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1 on, thereby encouraging prompt initiation of immunosuppressive therapy.
2  serum PLA2R antibodies who had not received immunosuppressive therapy.
3  aplastic anemia remain pancytopenic despite immunosuppressive therapy.
4 r of which may be particularly refractory to immunosuppressive therapy.
5 nt, which, in this series, required systemic immunosuppressive therapy.
6 intervention with ribavirin or alteration in immunosuppressive therapy.
7 standing of this entity in the era of modern immunosuppressive therapy.
8 e receiving conventional doses of first-line immunosuppressive therapy.
9 oping PTLD without the need for reduction in immunosuppressive therapy.
10 iopsy findings are reliable after initiating immunosuppressive therapy.
11 clinical practice and determine the need for immunosuppressive therapy.
12 higher disease activity and a more intensive immunosuppressive therapy.
13 r the withdrawal, or during the tapering, of immunosuppressive therapy.
14  to influence positively even under systemic immunosuppressive therapy.
15 ll patients received and failed conventional immunosuppressive therapy.
16 mitations of IGRAs in the setting of chronic immunosuppressive therapy.
17 of islet morphology and function without any immunosuppressive therapy.
18 d with intrinsic risk factors and concurrent immunosuppressive therapy.
19 d in transplant patients taking rapamycin as immunosuppressive therapy.
20 n alpha-N-acetylglucosaminidase (NAGLU) plus immunosuppressive therapy.
21 nerate tumors, especially in the presence of immunosuppressive therapy.
22 d in patients with AIE who receive long-term immunosuppressive therapy.
23 -M2 antibodies they decrease during UDCA and immunosuppressive therapy.
24 fractory celiac disease that is sensitive to immunosuppressive therapy.
25 hibitor induced carcinoma, a complication of immunosuppressive therapy.
26 with a poor prognosis and modest response to immunosuppressive therapy.
27  prior statin use and should be treated with immunosuppressive therapy.
28 mmon and major problem in patients receiving immunosuppressive therapy.
29 ors or erythropoietin, or discontinuation of immunosuppressive therapy.
30  is important, as these patients may require immunosuppressive therapy.
31 equired chronic glucocorticosteroid or other immunosuppressive therapy.
32 ow individual tailoring of potentially toxic immunosuppressive therapy.
33 limited by the lack of information regarding immunosuppressive therapy.
34 se disease has failed to respond to standard immunosuppressive therapy.
35 lem and is thought to be secondary to potent immunosuppressive therapy.
36 immunodeficiency states or who are receiving immunosuppressive therapy.
37 MHC mismatch and in the absence of continued immunosuppressive therapy.
38 temic autoimmunity and allowed evaluation of immunosuppressive therapy.
39 BKV infection when treated with reduction in immunosuppressive therapy.
40 inical data hampers the optimal selection of immunosuppressive therapy.
41 s IL-14 transcript levels are not reduced by immunosuppressive therapy.
42 fluence on graft survival, without continued immunosuppressive therapy.
43        All baboons were treated with chronic immunosuppressive therapy.
44 mmation necessitating corticosteroid-sparing immunosuppressive therapy.
45 peutic approach than the current practice of immunosuppressive therapy.
46 fections in the posttransplant period due to immunosuppressive therapy.
47 se many patients with the disease respond to immunosuppressive therapy.
48 gnosis of cancer and are often refractory to immunosuppressive therapy.
49  used to develop a new type of pro-tolerance immunosuppressive therapy.
50 r by age, underlying diagnosis, or amount of immunosuppressive therapy.
51 on the choice of calcineurin inhibitor (CNI) immunosuppressive therapy.
52 n is similar to the risk with other types of immunosuppressive therapy.
53 ive stress, and inflammation associated with immunosuppressive therapy.
54 n, even though recipients undergo aggressive immunosuppressive therapy.
55 ffects AIDS patients and patients undergoing immunosuppressive therapy.
56 is requiring systemic corticosteroid-sparing immunosuppressive therapy.
57 ecessarily prompt the discontinuation of the immunosuppressive therapy.
58 ly tolerant patients and patients on regular immunosuppressive therapy.
59  P = .009) than those receiving conservative/immunosuppressive therapy.
60 ade (RASB) compared with individuals without immunosuppressive therapy.
61  a target for development of organ-selective immunosuppressive therapies.
62 clinical syndrome was refractory to multiple immunosuppressive therapies.
63 ccurred in 50% of patients treated with mild immunosuppressive therapies.
64 osporin A (CsA) or FK506 is a cornerstone of immunosuppressive therapies.
65 mplications for the development of localized immunosuppressive therapies.
66 n of tissue pathology and may be amenable to immunosuppressive therapies.
67  more likely to be taking steroids and other immunosuppressive therapies.
68 ity from infectious diseases, independent of immunosuppressive therapies.
69  symptoms despite continued use of intensive immunosuppressive therapies.
70 presence of immunocompromising conditions or immunosuppressive therapies.
71 n important determinant of responsiveness to immunosuppressive therapies.
72 ients before they receive other, potentially immunosuppressive, therapies.
73  each given 2 weeks apart) nor withdrawal of immunosuppressive therapy (37 of 60 patients [62%]) infl
74 ion of prednisolone maintenance and/or other immunosuppressive therapy (50% versus 59%), steroid depe
75 ow-up (before transplant: 74.0+/-2.0; during immunosuppressive therapy: 75.4+/-2.8; and after withdra
76 cipients, it was possible to discontinue all immunosuppressive therapy 9 to 14 months after the trans
77 gic management is complicated by the risk of immunosuppressive therapy abrogating the antimalignancy
78 ng could be a useful tool in individualizing immunosuppressive therapy according to the risk of ACR o
79                                      Current immunosuppressive therapy after heart transplantation ei
80 rm graft survival that necessitates lifelong immunosuppressive therapy after renal transplant.
81         Tacrolimus (TAC), the cornerstone of immunosuppressive therapy after solid organ transplantat
82                                 Intensity of immunosuppressive therapies also influences the risk for
83 with cancer who undergo certain cytotoxic or immunosuppressive therapies and have HBV infection or pr
84 r, or who have other conditions that require immunosuppressive therapies and/or solid organ or stem c
85     Before tocilizumab therapy, conventional immunosuppressive therapy and 1 or more biologic agents
86 ase series of patients treated with systemic immunosuppressive therapy and additional amniotic membra
87 interesting trend toward better responses of immunosuppressive therapy and an association with the pr
88                                    High-dose immunosuppressive therapy and autologous hematopoietic s
89 least two immunosuppressive therapies or one immunosuppressive therapy and chronic intravenous immuno
90                                      Chronic immunosuppressive therapy and control groups had similar
91 al systemic toxicities of corticosteroid and immunosuppressive therapy and death.
92        The latter include patients receiving immunosuppressive therapy and elderly subjects, particul
93 risk is related to intensity and duration of immunosuppressive therapy and inversely to recipient age
94                              Less aggressive immunosuppressive therapy and lower average prednisone d
95 ethodologies also have direct application to immunosuppressive therapy and other immunosuppressive di
96 positive donor in this study received triple immunosuppressive therapy and prophylactic CMV treatment
97 o transplanted tissues with short courses of immunosuppressive therapy and that with regard to tolera
98 nor antibodies is taken to reflect effective immunosuppressive therapy and to predict a favorable out
99 vates in kidney transplant recipients during immunosuppressive therapy and triggers BKPyV-associated
100 ents with catastrophic APS also benefit from immunosuppressive therapy and/or plasma exchange, wherea
101 ission requiring escalation or resumption of immunosuppressive therapy), and deaths were recorded.
102 Altogether, 102 of the 110 patients received immunosuppressive therapy, and 56 received an intracardi
103 gnosis was associated with responsiveness to immunosuppressive therapy, and an elevated CD8(+) TSCM p
104                 Organ histology, response to immunosuppressive therapy, and biochemical and immunolog
105 be treated with bone marrow transplantation, immunosuppressive therapy, and high-dose cyclophosphamid
106                    All patients responded to immunosuppressive therapy, and many experienced a relaps
107              Vector was administered without immunosuppressive therapy, and participants were followe
108 nfections requiring more than 1 debridement, immunosuppressive therapy, and the exchange of removable
109 1A) rats were treated with a short course of immunosuppressive therapy (anti-alphabeta-TCR monoclonal
110 can move, and are affected by HIV infection, immunosuppressive therapies, antituberculosis treatments
111 e comprehensive understanding of how current immunosuppressive therapies applied to organ transplanta
112                                              Immunosuppressive therapies are effective, but reduced n
113 that patients with IED treated with systemic immunosuppressive therapy are at increased risk of malig
114 susceptibility to infection, and response to immunosuppressive therapy are influenced in part by his/
115 ge at the onset of first symptoms as well as immunosuppressive therapy are likely associated with mor
116 seroconstellation, HLA-DR7, and intensity of immunosuppressive therapy are significant risk factors f
117 sulting from HIV infection, chemotherapy, or immunosuppressive therapy, are the primary risk factors.
118 lowing antiretroviral therapy or reversal of immunosuppressive therapy, as the newly reconstituted im
119       Thirteen patients (43%) were receiving immunosuppressive therapy at the time of initiation of i
120        Only 5 patients were still undergoing immunosuppressive therapy at the time of last follow-up.
121                                     Although immunosuppressive therapy benefits some patients, trial
122  Adults with autoimmune disease treated with immunosuppressive therapy (biologic or nonbiologic) were
123 gy to avoid the side effects of conventional immunosuppressive therapies, but targeting CD28-mediated
124 network are investigated as drug targets for immunosuppressive therapy, but the selective action of S
125 ith hematologic malignancy, transplantation, immunosuppressive therapy (calcineurin inhibitors, antit
126                                              Immunosuppressive therapy can produce hematologic respon
127 dies to discuss whether mTOR inhibitor-based immunosuppressive therapy can reduce the magnitude of CM
128 urvival, once strongly linked to response to immunosuppressive therapy, can now be achieved even amon
129                                              Immunosuppressive therapy, chronic graft-versus-host dis
130                       The effects of chronic immunosuppressive therapy (CIST) on long-term oncologic
131 imab-tacrolimus-mycophenolate-corticosteroid immunosuppressive therapy, CMV disease rates increased i
132 mune checkpoint inhibitors and initiation of immunosuppressive therapy, consisting of intravenous met
133 and an elevated CD8(+) TSCM population after immunosuppressive therapy correlated with treatment fail
134     Two lung transplant recipients receiving immunosuppressive therapy developed pruritic, brown plaq
135                            Active disease or immunosuppressive therapy did not impair the assay perfo
136 in why patients receiving cyclosporine A for immunosuppressive therapy display excessive hair growth,
137 , steroidal anti-inflammatory drugs (SAIDs), immunosuppressive therapy drugs (immunomodulatory therap
138 majority of patients will ultimately require immunosuppressive therapy due to symptomatic neutropenia
139 ti-HBs]) for "persons receiving cytotoxic or immunosuppressive therapy (eg, chemotherapy for malignan
140                               In the current immunosuppressive therapy era, vessel thrombosis is the
141                        However, the required immunosuppressive therapy exposes patients to serious si
142   In more severe GVHD, prolonged exposure to immunosuppressive therapies, failure to achieve toleranc
143 rticipants were identified from the Systemic Immunosuppressive Therapy for Eye Diseases (SITE) cohort
144   Patients were identified from the Systemic Immunosuppressive Therapy for Eye Diseases Cohort Study.
145                         BACKGROUND AND AIMS: Immunosuppressive therapy for inflammatory bowel disease
146  bleeding episodes and prompt institution of immunosuppressive therapy for long-term inhibitor eradic
147 ath, in a patient who was receiving systemic immunosuppressive therapy for rheumatoid arthritis and w
148  was as effective as continuous conventional immunosuppressive therapy for the induction and maintena
149                     In the Supportive Versus Immunosuppressive Therapy for the Treatment of Progressi
150      There are limited data on the safety of immunosuppressive therapy for these patients.
151 vailable therapy (maintenance or increase in immunosuppressive therapy) for HCV-associated cryoglobul
152 ned > 5 mug/L, the trough level used in oral immunosuppressive therapy, for (95% credible interval) 1
153                                      Chronic immunosuppressive therapy group had significantly lower
154              Beneficial clinical response to immunosuppressive therapies has been demonstrated which
155 olled trial, although the evidence for other immunosuppressive therapies has been derived mainly from
156   However, to date most randomized trials of immunosuppressive therapy have had acute rejection as th
157 ion of posttransplant alloantibodies despite immunosuppressive therapy have not been fully elucidated
158      A phase 2 single-arm study of high-dose immunosuppressive therapy (HDIT) and autologous CD34-sel
159                                    High-dose immunosuppressive therapy (HDIT) with autologous hematop
160 n that all patients undergoing chemotherapy, immunosuppressive therapy, hematopoietic stem cell trans
161 ring allows individualization of a patient's immunosuppressive therapy; however, drug levels alone ma
162 s and their colitis is resistant to standard immunosuppressive therapy, HSCT should be considered ear
163                                              Immunosuppressive therapies (ie, intravenous cyclophosph
164                                    Induction immunosuppressive therapy (if any) was available in 3/10
165 pportive-care group) or supportive care plus immunosuppressive therapy (immunosuppression group) for
166 t questions about the development and use of immunosuppressive therapies in AGS and related phenotype
167 tion, which may occur with a wide variety of immunosuppressive therapies in benign or malignant disea
168 of toxicities of systemic corticosteroid and immunosuppressive therapies in the trial.
169 We assessed the longitudinal requirement for immunosuppressive therapy in 339 patients treated with t
170                      However it supports the immunosuppressive therapy in acute situations as in crit
171               There are anecdotal reports of immunosuppressive therapy in autoimmune retinopathy; how
172 should not be used as justification to delay immunosuppressive therapy in children with typical sympt
173                             Although current immunosuppressive therapy in kidney transplant recipient
174 thway, allows for calcineurin-inhibitor free immunosuppressive therapy in kidney transplantation but
175 to assess the clinical benefits of adjusting immunosuppressive therapy in liver recipients based on i
176 sregulation in MDS and summarize the role of immunosuppressive therapy in MDS.
177 t that Rtx might replace St-Cp as first-line immunosuppressive therapy in patients with idiopathic me
178 s represents a noninvasive way of monitoring immunosuppressive therapy in renal transplant patients.
179 steroid-free regimens compared with a triple immunosuppressive therapy in renal transplant recipients
180 risk of HBVr under different combinations of immunosuppressive therapy in rheumatic patients.
181 ng cell type for use as a cell-based adjunct immunosuppressive therapy in solid organ transplant reci
182                     The clinical response to immunosuppressive therapy in suspected autoimmune enceph
183 rventions such as immunoglobulin therapy and immunosuppressive therapy in the care of the patient wit
184 ts with particular focus on the evidence for immunosuppressive therapy in these patients.
185                  Available evidence to guide immunosuppressive therapy in this setting is limited but
186  T cell depletion has potential as a robust, immunosuppressive therapy in transplantation.
187 BcAb + HBsAg- NHL patients treated with mild immunosuppressive therapies, in order to detect an occul
188 r age, male sex, type of cardiomyopathy, and immunosuppressive therapy (including switch to mTOR inhi
189 s were undergoing varied mono or combination immunosuppressive therapy, including 36 who were receivi
190                    Daily plasma exchange and immunosuppressive therapies induce remission, but mortal
191 nd the clinical and radiological response to immunosuppressive therapies is consistent with an immune
192                         Corticosteroid-based immunosuppressive therapy is effective in eliminating mo
193 oung adults with severe aplastic anemia, and immunosuppressive therapy is employed when hematopoietic
194 cyte syndrome, is waning because anti-B-cell immunosuppressive therapy is increasingly a component of
195  risk for chronic HBV infection or if highly immunosuppressive therapy is planned.
196    Following organ transplantation, lifelong immunosuppressive therapy is required to prevent the hos
197 id organ transplantation and improvements in immunosuppressive therapy is the reality that long-term
198                                              Immunosuppressive therapy is the standard of care for th
199    Group 1 (Gp1) (controls, n=6) received no immunosuppressive therapy (IS) and no graft.
200  NAC, without concurrent plasma exchange and immunosuppressive therapy, is effective in preventing an
201          Growth factors can be combined with immunosuppressive therapy (IST) and may improve response
202 etween specific Treg subsets and response to immunosuppressive therapy (IST) as well as their in vitr
203  defined as a lack of response to first-line immunosuppressive therapy (IST) with antithymocyte globu
204 ed pathophysiology in some patients, in whom immunosuppressive therapy (IST) with horse antithymocyte
205  for second line after failure to respond to immunosuppressive therapy (IST).
206  been widely reported in patients undergoing immunosuppressive therapy (IT); however, few data are av
207                             Within 3 months, immunosuppressive therapy led to a sustained 81% reducti
208 r investigation into SPMs as alternatives to immunosuppressive therapies like steroids.
209  recalcitrant chronic itch that failed other immunosuppressive therapies markedly improve when treate
210  of anti-HLA IgG with FcMonoIgG may minimize immunosuppressive therapies, maximize the number of dono
211                                  Ultimately, immunosuppressive therapy may be only partially required
212 eactivation of hepatitis B in the context of immunosuppressive therapy may be severe and potentially
213 utcomes, uveitis patients receiving systemic immunosuppressive therapy may experience a deterioration
214 lled with or were intolerant to conventional immunosuppressive therapy (median number, 3 [1-5]).
215 ease activity (proteinuria) in patients with immunosuppressive therapy (n=101) or supportive care (n=
216 ve care unit (ICU) admissions, active use of immunosuppressive therapy, neutropenia, or bacteremia du
217 aneously, but more typically is triggered by immunosuppressive therapy of cancer, autoimmune disease,
218 cade emerges as a promising new strategy for immunosuppressive therapy of large-vessel vasculitis.
219 atients, we analyzed the impact of EVR-based immunosuppressive therapy on CMV replication and disease
220 es, and previous treatment with at least two immunosuppressive therapies or one immunosuppressive the
221 ancytopenia, can be treated effectively with immunosuppressive therapy or allogeneic transplantation.
222 hich can be successfully treated with either immunosuppressive therapy or hematopoietic stem-cell tra
223  namely, the reduction or discontinuation of immunosuppressive therapy or the switch from calcineurin
224 cancer who are about to receive cytotoxic or immunosuppressive therapy or who are already receiving t
225 OR, 5.65; P < .05), and the intensity of the immunosuppressive therapy (OR, 1.53; P < .01) as indepen
226  1.11; 95% CI, 1.08-1.14; P = .0001), use of immunosuppressive therapy (OR, 1.69; 95% CI, 1.18-2.44;
227 s that were subjected to diabetes induction, immunosuppressive therapy, or islet allotransplantation.
228 oaches are limited by the adverse effects of immunosuppressive therapy over the lifetime of the recip
229                   Nineteen patients received immunosuppressive therapies: overall response (OR) was 4
230 rvival of islet allografts without any other immunosuppressive therapy (P=0.0003), and the protection
231 t or refractory (p=0.048) and need long-term immunosuppressive therapy (p=0.0213).
232 e transplanted into baboons that received no immunosuppressive therapy, partial regimens, or a full r
233 ransplant recipients complicates maintenance immunosuppressive therapy, particularly in patients with
234 s of HBV-infected persons, persons requiring immunosuppressive therapy, persons with end-stage renal
235 patients in a prospective phase 1-2 study of immunosuppressive therapy plus eltrombopag.
236                       We addressed issues of immunosuppressive therapy, psychological and ethical out
237 enal function and were treated with the same immunosuppressive therapy, receiving a minimum dose of c
238                                              Immunosuppressive therapy remains an important treatment
239                                The effect of immunosuppressive therapy remains speculative.
240                  The intensive and prolonged immunosuppressive therapy required to prevent or treat g
241 d in candidate patients for chemotherapy and immunosuppressive therapy requires further investigation
242                             Belatacept-based immunosuppressive therapy resulted in higher and more se
243 l Vasculitis who was treated with aggressive immunosuppressive therapy resulting in a favorable visua
244                                  The current immunosuppressive therapies showed limited success in ma
245 ith the use of an intensified posttransplant immunosuppressive therapy starting at day 0 combined wit
246                                Various other immunosuppressive therapy studies have also reported suc
247 bidity and mortality in patients who receive immunosuppressive therapy, such as solid organ and hemat
248 ance between infectious risk and response to immunosuppressive therapy, such as that required for aut
249 tients with severe aplastic anemia receiving immunosuppressive therapy, telomere length was unrelated
250                                              Immunosuppressive therapies that block the CD40/CD154 co
251 nchiectasis, but also to avoid inappropriate immunosuppressive therapy that worsens the disease.
252                          Despite advances in immunosuppressive therapies, the rate of chronic transpl
253             In patients not receiving active immunosuppressive therapy, the most likely culprits are
254 resection of the teratoma and treatment with immunosuppressive therapy, the patient progressed to a m
255 graft biopsies, obtained after withdrawal of immunosuppressive therapy, there were high levels of P3
256                            With reduction in immunosuppressive therapy, three patients (13%) develope
257 or 6-12 months after discontinuation of such immunosuppressive therapies to protect against HBV react
258 otection, and the potential contributions of immunosuppressive therapies to tumor induction.
259 increased from 21% at the time of failure on immunosuppressive therapy to 68% by late PRA after weani
260                              The addition of immunosuppressive therapy to intensive supportive care i
261 t approaches seek to limit administration of immunosuppressive therapy to patients at risk for life-t
262  and in kidney transplant patients receiving immunosuppressive therapy to prevent organ rejection.
263                                              Immunosuppressive therapies using calcineurin inhibitors
264 e results may have clinical implications for immunosuppressive therapy using calcineurin inhibitors.
265                                   A systemic immunosuppressive therapy was administered in all patien
266 rly or rituximab late, and glucocorticoid or immunosuppressive therapy was allowed at study entry.
267               The addition of eltrombopag to immunosuppressive therapy was associated with markedly h
268                                              Immunosuppressive therapy was recommended in cases of de
269 ted to be due to the underlying disease, and immunosuppressive therapy was scheduled.
270                                              Immunosuppressive therapy was similar in both groups.
271      Cyclosporine as the sole posttransplant immunosuppressive therapy was tapered and discontinued a
272 ariate repeated-measures model incorporating immunosuppressive therapy was utilized.
273                                              Immunosuppressive therapy was with conventional agents (
274                                              Immunosuppressive therapy was withdrawn in 37 of 60 pati
275 combination with cyclosporine, as first-line immunosuppressive therapy, was evaluated prospectively i
276 oderate/severe scleritis, requiring systemic immunosuppressive therapy, was present in 25 eyes (69%).
277  patients who received SRL-based maintenance immunosuppressive therapy were determined using polymera
278                  In contrast, malignancy and immunosuppressive therapy were each assigned -1 point, o
279         Participants with a history of using immunosuppressive therapy were identified in clinics, an
280                              The outcomes of immunosuppressive therapy, when added to supportive care
281 h SLE have been managed largely with empiric immunosuppressive therapies, which are associated with s
282        In total, 124 patients (49%) received immunosuppressive therapy, which predominantly consisted
283  as it would avoid the toxicities of chronic immunosuppressive therapies while preventing acute and c
284 erance would avoid the toxicities of chronic immunosuppressive therapies while preventing graft rejec
285  concurrent anti-TNF-alpha therapy and other immunosuppressive therapy while she was living in an are
286                                              Immunosuppressive therapy with antithymocyte globulin (A
287  of the extrinsic coagulation pathway during immunosuppressive therapy with ATG may have broader impl
288 , in addition to conventional posttransplant immunosuppressive therapy with cyclosporine, markedly at
289         Many younger patients who respond to immunosuppressive therapy with drugs such as antithymocy
290                         We combined standard immunosuppressive therapy with eltrombopag in previously
291                                              Immunosuppressive therapy with mammalian target of rapam
292                                    Intensive immunosuppressive therapy with rituximab appears to be e
293 eatment groups (24/168 hr) received standard immunosuppressive therapy with tacrolimus.
294 cific inflammatory responses and complements immunosuppressive therapy with tacrolimus.
295                                              Immunosuppressive therapy, with cyclosporine, methotrexa
296  patients with aplastic anemia refractory to immunosuppressive therapy, with frequent multilineage re
297 ere observed among the patients who received immunosuppressive therapy, with no change in the rate of
298                  Only 21% (3 of 14) received immunosuppressive therapy within 1 year before lung tran
299 ction off immunosuppression were returned to immunosuppressive therapy without evidence of rejection
300       ERT was resumed 8 weeks after starting immunosuppressive therapy without inducing a rebound of

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