Histiocytes Research Articles

A Case of Histiocytic Necrotizing Lymphadenitis Complicated with Sjögren's Syndrome

A Case of Histiocytic Necrotizing Lymphadenitis Complicated with Sjögren's Syndrome

A case of skin infection caused by Mycobacterium szulgai

A 7-year-old girl presented with a plaque on the left side of the face for 4 years. Skin examination revealed a well-marginated circular firm plaque measuring 6 cm × 5 cm in size on the left side of the face with purulent crusts on the surface, which was nontender to palpation. Histopathologic study showed ulceration and necrosis in some areas in the epidermis, diffuse dermal infiltration of lymphocytes, histiocytes and epithelioid cells with the presence of many neutrophilic granulocytes in some regions. Both periodic acid-Schiff (PAS) staining and acid-fast staining were negative. After 25 days of tissue culture, scotochromogenic Mycobacterium colonies grew, and colony smears showed positive acid-fast staining. The sequences of 16S rRNA and hsp65 genes of the fungal isolate showed 100% and 99% homology with those of Mycobacterium szulgai, respectively. After the treatment with rifampicin, isoniazid and ethambutol, the patient's condition was improved. Key words: Skin; Nontuberculous mycobacteria; Infection; Mycobacterium szulgai; 16S rRNA; HSP65 heat-shock proteins

Visceral Leishmaniasis with renal involvement or Systemic lupus Erythematosus: Clinicians dilemma

Indian subcontinent is responsible for the largest proportion of global Visceral Leishmaniasis. 35 year old man watchman by occupation hailing from Nepal came with complaints of high grade fever on and off since two months. He also had pedal oedema, breathlessness, oliguria and distension of abdomen. On examination patient had pallor, pedal oedema, ascites and splenomegaly. His investigations showed proeteinuria (1.5 gm/day), raised Creatinine and pancytopenia. Bone marrow aspiration showed multiple Leishmania Donovani(LD) bodies, amastigote form scattered intracellular/extracellular form. Bone marrow Biopsy was suggestive of normocellular marrow with histiocytic infiltration with LD bodies. Patient was treated with Amphotericin B infusions. Patients condition deteriorated due to amphotericin induced nephrotoxicity. Report of ANA +2 (1:160) nucleolar was then received. Patient was given methyl prednisolone injection 1 gm /day for 5 days. Patient succumbed to hypo-proteinemia, sepsis and renal impairment. Visceral Leishmaniasis and Systemic Lupus Erythematosus (SLE) with flare both can mimic each other due to overlapping clinical features.SLE can have simultaneous infection with VL in endemic areas. A clinician will have to use is detailed history, thorough examination, battery of laboratory investigations and his clinical acumen to arrive at diagnosis and rule out the mimicker.

Progress in Langerhans-cell histiocytosis

Langerhans-cell histiocytosis (LCH), the most common histiocytic disorder, is a reactive clonal proliferation and accumulation of CD1a+/CD207+ dendritic cells in inflammatory lesion, characterized by its strong heterogeneity and changeable complexity including apparent inflammation and tumor features,which should be redefined as an inflammatory myeloid neoplasia. Recent research has shown that LCH is the consequence of misguided myeloid differentiation on account of genomic aberrances in the RAS-RAF-MEK-ERK pathway. These gene inhibitors may present more curative effects for the treatment of LCH. With further prospective clinical trial, molecular targeted therapy may combine with or even replace the traditional surgery plus chemotherapy as the first-line regimen in LCH. Key words: Histiocytosis, Langerhans-cell; Dendritic cells; Gene, BRAF; Molecular targeted therapy

Clinicopathologic analysis of extranodal Rosai-Dorfman disease of breast: a report of 12 cases

To investigate the clinicopathologic features, diagnosis and differential diagnosis of extranodal Rosai-Dorfman disease(RDD)of the breast. Twelve cases of extranodal RDD of the breast were analyzed using hematoxylin-eosin stain and immunohistochemical staining.The morphological features and immunophenotype were observed by light microscopy, accompanied with a review of the literature. Twelve cases of extranodal RDD of the breast are presented. The patients were women and their ages ranged from 15 to 55 years (mean =37 years). Except one patient with involvement of the right breast and ipsilateral axillary lymph nodes, other eleven patients' disease confined to the breast. Seven cases located in the right breast, the other five cases in the left breast. Microscopically, it showed a typical morphology, characterized by diffuse infiltration of large histiocytes, lymphocytes and plasmocytes that formed irregular nodular structure with light and dark appearance under microscope. Spindling of histiocytosis often arranged in a vague storiform with prominent fibrosis, accumulation of foamy histiocytes and scattered atypical nuclei. The characteristic histocytes and emperipolesis could not be seen obviously in extranodal RDD of the breast.Immunohistochemical staining showed histocytes were strongly positive for S-100 protein, CD68 and CD163, while negative for CD1a. Extranodal RDD of the breast is very rare. Because of unconspicuous emperipolesis and lack of specificity in clinic and images, extranodal RDD of the breast is easy to be misdiagnosed as other histiocytosis. The microscopic differential diagnosis includes idiopathic granulomatous mastitis, infective granulomas, langerhans cell histiocytosis, IgG4 related sclerosing disease, Erdheim-Chester disease, benign fibrous histiocytoma, malignant fibrous histiocytoma and Hodgkin Lymphoma. Light and dark appearance under microscope is the important clue in diagnosis of extranodal RDD in breast. Immunohistochemistry is also helpful.

Pathogenesis of Rosai-Dorfman disease

Rosai-Dorfman disease is a rare benign inflammatory cutaneous histiocytosis with the involvement of lymph nodes. It is histopathologically characterized by proliferation and emperipolesis of histiocytes with abundant cytoplasm that stain positive for CD68 and S100. The origin and pathogenesis of Rosai-Dorfman disease are unclear at present, and the most probable pathogeneses are that macrophage colony-stimulating factor induces the differentiation of immunosuppressive macrophages, hampers the activation of lymphocytes, and increases the expressions of multiple cytokines, including nuclear factor kappa B, tumor necrosis factor-alpha, interleukin-1β (IL-1β), IL-6 and various chemokine receptors. In addition, human herpes virus infection, malignant tumors and mutations in the SLC29A3 gene may contribute to the occurrence of Rosai-Dorfman disease. It usually undergoes spontaneous regression. Surgical excision, oral glucocorticoids, radiotherapy and chemotherapy are often used when lesions are extensive or systemic symptoms appear. Key words: Histiocytosis, sinus; Immunity; Heredity; Viruses; Treatment outcome

A case of cutaneous and systemic plasmacytosis

A 46-year-old male patient developed scatterred reddish-brown plaques and nodules on the back 6 years prior to the presentation. Then, the lesions gradually spread to the axillary fossa and protothorax, and became indurated with slight itching in winter. Laboratory examination revealed hypergammaglobulinemia. Computed tomography (CT) scan showed multiple nodular or patchy shadows in both lungs, lymphadenectasis in axillary, mediastinal and inguinal regions, and spleen enlargement. Histopathological examination of skin lesions showed granulomatous infiltrates with plenty of lymphocytes, histiocytes and mature plasma cells in the middle and lower dermis with the presence of lymphoid follicle-like structures, but no cell atypia was observed. Immunohistochemical study showed positive staining for CD38, CD138, CD79a, κ and λ light chains. According to clinical manifestations and laboratory examination results, the patient was diagnosed with cutaneous and systemic plasmacytosis. Key words: Neoplasms, plasma cell; Skin manifestations; Hypergammaglobulinemia; Plasmacytosis

Epigenetic regulation of nuclear PLCbeta1 and Cyclin D3 during Azacitidine treatment

The Myelodysplastic Syndromes (MDS) are a heterogeneous group of bone marrow disorders characterized by alterations of the hematopoietic stem cells that lead to anemia, neutropenia, bleeding problems and infections. The evidence of a clinical correlation between the presence of a monoallelic gene deletion of Phospholipase Cβ1 (PLCβ1) and the progression of MDS to Acute Myeloid Leukemia (AML) opened new perspectives of research and treatments. Patients affected by MDS with a higher risk of AML evolution have a reduction in the expression of the nuclear PLCβ1, which is also epigenetically relevant in MDS. This strengthens the importance of PLCβ1 localization. In fact, PLCβ1 is a molecular target for hypomethylating agents, such Azacitidine (AZA)(1). High-risk MDS patients that respond to the drug showed an increased expression of nuclear PLCβ1 and its downstream target Cyclin D3 (CCND3), an induction of normal myeloid differentiation, and a better prognosis. Stemming from these data, our goal was to analyze the correlation between CCND3, PLCβ1 and AZA treatment. Firstly, we treated two different cellular lines, AML HL60 and histiocytic lymphoma U937, with AZA 5μM (Ec50 for HL60 cells) for 24 hours. Then, we used Real-Time PCR and Western blot to quantify both gene and protein expression. Moreover, we showed that CCND3 promoter has one CpG island. For this reason, it is possible that AZA could directly affect both PLCβ1 and CCND3 promoters. Therefore, we studied PLCβ1 binding to CCND3 promoter by chromatin immunoprecipitation (CHIP), before and after AZA treatment. Our results evidenced that the recruitment of PLCβ1 to CCND3 promoter is specifically increased after AZA treatment, leading to suppose that PLCβ1 could have a pivotal role in MDS with either a direct or indirect effect on cell cycle, proliferation and differentiation. These complicate relations need future deepening in order to demonstrate how PLCβ1 binding actually regulates CCND3 expression and how much this expression depends on CCND3 direct promoter demethylation and PLCβ1 control.

Çocukluk Çağında İnmemiş Testis Dokusundan Gelişen Primer Histiyositik Sarkom

Çocukluk Çağında İnmemiş Testis Dokusundan Gelişen Primer Histiyositik Sarkom

Leiomyosarcoma with prominent osteoclast-like giant cells: a clinicopathologic analysis of 7 cases and review of literature

To study the clinicopathologic features of leiomyosarcoma with prominent osteoclast-like giant cells. The clinical and pathologic features of 7 cases of leiomyosarcoma with prominent osteoclast-like giant cells were analyzed. Immunohistochemical and ultrastructural studies were performed. The literature was reviewed. All cases occurred in adults, with a mean age of 63 years. There was no significant sex predilection (male-to-female ratio = 4:3). The tumor involved subcutaneous soft tissue of thigh (number = 2), left back (number = 1), retroperitoneum (number = 1), small intestine (number = 1), breast (number = 1) and uterus (number = 1). Histologic examination showed that the tumor was composed of relatively uniform spindly cells arranged in interlacing fascicles. The hallmark was the presence of prominent osteoclast-like giant cells, either intimately admixed with the spindly cells (number = 6) or forming giant cell tumor-like nodules (number = 1). Immunohistochemically, the spindly cells expressed smooth muscle actin, muscle-specific actin, desmin and h-caldesmon in various degrees, whereas the osteoclast-like giant cells expressed CD68. Ultrastructural study showed smooth muscle differentiation in the spindly cells and histiocytic differentiation in the osteoclast-like giant cells. Follow-up data were available in 6 cases. There were local recurrences and/or metastases in all the 6 patients. Three patients were alive with unresectable or recurrent/metastatic disease and two patients died of the disease. Leiomyosarcoma with prominent osteoclast-like giant cells is a rare variant of leiomyosarcoma which should be distinguished from the so-called giant cell variant of malignant fibrous histiocytoma. The osteoclast-like giant cells are of histiocytic differentiation. Surgical resection remains the mainstay of management of this high-grade sarcoma.

Clear cell papillary renal cell carcinoma: a distinct low-grade renal tumour

To study the clinicopathologic features of clear cell papillary renal cell carcinoma (CCPRCC). The clinical, morphologic and immunohistochemical characteristics of 6 cases of CCPRCC were reviewed, with analysis of follow-up data. There were altogether 3 men and 3 women. The mean age of patients was 56 years. The size of tumors ranged from 1.0 to 4.5 cm in greatest dimension. They had solid or solid-cystic cut surface. Histologically, the tumors were encapsulated and showed several morphologic patterns, with tubules, papillae, acini, interconnecting ribbons and macro/microcysts lined by single layer of cells with clear or small amount of eosinophilic cytoplasm and low-grade nuclei (corresponding to Fuhrman grade 1 or 2). Mitotic figures were rarely seen. Characteristically, there was linear arrangement of the nuclei away from the basement membrane, conferring an appearance similar to that of endometrial glands in early secretory phase. Tubules and cysts contained serosanguineous fluid or colloid-like secretion were identified. No foamy histiocytes, psammomatous calcifications or hemosiderin was present in the papillary areas. Two of the tumors showed focal or extensive angioleiomyoma/leiomyoma-like components. No coagulative necrosis, sarcomatoid dedifferentiation, nor microscopic vascular invasion was observed. Immunohistochemically, all tumors showed strong co-expression of CK7 and CA9 (with characteristic "goblet" staining pattern). The staining for EMA, CK (AE1/AE3), vimentin, CK8, CK18, CK19 and PAX-8 were also positive in all cases. Ki-67 was expressed in less than or about 5% of the tumor cell nuclei. The staining for CD10, P504S, CD117, TFE3 and TFEB was negative. Follow-up data were available in all patients, with mean duration of 14 months (range = 7 to 27 months). All of the patients were disease-free after operation. CCPRCC is a special type of low-grade renal neoplasm with characteristic histopathologic and immunohistochemical features. It needs to be distinguished from clear cell renal cell carcinoma or papillary renal cell carcinoma.

Clinical analysis of hard metal lung disease

To analyze the clinical features and investigate the clinical diagnostic methods of hard metal lung disease (HMLD), then provide reference for the diagnostic criteria of occupational HMLD. Retrieved the open published case reports associated with HMLD from January, 2000 to June, 2014. Regarding the ages, sex, types and years of work, clinical features and laboratory results for analyzing. Collected 21 clinical cases of HMLD belonged to 6 internal reports and 15 oversea reports. Among them 15 male and 6 female, ages were from 22 to 58, length of service between 1 year and 43 years. Clinical presentations included cough (20 cases), dyspnea on progressive (10 cases), and pulmonary function testing showed a restrictive abnormality. The imaging features presented as bilateral areas of ground-glass attenuation, diffuse small nodules, extensive reticular opacities and traction bronchiectasis. The finding of giant cell interstitial pneumonia (GIP) was almost pathognomonic for hard metal pneumoconiosis. The main pathological findings contained a different levels of lymphocyte, acidophilic cell infiltration, hyperplasia of fibrous tissue and numerous large multinucleated histiocytes which ingested inflammatory cells were admixed with macrophages. 16 cases of the 21 reports showed GIP. Clinical presentations include cough and dyspnea on progressive, and pulmonary function testing show a restrictive abnormality. The imaging features present as bilateral areas of ground-glass attenuation, areas of consolidation, diffuse small nodules, extensive reticular opacities and traction bronchiectasis. The prime pathological findings contain interstitial pneumonia with intra-alveolar macrophages and a large amount of multinucleated histiocytes.

Ceroid granuloma, a rare lesion mimicking breast carcinoma: Case report

Seroid granulomu; lipid ve lipoproteinlerin kismi oksidasyonu sonucu, kanama ve nekroz alanlarinda ortaya ci- kan, makrofajlar icinde depolanan, en sik kadin genital sisteminde ve genelde tesadufen rastlanan bir pigmenttir. Bizim hastamizin sag memesinden malignite suphesiyle eksize edilen kitlenin histopatolojisinde histiositlerde depolanan, Sudan Black B ile lipid oldugu saptanan ve granulom yapisi olusturan seroid saptandi ve olgu Seroid Granulomu tanisi aldi. Meme parankiminde ve duktuslarinda atipik bulgu saptanmadigindan malignite ekarte edildi. Hastamizda seroid granulomunun daha once Fibrokistik degisiklik nedeniyle ayni bolgeden gecirmis oldugu cerrahi isleme sekonder olarak olustugu dusu- nuldu. Maligniteyle klinik ve radyolojik olarak karisabilen, memede cok nadir gorulen Seroid granulomu klinisyenler ve patologlar tarafindan ayirici tanida akilda tutulmalidir. Anahtar kelimeler: Meme, seroid, granulom

Surgical pathology of revision after knee and hip arthroplasty

To investigate clinical characteristics and pathological changes of tissue surrounding prosthesis after hip and knee arthroplasty. A total of 67 patients receiving hip and knee arthroplasty were included in the study and pathological changes of the revision specimens were evaluated by microscopic examination. Of 67 patients, there were 25 males and 42 females (ratio of 0.6) with a mean age of 64 years. There were 42 cases of revision hip prosthesis and 25 cases of knee prosthesis. The primary causes for the revision varied, including 20 cases of infection (29.9%, within 3 months in 9 cases,3 to 24 months in 3 cases and over 24 months in 8 cases), 14 cases of pain (20.9%), 13 cases of loosening of the prosthesis (19:4%), 9 cases of joint stiffness (13.4%), 8 cases of prosthetic dislocation (11.9%), and 3 cases of prosthesis fracture (4.5%). Pathological findings in the tissue surrounding the prostheses included debris reaction, histiocytes, acute inflammatory, chronic non-specific inflammation, pigmented villonodular synovitis (PVNS), "pseudomembranous", calcification, necrosis, sequestrum, etc. These histological changes were frequently admixed. Various reasons may lead to hip and knee revision arthroplasty. The main pathological findings include infection, debris granulomas, chronic non-specific inflammatory changes, PVNS. The surgical pathology of the prosthesis provids guidances for clinical treatment and basic research.

Clinical and pathologic characteristics of Erdheim-Chester disease

To explore the clinicopathologic features, immunophenotype, differential diagnosis and gene mutation status of the Erdheim-Chester disease (ECD). Clinical and pathologic findings of 3 ECD cases were examined by gross, microscopic, immunohistochemical methods and BRAF V600E mutation. Related literatures were reviewed. Two male patients and one female patient presented clinically with multiple skin nodules, bone pain and bony lesions by imaging study. Microscopically, the lesions were composed of spindle-shaped fibroblasts, foamy histiocytes and scattered Touton-type giant cells embedded in reactive fibrous tissue. Lymphocytes, plasma cells, and multinucleated giant cells were also found. Immunohistochemically, all histiocytes were positive for CD68, none of which expressed CD1a, although 2 cases focally expressed weak S-100 stain. In 2 cases,BRAF V600E mutation was detected. ECD is a rare disease of xanthogranulomatous histiocytosis.Its diagnosis relies on pathological and immunohistochemical findings, but correlation with clinical information, especially radiographic findings should be performed.No effective treatment of the disease is currently available.

Clinicopathologic features and prognosis of T lymphoblastic lymphoma associated with Langerhans cell histiocytosis

To study the clinicopathologic features, immunophenotype and molecular genetic changes of T lymphoblastic lymphoma (T-LBL) associated with Langerhans cell histiocytosis (LCH). Three cases of T-LBL associated with LCH were included. The morphologic characteristics were reviewed along with immunohistochemical profiling using EnVision method and TCR gene rearrangement by PCR. A review of composite lymphoma previously reported in the literature was performed. All three patients were male with the mean age of 61.7 years. One was Hans and the other 2 were Uyguers. All presented with superficial lymph node enlargement. Biopsy of lymph node showed two abnormal cell populations: distended sinus by large, pale histiocytes with nuclear grooves, and the interfollicular region containing immature-appearing cells with irregular nuclei slightly larger than that of small lymphocyte, dispersed chromatin, inconspicuous nucleoli, scant cytoplasm, and scattered mitotic figures. These cells presented in aggregates and small sheets interspersed with normal-appearing lymphocyte. The histiocytes were positive for CD1a, S-100 protein and CD68. The lymphoma cells were positive for CD3, CD7, TdT and CD34. TCR-γ gene rearrangement was detected in one case by PCR technology. One case involved bone marrow with double phenotype acute leukemia. Amongst the 8 including 5 reported cases, there were 4 males and 4 females. The mean age of the patients and the median age were 54 years. Lymphoadenopathy was the most common presentation. Bone marrow was involved in 4 cases. The time of follow-up was 2 to 27 months. The median survival was 5.5 months and the one-year survival rate was 33.3%. Diagnosis of T-LBL and LCH should be based on typical morphology, immunophenotype and molecular genetic findings, with differential diagnoses including Langerhans cell hyperplasia originated from dermatopathic lymphadenopathy. When involving lymph node, extensive sampling supplemented by immunohistochemical staining is important to reach a correct diagnosis. Although coexistent T-LBL and LCH is clonally related, the understanding of its pathogenesis requires further investigation.

Current research of thrombospondin in eye

Thrombospondin(TSP) has five members with diversiform expressions and complicated biologic functions in different histiocytes all over the body.TSP also is widely expressed in different parts of eye,such as retinal pigment epithelial cells,corneal endothelial cells and lens epithelial cells,etc.,and sometimes TSP is secreted by trabecular meshwork cells.As a group of cytokines,TSP plays an important regulating role in the physiological and pathological activities of eye.Studies determined that TSP participates in the pathogenesis of age-related macular degeneration,repaired of corneal diseases,formation of cataract,development of open-angle glaucoma,pathological process of eye tumor,occurrence of proliferating vitroretinopathy and diabetic retinopathy.Studies towards their functions are helpful for revealing the pathogenesis of eye diseases and providing new ideas of prevention and therapy.The distribution,source and eye disease-related action of TSP were summarized. Key words: Thrombospondin; Eye; Physiology; Pathology

Radiological and clinicopathological analysis of intraspinal primary Rosai-Dorfman disease

Background Rosai-Dorfman disease (RDD), also known as sinus histiocytosis with massive lymphadenopathy (SHML), is a non-neoplastic histiocytic proliferation predominantly affecting lymph nodes, and usually presents with massive painless cervical lymphadenopathy accompanied by fever and weight loss. Extranodal involvement occurs in over 40% of patients; however, isolated extranodal disease without lymph node involvement is unusual. Although extranodal involvement has been reported in diverse sites, central nervous system manifestation, particularly in spinal cord is distinctly rare. It is a diagnostic challenge for radiologists and histopathologists to differentiate RDD from other spinal lesions because of its similarities in radiological and histological findings. Herein we describe a case of unusual isolated RDD in spinal cord. The radiology and clinicopathology of this lesion, as well as its differential diagnosis are discussed. Methods The clinical manifestation of a patient with intraspinal primary RDD occurring C 3-6 level was presented retrospectively. Gross resected mass was routinely paraffin-embedded and stained with hematoxylin and eosin. Dako EnVision immunohistochemical staining system was used to detect the tumor antigen expressions, including S-100 protein (S-100), CD1a and CD68 (KP-1). Results A 25-year-old female patient presented with 3-month history of numbness and weakness in both upper limbs associated with an increasing neck back pain. There was no fever and lymphadenopathy found in the patient. MRI of the whole spine revealed a subdural mass extending from C 3 to C 6 level of cervical spinal cord with homogeneous enhancement after contrast administration. Laminectomy and midline opening of the dura were performed. The subdural lesion appeared to have no capsule and attach the dura mater. The lesion was removed totally. Under the microscopic examination, dense fibrosis and intense chronic inflammation with focal neutrophilic infiltrates were noted. The clusters of large histiocytes with eosinophilic, finely granular cytoplasm and multinucleate giant cells were also observed in the lesion. Emperipolesis with intact lymphocytes within the cytoplasm of the large histiocytes were present. Mitotic activity and necrotic area were not observed. Special stains for organisms were negative. By immunohistochemical analysis, the characteristic histiocytes were positive for S-100 and CD68 and negative for CD1a. Based on clinical presentations and histological findings, a final histological diagnosis of primary RDD in spinal cord was made according to the criteria of WHO classification. The patient did not receive chemotherapy and radiotherapy, and attended follow-up for 12 months, without any neurological deficit or signs of recurrence. Conclusions Isolated intraspinal RDD is rare. The definite diagnosis of this lesion should be made under the microscopical examination because the preoperative radiological appearance of the lesion does not differ from other lesions occurring in spinal cord, such as inflammatory pseudotumor, meningioma and lymphoma. Although good prognosis is obtained from gross total resection in most of reported patients with this lesion, recurrence could be found in individual cases, and chemotherapy and (or) radiotherapy had been applied for a few cases with multiple organs involvement to control the progression of lesion. Due to the rarity of its site, the strictly differential diagnosis should be made when the isolated RDD is encountered in spinal cord. doi: 10.3969/j.issn.1672-6731.2014.04.011

Nodular histiocytic/mesothelial hyperplasia: a clinicopathologic analysis of 7 cases

To analyze the clinicopathologic and immunohistochemical features of nodular histiocytic/mesothelial hyperplasia (NHMH) and to improve the knowledge of this disease. Seven cases of NHMH were collected and the clinicopathologic and immunohistochemical data were analyzed with review of the literature. Seven male patients aged from 1.5 to 5.0 years (mean 2.8). The main clinical symptom was an inguinal mass.Grossly, main pathological changes were the mural nodule or free nodule in lumen, with diameter of 0.1-0.5 cm.Histologically, the tumor cell morphology was relatively single, cohesive polygonal or oval cells which were arranged in solid sheets or nests, usually with ovoid or deeply grooved nuclei and a moderate amount of pale pink cytoplasm in the nodular collection area. The nuclei had delicate chromatin and no obvious atypia, and mitosis was incidentally found. A few scattered lymphocytes were found in the stroma. The cyst wall was lined by a single layer of mesothelial cells.Immunohistochemically, the most cells in nodular lesion were strongly positive for the histiocytic marker CD68, vimentin and α1-antichymotrypsin, while lining mesothelial cells on the wall were positive for calretinin, MC, WT1, CK5/6, CKpan and EMA. NHMH is a rare and benign tumor-like lesion, and easy to be misdiagnozed, which should be distinguished from neuroendocrine tumors, Langerhans cell histiocytosis, seminoma, mesothelioma and so on. The correct diagnosis of this lesion depends on the clinical characteristics, morphology and immunohistochemistry.

A histological study of eosinophilic granuloma in mice following infestation with Anisakis larvae

Anisakidosis is a parasitic anthropozoonosis caused by the nematode larvae of the Anisakidae family. Anisakid nematodes belonging to the Anisakis pegreffii are highly prevalent in several fish species living in the Mediterranean sea. The larvae can accidentally infect humans following the ingestion of infected raw or undercooked sea fish. A migrating larva causes a clinical disease when it invades the stomach or intestinal wall and peritoneum, mimicking an eosinophilic gastroenteritis or an ulcer. In this preliminary experiment, the histopathology of the newly-formed parasitic granulomas in mice infested with third stage Anisakis pegreffii larvae, was studied and described. The larvae were morphologically identified as Anisakis type I by the presence of a boring tooth and a mucron, without ventriculus and caecum. The larval DNA was extracted and amplified by polymerase chain reaction (PCR). After PCR, the samples were processed to undergo restriction fragment length polymorphism analysis (RFLP). This was done to scan the restriction profiles for genetic identification. PCR products were purified and sequenced. The sequences were analysed to detect the relationship between nucleotides and perform a phylogenetic analysis. The paraffin-embedded granuloma samples showed worms having a diameter of 0.55 mm x 0.37 mm, polymyarian muscle cells and a circular intestine. The histological profiles showed a primary lesion at the site of anisakid penetration marked by oedema and neutrophil and eosinophil infiltration. The presence of histiocytes or epithelioid histiocytes, lymphocytes, monocytes, and plasma cells was also possible. Fibrinous exudation, hemorrhage, or vascular damage were detected within the first week of the acute intestine infection with a massive eosinophilic infiltration. Two weeks after the infestation, the infiltrating host cells formed a granuloma in the tissue surrounding the penetrated worm mainly consisting of eosinophils, a large number of fibroblasts and a varying number of admixed multinucleated giant cells. In order to explain the origin of the eosinophilic granulomas, a study into the produced substance attracting eosinophils and other host white blood cells to the area will carry out.