Chronic Active(만성 활성)란 무엇입니까?
Chronic Active 만성 활성 - Also there was significant difference in both microRNA 21 and 101 expression between patient and control group and a significant difference in these microRNAs between patients with chronic active and inactive HBV infections Conclusion: Both mico RNA and HBx Ag can be used as good prognostic biomarkers for disease progression and severity. [1] RESULTS Among 381 cases with complete 1-year follow-up, 49% had a chronic active or relapsing disease course, 40% achieved sustained remission after treatment and 11% had a quiescent course. [2] On histopathology, both chronic active and smoldering lesions exhibited more severe acute axonal damage at the lesion edge than in the lesion center (edge vs center: p = 0. [3] The inflammatory activity in each lesion was evaluated by immunohistochemistry for the myelin protein MOG and the HLA antigen to classify them as active, chronic inactive or chronic active. [4] OBJECTIVE Recently, there has been an increasing interest in "chronic enlarging" or "chronic active" multiple sclerosis (MS) lesions that are associated with clinical disability. [5] In multiple sclerosis (MS), chronic active/smoldering white matter lesions presenting with hypointense rims on susceptibility-weighted imaging (SWI) of the brain have been recognized as an important radiological feature. [6] 1,2 Subsequently, some lesions become chronic inactive, whereas up to 57% of lesions show persistent inflammation,1,2 and are defined as chronic active. [7] Multiple sclerosis (MS) is a chronic inflammatory, demyelinating and neurodegenerative disease of the central nervous system (CNS) characterized by the accumulation of focal white matter (WM) lesions that can be classified as active, chronic active (also referred to as mixed active/inactive lesions), inactive, and remyelinated, according to the presence and topography of ongoing demyelination and active inflammation or remyelination [1–3]. [8] About 20 years ago, John Prineas and colleagues described the neuropathology of “chronic active/ slowly expanding lesions” in secondary progressive multiple sclerosis (MS) autopsy cases pointing out their potential pathogenetic relevance to disease progression in MS. [9] Lesions were classified as active, chronic active or chronic silent. [10] Chronic active and slowly expanding/evolving lesions with smouldering inflammation are neuropathological correlates of progressive multiple sclerosis. [11] Different patterns of plasma cytokines can be expected in the case of chronic active-antibody-mediated (cAMR) and acute cellular rejection (AR) after kidney transplantation (KTx). [12] Aim: The purpose of this study was to evaluate the expression level of Interferon-stimulated Gene 15 (ISG15), Interleukin28B (IL28B) or IFN-lambda-3 and Ubiquitin specific peptidase 18 (USP18) genes in Peripheral Blood Mononuclear Cells (PBMCs) of patients with chronic active and inactive hepatitis B in comparison with healthy individuals. [13]또한 환자와 대조군 사이에 microRNA 21과 101 발현에 상당한 차이가 있었고 만성 활성 및 비활성 HBV 감염 환자 간에 이러한 microRNA에서 상당한 차이가 있었습니다. 결론: mico RNA와 HBx Ag 모두 질병에 대한 좋은 예후 바이오마커로 사용될 수 있습니다. 진행 및 심각도. [1] 결과 완전한 1년 추적 관찰을 한 381명의 사례 중, 49%는 만성 활동성 또는 재발성 질환 경과를 보였고, 40%는 치료 후 지속적인 관해에 도달했으며, 11%는 휴면 경과를 보였습니다. [2] 조직 병리학에서 만성 활동성 병변과 그을린 병변 모두 병변 중심보다 병변 가장자리에서 더 심각한 급성 축삭 손상을 나타냈다(가장자리 대 중심: p = 0. [3] 각 병변의 염증 활성은 수초 단백질 MOG 및 HLA 항원에 대한 면역조직화학에 의해 평가되어 이들을 활성, 만성 비활성 또는 만성 활성으로 분류하였다. [4] 목적 최근, 임상 장애와 관련된 "만성 확대" 또는 "만성 활성" 다발성 경화증(MS) 병변에 대한 관심이 증가하고 있습니다. [5] 다발성 경화증(MS)에서 뇌의 감수성 가중 영상(SWI)에서 저강도 테두리를 보이는 만성 활성/그을린 백질 병변은 중요한 방사선학적 특징으로 인식되었습니다. [6] 1,2 결과적으로 일부 병변은 만성 비활성 상태가 되는 반면 병변의 최대 57%는 지속적인 염증을 나타내며1,2 만성 활동성으로 정의됩니다. [7] 다발성 경화증(MS)은 활동성, 만성 활동성(혼합 활동성이라고도 함)으로 분류될 수 있는 국소 백질(WM) 병변의 축적을 특징으로 하는 중추신경계(CNS)의 만성 염증성, 탈수초화 및 신경퇴행성 질환입니다. /inactive lesions), inactive, remyelinated, 진행 중인 탈수초화 및 활동성 염증 또는 재수초화의 존재 및 지형에 따라 [1-3]. [8] 약 20년 전 John Prineas와 동료들은 이차 진행성 다발성 경화증(MS) 부검 사례에서 "만성 활동성/천천히 확장되는 병변"의 신경병리학을 설명하여 MS의 질병 진행에 대한 잠재적인 병리학적 관련성을 지적했습니다. [9] 병변은 활동성, 만성 활동성 또는 만성 침묵으로 분류되었습니다. [10] 염증을 동반한 만성 활동성 및 천천히 확장/진화하는 병변은 진행성 다발성 경화증의 신경병리학적 상관관계입니다. [11] 만성 활성 항체 매개(cAMR) 및 신장 이식(KTx) 후 급성 세포 거부 반응(AR)의 경우 다른 패턴의 혈장 사이토카인이 예상될 수 있습니다. [12] 목적: 이 연구의 목적은 말초 혈액 단핵 세포(PBMC)에서 인터페론 자극 유전자 15(ISG15), 인터루킨28B(IL28B) 또는 IFN-람다-3 및 유비퀴틴 특이적 펩티다제 18(USP18) 유전자의 발현 수준을 평가하는 것이었습니다. 건강한 사람과 비교하여 만성 활동성 및 비활동성 B형 간염 환자의 비율. [13]
antibody mediated rejection 항체 매개 거부반응
Clinical trials of biologic agents for chronic active antibody-mediated rejection (CAMR) in kidney transplant recipients (KTRs) have been disappointing. [1] Simple Summary The most common cause of late allograft failure is chronic active antibody-mediated rejection (ABMR), but no effective therapy is available. [2] Chronic active antibody-mediated rejection (CAAMR) is an intermediate process that occurs during the development of chronic antibody-mediated rejection (CAMR), which is a key problem associated with the long-term kidney grafts survival. [3] Objective To investigate the efficacy and safety of bone marrow-derived mesenchymal stem cells (BM-MSCs) on chronic active antibody-mediated rejection (cABMR) in the kidney allograft. [4] One year previously , the patient had an uneventful kidney allograft biopsy which revealed chronic active antibody-mediated rejection. [5] Chronic active antibody-mediated rejection (CAAMR) is a frequent cause of late graft loss. [6] The risk of infection associated with specific treatments of chronic active antibody-mediated rejection (cAMR) after kidney transplantation remains unknown. [7] Kidney transplant biopsy revealed de novo collapsing focal segmental glomerulosclerosis on a background of chronic active antibody mediated rejection. [8] Chronic active antibody-mediated rejection (AMR) in renal transplantation is usually refractory to current conventional treatment with rituximab, plasmapheresis (PP), and intravenous immunoglobulins (IVIG). [9] 3% of patients; 65% of these patients had C4d positivity in peritubular capillaries, and only 1 patient developed chronic active antibody-mediated rejection on follow-up. [10] However, 1 year after treatment, he developed chronic active antibody-mediated rejection without any donor-specific antibodies. [11] After KTx, the patient developed chronic active antibody-mediated rejection; however, the graft function was maintained throughout the follow-up period. [12] Chronic active antibody-mediated rejection is a major cause of allograft failure in kidney transplantation. [13] 1% in STD group developed chronic active antibody-mediated rejection. [14] We searched for distinctive cellular profiles that could be assigned to each rejection category of the Banff schema: antibody-mediated rejection (active and chronic active), borderline, T cell-mediated rejection (TCMR), and mixed rejection. [15] BACKGROUND Chronic active antibody-mediated rejection (CAMR) has unsatisfactory prognosis in spite of intensive standard antihumoral treatment. [16] In patients whose post-transplant period was less than 5 years, urine protein-to-creatinine ratio was significantly elevated in the glomerulonephritis and chronic active antibody-mediated rejection groups only. [17] Objective To evaluate the efficacy and safety of bortezomib in kidney transplant recipients with chronic active antibody-mediated rejection (cABMR). [18] BACKGROUND Linear C4d staining in the peritubular capillaries is considered a sensitive and useful marker of active or chronic active antibody-mediated rejection (ABMR) in transplanted kidneys. [19] The aim of this study was to identify potential proteomic biomarkers for chronic active antibody-mediated rejection (CAMR) in kidney transplant recipients (KTRs). [20]신장 이식 수용자(KTR)에서 만성 활성 항체 매개 거부 반응(CAMR)에 대한 생물학적 제제의 임상 시험은 실망스러웠습니다. [1] 간단한 요약 후기 동종이식 실패의 가장 흔한 원인은 만성 활성 항체 매개 거부반응(ABMR)이지만 효과적인 치료법이 없습니다. [2] nan [3] nan [4] 1년 전, 환자는 만성 활성 항체 매개 거부반응을 나타내는 사건이 없는 신장 동종이식편 생검을 받았습니다. [5] nan [6] nan [7] nan [8] nan [9] 환자의 3%; 이들 환자의 65%는 세뇨관 주위 모세혈관에서 C4d 양성이었고, 1명의 환자만이 추적 관찰에서 만성 활성 항체 매개 거부반응을 나타냈다. [10] 그러나 치료 1년 후 그는 기증자 특이적 항체 없이 만성 활성 항체 매개 거부 반응을 보였습니다. [11] KTx 후 환자는 만성 활성 항체 매개 거부 반응을 보였습니다. 그러나 이식 기능은 추적 기간 내내 유지되었습니다. [12] 만성 활성 항체 매개 거부반응은 신장 이식에서 동종이식 실패의 주요 원인입니다. [13] nan [14] nan [15] nan [16] nan [17] nan [18] nan [19] nan [20]
cell mediated rejection 세포 매개 거부 반응
Chronic active T cell-mediated rejection (CA TCMR) is a newly described variant of kidney allograft rejection associated with long-term graft loss. [1] Chronic active T cell mediated rejection (TCMR) and chronic active antibody-mediated rejection (ABMR) are classified as two principal subtypes of CKTR. [2] Chronic active T cell-mediated rejection, demonstrated by the presence of inflammation in areas of fibrosis, is associated with long-term allograft loss. [3] One had acute T-cell mediated rejection Banff 1B and the fourth had borderline T-cell mediated rejection with morphological changes suggestive of chronic active antibody mediated rejection (AMR). [4] Histopathology revealed grade II chronic active T cell mediated rejection. [5] The 2017 Banff meeting provided specific criteria for the diagnosis of tubulointerstitial changes in chronic active T cell-mediated rejection (CATCR), with an emphasis on inflammation in areas of interstitial fibrosis and tubular atrophy, which was thought to reflect an ongoing T cell-mediated alloimmunity. [6] The primary outcome at 12 months is a composite of death-censored graft loss, clinical biopsy-proven acute rejection, de novo donor-specific antibody, inflammation in areas of interstitial fibrosis and tubular atrophy (Banff i-IFTA, chronic active T-cell mediated rejection) and subclinical tubulitis on 12-month surveillance biopsy. [7]만성 활성 T 세포 매개 거부반응(CA TCMR)은 장기 이식 손실과 관련된 신장 동종이식 거부반응의 새로 설명된 변형입니다. [1] 만성 활성 T 세포 매개 거부 반응(TCMR) 및 만성 활성 항체 매개 거부 반응(ABMR)은 CKTR의 두 가지 주요 하위 유형으로 분류됩니다. [2] nan [3] nan [4] nan [5] 2017년 밴프 회의에서는 만성 활성 T 세포 매개 거부 반응(CATCR)의 세뇨관 간질 변화 진단에 대한 특정 기준을 제공했으며, 진행 중인 T 세포 매개 거부를 반영하는 것으로 생각되는 간질 섬유증 및 세뇨관 위축 영역의 염증에 중점을 둡니다. 동종면역. [6] 12 개월의 1차 결과는 사망 검열 이식편 손실, 임상 생검으로 입증된 급성 거부 반응, 새로운 기증자 특이적 항체, 간질 섬유증 및 세뇨관 위축 영역의 염증(Banff i-IFTA, 만성 활성 T-세포 중재 거부) 및 12개월 감시 생검에서 무증상 세뇨관염. [7]
severe mosquito bite
Methods Fifty-nine patients with EBV T/NK-LPD including chronic active EBV infection (CAEBV), severe mosquito bite allergy, hydroa vacciniforme-like lymphoproliferative disorder (HV), and EBV- hemophagocytic lymphohistiocytosis (EBV-HLH) were enrolled. [1] EBV-T/NK-LPDs include chronic active EBV infection, EBV-associated hemophagocytic lymphohistiocytosis, hydroa vacciniforme-like lymphoproliferative disease, and severe mosquito bite allergy. [2] Infection of T or NK cells with EBV is associated with extranodal NK/T cell lymphoma, aggressive NK-cell leukemia, systemic EBV-associated T-cell lymphoma, and chronic active EBV disease, which in some cases can include hydroa vacciniforme-like lymphoproliferative disease and severe mosquito bite allergy. [3]방법 만성 활동성 EBV 감염(CAEBV), 중증 모기에 물린 알레르기, 백신 유사 림프구 증식 장애(HV) 및 EBV-혈구포식성 림프조직구증(EBV-HLH)을 포함한 EBV T/NK-LPD 환자 59명이 등록되었습니다. [1] EBV-T/NK-LPD에는 만성 활동성 EBV 감염, EBV 관련 혈구포식성 림프조직구증가증, 수두백신종 유사 림프증식성 질환 및 중증 모기에 물린 알레르기가 포함됩니다. [2] nan [3]
quantitative susceptibility mapping 정량적 감수성 매핑
Background Chronic active MS lesions with paramagnetic rim can be identified by high-pass filtered (HPF) phase imaging or quantitative susceptibility mapping (QSM). [1] Objective: This study aimed to explore the association between chronic active rim+ lesions, identified as having a hyperintense rim on quantitative susceptibility mapping (QSM), on both clinical disability and imaging measures of neurodegeneration in patients with multiple sclerosis. [2] In MS patients, 80 chronic active lesions with hyperintense rim on quantitative susceptibility mapping were identified, and the mean OEF and χn within the rim and core were compared using linear mixed-effect model analysis. [3]배경 상자성 테두리가 있는 만성 활동성 다발성 경화증 병변은 고역 통과 필터링(HPF) 위상 영상 또는 정량적 감수성 매핑(QSM)으로 식별할 수 있습니다. [1] 목적: 이 연구는 임상적 장애와 다발성 경화증 환자의 신경퇴행성 영상 측정 모두에서 QSM(양적 감수성 매핑)에서 과강한 테두리가 있는 것으로 확인된 만성 활성 테두리+ 병변 사이의 연관성을 조사하는 것을 목표로 했습니다. [2] nan [3]
magnetic resonance imaging 자기 공명 영상
There has been an increasing interest in chronic active multiple sclerosis (MS) lesions as a new magnetic resonance imaging (MRI) marker of disease progression. [1] The presence of chronic active white matter lesions harbouring a paramagnetic rim on susceptibility-weighted magnetic resonance imaging has also been associated with an aggressive form of multiple sclerosis. [2]질병 진행의 새로운 자기 공명 영상(MRI) 마커로서 만성 활동성 다발성 경화증(MS) 병변에 대한 관심이 증가하고 있습니다. [1] 감수성 가중 자기 공명 영상에서 상자성 테두리가 있는 만성 활동성 백질 병변의 존재도 공격적인 형태의 다발성 경화증과 관련이 있습니다. [2]
Developed Chronic Active 개발된 만성 활성
3% of patients; 65% of these patients had C4d positivity in peritubular capillaries, and only 1 patient developed chronic active antibody-mediated rejection on follow-up. [1] However, 1 year after treatment, he developed chronic active antibody-mediated rejection without any donor-specific antibodies. [2] After KTx, the patient developed chronic active antibody-mediated rejection; however, the graft function was maintained throughout the follow-up period. [3] Results StCldn18-/- mice developed chronic active gastritis at middle age, with expression of the chemoattractant CCL28. [4] 1% in STD group developed chronic active antibody-mediated rejection. [5]환자의 3%; 이들 환자의 65%는 세뇨관 주위 모세혈관에서 C4d 양성이었고, 1명의 환자만이 추적 관찰에서 만성 활성 항체 매개 거부반응을 나타냈다. [1] 그러나 치료 1년 후 그는 기증자 특이적 항체 없이 만성 활성 항체 매개 거부 반응을 보였습니다. [2] KTx 후 환자는 만성 활성 항체 매개 거부 반응을 보였습니다. 그러나 이식 기능은 추적 기간 내내 유지되었습니다. [3] 결과 StCldn18-/- 마우스는 화학유인물질 CCL28의 발현과 함께 중년에 만성 활동성 위염을 발병했습니다. [4] nan [5]
Severe Chronic Active 심한 만성 활동성
A pancolonoscopy was performed (Figure B) and the biopsy showed severe chronic active inflammation in keeping with inflammatory bowel disease (IBD)-like colitis [1]. [1] Histopathological examination confirmed severe chronic active pyelonephritis with renal infarcts, multi-organ vasculitis and thrombosis suggestive of an infectious diseases of bacterial origin. [2] Post-mortem examination revealed severe chronic active pancreatitis with moderate chronic lymphocytic, plasmacytic cholangiohepatitis and mild chronic lymphocytic–plasmacytic duodenal enteritis (triaditis). [3] Colonoscopy showed severe chronic active colitis, stricture at 30 cm of anal verge, and a perianal fistula. [4]대장 내시경을 시행한 결과(그림 B), 조직 검사에서 염증성 장질환(IBD) 유사 대장염과 함께 심각한 만성 활동성 염증이 관찰되었습니다[1]. [1] 조직병리학적 검사에서 신장 경색, 다기관 혈관염 및 세균 기원의 전염병을 암시하는 혈전증을 동반한 심각한 만성 활동성 신우신염이 확인되었습니다. [2] nan [3] 대장 내시경 검사에서 심한 만성 활동성 대장염, 항문가장자리 30cm의 협착, 항문주위 누공이 관찰되었습니다. [4]
Revealed Chronic Active 공개된 만성 활성
Subsequent upper and lower GI endoscopy was macroscopically normal, and histology revealed chronic active oesophagitis/gastritis with a normal colon. [1] One year previously , the patient had an uneventful kidney allograft biopsy which revealed chronic active antibody-mediated rejection. [2] Endoscopic and histologic evaluation revealed chronic active ileitis, granulomatous inflammation, multinucleated giant cells, and a rare, equivocal acid-fast bacterium in the terminal ileum. [3] Biopsies of the colon revealed chronic active colitis; biopsies of the lesion revealed highgrade dysplasia (HGD). [4]이후의 상부 및 하부 위장관 내시경은 육안상 정상이었으며, 조직학적 소견은 정상 결장을 동반한 만성 활동성 식도염/위염을 나타냈다. [1] 1년 전, 환자는 만성 활성 항체 매개 거부반응을 나타내는 사건이 없는 신장 동종이식편 생검을 받았습니다. [2] nan [3] nan [4]
Background Chronic Active 백그라운드 만성 활성
BACKGROUND Chronic active Epstein-Barr virus infection (EBV) is a systemic EBV-positive lymphoproliferative disease, which may lead to fatal illness. [1] Background Chronic active MS lesions with paramagnetic rim can be identified by high-pass filtered (HPF) phase imaging or quantitative susceptibility mapping (QSM). [2] Background Chronic active Epstein–Barr virus infection (CAEBV) is defined as Epstein–Barr virus (EBV)-positive T/NK cell-related neoplasia, and its major clinical symptom is systemic inflammation presenting as infectious mononucleocytosis, whereas enteritis and diarrhea are minor clinical symptoms. [3] Background Chronic active hepatitis C virus (HCV) infection is a major public health problem and causes liver fibrosis (LF) up to liver cirrhosis (LC). [4]배경 만성 활동성 엡스타인-바 바이러스 감염(EBV)은 치명적인 질병으로 이어질 수 있는 전신 EBV-양성 림프증식성 질환이다. [1] 배경 상자성 테두리가 있는 만성 활동성 다발성 경화증 병변은 고역 통과 필터링(HPF) 위상 영상 또는 정량적 감수성 매핑(QSM)으로 식별할 수 있습니다. [2] nan [3] nan [4]
Demonstrated Chronic Active
Pathological evaluation of the specimen demonstrated chronic active transmural inflammation, vascular congestion and acute serositis. [1] Histopathological evaluation of the bladder demonstrated chronic active polypoid cystitis. [2] However, the pathology of bone marrow, lymph nodes, and the spleen demonstrated chronic active Epstein-Barr virus-associated T-cell lymphoproliferative disorders. [3]표본의 병리학적 평가는 만성 활동성 경벽 염증, 혈관 울혈 및 급성 장막염을 보여주었습니다. [1] 방광의 조직병리학적 평가는 만성 활동성 폴립성 방광염을 보여주었습니다. [2] 그러나 골수, 림프절 및 비장의 병리학은 만성 활성 엡스타인-바 바이러스 관련 T 세포 림프 증식성 장애를 보여주었습니다. [3]
Showed Chronic Active 만성 활성을 보임
Histopathology of the molar and mandibular and sublingual glands showed chronic active sialoadenitis with more severe changes in the molar gland. [1] Nine patients had pouch biopsies to rule out inflammation: all showed chronic active enteritis, a normal finding in ileal pouches. [2] The vacA subtypes: s1as1bm2, s1a1b and s2 m2 showed chronic active gastritis in percentages of 90. [3]어금니와 하악 및 설하 샘의 조직 병리학은 어금니에 더 심각한 변화와 함께 만성 활동성 시알 덴염을 보였다. [1] 9명의 환자는 염증을 배제하기 위해 주머니 생검을 받았습니다. 모든 환자는 회장 주머니에서 정상적인 소견인 만성 활동성 장염을 보였습니다. [2] nan [3]
Systemic Chronic Active
Systemic chronic active Epstein-Barr virus (EBV; sCAEBV) infection, T- and natural killer (NK)-cell type (sCAEBV), is a fatal disorder accompanied by persisting inflammation harboring clonal proliferation of EBV-infected T or NK cells. [1] Systemic forms of EBV‐associated T‐cell lymphoproliferative disorders of childhood (S‐EBV‐T‐LPD) comprise three major forms: EBV‐positive hemophagocytic lymphohistiocytosis (EBV‐HLH), systemic EBV‐positive T‐cell lymphoma (S‐EBV‐TCL), and systemic chronic active EBV infection (S‐CAEBV). [2]전신 만성 활성 엡스타인-바 바이러스(EBV; sCAEBV) 감염, T 세포 및 자연 살해(NK) 세포 유형(sCAEBV)은 EBV에 감염된 T 또는 NK 세포의 클론 증식을 포함하는 지속적인 염증을 동반하는 치명적인 장애입니다. [1] nan [2]
Include Chronic Active
EBV-T/NK-LPDs include chronic active EBV infection, EBV-associated hemophagocytic lymphohistiocytosis, hydroa vacciniforme-like lymphoproliferative disease, and severe mosquito bite allergy. [1] Disorders presenting mainly in children and young adults include chronic active EBV infection (CAEBV) - systemic and cutaneous forms - which are not considered malignant disorders but were included in the WHO classification for the first time because of the differential diagnosis with other T- or NK-cell lymphomas. [2]EBV-T/NK-LPD에는 만성 활동성 EBV 감염, EBV 관련 혈구포식성 림프조직구증가증, 수두백신종 유사 림프증식성 질환 및 중증 모기에 물린 알레르기가 포함됩니다. [1] 주로 소아 및 젊은 성인에게 나타나는 장애는 만성 활동성 EBV 감염(전신 및 피부 형태)을 포함하며, 이는 악성 장애로 간주되지 않지만 다른 T- 또는 NK와의 감별 진단으로 인해 처음으로 WHO 분류에 포함되었습니다. - 세포 림프종. [2]
Diffuse Chronic Active
Biopsies showed moderate diffuse chronic active colitis with crypt abscesses and apoptotic bodies. [1] Microscopic investigation revealed a diffuse chronic active endomyometritis with sporadic Actinomycetes colonies. [2]생검 결과 음와 농양과 세포 사멸체를 동반한 중등도 미만성 만성 활동성 대장염이 나타났습니다. [1] nan [2]
chronic active epstein 만성 활성 엡스타인
Chronic active Epstein-Barr virus (CAEBV) typically presents as persistent infectious mononucleosis-like disease and/or hemophagocytic lymphohistocytosis (HLH), reflecting ectopic Epstein-Barr virus (EBV) infection and lymphoproliferation of T and/or NK cells. [1] Chronic active Epstein–Barr virus infection (CAEBV) is a disease where Epstein–Barr virus (EBV)-infected T- or NK-cells are activated and proliferate clonally. [2] Chronic active Epstein–Barr virus (CAEBV) infection is a rare disease with a high mortality rate. [3] Thereafter, she was diagnosed with extranodal NK/T-cell lymphoma related to chronic active Epstein–Barr virus (CAEBV). [4] Purpose We intended to investigate the clinical features of pediatric patients with chronic active Epstein-Barr virus infection (CAEBV) and effectiveness of the L-DEP regimen before HSCT (hematopoietic stem cell transplantation). [5] Chronic active Epstein-Barr virus (CAEBV) infection is a progressive disease characterized by persistent inflammatory symptoms accompanied by clonally proliferating EBV-positive T or NK cells. [6] BACKGROUND Chronic active Epstein-Barr virus infection (EBV) is a systemic EBV-positive lymphoproliferative disease, which may lead to fatal illness. [7] OBJECTIVE To analyze the clinical characteristics, prognosis factors and risk factors of chronic active Epstein-Barr virus (EBV) infection in children. [8] Background: Chronic active Epstein-Barr virus (CAEBV) infection is one of the EBV-positive T- or NK-cell lymphoproliferative diseases. [9] Chronic active Epstein-Barr virus (CAEBV) infection characterized by persistent infectious mononucleosis-like symptoms can lead to cardiovascular diseases. [10] When these situations persist for more than 3 months, it is determined as chronic active Epstein–Barr virus infection (CAEBV). [11] Objective To investigate the clinical characteristics, treatment, prognosis and risk factors for chronic active Epstein–Barr Virus infection (CAEBV) associated with coronary artery dilatation (CAD) in children. [12] Background Chronic active Epstein–Barr virus infection (CAEBV) is defined as Epstein–Barr virus (EBV)-positive T/NK cell-related neoplasia, and its major clinical symptom is systemic inflammation presenting as infectious mononucleocytosis, whereas enteritis and diarrhea are minor clinical symptoms. [13] Chronic active Epstein-Barr virus (EBV) disease (CAEBV) is characterized by high levels of EBV predominantly in T and/or NK cells with lymphoproliferation, organ failure due to infiltration of tissues with virus-infected cells, hemophagocytic lymphohistiocytosis (HLH) and/or lymphoma. [14] Chronic active Epstein–Barr virus infection (CAEBV) is relatively uncommon and can be associated with lymphoproliferative diseases (LPD's) of NK/T cell and B cell type. [15] Chronic active Epstein-Barr virus (CAEBV) infection is a very rare and potentially lifethreatening illness caused by long-term EBV infection. [16] Purpose We intended to investigate the clinical features of paediatric patients with chronic active Epstein–Barr virus infection (CAEBV) and to examine the effectiveness of the L-DEP regimen before haematopoietic stem cell transplantation (HSCT). [17] Chronic active Epstein–Barr virus (CAEBV) disease is a rare condition characterised by persistent EBV infection in previously healthy individuals. [18] Chronic active Epstein-Barr virus infection (CAEBV) is a prototype of EBV-associated Tand NK-cell lymphoproliferative diseases (T/NK-cell LPDs). [19] Background: Chronic active Epstein-Barr virus hepatitis (CAEBVH) in adult patients is a rare and highly lethal disease characterized by hepatitis and hepatomegaly. [20] Patient 4: An 18-year-old female patient, who had combined immunodeficiency, was diagnosed with EBV infection with clinical manifestations of chronic active Epstein-Barr virus infection and haemophagocytic lymphohistiocytosis. [21] Systemic chronic active Epstein-Barr virus (EBV; sCAEBV) infection, T- and natural killer (NK)-cell type (sCAEBV), is a fatal disorder accompanied by persisting inflammation harboring clonal proliferation of EBV-infected T or NK cells. [22] Pediatric coronary artery aneurysms (CAAs) are mainly detected in Kawasaki disease and in chronic active Epstein-Barr virus (EBV) infection sometimes, and cardiac complications are rare in viral-associated hemophagocytic lymphohistiocytosis (HLH) patients. [23] Identification of biallelic loss-of-function mutations in TNFRSF9 and PIK3CD in a kindred with chronic active Epstein-Barr virus infection of T cells (CAEBV) suggests that CAEBV is the consequence of factors providing growth advantage to EBV-infected T cells combined with defective cell immunity toward EBV-infected cells. [24] Rationale: Chronic active Epstein-Barr virus infection (CAEBV) is a common infectious disease that often affects multiple organs or systems. [25] Chronic active Epstein-Barr virus (EBV) infection (CAEBV) is an EBV-associated lymphoproliferative disease characterized by repeated or sustainable infectious mononucleosis (IM)-like symptoms. [26] Introduction: A chronic active Epstein–Barr virus (EBV) infection (CAEBV), which is characterized by persistent “infectious mononucleosis-like” symptoms, can lead to cardiovascular complications, including coronary artery aneurysms. [27] Hydroa vacciniforme-like lymphoproliferative disorder (HV-LPD) is a cutaneous form of chronic active Epstein-Barr virus (EBV) infection, which occurs mainly in children in Latin America and Asia. [28] Chronic active Epstein-Barr virus infection (CAEBV) presents with mononucleosis-like symptoms such as chronic persistent or recurrent pyrexia, lymphadenopathy, and hepatosplenomegaly because of the reactivation of Epstein-Barr virus (EBV) as demonstrated by the recurrence of EBV-infected cells. [29] BackgroundTo report 2 cases of bilateral granulomatous panuveitis accompanied by chronic active Epstein-Barr virus infection (CAEBV). [30] BackgroundSystemic chronic active Epstein-Barr virus infection is an extremely rare childhood disease. [31] Chronic active Epstein-Barr virus infection (CAEBV) is critical owing to lethal complications such as hemophagocytic lymphohistiocytosis (HLH), multiple organ failure, and malignant lymphoma. [32] Main textIn the present review, these included three early complications; hepatitis, splenic rupture and airway compromise, as well as possible late conditions; lymphoproliferative cancers, multiple sclerosis, rheumatoid arthritis, and chronic active Epstein-Barr virus infection. [33] However, the pathology of bone marrow, lymph nodes, and the spleen demonstrated chronic active Epstein-Barr virus-associated T-cell lymphoproliferative disorders. [34] Dear Editor, Chronic active Epstein–Barr virus (CAEBV) often succumbs to hemophagocytic lymphohistiocytosis, multi-organ failure, or Epstein–Barr virus–positive lymphomas if untreated. [35] Chronic active Epstein-Barr virus (EBV) infection of T-cell and NK-cell type, systemic form (CAEBV-T/NK-S) is characterized by EBV+ T-cell and/or NK-cell proliferation with no changes suggesting malignancy. [36] We report a case of ceftriaxone-induced immune hemolytic anemia in a 10-year-old with chronic active Epstein–Barr virus disease and hemophagocytic lymphohistiocytosis. [37] The presence of clinical symptoms and viral load in a patient in 6 months after the infectious mononucleosis disease indicates the formation of chronic active Epstein – Barr viral infection. [38] Case presentationWe report a 30-year-old Chinese female patient who was diagnosed with chronic active Epstein-Barr virus infection more than 9 months prior and has since been presenting with cutaneous lymphoproliferative disorders mimicking hydroa vacciniforme and subsequent haemophagocytic lymphohistiocytosis. [39] dermatitidis infection in an adult patient that developed after allogeneic hematopoietic stem cell transplantation for chronic active Epstein-Barr virus infection. [40] Chronic active Epstein-Barr virus (CAEBV) T-cell type infection, systemic form, is characterized by persistent infectious mononucleosis-like symptoms, high Epstein-Barr virus (EBV) DNA levels in the peripheral blood, organ damage, and a poor prognosis. [41] Chronic active Epstein-Barr virus (CAEBV) infection is an EBV-associated lymphoproliferative disease defined by (1) illness lasting > 6 months; (2) infiltration of tissues with lymphocytes; (3) elevated EBV DNA, RNA, or proteins in affected tissues; and (4) the absence of any other immunosuppressive condition1,2. [42] The lacrimal gland biopsy showed atypical EBV positive T-cell lymphoid proliferation with features suggestive of chronic active Epstein–Barr virus (EBV) infection and serum EBV polymerase chain reaction was 825 000 copies/mL. [43] Chronic active Epstein-Barr virus infection (CAEBV) is one of the Epstein-Barr virus (EBV)-positive T- or NK-lymphoproliferative diseases. [44]만성 활성 엡스타인-바 바이러스(CAEBV)는 일반적으로 이소성 엡스타인-바 바이러스(EBV) 감염 및 T 및/또는 NK 세포의 림프 증식을 반영하는 지속적인 감염성 단핵구증 유사 질환 및/또는 혈구탐식성 림프조직구증(HLH)으로 나타납니다. [1] CAEBV(만성 활성 엡스타인-바 바이러스 감염)는 엡스타인-바 바이러스(EBV)에 감염된 T 또는 NK 세포가 활성화되어 클론적으로 증식하는 질병입니다. [2] CAEBV(만성 활성 엡스타인-바 바이러스) 감염은 사망률이 높은 희귀 질환입니다. [3] 그 후 그녀는 만성 활성 엡스타인-바 바이러스(CAEBV)와 관련된 림프절 외 NK/T 세포 림프종 진단을 받았습니다. [4] 목 적 소아 만성 활성 엡스타인-바 바이러스 감염(CAEBV) 환자의 임상 양상과 조혈모세포 이식(HSCT) 전 L-DEP 요법의 효과를 조사하고자 하였다. [5] CAEBV(만성 활성 엡스타인-바 바이러스) 감염은 클론적으로 증식하는 EBV 양성 T 또는 NK 세포를 동반하는 지속적인 염증 증상을 특징으로 하는 진행성 질환입니다. [6] 배경 만성 활동성 엡스타인-바 바이러스 감염(EBV)은 치명적인 질병으로 이어질 수 있는 전신 EBV-양성 림프증식성 질환이다. [7] 목적 소아에서 만성 활성 엡스타인-바 바이러스(EBV) 감염의 임상적 특징, 예후 인자 및 위험 인자를 분석합니다. [8] 배경: CAEBV(만성 활성 엡스타인-바 바이러스) 감염은 EBV 양성 T 또는 NK 세포 림프 증식성 질환 중 하나입니다. [9] 지속적인 전염성 단핵구증과 유사한 증상을 특징으로 하는 만성 활성 엡스타인-바 바이러스(CAEBV) 감염은 심혈관 질환을 유발할 수 있습니다. [10] 이러한 상황이 3개월 이상 지속되면 만성 활성 엡스타인-바 바이러스 감염(CAEBV)으로 판정됩니다. [11] nan [12] nan [13] nan [14] nan [15] nan [16] nan [17] nan [18] nan [19] nan [20] nan [21] 전신 만성 활성 엡스타인-바 바이러스(EBV; sCAEBV) 감염, T 세포 및 자연 살해(NK) 세포 유형(sCAEBV)은 EBV에 감염된 T 또는 NK 세포의 클론 증식을 포함하는 지속적인 염증을 동반하는 치명적인 장애입니다. [22] 소아 관상동맥류(CAA)는 주로 가와사키병 및 만성 활동성 엡스타인-바 바이러스(EBV) 감염에서 종종 발견되며, 심장 합병증은 바이러스 관련 혈구포식성 림프조직구증(HLH) 환자에서 드뭅니다. [23] T 세포의 만성 활성 엡스타인-바 바이러스 감염(CAEBV)이 있는 친척에서 TNFRSF9 및 PIK3CD에서 이대립유전자 기능 상실 돌연변이의 확인은 CAEBV가 결함이 있는 EBV에 감염된 T 세포에 성장 이점을 제공하는 요인의 결과임을 시사합니다 EBV에 감염된 세포에 대한 세포 면역. [24] nan [25] nan [26] nan [27] nan [28] nan [29] nan [30] nan [31] nan [32] nan [33] 그러나 골수, 림프절 및 비장의 병리학은 만성 활성 엡스타인-바 바이러스 관련 T 세포 림프 증식성 장애를 보여주었습니다. [34] nan [35] nan [36] nan [37] nan [38] nan [39] nan [40] nan [41] nan [42] nan [43] nan [44]
chronic active ebv 만성 활성 Ebv
The 2017 World Health Organization (WHO) classification recognizes the following entities characterized by different outcomes: chronic active EBV infection of T- or NK-cell types (cutaneous and systemic forms), systemic EBV-positive T-cell lymphoma of childhood, EBV-positive aggressive NK-cell leukemia, extra nodal NK/T-cell lymphoma nasal type, and the new provisional entity known as primary EBV-positive nodal T/NK-cell lymphoma. [1] Epstein-Barr virus (EBV) infection is prevalent and associated with distinct diseases including infectious mononucleosis (IM), chronic active EBV infection (CAEBV) and NK/T-cell lymphoma (NKTL). [2] Some cases of EBV-driven HLH are due to chronic active EBV (CA-EBV), wherein EBVmay infect T andNKwith progression to lymphoproliferative neoplasms. [3] Chronic active EBV infection is a rare condition with considerable diagnostic and treatment difficulties. [4] These findings directly implicate Tsg101 in EBV nuclear egress and identify prazoles as potential therapeutic candidates for conditions that rely on EBV replication, such as chronic active EBV infection and posttransplant lymphoproliferative disorders. [5] Epstein-Barr virus (EBV) T/NK-cell lymphoproliferative diseases are characterized by clonal expansion of EBV-infected T or NK cells, including chronic active EBV infection of T/NK-cell type (CAEBV+T/NK), EBV-associated hemophagocytic lymphohistiocytosis (EBV+HLH), extranodal NK/T-cell lymphoma of nasal type (ENKTL), and aggressive NK-cell leukemia (ANKL). [6] No cases of lymphoproliferative disorder, hemophagocytic lymphohistiocytosis, or chronic active EBV infection were reported. [7] Epstein-Barr virus-positive T-cell and NK-cell lymphoproliferative diseases (EBV-T/NK-LPD) is categorized into two major groups: systemic Epstein-Barr virus-positive T-cell lymphoma of childhood (SETL) and chronic active EBV infection (CAEBV) [1]. [8] The patient was thus diagnosed with chronic active EBV infection (CAEBV) associated with hemophagocytic lymphohistiocytosis (HLH). [9] ABSTRACT A 7-year-old girl with chronic active EBV (CAEBV) infection-associated hemophagocytic lymphohistiocytosis presented with fever. [10] EBV‐HLH may occur heterogeneously associated with the primary infection, with chronic active EBV infection or with underlying primary HLH. [11] A further two patients demonstrated EBV + node-based CD8 + large TCL without HLH, while the remaining two had the systemic form of chronic active EBV infection (sCAEBV) with CD8 + small lymphocytes. [12] Hence, HMB may progress to systemic diseases, such as hemophagocytic lymphohistiocytosis, chronic active EBV disease, and EBV-associated malignancies. [13] Non-familial EBV-associated HLH is a major diagnostic dilemma, as it represents a diverse spectrum of disease ranging from highly curable (non-neoplastic EBV-HLH) to indolent but incurable (chronic active EBV) to acutely fatal (systemic EBV-positive T-cell lymphoma of childhood). [14] The monoclonal proliferation of EBV-infected T cells was confirmed by Southern blotting, and the patient was diagnosed with chronic active EBV-associated sHLH and T-cell lymphoproliferative disease. [15] EBV-positive NK-cell neoplasms, such as extranodal NK/T-cell lymphoma of nasal type, aggressive NK-cell leukemia, and chronic active EBV infection, are relatively rare but lethal disorders. [16] In this classification, primary cutaneous acral CD8+ T-cell lymphoma and Epstein-Barr virus positive (EBV+) mucocutaneous ulcer are included as new provisional entities, and a new section on cutaneous forms of chronic active EBV disease has been added. [17] Pathways promoting proliferation, such as Janus associated kinase/ Signal Transducer and Activator of Transcription (JAK/STAT) and nuclear factor kB, are upregulated in ENKTL while upregulation of survivin and deregulation of p53 inhibit apoptosis in both ENKTL and chronic active EBV infection (CAEBV). [18] Methods Fifty-nine patients with EBV T/NK-LPD including chronic active EBV infection (CAEBV), severe mosquito bite allergy, hydroa vacciniforme-like lymphoproliferative disorder (HV), and EBV- hemophagocytic lymphohistiocytosis (EBV-HLH) were enrolled. [19] Our previous case series study clearly showed a clinical spectrum of EBV-associated T/NK LPDs including HV, hypersensitivity to mosquito bites (HMB), chronic active EBV infection (CAEBV), and hemophagocytic lymphohistiocytosis (HLH). [20] Systemic forms of EBV‐associated T‐cell lymphoproliferative disorders of childhood (S‐EBV‐T‐LPD) comprise three major forms: EBV‐positive hemophagocytic lymphohistiocytosis (EBV‐HLH), systemic EBV‐positive T‐cell lymphoma (S‐EBV‐TCL), and systemic chronic active EBV infection (S‐CAEBV). [21] They encompass a spectrum of entities that range from non-neoplastic lesions such as EBV-associated haemophagocytic lymphohistiocytosis (EBV-HLH) to more chronic conditions with variable outcomes such as chronic active EBV infections (CAEBV) of T- and NK-cell type (cutaneous and systemic forms) and malignant diseases such as systemic EBV-positive T-cell lymphoma of childhood, aggressive NK-cell leukaemia, extranodal NK/T-cell lymphoma, nasal-type, and primary EBV-positive nodal T/NK-cell lymphoma. [22] Accordingly, we made a diagnosis of NK-cell post-transplant lymphoproliferative disease with chronic active EBV infection-like clinical findings (CAEBV-like NK-cell PTLD). [23] We recently reported genomic analyses of chronic active EBV infection (CAEBV), a proliferative disorder of T and/or NK cells, as well as other lymphoid malignancies. [24] This study was aimed at describing the pathologic changes of nonlymphomatous gastrointestinal EBV lymphoproliferative diseases in both immunocompetent and immunocompromised settings; the former was focused on chronic active EBV infection, and the latter was about the infection in posttransplantation patients. [25] Hydroa vacciniforme-like lymphoproliferative disorder and hypersensitivity reactions to mosquito bites are cutaneous manifestations of chronic active EBV infection, which are seen mainly in children and adolescents in Central and South America and Asia. [26] ABSTRACT Epstein–Barr virus (EBV) associated with several diseases such as contagious mononucleosis chronic active EBV infection, and diverse sorts of malignant tumors. [27] EBV-T/NK-LPDs include chronic active EBV infection, EBV-associated hemophagocytic lymphohistiocytosis, hydroa vacciniforme-like lymphoproliferative disease, and severe mosquito bite allergy. [28] The EBV-LPD of childhood is divided into several types, such as chronic active EBV-LPD, hypersensitivity to mosquito bite, hydroa vacciniforme-like lymphoma, and systemic EBV+ T-cell lymphoma of childhood. [29] Chronic active EBV infection (CAEBV) and EBV-hemophagocytic lymphohistiocytosis (HLH) are recognized as systemic EBV-positive T-cell and natural killer (NK)-cell lymphoproliferative diseases (LPDs) arising from the clonal proliferations of EBV-infected T cells and NK cells. [30] Plasma viral loads were significantly higher in "active" disease in chronic active EBV infection (CAEBV). [31] Disorders presenting mainly in children and young adults include chronic active EBV infection (CAEBV) - systemic and cutaneous forms - which are not considered malignant disorders but were included in the WHO classification for the first time because of the differential diagnosis with other T- or NK-cell lymphomas. [32] Chronic active EBV infection (CAEBV) is one of the EBV-associated T/NK lymphoproliferative diseases. [33] Infection of T or NK cells with EBV is associated with extranodal NK/T cell lymphoma, aggressive NK-cell leukemia, systemic EBV-associated T-cell lymphoma, and chronic active EBV disease, which in some cases can include hydroa vacciniforme-like lymphoproliferative disease and severe mosquito bite allergy. [34] The 2016 revised World Health Organization classification recognizes the following EBV-positive lymphoproliferative disorders (LPD): chronic active EBV infection (CAEBV) of T- and NK-cell type (cutaneous and systemic forms), systemic EBV-positive T-cell lymphoma of childhood, aggressive NK-cell leukemia, extranodal NK/T-cell lymphoma, nasal type, and the new provisional entity primary EBV-positive nodal T/NK-cell lymphoma. [35] Chronic active EBV infection (CAEBV) is an intractable disease classified as a lymphoproliferative disorder in the 2016 World Health Organization lymphoma classification1,2. [36] Here, we review the normal immune response to EBV and discuss several CSS associated with EBV, such as chronic active EBV infection, hemophagocytic lymphohistiocytosis, and posttransplant lymphoproliferative disorder. [37] She was diagnosed with NK-cell chronic active EBV infection. [38] Conclusions HVLPD is closely associated with chronic active EBV infection. [39] The patient had a long history of chronic active EBV infection (CAEBV) presenting with recurrent fever, multiple enlarged lymph nodes and elevated EBV-DNA load. [40]2017년 세계 보건 기구(WHO) 분류에서는 T 세포 또는 NK 세포 유형(피부 및 전신 형태)의 만성 활동성 EBV 감염, 아동기의 전신 EBV 양성 T 세포 림프종, EBV- 양성 공격성 NK 세포 백혈병, 추가 결절 NK/T 세포 림프종 비강 유형 및 원발성 EBV 양성 결절 T/NK 세포 림프종으로 알려진 새로운 임시 개체. [1] 엡스타인-바 바이러스(EBV) 감염은 만연하고 전염성 단핵구증(IM), 만성 활동성 EBV 감염(CAEBV) 및 NK/T 세포 림프종(NKTL)을 포함한 별개의 질병과 관련이 있습니다. [2] EBV에 의한 HLH의 일부 사례는 만성 활성 EBV(CA-EBV)에 기인하며, 여기서 EBV는 T 및 NK를 감염시키고 림프 증식성 신생물로 진행합니다. [3] 만성 활동성 EBV 감염은 진단 및 치료에 상당한 어려움이 있는 드문 질환입니다. [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10] nan [11] nan [12] nan [13] nan [14] nan [15] nan [16] 이 분류에서 원발성 피부 선단 CD8+ T 세포 림프종 및 Epstein-Barr 바이러스 양성(EBV+) 점막 피부 궤양이 새로운 임시 항목으로 포함되었으며 만성 활동성 EBV 질환의 피부 형태에 대한 새로운 섹션이 추가되었습니다. [17] Janus 관련 키나제/신호 변환기 및 전사 활성화제(JAK/STAT) 및 핵 인자 kB와 같은 증식을 촉진하는 경로는 ENKTL에서 상향 조절되는 반면 서바이빈의 상향 조절 및 p53의 조절 완화는 ENKTL 및 만성 활성 EBV 감염(CAEBV)에서 세포자멸사를 억제합니다. ). [18] 방법 만성 활동성 EBV 감염(CAEBV), 중증 모기에 물린 알레르기, 백신 유사 림프구 증식 장애(HV) 및 EBV-혈구포식성 림프조직구증(EBV-HLH)을 포함한 EBV T/NK-LPD 환자 59명이 등록되었습니다. [19] nan [20] nan [21] nan [22] nan [23] nan [24] nan [25] nan [26] nan [27] EBV-T/NK-LPD에는 만성 활동성 EBV 감염, EBV 관련 혈구포식성 림프조직구증가증, 수두백신종 유사 림프증식성 질환 및 중증 모기에 물린 알레르기가 포함됩니다. [28] nan [29] nan [30] nan [31] 주로 소아 및 젊은 성인에게 나타나는 장애는 만성 활동성 EBV 감염(전신 및 피부 형태)을 포함하며, 이는 악성 장애로 간주되지 않지만 다른 T- 또는 NK와의 감별 진단으로 인해 처음으로 WHO 분류에 포함되었습니다. - 세포 림프종. [32] nan [33] nan [34] nan [35] nan [36] nan [37] nan [38] nan [39] nan [40]