodies, and mixed cryoglobulinemia is increasingly reported in different p
77 f HCV with the extrahepatic complications of cryoglobulinemia is widely recognized, the relationship
78 lymphoproliferative disorders such as mixed cryoglobulinemia (MC) and B-cell non-Hodgkin lymphoma (B
83 Hepatitis C virus (HCV)-associated mixed cryoglobulinemia (MC) vasculitis commonly regresses upon
84 titis C virus (HCV) frequently develop mixed cryoglobulinemia (MC), a monoclonal expansion of immunog
85 in hepatitis C virus (HCV)-associated mixed cryoglobulinemia (MC), especially concerning the long-te
87 Waldenstrom macroglobulinemia (n = 165), and cryoglobulinemia (n = 551) were increased with HCV infec
88 9%) of 34 patients with HCV-infected type II cryoglobulinemia, none of 29 patients with type III cryo
89 drome (P = 0.05), hypertension (P < 0.0001), cryoglobulinemia (P = 0.05), and preexisting intraocular
92 sociated with resolution of complications of cryoglobulinemia, reduced levels of insulin resistance,
93 m 50 patients with HCV infection but without cryoglobulinemia, sera from 29 patients with mixed cryog
96 asculitis of low/medium sized vessels (mixed cryoglobulinemia syndrome or cryoglobulinemic vasculitis
99 ransgenic animals developed polyclonal mixed cryoglobulinemia (type III) and a systemic inflammatory
100 There was no apparent difference between cryoglobulinemia types I and II regarding the role of co
101 hepatitis C virus (HCV) infection, and overt cryoglobulinemia vasculitis (CryoVas) develops in approx
102 herapeutic management of noninfectious mixed cryoglobulinemia vasculitis (CryoVas) in the era of hepa
106 irty-six HCV patients with and without mixed cryoglobulinemia were compared with 18 healthy control v
108 le mouse model of renal involvement in mixed cryoglobulinemia, which enables detailed studies of a me
110 on for end-stage chronic hepatitis C in whom cryoglobulinemia with vasculitis developed after transpl