新生儿红斑狼疮1例

报告1例新生儿红斑狼疮。患儿男,出生56天,头面部、躯干四肢出现环形红斑1月余。肝功能轻度异常,中度贫血,窦性心动过速,患儿及其母亲抗Ro/SSA抗体、抗La/SSB抗体阳性。     

新生儿红斑狼疮1例

报告1例新生儿红斑狼疮。患儿男,出生56天,头面部、躯干四肢出现环形红斑1月余。肝功能轻度异常,中度贫血,窦性心动过速,患儿及其母亲抗Ro/SSA抗体、抗La/SSB抗体阳性。     

新生儿红斑狼疮1例

报道1例新生儿红斑狼疮,患儿男,4个月15天,头面部蝶形红斑1月余。抗SSA抗体阳性（＋＋＋）、抗重组Ro－52阳性（＋＋＋）。其母亲抗Ro／SSA抗体阳性（＋）,无临床症状。患儿入院后诊断为：①新生儿红斑狼疮;②急性细支气管炎;③泌尿道感染。给予护肝、护心、抗感染、化痰平喘等对症治疗,颜面外用丁酸氢化可的松软膏7天后皮损逐渐消退,经内科治疗咳嗽等临床症状好转。     

新生儿红斑狼疮1例

报道1例新生儿红斑狼疮,患儿男,4个月15天,头面部蝶形红斑1月余。抗SSA抗体阳性(+++)、抗重组Ro-52阳性(+++)。其母亲抗Ro/SSA抗体阳性(+),无临床症状。患儿入院后诊断为:1新生儿红斑狼疮;2急性细支气管炎;3泌尿道感染。给予护肝、护心、抗感染、化痰平喘等对症治疗,颜面外用丁酸氢化可的松软膏7天后皮损逐渐消退,经内科治疗咳嗽等临床症状好转。     

6例新生儿红斑狼疮临床分析

目的：探索新生儿红斑狼疮（NLE）的临床特点和远期并发症。方法：追踪和观察我科近6年来诊断为新生儿红斑狼疮的患儿。结果：近6年来我科共诊治新生儿红斑狼疮6例,包括男婴2例,女婴4例。6例NLE患儿分别于出生后第28、15、14、48、20和65天出现皮损,主要位于颜面、颈部等暴露部位,多表现为圆形、环形或半环形红斑、斑块,表面有细碎鳞屑。1例男婴出生时患有I度房室传导阻滞,1例患儿出生7天时出现高胆红素血症,1例患儿出现肝转氨酶升高。所有患儿和患儿母亲抗Ro／SSA抗体阳性,所有患儿抗Ro／SSA抗体均在9个月内消失。1例患儿母亲孕前已患有亚急性皮肤型红斑狼疮,1例患儿母亲在小孩出生2年后发生干燥综合征。所有患儿均未治疗,皮损均在6个月内消失,无后遗症。结论：新生儿红斑狼疮具有自限性,整体愈后良好,但仍需长期随访观察。     

新生儿红斑狼疮15例临床分析及文献回顾

目的 探讨新生儿红斑狼疮的临床特点并进行文献回顾.方法 回顾性分析徐州市儿童医院15例新生儿红斑狼疮患儿的临床资料,对新生儿红斑狼疮的临床特点进行分析总结,并进行随访.结果 15例患儿中女11例,男4例,就诊年龄8 d～3个月.皮损位于头面部14例,位于非曝光部位8例;皮损表现为水肿性红斑样13例,表现为脂溢性皮炎2例...     

新生儿红斑狼疮一例

正临床资料患儿,女,20天龄。主因头面部红斑10 d,躯干、四肢红斑4 d,于2015年1月26日就诊。10 d前,无明显诱因患儿头面部出现数个环状红斑,上覆少许鳞屑,皮损渐累及躯干及四肢,无发热、喘息等。患儿系第二胎,足月剖宫产,出生时Apgar评分10分。其兄无类似病史。父母非近亲结婚。其母亲有亚急性皮肤型红斑狼疮病史20年,曾口服醋酸泼尼松1~2     

新生儿红斑狼疮与抗Ro/SSA和抗La/SSB抗体阳性2例

报告了 2例新生儿红斑狼疮。 1例出生后发现有心脏房室传导阻滞和室间隔缺损 ,脐血检测有抗Ro/SSA和抗U1RNP抗体 ,母亲为SLE患者。 1例出生后 1个月于面部、颈部及躯干上部出现环形红斑样皮疹 ,脐血检测有抗Ro/SSA和抗La/SSB抗体 ,母亲为SCLE患者。 2例患儿皮疹和心脏传导阻滞于生后 3个月内消退 ,自身抗体于生后 6个月内消退 ,随访 7年和 1 5年后均健康。     

新生儿红斑狼疮

报告1例新生儿红斑狼疮。患儿女,出生24d。头部、躯干、外阴及四肢出现环形红斑10余天。肝功能异常．心脏室间隔缺损,抗La／SSB抗体阳性,其母亲抗La／SSB抗体亦阳性。     

宫内发病的新生儿红斑狼疮一例

新生儿红斑狼疮(neonatallupuserythematosus,NLE)是一种母体自身抗体经过胎盘进入胎儿体内造成的自身免疫性疾病,临床主要特征为皮肤类似亚急性皮肤性红斑狼疮(SCLE)样的环形红斑和先天性心脏传导阻滞,有时有其他系统损害。我们在对1例抗Ro/SSA抗体阳性的SCLE患者的妊娠随访中,发现1例宫内发病的NLE,现报道如下。患儿母亲,29岁,5年前出现面部皮疹,ANA阳性,抗Ro/SSA、抗La/SSB阳性,在我院诊断为SCLE,环形红斑型,给予泼尼松30mg/d,服药2个月后病情好转,之后泼尼松逐渐减量至10mg/d,其间曾人工流产2次。患者于2002年1月妊娠,当…     

Central nervous system involvement in neonatal lupus erythematosus

Computerized tomography (CT) of the brain was performed in 10 of 11 consecutive infants with neonatal lupus erythematosus (NLE) (five boys and six girls). Ten of the 11 infants had brain neurosonography. Nine of 10 infants had abnormal CT scans. There was diffuse, markedly reduced attenuation of the cerebral white matter in four infants studied in the first week of life, and also in an infant 5 weeks of age. Patchy reduced subcortical white matter attenuation was observed in another 5-week-old infant. Basal ganglia calcifications were present in two infants at 2 months of age, one of whom also had mild ventriculomegaly. A patient with macrocephaly studied at 4 months of age had enlarged ventricles and subarachnoid spaces consistent with benign macrocephaly of infancy. Cerebral ultrasound examination was abnormal in all five infants studied in the first week of life and in one infant at 2 months of age. Findings included subependymal cysts (4), echogenic white matter (3), and echogenic lenticulostriate vessels (3). Apart from one case of macrocephaly, there was no clinical evidence of neurologic disease and the subsequent development of these infants has been normal. Subclinical central nervous system (CNS) disease in NLE is likely to be a transient phenomenon that resolves as maternal antibodies are cleared from the infant's circulation. It is important to be aware of these neuroimaging abnormalities to avoid misdiagnosis of congenital viral infection in a newborn with multisystem NLE. The potential for neurologic sequelae is uncertain.     

Livedoid vasculitis and central nervous system involvement in systemic lupus erythematosus

Of 66 patients with systemic lupus erythematosus (SLE), 11 (16.7%) had livedoid vasculitis. The sites of predilection included the elbows, knees, fingers, soles, and back, which are not those of common livedoid vasculitis. Livedoid vasculitis developed in ten (90.9%) of the 11 patients with SLE who eventually developed central nervous system (CNS) lupus. In contrast, such preceding livedoid vasculitis occurred in only three (11.5%) of the 26 patients with severe nephrotic lupus nephritis. Livedoid vasculitis did not occur in any patient with neither CNS lupus nor severe lupus nephritis. These results indicate that livedoid vasculitis in SLE is a very important cutaneous manifestation that may possibly be prodromal to CNS lupus.     

新生儿红斑狼疮1例

临床资料患儿,男,52天。生后20天右足底出现一黄豆大小红斑,10余天后左上肢也出现一类似红斑。患儿系头胎足月顺产,出生时体重2700g,Apgar评分10分。家族史:其母30岁,近一个月来自觉口干、乏力,双手关节疼痛,抗SSA抗体和抗SSB抗     

A case of multiple cavernous hemangiomas with skin and central nervous system involvement

A 47-year-old woman presented with multiple bluish subcutaneous nodules on the trunk and upper extremities. The histological diagnosis of a subcutaneous nodule was cavernous hemangioma. Multiple cavernous hemangiomas were also found in her cerebrum, cerebellum, and medulla oblongata on magnetic resonance imaging examination. We did not detect any mutations in the two loci of the TIE2 gene that have been reported in familial venous malformations.     

A case of systemic lupus erythematosus with the central nervous system manifestations (CNS-lupus) mimicking herpes simplex encephalitis (HSE)

A 21-year-old male with SLE developed seizure, loss of consciousness and focal signs referable to involvement of the front-temporal brain regions. MRI (magnetic response imaging) image revealed high signal areas in the temporal lobes. By these findings, herpes simplex encephalitis (HSE) was suspected at first. But neither isolation of herpes simplex virus nor HSV specific IgM by ELISA was detected. Acyclovir administration by intravenous infusion was'nt effective but corticosteroid pulse therapy was effective. The level of anticardiolipin antibody was very high. Finally, the diagnosis of CNS-lupus with HSE-like characteristics was made in this case.     

A case of blue rubber bleb nevus syndrome with gastrointestinal and central nervous system involvement

Blue rubber bleb nevus syndrome, or Bean syndrome, is a rare sporadic disorder of venous malformations of the skin and internal viscera. We report a rare case of blue rubber bleb nevus syndrome with gastrointestinal and central nervous system involvement.