与结核相关的脂膜炎研究进展

【摘要】 脂膜炎病因繁多而复杂,感染为重要病因之一,在欧美等结核低发区,以链球菌感染最为常见,但在结核高发地区如我国,结核杆菌感染是脂膜炎的重要因素,以Bazin硬红斑和结节性红斑最为常见。Bazin硬红斑与结核关系最为密切,常表现为下肢屈侧结节、斑块,可出现溃疡,病理表现为小叶性脂膜炎。结节性红斑可作为结核的早期症状出现,可作为结核的预测指标,常表现为双下肢伸侧红斑、结节,极少破溃,间隔性脂膜炎是其病理特征。Bazin硬红斑和结节性红斑的抗结核治疗常可取得理想效果。因此,明确结核分支杆菌与脂膜炎的关系,在脂膜炎的治疗及预后方面,尤其在结核高发地区有着重要意义。     

下肢红斑结节性皮损与结核关系的探讨

目的 了解下肢红斑结节性皮损与结核的关系。方法 对50例下肢红斑结节性皮损的患者进行结核菌素及X线胸片检查。结核菌素试验强阳性者进行抗结核治疗。结果 结核菌素试验强阳性的有42例，占总数的84.0%。其中10例有明确肺结核病史。经抗结核治疗后41病例1月内明显好转，2月内原发皮损消退而痊愈。无肺结核的患者疗程为3个月，有肺结核者疗程为6个月。所有病例治疗完成后，半年内未见复发。结论 结核杆菌感染可能是下肢红斑结节性皮损最常见的原因。     

结节性红斑与结核病的关系探讨

为探讨结节性红斑与结核病的关系,回顾分析56例结节性红斑病例的PPD试验、抗结核抗体结果,并与40例正常人做对照。结果:结节性红斑组的PPD试验强阳性率与正常对照组比较有显著差异,结节性红斑组的抗结核抗体的阳性率与正常对照组比较无显著差异,对PPD试验强阳性的结节性红斑患者,单纯抗结核治疗具有肯定疗效。结节性红斑与结核病的关系密切,抗结核治疗对于结核及其诱发的结节性红斑具有重要意义。     

近25年结节性红斑患者中结核感染特点的Meta分析

目的：明确1993-2018年结节性红斑(EN)患者中结核(TB)感染特点。方法：2位研究者独立检索1993年1月至2018年9月PubMed、Embase、MEDLINE、CNKI、CBM、万方数据库筛选出符合纳入标准的文献，采用STATA 12.0软件通过Meta分析方法进行单个率的合并分析。结果：共纳入27篇文献，包括国内11篇（1019例患者，其中结核性结节性红斑患者277例，感染率25.4%），国外16篇（995例，其中结核性结节性红斑患者52例，感染率6%）。国内亚组分析显示东部、中部及西部地区EN患者中结核感染率分别为16.0%、27.9%和32.5%，Meta回归显示地区因素而非年份因素可解释异质性来源(P=0.02)。结节性红斑患者结核病灶为肺结核、淋巴结核、其他类型结核（如：结核性胸膜炎、卵巢结核等）、仅PPD强阳性，分别占44.4%、11.1%、7.1%及38.2%。结论：大多数EN患者没有明显的结核症状，因此应尽量寻找潜在的结核病感染病灶。     

结核相关结节性红斑的研究进展

结节性红斑(erythema nodosum,EN)是一种常见的间隔性脂膜炎,以红斑、炎症性皮下结节为主要表现。其病因复杂,目前认为部分EN与结核菌感染关系密切。结核相关EN好发于女性及青少年,最常见的结核病类型是原发型结核和淋巴结结核,但大多数患者缺乏相应结核病表现。其发病机制认为与免疫复合物介导的以及细胞介导的免疫机制有关。EN主要根据皮损病理诊断确诊,其组织学表现为不伴血管炎的间隔性脂膜炎,多有间隔增厚,伴各种炎性细胞浸润。当怀疑结核菌感染时,则需完善结核菌素试验、结核抗体、胸片、痰培养等相关检查以明确诊断。认为即使缺乏明确的结核感染证据,对于结核菌素皮肤试验强阳性的患者,尤其是在结核流行病区,应该进行抗痨治疗。     

结节性血管炎的研究进展

结节性血管炎和硬红斑在临床和病理上相似,是否和硬红斑为同一疾病尚无定论,目前认为,结节性血管炎找到结核杆菌感染的证据即为硬红斑.临床上中年女性下肢尤其是小腿后侧的疼痛性复发性紫红色结节或斑块,应高度怀疑本病.确切病因不明,曾认为是结核感染引起,目前推测可能与结核、衣原体、链球菌等感染、自身免疫性疾病、肿瘤等都有一定联系.多数患者的组织病理显示为小叶性脂膜炎.治疗上应尽可能找出潜在的病因,治疗的药物有碘化钾、糖皮质激素、非甾体抗炎药等.     

以硬红斑为首发表现的肺结核一例

现将我院诊治的以硬红斑为首发表现的肺结核一例报道如下。患者，女，79岁，双小腿屈侧斑块1个月，无痛痒。皮肤组织病理检查示：皮下脂肪小叶及间隔可见由上皮样细胞、朗汉斯巨细胞、多核巨细胞及淋巴细胞所组成的结核样结节。行支气管镜肺组织活检示：（右肺中叶）大量尘埃颗粒沉着及凝固性坏死，坏死周边见上皮样细胞；支气管灌洗液刷片找到抗酸杆菌。     

45例结核菌素试验阳性的结节性红斑回顾性临床分析

目的:探讨结核菌素试验阳性的结节性红斑的可能诱因和临床特点。方法:回顾性分析45例结核菌素试验阳性的结节性红斑的临床和实验室资料。结果:45例患者均具有典型的结节性红斑皮损,PPD试验阳性或强阳性;男女之比为1∶4.5,平均年龄34.5岁,平均病程1.2年。45例X光胸片检查合并肺结核6例(13.4%),淋巴结核4例(8.9%),胸膜炎4例(8.9%),肺部阴影灶8例(17.8%);无异常者23例(51.1%)。实验室检查:45例中血沉增快32例,抗"O"阳性2例,Ig G较正常升高3例,类风湿因子阳性2例,痰菌涂片阳性1例,其余各项均为阴性。结论:结节性红斑病因复杂,结核菌感染是原因之一。对结核菌素试验阳性的结节性红斑,抗结核药联合糖皮质激素治疗有良好的临床疗效。     

102例结节性红斑的病因和临床表现分析

分析了102例结节性红斑的病因和临床表现，发现病因未明的占30例（占29.4%)，感染引起者18例（占17.6%)，风湿病引起者54例（占53%），风湿病既可以结节性红斑为首发，也可继发，且皮疹的分布多较广泛。对多部位结节性红斑，特别是伴ESR，CRP，肝功能明显异常的患者要注意合并风湿病的可能。     

抗结核药联合糖皮质激素治疗结核菌素试验阳性的结节性红斑临床观察

目的：观察抗结核药联合糖皮质激素治疗结核菌素试验（PPD）阳性的结节性红斑的疗效和安全性。方法：采用随机、开放平行对照的方法，对45例除有结节性红斑的临床症状外，且PPD试验强阳性患者，按1：1：1比例分成A、B、c三组，分别随机接受A组2HRZ／4HR＋P；B组P；C组2HRZ／4HR治疗。观察第14天、第28天的临床疗效及一年内复发率。结果：治疗结节性红斑第14天和第28天的有效率分别为：A组80％和93．3％；B组66．6％和80．6％；C组73．3％和86．6％。三组之间差异无统计学意义（P〉0．05）。观察1年内复发率：A组8．3％；B组50％、C组22．2％。结论：抗结核药联合糖皮质激素治疗PPD阳性的结节性红斑疗效好，治愈率高，有减少复发的作用。     

Panniculitis in tuberculosis: a clinicopathologic study of nodular panniculitis associated with tuberculosis

Background Certain types of panniculitis, erythema induratum of Bazin and erythema nodosum, have been well documented as tuberculids. Many histopathologic diagnoses of panniculitis have been reported in tuberculosis patients. This study investigates the correlation between underlying tuberculosis and clinicopathologic findings of panniculitis.
Methods We retrospectively reviewed the clinical files of histologic-proven panniculitis cases at the Dermatologic Clinic, Siriraj Hospital from January 1992 to December 1995; only cases with active tuberculous foci were analyzed.
Results The incidence of panniculitis caused by tuberculosis was 8.2%. The ratio of men to women was 1 : 1. The mean age of onset was 35.3 years. The average duration of the nodules was 35.5 days. There was a history of contact tuberculosis in 16.6%. Constitutional symptoms and a strongly positive purified protein derivative (PPD) reaction were found in 66.6%. Chest roentgenograms were abnormal in 83.3%. The erythrocyte sedimentation rate was elevated in all tested cases. The histopathologic diagnoses were nodular vasculitis (33.3%), erythema nodosum (50%), and cutaneous periarteritis nodosa (16.4%). The panniculitis lesion responded to standard antituberculous regimens in 4.6 weeks, on average, with residual hyperpigmentation.
Conclusions In panniculitis patients, clues for the investigation of tuberculosis included constitutional symptoms, elevated erythrocyte sedimentation rate, and abnormal chest roentgenograms. Histopathologic changes of panniculitis did not seem to correlate with underlying tuberculosis. The clinician should be aware of the tuberculosis, however, and should carefully search for active foci in all panniculitis patients.     

Nodules on the legs. A clinical, histological and immunohistological study of 82 patients representing different types of nodular panniculitis.

Eighty-two cases of nodular panniculitis of the legs were examined clinically, histologically and immunohistologically. Clinically the cases could be divided into four groups: typical erythema nodosum (ENty) (35 cases), erythema nodosum migrans (ENmi) (11 cases), erythema induratum (EI) (11 cases) and the remaining 25 cases not consistent with the others as "non-definite panniculitis" (NDP). The main histological categories were septal panniculitis and lobular panniculitis, the former including erythema nodosum, both typical and migrans, the latter EI and NDP. Lobular panniculitis was divided into three subgroups in which the most prominent histological features were epithelioid cell granuloma, vasculitis and palissading granuloma, respectively. Immunoglobulins in the vessel walls were found in 5 of the 46 cases of erythema nodosum, in 19 of the 36 EI and NDP cases and, in the histological groups in 4 of the 43 cases of septal panniculitis and in 19 of the 35 cases of lobular panniculitis, respectively. Fibrin was found in the walls of the papillary capillaries and deep dermal vessels in the majority of cases of lobular panniculitis. In EI and NDP the follow-up time was 40 months, on average. Twenty-two patients were treated with antituberculous drugs, 15 became symptomless, as did 5 of the 12 patients who were not treated at all.     

Erythema nodosum-like lesions in Behçet''s syndrome: a histopathologic study of 30 cases

Thirty patients who fulfilled the criteria for complete and incomplete types of Behçet's syndrome were studied to determine the histopathologic changes of erythema nodosum-like lesions. Lymphocytic vasculitis was observed in 12 (40%) of the cases, but it was only focal in areas of severe lymphocytic inflammation and only mild in degree. No diffuse vasculitis was seen. It is our opinion that the observed lymphocytic vasculitis is only secondary to moderate or severe lymphocytic inflammation. Twelve cases (40%) revealed septal panniculitis, 10 cases (33%) demonstrated lobular panniculitis with moderate to marked inflammation and fat cell necrosis, and 8 cases (27%) showed mild and nonspecific inflammation in the panniculus. Therefore, there is a spectrum of histopathologic changes of erythema nodosum-like lesions in Behçet's syndrome, similar to that of erythema nodosum secondary to other systemic disorders.     

Septal granulomatous panniculitis: comparison of the pathology of erythema nodosum migrans (migratory panniculitis) and chronic erythema nodosum

Fifty-eight cases of septal granulomatous panniculitis were reviewed; 14 cases were diagnosed as erythema nodosum migrans (migratory panniculitis) and 36 as chronic erythema nodosum on the basis of clinical and histopathologic features. Erythema nodosum migrans was characterized by markedly thickened and fibrotic septae, marked capillary proliferation (like granulation tissue), and massive granulomatous reaction (with giant cells) along the borders of the widened septa. Hemorrhage was rare, and phlebitis was not seen. Chronic erythema nodosum showed mild septal change, little fibrosis, and lymphohistiocytic perivascular inflammation with only focal granulomatous formation. Phlebitis and hemorrhage were common. The condition termed erythema nodosum migrans has many of the same clinical features as chronic erythema nodosum, and we think this term is preferable to migratory panniculitis. We believe that there are sufficient clinical and histopathologic features to justify considering erythema nodosum migrans as a unique clinicopathologic entity.     

A Case of Assisted Reproductive Therapy-induced Erythema Nodosum

Erythema nodosum is a common variant of panniculitis. It is characterized by tender erythematous nodule and plaque on the anterior aspect of the leg. The etiology is not fully understood. It may be associated with a variety of disorders, including infection, medication, autoimmune disorders, pregnancy, and malignancy. A 33-year-old Korean woman presented with 1 week history of painful erythematous plaques on both knees. She was 7 weeks pregnant with assisted reproductive therapy, and had been maintained on daily intramuscular progesterone injection for 4 weeks. Histological examination of the lesions revealed septal panniculitis without vasculitis. Two days after discontinuing progesterone injection, the symptoms and lesions started to resolve. Herein we present a case of erythema nodosum caused by progesterone injection for endometrial preparation.     

Eosinophilic panniculitis: a clinicopathologic study

Study of 18 patients with biopsy diagnoses of eosinophilic panniculitis revealed diverse patterns of systemic disease, including Wells' syndrome, vasculitis, atopy, and erythema nodosum as well as localized panniculitis. Significant associated diseases included psychiatric illness, 6 (drug dependency, 4); atopy, 5 (asthma, 3); malignancies, 5; immune complex vasculitis, 4; thyroid disease, 2; Wells' eosinophilic cellulitis, 2; glomerulonephritis and sarcoidosis, 1 each. The skin lesions varied from urticarial papules and plaques to purpura, pustules, and ulcerative lesions but always included a nodular subcutaneous component, frequently as a presenting complaint. Eosinophilic panniculitis is a non-specific finding that can signify localized disease, such as an insect bite or injection lipophagic granuloma in a drug-dependent patient, or systemic lymphoma or immune reactive disease. Eosinophilic panniculitis in erythema nodosum is perhaps its most confusing presentation.     

Erythema nodosum

Erythema nodosum is the most frequent clinicopathologic variant of panniculitis. The process is a cutaneous reaction that may be associated with a wide variety of disorders, including infections, sarcoidosis, rheumatologic diseases, inflammatory bowel diseases, medications, autoimmune disorders, pregnancy, and malignancies. Erythema nodosum typically manifest by the sudden onset of symmetrical, tender, erythematous, warm nodules and raised plaques usually located on the lower limbs. Often the lesions are bilaterally distributed. At first, the nodules show a bright red color, but within a few days they become livid red or purplish and, finally, they exhibit a yellow or greenish appearance, taking on the look of a deep bruise. Ulceration is never seen, and the nodules heal without atrophy or scarring. Histopathologically, erythema nodosum is the stereotypical example of a mostly septal panniculitis with no vasculitis. The septa of subcutaneous fat are always thickened and variously infiltrated by inflammatory cells that extend to the periseptal areas of the fat lobules. The composition of the inflammatory infiltrate in the septa varies with age of the lesion. In early lesions edema, hemorrhage, and neutrophils are responsible for the septal thickening, whereas fibrosis, periseptal granulation tissue, lymphocytes, and multinucleated giant cells are the main findings in late stage lesions of erythema nodosum. A histopathologic hallmark of erythema nodosum is the presence of the so-called Miescher's radial granulomas, which consist of small, well-defined nodular aggregations of small histiocytes arranged radially around a central cleft of variable shape. Treatment of erythema nodosum should be directed to the underlying associated condition, if identified. Usually, nodules of erythema nodosum regress spontaneously within a few weeks, and bed rest is often sufficient treatment. Aspirin, nonsteroidal antiinflammatory drugs, such as oxyphenbutazone, indomethacin or naproxen, and potassium iodide may be helpful drugs to enhance analgesia and resolution. Systemic corticosteroids are rarely indicated in erythema nodosum and before these drugs are administered an underlying infection should be ruled out.     

Panniculitis: clinical overlap and the significance of biopsy findings

Background: Panniculitides are well-recognized clinicopathologic entities but the non-specificity of their clinical and pathological features often troubles the diagnostician.
Methods: This study retrospectively evaluates the clinical overlaps and the significance of histological findings among various panniculitides.
Results: The clinical evaluation in 55 panniculitides cases suggested the diagnosis of typical erythema nodosum (EN) in 26 cases, atypical EN in 17 cases, atypical nodular vasculitis (NV) in two cases, soft tissue infection in five cases and five cases remained unclassified. Skin biopsy evaluation provided definite panniculitis diagnosis in 53 cases including EN (28 cases), leukocytoclastic vasculitis (seven cases), NV (four cases), superficial thrombophlebitis (ST) (two cases), eosinophillic panniculitis (EP) (three cases), infection-related panniculitis (five cases), and one case each of erythema nodosum leprosum (ENL), lupus panniculitis (LP), pancreatic fat necrosis and acne conglobata with two cases remaining unclassified. Histologically, 'predominantly septal' and 'mixed panniculitis' were the chief inflammatory patterns in EN cases, while mixed panniculitis was seen in most LCV cases and predominantly lobular and mixed panniculitis in NV cases.
Conclusions: Biopsy evaluation of a panniculitis lesion is usually significant, and the application of a combination of histologic features rather than of a single biopsy finding or an inflammatory pattern is helpful in the diagnosis of panniculitis.