结节性淋巴细胞为主型霍奇金淋巴瘤

1.病例简介:患者男,70岁,偶然发现右腋下无痛性肿物3年,逐渐增大。于1997年10月24日入院。体检:右腋下肿物10cm×10cm×4cm,无触痛。质软,部分坚实,可活动。全身其余部位浅表淋巴结未扪及。肝脾肋下未及。实验室及影像学检查均未见异常。临床诊断:脂肪瘤。行肿物手术切除。2.病理检查:肉眼观察:灰红灰黄组织13·0cm×12·0cm×4·5cm,多结节状,切面灰红色,均质,质软。光镜观察:淋巴结结构破坏,低倍镜下可见多个大小不一深染模糊结节,边界不清,无生发中心(图1)。结节与结节之间较拥挤,有的结节较大,周围有少许纤维组织围绕,大多数结节间不见…     

类似结节硬化型Hodgkin淋巴瘤的ALK阳性的间变性大细胞性淋巴瘤

间变性大细胞性淋巴瘤(ALCL)和Hodgkin淋巴瘤(HL)虽然是两种具有不同生物学行为的独立的疾病实体,但有时这两种疾病的形态学特征比较相似,该诊断带来了困难。作者从其收集的380例ALCL中发现有10例具有Hodgkin样特点,其中男性7例,女性3例,年龄3~92岁,平均年龄11岁。病变位于颈部     

霍奇金样型间变性大细胞淋巴瘤1例

正患者男性,78岁,发现左侧腹股沟肿块4个月,增大2个月。CT示:腹膜后、左侧髂血管旁见多发增大、肿大淋巴结;左侧腹股沟区见数个结节影,部分融合,见坏死,较大者大小6.0 cm×4.9 cm,强化均匀,坏死部分无强化。考虑肿大淋巴结可能性大,建议随访或进一步排外淋巴瘤可能。切除左侧腹股沟淋巴结送病理检查。病理检查眼观:不规则组织2块,大小4 cm×3.5 cm×2.5 cm,切面灰白色,实性,质硬。镜检:胶原束同心圆状围绕形成细胞结节。结节似呈斑驳状表现(图1),其内见少     

小肠非霍奇金CD30阳性的弥漫大B细胞淋巴瘤合并直肠管状腺癌一例

患者男,72岁。因便血3个月于2006年5月3日人院。肠镜检查发现直肠肿瘤,3cm×3cm,向肠腔突起,基底宽,表面高低不平,有糜烂,未见明显溃疡。CT和MRI检查发现腹腔多处淋巴结肿大,小肠肠管间有界线不清肿块,肝内多发占位,大者直径3cm。临床诊断为小肠恶性肿瘤伴腹腔广泛转移及直肠癌。术中所见：肝脏边缘锐利,可触及多个质硬结节直径约0．2～0．5cm。[第一段]     

富于T细胞/组织细胞的大B细胞淋巴瘤

1.病例简介:患者男,65岁。左侧颌下淋巴结肿大1个月,于2004年8月2日入院行肿物切除术。术中所见:肿物大小约为3.5cm×2.5cm×2.0cm,灰白色,质硬,与周围组织粘连、固定,活动度较差。患者曾于9年前发现右颌下淋巴结肿大而行肿物切除术,术后病理诊断为非霍奇金淋巴瘤,B免疫母细胞型,高度恶性。在随后半年内应用CHOP方案化疗4疗程,放疗25次(总放射计量5000cGy),肿物消失。3年前右颌下淋巴瘤复发,予以CHOP方案化疗6疗程,肿物消失。1年前右颌下淋巴瘤再次复发,化疗效果不明显。2.病理检查:结节状肿物一个,大小3.5cm×2.5cm×2.0cm,切面灰粉、…     

A critique and case study of nodular sclerosing Hodgkin's disease.

This paper presents a critique of the present concepts of the pathology of nodular sclerosing Hodgkin's disease and particularly of the criteria required for diagnosis for the condition and its separation from other types of Hodgkin's disease. In addition, the natural history and histopathology of the condition have been studied among 104 cases of Hodgkin's disease presenting at The London Hospital, and the significance of the appearance is discussed.     

Leu 7 (CD57) reactivity distinguishes nodular lymphocyte predominance Hodgkin's disease from nodular sclerosing Hodgkin's disease, T-cell-rich B-cell lymphoma and follicular lymphoma.

Several recent reports have suggested that nodular lymphocyte predominance Hodgkin's disease (NLPHD) may be distinct from other forms of Hodgkin's disease and may be more closely related to B-cell non-Hodgkin's lymphoma. This is primarily based on immunophenotypic studies that have shown that the L & H cells in NLPHD demonstrate a B-cell phenotype. In 1989, Poppema reported that the T cells in NLPHD differ from T cells in other forms of Hodgkin's disease in that they demonstrate reactivity for Leu 7 (CD57). In this study we tested the hypothesis that Leu 7 (CD57) reactivity of small lymphocytes in NLPHD is an immunophenotypic feature that distinguishes NLPHD from nodular sclerosing Hodgkin's disease and from certain B-cell lymphomas that may histologically simulate NLPHD, namely T-cell-rich B-cell lymphoma and follicular lymphoma. Using an image analysis method, we found Leu 7 (CD57) reactivity in an average of 18.9% of the small lymphocytes in the nodules of NLPHD compared with 3.9% in nodular sclerosing Hodgkin's disease, 4.3% in T-cell-rich B-cell lymphoma, and 2.1% in follicular lymphoma. Moreover, Leu 7 (CD57)-reactive small lymphocytes often showed a distinctive pattern in NLPHD, forming a ring of cells around the large L & H cells. While scattered Leu 7 (CD57)-reactive lymphocytes were found in the other disorders, the percentage of reactive cells and the pattern of reactivity were significantly different in NLPHD. These results suggest that Leu 7 (CD57) reactivity may be used as an additional immunophenotypic criterion in distinguishing NLPHD from nodular sclerosing Hodgkin's disease, T-cell-rich B-cell lymphoma, and follicular lymphoma. The clinical and biological significance of Leu 7 (CD57) reactivity of small lymphocytes in NLPHD merits further investigation.     

Syncytial variant of nodular sclerosing Hodgkin's disease: Fine-needle aspiration findings in two cases

The syncytial variant is a recently described, uncommon form of nodular sclerosing Hodgkin's disease that was previously termed “sarcomatoid.” In addition to foci of typical sclerosis, it is characterized histologically by sheets or clusters of mononuclear Reed-Sternberg variants. These may be arranged around areas of necrosis with variable numbers of neutrophils. In excised material, differential diagnostic considerations include non-Hodgkin's malignant lymphoma, granulocytic sarcoma, malignant melanoma, metastatic carcinoma, thymoma, and metastatic germ cell tumor. We describe the fine-needle aspiration cytologic finding in two examples of this entity. Cohesive clusters and sheets of malignant cells with clear cytoplasm, vesicular nuclei, and prominent nucleoli are easily mistaken for metastatic carcinoma or germ cell tumor. Ancillary tests useful in this differential diagnosis are discussed. Diagn. Cytopathol. 1997;17:477–479. © 1997 Wiley-Liss, Inc.     

Eosinophils are the major source of transforming growth factor-beta 1 in nodular sclerosing Hodgkin's disease.

Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional cytokine which promotes fibroblast growth and collagen synthesis, but suppresses growth and differentiation of immune lymphocytes and killer cells. Immunohistochemical detection of TGF-beta 1 in Hodgkin's disease (HD) has been shown to correlate with the histologic feature of nodular sclerosis, which is associated with a favorable prognosis (American Journal of Pathology 1990, 136:1209). In that study, TGF-beta 1 was localized mainly at the margins of broad collagen bands (presumably sites of new collagen synthesis) and in areas containing numerous Hodgkin/Reed-Sternberg cells (H/RS). In these areas, TGF-beta 1 protein was found on the membrane and occasionally within the cytoplasm of H/RS cells. To determine whether TGF-beta 1 is synthesized by H/RS cells or secondarily bound to their membrane and sometimes internalized, we performed in situ hybridization (ISH) using 1.5 Kb 35S-labeled anti-sense and sense RNA probes to TGF-beta 1. Paraffin-embedded tissues of 10 cases from all histologic types of HD were examined. Somewhat unexpectedly, the major site of TGF-beta 1 mRNA was in eosinophils; TGF-beta 1 mRNA was not detected in H/RS cells. TGF-beta 1 mRNA was found in eosinophils in all cases of nodular sclerosis but not in other types of HD, despite the presence of numerous eosinophils in mixed cellularity cases. The presence of TGF-beta 1 mRNA coincided with immunohistochemical detection of TGF-beta 1 protein using antibody CC (1-30). These results confirm the role of TGF-beta 1 in the histogenesis of nodular sclerosing HD and indicate that eosinophils are the major source of TGF-beta 1 in this type of HD.     

Metastatic carcinoma in lymph nodes simulating "syncytial variant" of nodular sclerosing Hodgkin's disease.

The authors report the histories of two patients with undifferentiated carcinoma metastatic to lymph nodes simulating the "syncytial variant" of nodular sclerosing Hodgkin's disease. One of the patients initially was treated for Hodgkin's disease, but the clinical evolution was more typical of carcinoma. Both lesions were characterized histologically by noncohesive aggregates of large neoplastic cells with abundant eosinophilic cytoplasm and conspicuous nucleoli. Although cells compatible with diagnostic Reed-Sternberg cells were identified in an "appropriate" cellular background in both patients, the diagnosis of carcinoma was supported by intense cytokeratin immunoreactivity. Subtle histologic clues that should suggest the possibility of metastatic carcinoma in a patient whose morphologic data suggests the syncytial variant of nodular sclerosing Hodgkin's disease include sinus infiltration, phagocytosis of neutrophils by tumor cells, marked nuclear anaplasia, and the presence of spindle-shaped tumor cells.     

Transforming growth factor beta 1 messenger RNA in Reed-Sternberg cells in nodular sclerosing Hodgkin's disease.

AIMS--To determine the cellular origin of the most potent cytokine present in Hodgkin's disease, transforming growth factor (TGF) beta, the polycellular population of Hodgkin's tissue was studied using in situ hybridisation. METHODS--A biotin labelled oligo-complementary DNA (cDNA) was constructed according to the previously determined sequence for TGF beta 1 cDNA. Forty three frozen and paraffin wax embedded tissue samples replaced by Hodgkin's disease or non-Hodgkin's lymphoma, three Reed-Sternberg cell lines, one Ki1 positive lymphoma cell line, and an epithelial cell line were studied for expression of TGF beta 1 messenger RNA (mRNA) as well as secretion of the TGF beta 1 protein and expression of the CD30 epitope. RESULTS--The results obtained with the 24 frozen tissue samples confirmed that the TGF beta antigen is found predominantly in the nodular sclerosing Hodgkin's disease (NSHD) subtype. Nineteen paraffin wax embedded tissue samples were used to measure the simultaneous expression of CD30 and TGF beta 1 mRNA. The latter was found in eight of eight NSHD samples, two of six mixed cellularity samples, and two of five non-Hodgkin's lymphoma samples. No evidence of fibroblast expression of TGF beta 1 mRNA was noted. CONCLUSIONS--Activated lymphocytes in NSHD express TGF beta 1 mRNA, but binucleate Reed-Sternberg cells and mononuclear Hodgkin's cells are the primary sources of activated TGF beta in Hodgkin's disease.     

On the pathogenesis of sclerosis and nodularity in nodular sclerosing Hodgkin's Disease

Summary Ten cases of nodular sclerosing Hodgkin's disease involving lymph nodes were studied by electron microscopy to determine the ultrastructural composition of the nodule-stromal interphase and the collagenized regions. In addition to a few lymphocytes, rare eosinophils and neutrophils, abundant filamentous and granular electron dense material, collagen fibers and myofibroblasts were observed in all instances. Since myofibroblasts possess contractile and synthetic properties, it is likely they contribute to the retraction and sclerosis which together represent one of the morphologic hallmarks of the disease. The dense fibrosis and contractile state of such tissue may constitute a beneficial host response to contain and limit local and vascular invasion by the neoplastic cellular population, thus contributing to the relative benignity of this form of Hodgkin's disease.