SARS肺部病变胶原纤维的检测及其意义

目的 研究SARS肺部病变形态特征和探讨胶原纤维在SARS肺部病变中的变化规律。方法 4例SARS肺标本组织，经HE、苦味酸天狼猩红和免疫组化染色、光镜或偏振光观察胶原纤维的分布及表达。结果 SARS肺部病变发展过程分3期：急性渗出期、纤维增殖期、胶原化期。急性渗出期：胶原纤维较正常稍增多，可见Ⅰ、Ⅲ、Ⅳ型，Ⅰ型较多；纤维增殖期：Ⅰ、Ⅲ、Ⅳ型胶原纤维增多；胶原化期：基膜及肺间质Ⅳ型胶原显著增多，而Ⅰ型胶原明显减少。结论 胶原纤维过度增生及代谢异常是导致肺纤维化重要因素之一，苦味酸天狼猩红和免疫组化联合应用对认识胶原纤维的变化规律起到互补作用。     

严重急性呼吸综合征的病理改变

目的 探讨严重急性呼吸综合征(SARS)的主要脏器的病理改变特点及发病机制。方法 详细检查7例SARS患者的肺、心、脾、肝、肾等标本的大体特点及用常规方法研究光镜下SARS累及各脏器的病变特点。结果 7例中,病程短(5d)的患者肺部表现以肺水肿为主。与通常的肺水肿相比,其水肿液中纤维素成分多,可见透明膜形成。5例病程超过3周的患者出现肺泡内机化及肺泡间隔内的纤维母细胞增生,造成肺泡的实变和闭塞。6例可见到肺小血管内的微血栓。7例均可见到散在的肺出血、小叶性肺炎、肺泡上皮脱落、增生等病变。2例可见真菌感染,1例累及左全肺及右肺部分区域,还累及心脏和肾脏,1例出现在肺门淋巴结。肺门淋巴结多表现为充血、出血及淋巴组织减少,窦组织细胞增多。5例心脏有明显的肥大,2例有心内血栓,1例有灶性心肌炎,1例为真菌性心肌炎。7例中有1例为结节性肝硬化,另1例出现广泛的肝细胞带状坏死。脾内均有白髓变小或消失,红髓明显充血和出血。1例腹腔内淋巴结肿大,但其内淋巴滤泡亦减少,有明显充血和出血及窦组织细胞增生。结论 SARS的主要病变为肺,以各期弥漫性肺泡损伤的病变为基本特征。发病机制可能为病毒造成肺泡上皮及毛细血管的严重损伤导致肺水肿及肺泡及细支气管的纤维素性渗出性炎,出现透明膜,继而出现肺泡内机化及肺泡间隔的纤维化,导致肺泡萎陷,最终形成纤维化、实变。脾和淋巴结的淋巴组织减少是此病影响免疫系统的形态学表现。     

脾脏硬化性血管瘤样结节性转化临床病理分析

目的 探讨脾脏硬化性血管瘤样结节性转化的病理形态特征、形成原因及鉴别诊断.方法 对10例脾脏硬化性血管瘤样结节性转化病例进行病理形态观察,EnVision法行免疫组织化学染色,并行网状纤维染色和PAS染色,1例行电子显微镜观察.结果 脾脏硬化性血管瘤样结节性转化有其特征性血管瘤样结节,免疫组织化学显示结节内内皮细胞异质性表达,即小叶状分布毛细血管免疫表型为CD34~+/CD31~+/CD8~-,窦岸样细胞免疫表型为CD8~+/CD31~+/CD34~-,小静脉样血管免疫表型为CD31~+/CD8~-/CD34~-,结节内梭形细胞混合表达CD31、平滑肌肌动蛋白(SMA)和CD68,结节间梭形细胞混合表达SMA和CD68.网状纤维染色显示结节轮廓和结节内血管,PAS染色显示结节周围胶原沉积物.电镜显示淋巴窦扩大,胶原丰富等特征.结论 该病是一种少见的脾脏良性病变,可能是一种反应性病变,与血管瘤出血坏死机化关系密切.尤其需要与脾脏交界性或恶性肿瘤鉴别.     

泛发性皮肤肌纤维瘤1例并文献复习

报道1例泛发性皮肤肌纤维瘤,并对国内外相关文献进行复习回顾.本例患者以躯干泛发暗红色丘疹、斑块、结节为主要临床表现.病理见真皮内界限清晰的结节,梭形细胞周围充盈嗜伊红染色的胶原纤维.免疫组织化学:波形蛋白(vimentin)和平滑肌肌动蛋白(smooth muscle actin,SMA)均为阳性,CD34局灶性阳性,结蛋白(Desmin)和S-100均阴性.根据临床表现,组织病理和免疫组织化学结果可诊断.     

肢端黏液样炎性纤维母细胞肉瘤2例及文献复习

目的探讨肢端黏液样炎性纤维母细胞肉瘤的临床病理学特征及鉴别诊断。方法对2例发生在下肢末端的黏液样炎性纤维母细胞肉瘤进行光镜观察和免疫组化标记，并复习文献。结果2例发生在下肢末端的病程较长的渐进性肿块，术后局部复发。镜检：病变呈多结节状，边界不清；黏液样基质中见数量不等的各类炎细胞浸润，散在或灶性分布梭形、奇异形和多空泡状脂肪母细胞样3种形态的瘤细胞。免疫表型：肿瘤细胞Vim弥漫阳性，CD68和CD34灶性阳性，CK、SMA、HHF-35、S-100蛋白、CD45、CD45R0、CD15、CD30均阴性。结论此病病程较长，术后易局部复发，是一种低度恶性的肿瘤。鉴于病变黏液样基质及各类炎细胞浸润的背景较为突出，而特征性的瘤细胞稀疏，应注意与炎症性病变或具有相似组织形态的良性或恶性肿瘤鉴别。     

SARS尸检组织的病理变化和超微结构观察

目的 研究严重急性呼吸综合征(SARS)尸检组织的临床病理和超微结构特征。方法 对1例SARS死亡患者做即刻肺穿刺和12h后尸检,进行病理形态和超微结构的观察;用Macchiavello法做病毒包涵体染色;并对淋巴结、脾脏、结肠、小肠及骨髓组织行CD20、CD45RO(UCHL-1)、CD4、CD8、CD68、CD34免疫组织化学标记。结果 SARS肺的主要病变为急性弥漫性全小叶性间质性炎,可见肺泡腔内透明膜形成和增生及脱落的肺泡上皮,偶见胞质内病毒包涵体样结构,病毒包涵体染色阳性,肺内小血管增生、扩张,呈血管炎性改变。淋巴结、脾脏结构破坏,淋巴滤泡消失,脾小体萎缩,淋巴细胞明显减少,组织细胞增生;结肠、小肠孤立和集合淋巴结淋巴滤泡消失;骨髓增生减低,巨核细胞增多。免疫组织化学染色：淋巴结、脾脏B细胞CD20弥漫散在阳性,CD45RO(UCHL-1)散在阳性,CD4辅助T细胞显著减少,CD8毒性T细胞稍增加,CD4／CD8比例明显小于0．5。电镜观察：肺泡内的单核巨噬细胞、肺泡上皮胞质内可见病毒样颗粒,大小80～160nm,有光晕或花环状包膜。结论 肺部明显急性弥漫性全小叶性间质性炎,肺泡腔透明膜形成,肺外淋巴造血系统明显损害,尤T细胞明显;内脏器官出血、坏死和血管炎改变等为急性SARS的形态特征;肺内所见病毒样颗粒可能为新型冠状病毒,推测其为此次SARS流行的主要病原体。     

SARS肺间质血管病变的病理观察

目的 观察分析严重急性呼吸综合征(severe acute respiratory syndrome，SARS)肺间质血管病变的病理形态学特征。方法 对3例行尸体解剖的SARS病例肺组织进行常规HE染色、组织化学染色和免疫组织化学染色，并探讨其病理形态学特征。结果 死亡的SARS病人肺部病变除弥漫性的肺部损伤(肺泡腔内可见细颗粒样或泡状水肿液、脱落的肺泡上皮细胞；肺泡间隔内表面可见透明膜覆盖，有的区域肺泡腔内出现机化性改变等)外，肺间质内的毛细血管簇状增生及血管壁出现明显的损伤性改变。结论 SARS的肺部血管病变是一个特征性病理形态学变化，可能与SARS病毒的蛋白导致的剧烈免疫反应有关。     

乳腺纤维瘤病12例临床病理学观察

目的 探讨乳腺纤维瘤病的临床病理学特征.方法 回顾性分析12例乳腺纤维瘤病临床病理资料,总结其临床、组织学特点并复习相关文献.结果乳腺纤维瘤病由梭形细胞和胶原纤维构成.梭形细胞为增生的纤维母细胞和肌纤维母细胞,构成束状交错形态,瘤细胞呈特征性"指样突起"浸润病灶周围的乳腺组织.瘤细胞vimentin和SMA阳性,Calponin、desmin少数细胞阳性,CK(AE1/AE3)、ER、PR、p63、CK5/6、CD34和S-100蛋白均阴性,Ki-67增殖指数<5%.结论乳腺纤维瘤病为少见的乳腺肿瘤,由增生的纤维母细胞、肌纤维母细胞和胶原纤维共同组成.结合临床特点、钼靶和超声检查也与乳腺癌难以区分,诊断主要依靠病理组织切片,在形态上应注意与乳房的其他梭形细胞病变鉴别.     

四氯化碳诱导性肝纤维化大鼠肝组织骨形态发生蛋白-7的表达

目的 探讨四氯化碳(CCl4)诱导性肝纤维化大鼠的肝组织纤维化与骨形态发生蛋白-7(BMP-7)表达的相互关系.方法 将健康雄性 Wistar 大鼠随机分为对照组和肝纤维化组.对照组大鼠每周一、四背部皮下注射橄榄油(0.12ml/100g),肝纤维化组每周一、四背部皮下注射60% CCl4橄榄油(0.3ml/100g),连续注射6、10、16 和21周.实验结束时处死大鼠,取肝中叶,石蜡包埋、切片.行天狼猩红染色,观察肝组织胶原纤维的增生情况;行BMP-7免疫组织化学染色和 Western blotting 检测,观察肝组织.BMP-7的表达.结果 天狼猩红染色显示对照组大鼠仅在肝门静脉及门管区看到少量的胶原纤维,各肝纤维化组大鼠均可见肝组织呈明显的胶原纤维增生,且随着时间的延长,肝纤维化程度逐渐加重;免疫组织化学染色显示,对照组大鼠肝组织中可见极少量的BMP-7表达阳性的细胞,6周肝纤维化组大鼠可见较多的BMP-7阳性表达细胞,但随着实验时间的延长,BMP-7阳性细胞呈递减的趋势,至21周肝纤维化组大鼠肝组织中基本呈阴性表达;Western blotting 法检测大鼠肝组织BMP-7的表达结果与免疫组织化学的结果基本一致.结论 CC14诱导性肝纤维化大鼠肝组织BMP-7的表达与肝纤维化的程度呈负相关的趋势,推测BMP-7可能对肝纤维化具有一定的保护作用.     

子宫Müllerian腺肉瘤伴间质横纹肌样瘤分化1例并文献复习

目的探讨子宫Muellerian腺肉瘤伴间质横纹肌样瘤分化的临床病理特征。方法用光镜、组织化学及免疫组化方法观察其病理组织学表现。结果肿瘤由良性上皮成分和肉瘤性间质成分组成，肉瘤成分过度生长。肿瘤细胞弥漫浸润性分布，细胞大，胞质丰富嗜酸性并可见嗜伊红包涵体。免疫表型：vimentin、CK、NF、CD57、CD99、CgA、Syn阳性，SMA散在阳性，而desmin、EMA、CD10、GFAP、MyoD1、Inhibin—α、HMB45和S-100蛋白阴性。组织化学染色PAS阴性，网状纤维染色显示网状纤维包绕单个或小巢肉瘤性间质细胞。结论子宫腺肉瘤伴间质横纹肌样瘤分化是一种罕见的混合性Muellerian肿瘤，应与子宫内膜间质肉瘤、子宫横纹肌肉瘤和低分化癌等鉴别。     

Thy-1 expression,a possible marker of early myofibroblast development,in renal tubulointerstitial fibrosis induced in rats by cisplatin

Interstitial fibrosis is regarded as the common final pathway in chronic renal failure. Myofibroblasts play an important role in the renal fibrosis through producing extracellular matrices. In addition to expressions of cytoskeletons such as vimentin, desmin and α-smooth muscle actin (α-SMA), Thy-1 expression was investigated in cisplatin-induced rat renal interstitial fibrosis, to clarify the characteristics of myofibroblasts. Immunohistochemically, myofibroblasts in the renal fibrotic lesions reacted to vimentin, desmin and α-SMA in varying degrees, and the expression degrees were increased with advancing fibrosis. Vimentin expression was the greatest and the increased expression retained even in scar at end stages, whereas desmin and α-SMA expressions were almost completely decreased in scar. In double immunofluorescence, there were myofibroblasts reacting to both vimentin/desmin, desmin/α-SMA or α-SMA/vimentin, indicating that renal myofibroblasts can simultaneously express different cytoskeletons. Thy-1 expression in renal myofibroblasts was increased according to progressing fibrosis; however, the increased expression was decreased in scar, similar to desmin and α-SMA expressions. Some myofibroblasts expressing Thy-1 reacted simultaneously to vimentin or desmin, but there were no cells reacting to both Thy-1 and α-SMA. Because well-differentiated myofibroblasts are characterized mainly by α-SMA expression and the pericytes (immature stromal stem cells) showed a positive reaction to Thy-1, renal myofibroblasts might be originated from immature mesenchymal cells through loosing Thy-1 expression. This study for the first time shows that renal myofibroblasts can variously exhibit such mesenchymal markers as vimentin, desmin, α-SMA and Thy-1; particularly, Thy-1 immunohistochemistry would be used to detect myofibroblasts at early stages in analyzing chemically induced renal lesions.     

严重急性呼吸综合征的临床病理及发病机制研究

目的　研究严重急性呼吸综合征 (SARS)的病理学特征及临床治疗的病理学基础 ,并探讨SARS的发病机制。方法　采用光、电镜观察 ,对 2例SARS系统尸检病例和 4例多器官多部位穿刺标本进行病理学观察 ;应用免疫组化标记并分析肺组织及免疫器官中各淋巴亚群的分布及数量变化 ;核酸原位杂交结合电镜观察 ,作SARS冠状病毒 (SARS CoV)在体病原学定位及定量检测。结果　 6例SARS肺组织均呈弥漫性肺泡上皮损伤 ,2例尸检肺组织呈急性间质性炎和区域性肺水肿 ,2例尸检和1例穿刺肺组织中肺泡腔内透明膜形成 ,1例尸检和 2例穿刺肺组织呈脱屑性终末细支气管炎及肺泡炎 ,2例穿刺病例见早期肺纤维化及肺泡腔机化。SARS肺外器官 ,2例病程 <12dSARS病例免疫器官呈较广泛的出血坏死性炎 ,组织细胞及单核细胞样免疫母细胞反应性增生 ,骨髓组织内单核 粒细胞系统相对抑制 ,而 4例病程 >2 1dSRAS病例脾脏中央动脉周围T淋巴细胞增生 ,骨髓像大致正常。体内SARS CoV存在多种感染靶细胞和靶器官 ,其中肺脏为主要靶器官 ,支气管、肾、肾上腺、心肌、胃肠道、淋巴组织及睾丸等也为靶器官。肺组织内以CD8+ 细胞浸润为主 ,杂以少数CD4 + 细胞 ;淋巴结及脾脏中CD3+ 、CD4 + 、CD8+ 和CD2 0 + 淋巴细胞亚群呈不同程度减少及比例失衡 ,而     

Co-expression of TNF alpha and IL-1 beta in human acute pulmonary fibrotic diseases: an immunohistochemical analysis

To clarify the involvement of TNF alpha and IL-1 beta in the initiation of fibrotic lung diseases, their localization was examined by immunohistochemistry. Fibrotic lung diseases observed were classified into acute and old pulmonary fibrotic changes. The acute fibrotic changes included adult respiratory distress syndrome, acute interstitial pneumonia and idiopathic pulmonary fibrosis with acute exacerbation. Acute pulmonary fibrotic changes histopathologically corresponded to a mixture of the exudative and proliferative phases of diffuse alveolar damage. Both TNF alpha and IL-1 beta were positive in the alveolar macrophages and proliferating type II pneumocytes in acute fibrotic changes. In contrast, positive cells for TNF alpha and IL-1 beta were sparse in the areas of old fibrotic change and in the normal tissue. These findings suggest that TNF alpha and IL-1 beta play an important role in the initiation of pulmonary fibrotic responses and in the architectural remodeling, irrespective of the etiology of fibrotic lung diseases.     

Pathological post‐mortem findings in lungs infected with SARS‐CoV‐2

Italy was the first European nation to be massively infected by SARS‐CoV‐2. Up to the end of May 2020, more than 33,000 deaths had been recorded in Italy, with a large prevalence among males, those over 75 years of age, and in association with co‐morbidities. We describe the lung pathological and immunohistochemical post‐mortem findings at the autopsy of nine patients who died of SARS‐CoV‐2‐associated disease. We found in the lung tissues of all patients histological changes consistent with diffuse alveolar damage in various evolution phases ranging from acute exudative to acute proliferative to fibrotic phase. Alveolar damage was associated with prominent involvement of the vascular component in both the interstitial capillaries and the mid‐size vessels, with capillary fibrin micro‐thrombi, as well as organized thrombi even in medium‐sized arteries, in most cases not related to sources of embolism. Eosinophilic infiltrate was also seen, probably reactive to pharmacological treatment. Viral RNA of SARS‐CoV‐2 was detected from the lung tissues of all the nine patients. Immunohistochemistry for the receptor of the SARS‐CoV‐2, ACE2, and its priming activator TMPRSS2 revealed that both proteins co‐localize in airway cells. In particular, the ACE2 protein was expressed in both endothelial cells and alveolar type I and II pneumocytes in the areas of histological diffuse alveolar damage (DAD). Pneumocytes, but not endothelial cells, also expressed TMPRSS2. There are no distinctive histological features of SARS‐CoV‐2 infection with respect to SARS‐CoV‐1 and other DAD with different aetiology. The identification of the cause of death in the course of SARS‐CoV‐2 infection is more likely multi‐factorial. © 2020 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.     

Arrhythmic sudden cardiac death in a 3-year-old child with intimal fibroplasia of coronary arteries, aorta, and its branches.

We report an unusual case of "arrhythmic" sudden cardiac death in a 3-year-old child who died of ischemic myocardial lesions as a result of intimal fibroplasia of the coronary arteries. Also affected were the aorta and its major branches, whereas renal and mesenteric arteries, celiac trunk, and systemic veins were normal. Histopathologic examination showed severe concentric thickening of intima because of a proliferation of spindle-shaped cells (mesenchymal cells) set in an abundant extracellular matrix. In some vascular segments the intima was densely fibrotic and hyalinized. No significant inflammation, foam cells, cholesterol clefts, or other evidence of atheroma were present. The intimal lesions did not involve the media and/or the adventitia. Immunohistochemical staining of intima showed the proliferating mesenchimal cells to be myofibroblastic. Reactions for vimentin and smooth muscle actin were positive, while those for desmin, myosin, CD34, and Factor VIII were negative.     

Demonstration of perycriptal fibroblasts in inflammatory-regenerative and dysplastic epithelial lesions of the flat colonic mucosa

The aim of the paper is the definition of perycriptal fibroblasts (PCFs) distribution in inflammatory-regenerative and dysplastic epithelial lesions of flat bowel mucosa. The relationship between the presentation of PCFs and the grade of inflammatory-regenerative and dysplastic process in the flat colon mucosa is also examined. Biopsy specimens from 270 patients were examined: 74 were classified as inflammatory-regenerative and 196 as dysplastic lesions (108 mild, 58 moderate, and 30 severe dysplasia). The demonstration of PCFs in biopsy specimens was performed by immunohistochemistry using monoclonal antibody for alpha smooth muscle actin, muscle-specific actin (HHF-35), vimentin and desmin, in comparison with normal mucosa and adenocarcinoma. The PCFs were reduced in inflammatory-regenerative and dysplastic mucosa. The reduction was significantly related with the grade of epithelial dysplasia. The carcinomas tended to lack PCF network. During inflammatory-regenerative and dysplastic process in flat bowel mucosa, PCFs express alpha smooth muscle actin, muscle specific actin, vimentin and desmin, showing the phenotypical growing expression of potentially present smooth muscle differentation features of fibroblasts. These findings suggest that the reduction of PCFs in dysplastic epithelial lesions may relate to the development of dysplasia in flat bowel mucosa. Reduced number of PCFs in dysplastic mucosa may be a marker for the risk of preneoplastic and neoplastic progression in bowel mucosa.     

Differential immunoexpressions of cytoskeletons in renal epithelial and interstitial cells in rat and canine fibrotic kidneys, and in kidney-related cell lines under fibrogenic stimuli

Myofibroblasts play an important role in chronic renal interstitial fibrosis. However, the origin and developmental mechanisms remain to be elucidated. The myofibroblasts may express various cytoskeletons during the development. Immunoexpressions of vimentin, desmin and alpha-smooth muscle actin (alpha-SMA) were analyzed using experimentally (cisplatin and unilateral ureteral obstruction) induced rat and spontaneous canine fibrotic kidneys or kidney-related cell lines incubated with transforming growth factor-beta1 (TGF-beta1), platelet-derived growth factor-BB (PDGF-BB) or their combination at various concentrations. In rat fibrotic kidneys, both renal epithelia and interstitial cells showed positive reactions to alpha-SMA and vimentin, supporting epithelial-mesenchymal transition (EMT) theory; however, renal epithelia did not react to desmin, though interstitial cells were reactive. Renal epithelia in canine fibrotic kidneys did not show a positive reaction to alpha-SMA, whereas interstitial cells reacted strongly to alpha-SMA; conversely, renal epithelia reacted strongly to desmin, but interstitial cells did not; vimentin expression was infrequently seen in renal epithelia and interstitial cells of canine kidneys. Exposure of TGF-beta1 to porcine renal epithelial cells (LLC-PK1), rat renal interstitial cells (NRK-49F), and rat immature mesenchymal cells (MT-9) dose-dependently increased selectively alpha-SMA-positive cell numbers. Moreover, PDGF-BB exhibited an additive effect on TGF-beta1-induced alpha-SMA expression in these cell lines when simultaneously added. alpha-SMA was the most plastic cytoskeleton under fibrogenic stimuli. This study shows that there are interspecies differences in cytoskeletal immunoexpressions of renal epithelia or interstitial cells between rat and canine fibrotic kidneys, and that the derivation of renal myofibroblasts may be heterogeneous, such as renal epithelia, interstitial cells or immature mesenchymal cells.     

Shock lung and diffuse alveolar damage pathological and pathogenetic considerations

Diffuse alveolar damage may be caused by any one or more of a large number of injurious agents. While the etiology may be diverse, the pathology is relatively uniform ranging from an acute exudative phase characterized by protein-rich interstitial and alveolar edema, through to a reactive subacute proliferative phase characterized by interstitial fibroplasia and collagenization together with granular pneumocyte hyperplasia. Interstitial inflammation is a variable feature and of course mixed exudative and proliferative features are common. In the clinically overt adult respiratory distress syndrome, the mortality is formidable. The pathogenesis is damage to endothelial cells and membranous pneumocytes. This may be caused by direct chemical action or indirectly through the mediation of oxidizing free radicles or leukotrienes. In diffuse alveolar damage associated with shock, recent work suggests mediation of the cellular injury via complement activation following tissue injury, with the major pathology being due to lysosomal enzyme damage from phagocytes chemotactically attracted to the lung. Etiological factors in diffuse alveolar damage are numerous and details of appropriate primary therapy are therefore diverse. The pathogenesis and pathology are however relatively uniform, calling for uniform supportive therapeutic measures of the clinical adult respiratory distress syndrome.     

Histological, immunohistochemical and biological data in assessing interstitial fibrosis in patients with chronic glomerulonephritis

The aim of this study was to determine the relationship between histological, immunohistochemical (IHC) and biological data in the assessment of interstitial fibrosis in patients with glomerular diseases. A group of 41 patients with primary and secondary glomerulonephritis was studied. In order to quantify the histological changes and to assess the extent of active-inflammatory and chronic-sclerotic/fibrotic interstitial lesions, we adapted a scoring system, initially used for lupus nephritis, and ANCA-associated vasculitis. IHC labeling procedures with monoclonal antibodies anti-smooth muscle actin (SMA), anti-vimentin and anti-transforming growth factor beta (TGFbeta) were assessed using a semi-quantitative score, correlated with the histological and biological data. Our results showed that interstitial labeling of SMA correlated with scores for sclerotic/fibrotic lesions (chronicity index) and with active-inflammatory lesions (interstitial infiltrate, activity index). Interstitial vimentin correlated with the score for interstitial infiltrate. Both interstitial vimentin and TGFbeta immunopositivity correlated with sclerotic/fibrotic lesions (interstitial fibrosis, tubular atrophies, vascular hyalinosis/fibrosis, chronicity index), and negatively with glomerular filtration rate. An important correlation was found between the interstitial labeling of the two IHC markers of myofibroblasts (SMA and vimentin). We conclude that IHC studies related to clinico-biological and histological data can have an important role in the evaluation of the glomerular diseases, but the classical histological investigation assessed through quantification has still not lost its importance.     

Serum marker of type III procollagen in patients with idiopathic hemochromatosis and its relationship to hepatic fibrosis

A radioimmunoassay for serum procollagen III aminopeptide (sPIIIP) was proposed recently for monitoring hepatic fibroplasia in patients with various inflammatory hepatic lesions. To determine whether sPIIIP also can detect fibroplasia in noninflammatory liver disorders, we measured this index in 16 patients with idiopathic hemochromatosis (IHC) at various stages of the disease and iron overload. Interestingly, we found normal levels of sPIIIP in 12 out of 16 patients examined (75%), despite clear histologic features of fibrosis or cirrhosis. The levels of sPIIIP exhibited no relationship to any of the clinical, laboratory, or histologic parameters of the disease. Thus, unlike other types of cirrhosis, in which sPIIIP is increased, the liver disease in IHC may be a fibrotic process unrelated to type III collagen stimulation. Accordingly, the determination of sPIIIP in these patients is of no value for monitoring the fibrosis associated with the liver disease.