结节性多动脉炎与显微镜下型多血管炎的研究进展

18 5 2年Ｒｏｋｉｔａｎｓｋｙ首次描述多血管炎 ,186 6年Ｋｕｓｓｍａｕｌ根据病理特点进一步将其命名为结节性多动脉炎 (ｐｏｌｙａｒｔｅｒｉｔｉｓｎｏｄｏｓａ ,ＰＡＮ) ,其特点为血管炎主要侵犯中等动脉 ,多累及肾脏和心脏 ,肾脏受累表现为肾梗死 ,又称之为经典型ＰＡＮ。 194 8年Ｄａｖｓｏｎ等报道了一组以节段坏死性肾小球肾炎病理改变为特点的血管炎 ,并提出此病不同于经典型ＰＡＮ ,并将其命名为显微镜下型多血管炎 (ｍｉｃｒｏｓｃｏｐｉｃｐｏｌｙａｒｔｅｒｉｔｉｓｎｏ ｄｏｓａ ,ＭＰＡ)。许多情况下ＭＰＡ可能被诊断为ＰＡ…     

结节性多动脉炎的诊断进展

结节性多动脉炎(polyarteritis nodosa,PAN)是一种罕见的原发性的坏死性血管炎(necrotizing vasculitis),患者通常为抗中性粒细胞胞浆抗体阴性,影响中等大小的肌动脉,尤其是心脏、肾脏等的血管组织.PAN临床表现、病程及治疗方法均不相同,几乎可侵犯每个器官,但较少累及肺部.PAN可...     

显微镜下多血管炎一例诊治分析

显微镜下多血管炎(MPA)是一种主要累及小血管的系统性坏死性血管炎,病理主要表现为局灶性坏死性的全层血管炎,新月体肾小球肾炎是其肾脏特征性改变。笔者对我院2010年收治的一例MPA的临床特点及治疗进行分析。     

结节性多动脉炎治疗进展

结节性多动脉炎(polyarteritis nodosa,PAN)是一种罕见的、主要累及中、小动脉的坏死性血管炎(necrotizing vasculitis),呈节段性分布,易发生于血管分叉处,病因尚不明确.目前,PAN的治疗方案主要为糖皮质激素,必要时联合环磷酰胺(cyclophosphamide).另外,各类生物...     

迟发性结节性多动脉炎1例及相关文献复习

结节性多动脉炎(PAN)是一组主要侵犯中等度大小肌肉动脉和肌层小动脉的以呈节段性炎症和坏死为特征,伴受累血管的供血组织发生继发性缺血。病因可能与免疫机制有关,药物及病毒感染均可致病[1,2]。病变可发生于任何部位,但以动脉多见,特点为坏死性血管炎。随医护人员对风湿免疫疾病认     

结节性多动脉炎误诊2例

结节性多动脉炎(PAN)是一种以中小动脉的节段性炎症与坏死为特征的非肉芽肿性血管炎.临床表现复杂多变,常被误诊为肾炎,胃肠道肿瘤,病毒感染,多发性肌炎等.本文2例均误诊,现报道如下: 1 病例介绍     

结节性多动脉炎发病机制解析

结节性多动脉炎(polyarteritis nodosa,PAN)作为一类累及中、小动脉全层的坏死性血管炎(necrotizing vasculitis),其发病机制尚不明确,存在病程长、诊断困难的问题,导致患者病情无法及时得到有效控制,最终可能发生重要脏器受侵,严重影响其生活质量,甚至威胁生命.本文结合既往研究,围绕...     

抗中性粒细胞胞质抗体相关性血管炎25例肺部CT表现分析

<正>抗中性粒细胞胞质抗体相关性血管炎(AAV)是一组以小血管壁的炎症及纤维素样坏死为主要表现的自身免疫病[1],但其具体发病机制、原因并不明确。2012年最新血管炎分类诊断共识中,AAV主要包括显微镜下多血管炎(MPA)、肉芽肿性多血管炎(GPA)和嗜酸性肉芽肿性多血管炎(EGPA)[2]。其累及全身多个系统脏器,并肺脏及肾脏是其主要靶器官[3]。由于其早期缺乏典型临床表现,易造成漏诊、误诊,因     

结节性多动脉炎误诊2例分析

结节性多动脉炎（PAN）是以中小动脉坏死性炎症为特征的一种全身性疾病,是临床上少见的风湿病中血管炎的一种。临床表现复杂多样,取决于受累血管的部位和程度,因而临床诊断困难,误诊可能性大。误诊是影响患者预后甚至引起死亡的重要原因之一。本院经组织活检证实2例,均被误诊。     

小儿结节性多动脉炎一例报告

结节性多动脉炎(PAN)是一种全身性中,小动脉坏死性血管炎,儿科较少见。现将我科收治的一例报告如下。患儿女,4岁。于6个月前无何诱因出现阵发性上腹痛伴呕吐。5个半月前发热,为弛张热,体温37.5～41℃之间,伴髋及膝关节非游走性痛,     

Concurrent polyarteritis nodosa and temporal arteritis

A patient is described in which features of both giant cell arteritis and polyarteritis nodosa were present simultaneously. The case emphasises our lack of an aetiologic classification for arteritis and that on occasions typical clinical presentations may be misleading.     

Cutaneous polyarteritis nodosa after streptococcal necrotizing fasciitis

Polyarteritis nodosa (PAN) is a necrotizing arteritis of small and medium-sized vessels. It may present with hypertension and/or renal insufficiency. Peripheral neuropathy, myopathy, joint pains, testicular pain, and ischemic myalgias may also be seen. Gastrointestinal involvement may lead to gangrene of the bowel, peritonitis, perforation, intra-abdominal hemorrhage, and pancreatitis. The cutaneous manifestations include tender subcutaneous nodules grouped along the course of superficial arteries of the lower extremities, with or without an overlying livedo reticularis. Although multisystem involvement is characteristic, sometimes only one organ or system may be involved. Associations with viral hepatitis (both B and C) and streptococcal infection have been established for PAN. Recurrent strep infections of the upper respiratory tract, streptococcal glomerulonephritis and rheumatic fever have previously been linked to PAN. This report extends the spectrum of associated streptococcal infections to include necrotizing fasciitis.     

Diclofenac, paracetamol, and vidarabine removal during plasma exchange in polyarteritis nodosa patients.

Since plasma exchange (PE) represents a major treatment for patients suffering from systemic diseases, its influence on the kinetics of three drugs was investigated: vidarabine, used in patients with polyarteritis nodosa associated with hepatitis B virus (eight subjects), and diclofenac and paracetamol for investigative purposes (five subjects). This study confirmed that vidarabine is so rapidly deaminated to form hypoxanthine arabinoside (Hx-Ara) that no detectable concentrations were measured. Hx-Ara levels were used to evaluate vidarabine kinetics; 19.5 +/- 14.6 mg of Hx-Ara were removed by one PE during the first week of treatment (15 mg kg-1 d-1, continuous infusion) and 7.8 +/- 10.2 mg were eliminated by one PE during the second week of treatment (7.5 mg kg-1 d-1, continuous infusion). Based on the vidarabine intake per hour and the resulting quantity of Hx-Ara removed per hour, PE recovery was quite important (ca. 30 per cent), during both the first and second weeks of continuous infusion. Data were subject to large interindividual variability. However, these results do not favor vidarabine dosage supplementation in this indication because the duration of PE is less than 8 per cent of a daily administration period. For paracetamol (1 g, single oral dose) and diclofenac (100 mg, single oral dose), the fractions of drug removed during PE effected within 2 h of drug intake, were respectively 5.0 +/- 3.1 per cent and 13.6 +/- 9.5 per cent, while plasmapheretic clearance reached, respectively, 13.0 +/- 10.7 per cent of the systemic clearance for paracetamol and 23.0 +/- 1.0 per cent for diclofenac.