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1 th chronic lymphocytic leukemia and acquired hypogammaglobulinemia.
2 lity to control Epstein-Barr virus (EBV) and hypogammaglobulinemia.
3  risk factors and outcomes of posttransplant hypogammaglobulinemia.
4 onoclonal, which is typical of patients with hypogammaglobulinemia.
5 bnormal antiviral and antitumor immunity and hypogammaglobulinemia.
6 Ig production and lead to disease-associated hypogammaglobulinemia.
7 tory was on pathogenic mechanisms underlying hypogammaglobulinemia.
8 association with celiac sprue, lymphoma, and hypogammaglobulinemia.
9 nd impaired immune responses as the cause of hypogammaglobulinemia.
10 here is the potential for B-cell aplasia and hypogammaglobulinemia.
11 s) had lymphopenia, and 178 (48%) of 368 had hypogammaglobulinemia.
12 vealed hypoalbuminemia (albumin 2 g/dl), and hypogammaglobulinemia.
13 ropic hormone deficiency (ACTHD) and primary hypogammaglobulinemia.
14  patients from a multigeneration family with hypogammaglobulinemia.
15 REGN-COV in a kidney transplant patient with hypogammaglobulinemia.
16 um as a novel PJI pathogen in a patient with hypogammaglobulinemia.
17 ive CMVIG can be considered in patients with hypogammaglobulinemia.
18 ganciclovir intolerance; (vii) patients with hypogammaglobulinemia.
19 ed depletion of endogenous CD19+ B cells and hypogammaglobulinemia.
20 so depletes normal B cells and causes severe hypogammaglobulinemia.
21 ondition in which thymoma is associated with hypogammaglobulinemia.
22 ical descriptions of 690 adults with primary hypogammaglobulinemia.
23 after each session to avoid coagulopathy and hypogammaglobulinemia.
24  fungal, viral, and bacterial infections and hypogammaglobulinemia.
25 etermined to be the mechanism underlying the hypogammaglobulinemia.
26 electrolyte disturbance, hypoproteinemia and hypogammaglobulinemia.
27 e seen in patients with classical AT without hypogammaglobulinemia.
28 predominantly found in patients with AT plus hypogammaglobulinemia.
29 electrolyte disturbance, hypoproteinemia and hypogammaglobulinemia.
30 s were rare, except for B-cell depletion and hypogammaglobulinemia.
31 lysis in consanguineous families affected by hypogammaglobulinemia.
32 ular defects observed in human subjects with hypogammaglobulinemia.
33 dered CD27 a candidate gene in patients with hypogammaglobulinemia.
34 , reduced class-switched memory B cells, and hypogammaglobulinemia.
35 psulated organisms, lymphoproliferation, and hypogammaglobulinemia.
36 ten showed a progressive loss of B cells and hypogammaglobulinemia.
37 ed as potential risk factors and outcomes of hypogammaglobulinemia.
38 rejection were significantly associated with hypogammaglobulinemia.
39 wenty-nine (26%) patients had posttransplant hypogammaglobulinemia.
40 s we found a 26% incidence of posttransplant hypogammaglobulinemia.
41 erum free light chains to identify secondary hypogammaglobulinemias.
42     Risk factors for mortality included mild hypogammaglobulinemia (400 mg/dL < IgG <= 600 mg/dL), in
43 of 56, OR 13.33 [3.71-47.84], p<0.0001), and hypogammaglobulinemia (67 [71%] of 95 vs 37 [47%] of 79,
44                       The phenotype included hypogammaglobulinemia (88.9%), reduced switched memory B
45 therapy was strongly predictive of worsening hypogammaglobulinemia after CAR-T therapy, which was ass
46  CAR-T therapy was associated with worsening hypogammaglobulinemia after CAR-T therapy.
47          We identified ~90% of patients with hypogammaglobulinemia after CAR-T therapy.
48                        We sought to evaluate hypogammaglobulinemia after CD19-targeted CAR-T therapy
49 ular and humoral rejections in patients with hypogammaglobulinemia after LT.
50 apy with rituximab were at risk of prolonged hypogammaglobulinemia, although severe infections were r
51 milar features, such as a failure to thrive, hypogammaglobulinemia, an absent T cell mitogenic respon
52                Most patients with congenital hypogammaglobulinemia and absent B cells are males with
53 ount for 85-90% of patients with early onset hypogammaglobulinemia and absent B cells.
54 st a substantial incidence of posttransplant hypogammaglobulinemia and an association with infection.
55               Here, we report a patient with hypogammaglobulinemia and ASD who carries biallelic muta
56                                              Hypogammaglobulinemia and autoimmune phenomena are both
57 isease because homozygous individuals showed hypogammaglobulinemia and autoimmunity, whereas heterozy
58  are associated with a clinical phenotype of hypogammaglobulinemia and autoimmunity.
59 sistence of CAR-T, incidence and duration of hypogammaglobulinemia and B-cell aplasia, and event-free
60       There was a strong association between hypogammaglobulinemia and both one-year (P=0.0490) and f
61 a monogenic disorder that is associated with hypogammaglobulinemia and characterized by a deficiency
62 onatremia, hyperpotassemia, hypoproteinemia, hypogammaglobulinemia and elevated levels of serum IL-18
63 ciation of chronic G. lamblia infection with hypogammaglobulinemia and experimental infections of mic
64 ciency disease characterized by neutropenia, hypogammaglobulinemia and extensive human papillomavirus
65 y immunodeficiency diseases characterized by hypogammaglobulinemia and impaired specific Ab response,
66 s of persistent symptomatic EBV viremia with hypogammaglobulinemia and impaired T cell-dependent anti
67 fectious mononucleosis phenotype of XLP with hypogammaglobulinemia and malignant lymphoma, a deletion
68  or fatal infectious mononucleosis, acquired hypogammaglobulinemia and malignant lymphoma.
69                 A strong association between hypogammaglobulinemia and mortality was seen.
70 odels demonstrate a CVID-like phenotype with hypogammaglobulinemia and poor humoral response to antig
71 nts from 3 unrelated families diagnosed with hypogammaglobulinemia and recurrent infections.
72 nd was associated with a higher incidence of hypogammaglobulinemia and, potentially, more episodes of
73                   Some patients present with hypogammaglobulinemia and/or refractory warts of skin an
74 penia and lymphopenia despite the absence of hypogammaglobulinemia and/or warts.
75 tients with early onset infections, profound hypogammaglobulinemia, and absent B cells.
76 ions showed the presence of hypoalbuminemia, hypogammaglobulinemia, and an elevated CRP level.
77 FATC1, presenting with recurrent infections, hypogammaglobulinemia, and decreased antibody responses.
78 d by increased susceptibility to infections, hypogammaglobulinemia, and immune dysregulation.
79 l recurrent infections, severe autoimmunity, hypogammaglobulinemia, and impaired B cell function in t
80  Immunophenotyping revealed loss of B cells, hypogammaglobulinemia, and impairments in cytotoxic T an
81 iciency characterized by B-cell lymphopenia, hypogammaglobulinemia, and increased radiosensitivity.
82 lastic syndromes, such as myasthenia gravis, hypogammaglobulinemia, and pure red cell aplasia.
83 by poor wound healing, fibrosis, cytopenias, hypogammaglobulinemia, and squamous-cell carcinoma.
84  autosomal genetic causes of childhood-onset hypogammaglobulinemia are currently not well understood.
85 a on the degree and clinical significance of hypogammaglobulinemia are sparse.
86 al and CLAD-free survival in recipients with hypogammaglobulinemia as compared to those with normal I
87                         Fourteen (12.5%) had hypogammaglobulinemia at the time of their baseline meas
88 VID-associated CD4(+) T-cell derangements to hypogammaglobulinemia, autoantibody production, or both
89                                              Hypogammaglobulinemia before CAR-T therapy was strongly
90 mmunologic phenotype characterized by severe hypogammaglobulinemia but limited clinical evidence of a
91 of infections is multifactorial and includes hypogammaglobulinemia, conventional therapy with alkylat
92 e homeostasis is needed to address the human hypogammaglobulinemia diseases.
93 uencies of class-switched memory B cells and hypogammaglobulinemia due to impaired B-cell survival, a
94  In several FHL-4 patients, we also observed hypogammaglobulinemia, elevated frequencies of naive B c
95 ilies) presenting with profound lymphopenia, hypogammaglobulinemia, fluctuating monocytopenia and neu
96 , risk factors, and clinical significance of hypogammaglobulinemia following rituximab therapy in chi
97 tients may develop prolonged and symptomatic hypogammaglobulinemia following rituximab treatment.
98 childhood cataracts, short dental roots, and hypogammaglobulinemia have also been reported in this di
99 n immunodeficiency phenotype associated with hypogammaglobulinemia, hepatopathy and a spectrum of neu
100 f common variable immunodeficiency (CVID) is hypogammaglobulinemia (HG).
101                                              Hypogammaglobulinemia (HGG) frequently occurs after soli
102 immunoglobulin G (IgG) level and the risk of hypogammaglobulinemia (HGG) in patients with severe lung
103                                              Hypogammaglobulinemia (HGG) was defined as IgG levels be
104 ed CAR-T therapy and evaluated demographics, hypogammaglobulinemia (IgG <=600 mg/dL), infections prio
105                                        Warts hypogammaglobulinemia immunodeficiency myelokathexis (WH
106 uestration in the BM of patients with warts, hypogammaglobulinemia, immunodeficiency, and myelokathex
107 lying recurrent sinopulmonary infections and hypogammaglobulinemia in 15 patients, ranging from 3 to
108                                  We detected hypogammaglobulinemia in 65% of patients with DADA2 (34
109     In summary, the observed lymphopenia and hypogammaglobulinemia in AD DC is likely a consequence o
110 ls, inactivate bacterial toxins or "correct" hypogammaglobulinemia in immunocompromised hosts.
111                                              Hypogammaglobulinemia in lung transplant recipients is m
112  objectives were to define the prevalence of hypogammaglobulinemia in lung transplant recipients, ass
113 ciency (CVID) is characterized by late-onset hypogammaglobulinemia in the absence of predisposing fac
114                             The treatment of hypogammaglobulinemia in transplant recipients with recu
115 sion done in the late 1970s in patients with hypogammaglobulinemia in which we documented the short h
116  Significant risk factors for persistent IgG hypogammaglobulinemia included low IgG and IgA levels pr
117                             Risk factors for hypogammaglobulinemia included only non A/non B hepatiti
118 a potentially useful treatment in the warts, hypogammaglobulinemia, infection, and myelokathexis synd
119 ctivating mutation L265P in MYD88 and warts, hypogammaglobulinemia, infection, and myelokathexis-synd
120 nd after CAR-T therapy, and risk factors for hypogammaglobulinemia, infection, hospitalizations, and
121 hift (FS) germline mutations found in warts, hypogammaglobulinemia, infections and myelokathexis (WHI
122 -targeted CAR-T therapy and risk factors for hypogammaglobulinemia, infections, and mortality.
123 -named because it is characterized by warts, hypogammaglobulinemia, infections, and myelokathexis (de
124 odeficiency disorder characterized by warts, hypogammaglobulinemia, infections, and myelokathexis (ne
125                             BACKGROUNDWarts, hypogammaglobulinemia, infections, and myelokathexis (WH
126 bed in 2 human hematologic disorders, warts, hypogammaglobulinemia, infections, and myelokathexis (WH
127                                       Warts, hypogammaglobulinemia, infections, and myelokathexis (WH
128 ing a gain of function that cause the warts, hypogammaglobulinemia, infections, and myelokathexis (WH
129 XCR4 antagonist, in participants with warts, hypogammaglobulinemia, infections, and myelokathexis (WH
130                                       Warts, hypogammaglobulinemia, infections, and myelokathexis (WH
131                                       Warts, hypogammaglobulinemia, infections, and myelokathexis (WH
132                                       Warts, hypogammaglobulinemia, infections, and myelokathexis (WH
133                                       Warts, hypogammaglobulinemia, infections, and myelokathexis (WH
134 plerixafor treatment of patients with warts, hypogammaglobulinemia, infections, and myelokathexis (WH
135 ndyloma specimens from a patient with warts, hypogammaglobulinemia, infections, and myelokathexis (WH
136 ly active CXCR4 mutation in zebrafish warts, hypogammaglobulinemia, infections, and myelokathexis (WH
137                        WHIM syndrome (warts, hypogammaglobulinemia, infections, and myelokathexis), a
138 ibed the presence of the C1013G/CXCR4 warts, hypogammaglobulinemia, infections, and myelokathexis-ass
139 ncy disorder that is characterized by warts, hypogammaglobulinemia, infections, and myelokathexis.
140         Such anomaly is linked to the warts, hypogammaglobulinemia, infections, myelokathexis (WHIM)
141                       MYD88 and CXCR4 warts, hypogammaglobulinemia, infections, myelokathexis syndrom
142                                 WHIM (warts, hypogammaglobulinemia, infections, myelokathexis) syndro
143 ine receptor linked to WHIM syndrome (warts, hypogammaglobulinemia, infections, myelokathexis), fails
144          Clarification regarding whether the hypogammaglobulinemia is secondary or primary is importa
145 variable immunodeficiency (CVID) suffer from hypogammaglobulinemia linked to an inadequate differenti
146 sms driving KS-associated immune deficiency (hypogammaglobulinemia [low IgA], splenomegaly, and dimin
147  patients with classical AT plus early-onset hypogammaglobulinemia (n = 3), classical AT (n = 8), and
148 d with EBV-associated Hodgkin's lymphoma and hypogammaglobulinemia; one also had severe varicella inf
149           Differences remained at 1 year for hypogammaglobulinemia only (52 [55%] of 94 vs 16 [25%] o
150                             The patients had hypogammaglobulinemia or agammaglobulinemia, and their p
151  blood mononuclear cells from 11 RV-infected hypogammaglobulinemia patients, 7 RV-infected control su
152 ce prolonged and profound B-cell aplasia and hypogammaglobulinemia, placing them at a higher risk for
153  descent presenting at 13 months of age with hypogammaglobulinemia, Pneumocystis jirovecii pneumonia,
154 revalent primary immunodeficiency, marked by hypogammaglobulinemia, poor antibody responses, and incr
155                                              Hypogammaglobulinemia post CAR-T therapy was associated
156  values, there was a significant increase in hypogammaglobulinemia post-rituximab therapy, with an in
157                                              Hypogammaglobulinemia post-rituximab treatment is freque
158 s group of patients with different causes of hypogammaglobulinemia predisposing to recurrent infectio
159                                              Hypogammaglobulinemia prior to CAR-T therapy was associa
160                                  WHIM(warts, hypogammaglobulinemia, recurrent bacterial infection, an
161 mune dysregulation syndrome characterized by hypogammaglobulinemia, recurrent infections and multiple
162 y immunodeficiency disease, characterized by hypogammaglobulinemia, recurrent infections and various
163 tients with AIOLOS haploinsufficiency showed hypogammaglobulinemia, recurrent infections, autoimmunit
164  domain of IKKalpha in a female patient with hypogammaglobulinemia, recurrent lung infections, and Ha
165 oimmunity, inflammatory bowel disease (IBD), hypogammaglobulinemia, regulatory T (T(reg)) cell defect
166  numbers of T and B lymphocytes, reversal of hypogammaglobulinemia, restoration of T-cell activation
167        The rare immunodeficient patient with hypogammaglobulinemia retains a nearly unique susceptibi
168                             In patients with hypogammaglobulinemia secondary to chronic lymphocytic l
169                                    Secondary hypogammaglobulinemia (SHG) is characterized by reduced
170              Key clinical features comprised hypogammaglobulinemia, short stature with microcephaly,
171 y syndrome (VODI), which is characterized by hypogammaglobulinemia, T-cell dysfunction, and a high fr
172 natural killer cell developmental defect and hypogammaglobulinemia that is associated with signs of i
173  flow cytometry revealed that in addition to hypogammaglobulinemia, the patient had low frequencies o
174 ther than being accompanied by a generalized hypogammaglobulinemia, this B-cell deficiency was accomp
175                                              Hypogammaglobulinemia was an expected chronic toxic effe
176                                              Hypogammaglobulinemia was defined as having at least one
177 atients with KMT2D mutations (KMT2D(Mut/+)), hypogammaglobulinemia was detected in all but 1 patient,
178                                              Hypogammaglobulinemia was not present until 3 years befo
179                               Persistent IgG hypogammaglobulinemia was observed in 27 of 101 evaluabl
180 ve in chronically infected SAP- animals, and hypogammaglobulinemia was observed.
181 zed by immune dysregulation, often including hypogammaglobulinemia, which contributes to a high rate
182  Prior to CAR-T therapy, 60% of patients had hypogammaglobulinemia, which increased to 91% post-CAR-T
183             Here, we describe a patient with hypogammaglobulinemia whose acute hepatitis C virus (HCV
184 th an unusual combination of childhood-onset hypogammaglobulinemia with recurrent infections, autoimm
185                    Immunologically, we noted hypogammaglobulinemia with terminal B-cell maturation ar

 
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