Shah Kabeer K, Pritt Bobbi S, Alexander Mariam P
Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN USA.
Mayo School of Graduate Medical Education, Mayo Clinic, Rochester, MN USA.
J Clin Tuberc Other Mycobact Dis. 2017 Feb 10;7:1-12. doi: 10.1016/j.jctube.2017.02.001. eCollection 2017 May.
Granulomatous inflammation is a histologic pattern of tissue reaction which appears following cell injury. Granulomatous inflammation is caused by a variety of conditions including infection, autoimmune, toxic, allergic, drug, and neoplastic conditions. The tissue reaction pattern narrows the pathologic and clinical differential diagnosis and subsequent clinical management. Common reaction patterns include necrotizing granulomas, non necrotizing granulomas, suppurative granulomas, diffuse granulomatous inflammation, and foreign body giant cell reaction. Prototypical examples of necrotizing granulomas are seen with infections and non-necrotizing granulomas with sarcoidosis. However, broad differential diagnoses exist within each category. Using a pattern based algorithmic approach, identification of the etiology becomes apparent when taken with clinical context. The pulmonary system is one of the most commonly affected sites to encounter granulomatous inflammation. Infectious causes of granuloma are most prevalent with mycobacteria and dimorphic fungi leading the differential diagnoses. Unlike the lung, skin can be affected by several routes, including direct inoculation, endogenous sources, and hematogenous spread. This broad basis of involvement introduces a variety of infectious agents, which can present as necrotizing or non-necrotizing granulomatous inflammation. Non-infectious etiologies require a thorough clinicopathologic review to narrow the scope of the pathogenesis which include: foreign body reaction, autoimmune, neoplastic, and drug related etiologies. Granulomatous inflammation of the kidney, often referred to as granulomatous interstitial nephritis (GIN) is unlike organ systems such as the skin or lungs. The differential diagnosis of GIN is more frequently due to drugs and sarcoidosis as compared to infections (fungal and mycobacterial). Herein we discuss the pathogenesis and histologic patterns seen in a variety of organ systems and clinical conditions.
肉芽肿性炎症是细胞损伤后出现的一种组织反应的组织学模式。肉芽肿性炎症由多种情况引起,包括感染、自身免疫、中毒、过敏、药物和肿瘤性疾病。这种组织反应模式缩小了病理和临床鉴别诊断及后续临床管理的范围。常见的反应模式包括坏死性肉芽肿、非坏死性肉芽肿、化脓性肉芽肿、弥漫性肉芽肿性炎症和异物巨细胞反应。坏死性肉芽肿的典型例子见于感染,而非坏死性肉芽肿见于结节病。然而,每个类别中都存在广泛的鉴别诊断。采用基于模式的算法方法,结合临床背景时病因的识别就会变得明显。肺部系统是最常遇到肉芽肿性炎症的受累部位之一。肉芽肿的感染原因以分枝杆菌和双相真菌最为常见,是鉴别诊断的主要因素。与肺部不同,皮肤可通过多种途径受累,包括直接接种、内源性来源和血行播散。这种广泛的受累基础引入了多种感染因子,可表现为坏死性或非坏死性肉芽肿性炎症。非感染性病因需要进行全面的临床病理检查以缩小发病机制的范围,包括:异物反应、自身免疫、肿瘤和药物相关病因。肾脏的肉芽肿性炎症,通常称为肉芽肿性间质性肾炎(GIN),与皮肤或肺部等器官系统不同。与感染(真菌和分枝杆菌)相比,GIN的鉴别诊断更常见于药物和结节病。在此我们讨论在各种器官系统和临床情况下所见的发病机制和组织学模式。