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PubMed1981

Histiocytes in vaginal smears: as prognostic parameter in carcinoma of the uterine cervix.

Pretreatment vaginal smears of 251 patients with carcinoma of the cervix were counted for the percentage of histiocyte count in relation to benign squamous epithelial cells. No correlation was found between the percentage of histiocyte count and the age of the patient, clinical stage, cell type of squamous cell carcinoma, and clinical radiation response. Also a high histiocyte count is found to be unrelated to 5-year survival, recurrence, metastasis, or death of these patients. The present study indicates that the histiocyte number appears to have no relationship with immediate or remote prognosis in patients with carcinoma of cervix uteri.

Carcinoma, Squamous Cell↗

PubMed1986

Enzyme- and immunohistochemical study of a case of histiocytic necrotizing lymphadenitis.

A combined morphological, immunohistological, and enzyme histochemical analysis was performed on frozen and fixed lymph node tissue in a case of histiocytic necrotizing lymphadenitis (HNL) using conventional histology, a panel of monoclonal and polyclonal antibodies, and a series of common haematological enzyme reactions. Histology showed multiple paracortical necrotizing foci which, in a prominently necrobiotic background devoid of granulocytes, contained large numbers of foamy histiocytes and macrophages intermingled with cells resembling degenerating plasmacytoid T-cells. Most of the histiocytes were alpha1-antichymotrypsin positive and foamy cells were also distinctly Leu-M1 positive. Strong granular acid phosphatase (AP) positivity was present in the cytoplasm of the macrophages and histiocytes. The cells with plasmacytoid features showed weaker and homogeneously diffuse AP staining. Alpha-naphthyl acetate esterase (ANAE) activity was much less striking than AP in the necrotizing foci and most of the ANAE negative cells corresponded to those with plasmacytoid features. No cells with B-cell lineage markers were present within the necrotizing foci; most of the occasional T-cells (Leu-1+, Leu-4+) present in the foci were Leu-2a+ (OKT8+) whereas OKT10+ lymphoid cells were abundant and appeared to correspond with the cells with plasmacytoid features. Our combined data confirm that the special type of necrosis found in HNL develops within foci of plasmacytoid T-cells undergoing regressive changes and apparently exhibiting distinct immunohistological and enzyme histochemical features.

Adult↗

PubMed2002

A case of true malignant histiocytosis: identification of histiocytic origin with use of immunohistochemical and immunocytogenetic methods.

We report here an autopsy case of true malignant histiocytosis. The patient was a 67-year-old woman who exhibited fever, wasting, hepatosplenomegaly, and progressive pancytopenia. The bone marrow aspiration disclosed hemophagocytosing cells, which resembled histiocytes. The molecular analysis did not show the clonal gene rearrangement of T-cell receptor or immunoglobulin heavy chain. Although the patient had been started on methylprednisolone pulse therapy and chemotherapy with etoposide, she died from cerebral hemorrhage. The autopsy specimens of spleen and liver showed extensive infiltration of atypical cells, for which histiocytic origin was identified with an immunohistochemical method using monoclonal antibodies against CD11c, CD68, macrophage colony-stimulating factor (M-CSF), M-CSF receptor, lysozyme, antitrypsin and alpha1-antichymotrypsin. Recent investigations have disclosed that in most cases diagnosed as malignant histiocytosis, hemophagocytosis was reactive and not evoked by histiocytic malignancy. True malignant histiocytosis, for which histiocytic origin is confirmed, is extremely rare.

Aged↗

PubMed1975

A scanning electron microscopic study of 34 cases of acute granulocytic, myelomonocytic, monoblastic and histiocytic leukemia.

This report describes the surface architecture of leukemic cells, as seen by scanning electron microscopy in 34 patients with acute nonlymphoblastic leukemia. Six patients with myeloblastic, 4 with promyelocytic, 10 with myelomonocytic, 8 with monocytic, 4 with histiocytic and 2 with undifferentiated leukemia were studied. Under the scanning electron microscope most leukemia histiocytes and monocytes appeared similar and were characterized by the presence of large, well developed broad-based ruffled membranes or prominent raised ridge-like profiles, resembling ithis respect normal monocytes. Most cells from patients with acute promyelocytic or myeloblastic leukemia exhibited narrower ridge-like profiles whereas some showed ruffles or microvilli. Patients with myelomonocytic leukemia showed mixed populations of cells with ridge-like profiles and ruffled membranes whereas cells from two patients with undifferentiated leukemia had smooth surfaces, similar to those encountered in cells from patients with acute lymphoblastic leukemia. It appears that nonlymphoblastic and lymphoblastic leukemia cells (particularly histiocytes and monocytes) can frequently be distinquished on the basis of their surface architecture. The surface features of leukemic histiocytes and monocytes are similar, suggesting that they may belong to the same cell series. The monocytes seem to have characteristic surface features recognizable with the scanning electron microscope and differ from most cells from patients with acute granulocytic leukemia. Although overlap of surface features and misidentification can occur, scanning electron microscopy is a useful adjunct to other modes of microscopy in the study and diagnosis of acute leukemia.

Acute Disease↗

PubMed1978

Sea-blue histiocytes in a patient with lymphoma.

A middle-aged man with lymphocytic lymphoma had numerous sea-blue histiocytes in his bone marrow, splenomegaly and thrombocytopenia. Thus, his illness mimicked that of patients with the primary syndrome of the sea-blue histiocyte. However, the paucity of sea-blue histiocytes in his spleen, the absence of neurologic disease, his age and the ultrastructure of his abnormal histiocytes were all evidence for the presence of the acquired syndrome. The pathogenesis of sea-blue histiocytosis and the relationship between acquired cases and the primary syndrome are discussed.

Biopsy↗

PubMed1978

Development of a histiocytic medullary reticulosis-like syndrome during the course of acute lymphocytic leukemia.

A 54 year old woman presented with acute lymphocytic leukemia. Following an initial response to chemotherapy with vincristine and prednisone, progressive pancytopenia developed coincident with intense bone marrow infiltration by abnormal histiocytes. At autopsy two months later, no evidence of leukemia was found, but the bone marrow was replaced by abnormal histiocytes showing active erythrophagocytosis, consistent with histiocytic medullary reticulosis. Detailed morphologic, ultrastructural and histochemical studies performed throughout the course of the patient's illness served to confirm the transition from leukemia to histiocytosis. Four similar cases of acute lymphocytic leukemia terminating in histiocytic medullary reticulosis have been reported. This association may represent a distinct clinicopathologic syndrome.

Bone Marrow↗

PubMed1975

Sea-blue histiocytes and sural nerve in neurovisceral storage disorder with vertical ophthalmoplegia.

Ultrastructural investigation of bone marrow histiocytes in neurovisceral storage disorder associated with vertical ophthalmoplegia revealed 3 types of cytosomes: (1) lamellar cytosomes; (2) larger cytosomes composed of lamellar fragments and a granular component; and (3) large irregular cytosomes with amorphous and granular portions, often including fingerprint profiles--in some of these, lysosome-like bodies were numerous. The lamellar cytosomes corresponded to vacuoles seen by light microscopy. The Type 2 and 3 cytosomes were the ultrastructural substract of Wright-Giemsa stained blue granules. Histiocytes having a predominance of Type 2 cytosomes in a cytoplasm rich in free ribosomes had the appearance of sea-blue histiocytes at the light-microscopic level. Transformed Type 1 cytostomes served as building blocks for Type 2 and 3 cytosomes. In the sural nerve, Schwann cells and endoneurial fibroblasts accumulated autofluorescent lipopigment but no lamellar cytosomes or their fragments were found on electron-microscopic examination. Ultrastructure of sea-blue histiocytes in this disease differed from that observed in some other diseases.

Adult↗

PubMed1995

Colonic histiocytic neoplasm mimicking malignant histiocytosis and presenting as intussusception.

It is now apparent that distinction between the so-called malignant histiocytosis and lymphoma can be made using panels of established immunohistochemical markers and/or genotypic analysis. Many, if not all, of the previously diagnosed cases of malignant histiocytosis have been shown to be of lymphoid, rather than histiocytic, lineage. We report a rare case of colonic histiocytic neoplasm accompanied by a lymphoreticular dissemination that mimicked that of malignant histiocytosis. In addition, barium studies and computed axial tomography confirmed an intussusception that subsequently developed. The histiocytic nature of the neoplastic cells was supported by immunohistochemical, ultrastructural, and cytochemical studies. To our knowledge our case may represent the fifth documented case of a histiocytic malignancy reported in the literature. The relationship among the various cases will be discussed as well as the significance of the focal S-100 immunoreactivity observed in the present case.

Colonic Diseases↗

PubMed1992

Histiocytic cytophagic panniculitis: molecular evidence for a clonal T-cell disorder.

Histiocytic cytophagic panniculitis is a systemic disease of unknown etiopathogenesis that invariably involves the subcutaneous fat and is histologically characterized by phagocytosis of blood elements by histiocytes that appear to be benign. Immunophenotypic and genotypic studies of biopsy specimens of the lesions of a 58-year-old woman showed that the lymphocytic infiltrates accompanying the histiocytes in the subcutis were composed of clonal T-cells with rearrangement of the surface receptor gene. Our findings suggest that the primary abnormality in histiocytic cytophagic panniculitis may be a clonal T-cell proliferation.

Biopsy↗

PubMed2004

Pseudoneoplastic proliferation of histiocytes with paclitaxel-induced ultrastructural changes in a mastectomy specimen.

A 49-year-old Hispanic woman with a T4N1M0 infiltrating duct carcinoma of the left breast underwent four courses of FAC (doxorubicin 86 mg, 5-fluorouracil 860 mg, cyclophosphamide 86 mg, and dexamethasone 10 mg) adjuvant chemotherapy plus four courses of paclitaxel (Taxol; Bristol-Myers Squibb Oncology, Princeton, NJ) and subsequent mastectomy. The tumor shrunk from 6.5 cm to 2.5 cm after the treatment. The residual tumor in the surgical specimen measured 1.5 cm with eight positive out of 24 axillary lymph nodes. The tumor showed typical chemotherapy changes and a massive proliferation of histiocytes that mimicked a neoplasm. A nodular proliferation of the same cells in one axillary node raised the impression of a second malignant tumor in the breast spreading to the node. The histiocytic cells contained lamellar and coarse periodic acid-Schiff-positive material distending their cytoplasm and they were strongly positive for CD68 and negative for CD1a, pan keratin, and S-100. These findings ruled out histiocytoid carcinoma, granular cell tumor, and Erdheim-Chester disease. The proliferating histiocytes had ultrastructural findings of paclitaxel-induced cytotoxicity with disorganized stacks of intermediate filaments positive for vimentin by immunostains and fewer masses of tubulin. The treated breast carcinoma cells were tubulin-positive but the proliferating histiocytes were tubulin-negative.

Antineoplastic Agents, Phytogenic↗

PubMed2006

Aggressive histiocytic disorders that can involve the skin.

Histiocytoses are a heterogeneous group of disorders that are characterized by the proliferation and accumulation of reactive or neoplastic histiocytes. Three classes of histiocytoses have been defined: class I, Langerhans cell disease; class II, non-Langerhans cell histiocytic disease without features of malignancy; and class III, malignant histiocytic disorders. Although the disorders in classes I and II usually have a benign appearance on histology and are commonly non-aggressive and self-healing, some can cause debilitating or even fatal outcomes. Such cases beg the question: what stimulates aggressive behavior of a classically benign disease? New molecular information may now provide insight into the driving force behind many of the aggressive histiocytoses. In this article, we review Langerhans cell disease and seven aggressive histiocytoses that can involve skin, discuss histologic features that may forecast a poor prognosis, and discuss the molecular findings that help to explain the pathophysiology of these aggressive histiocytic disorders.

Histiocytosis↗

PubMed2004

Histiocytic sarcoma with fatal duodenal ulcers.

Histiocytic sarcoma is an uncommon neoplasm of mature histiocytes with very poor outcome. We report an autopsy case of a true histiocytic sarcoma with characteristic symptoms of so-called "malignant histiocytosis of the intestine". The liver and spleen were enlarged, with remarkable tumor cell infiltration in the hepatic sinusoids and splenic sinuses. Tumor cells aggregated to form sporadic nodular lesions in the liver, which often showed coagulative necrosis. Infarcted lesions also occurred at the splenic subcapsular area. In addition, tumor cell infiltration was noted in the sinuses of bone marrow and lymph node. Tumor cells often demonstrated moderate pleomorphism with multinucleated giant cells. They were positive for CD68 and negative for T- and B-cell lineage markers, megakaryocytic markers, and CD30. Various examinations were done to rule out infection-associated hemophagocytic syndrome, and the absence of infectious diseases was revealed. Thus, the diagnosis of histiocytic sarcoma was made. Apart from these lesions, multiple ulcerations, some with fatal perforation, were found in the esophagus and duodenum. They showed only non-specific inflammatory changes without tumor cell involvement. The ulcers probably derived from ischemic condition through an embolic process caused by tumor cell infiltration elsewhere in the blood vessels at the periphery of the ulcers.

Antigens, CD↗

PubMed2002

Expression of the histiocytic marker PG-M1 in granuloma annulare and rheumatoid nodules of the skin.

BACKGROUND: The expression of PG-M1, the most specific histiocytic marker, has not yet been studied in granuloma annulare (GA) and other palisaded granulomas of the skin. We evaluated the reactivity of PG-M1 with a series of GA and rheumatoid nodules (RN) to establish the sensitivity and potential usefulness of this marker in the diagnosis and characterization of these entities. METHODS: Histological sections from 30 GA and 15 RN were immunostained with PG-M1. For comparison, additional sections were stained with KP-1 and lysozyme. The stains were recorded as negative, weakly positive (1+) and strongly positive (2+). RESULTS: PG-M1 stained all cases of GA (100%). KP-1 and lysozyme stained 26 (86%) and 18 (60%) GA cases, respectively. PG-M1 exhibited a significantly stronger staining intensity (1.8 +/- 0.07) when compared with KP-1 (1.4 +/- 0.13) (p = 0.018) and with lysozyme (0.9 +/- 0.15) (p < 0.0001). All RN were stained by PG-M1 (100%). KP-1 and lysozyme stained 14 (93%) and six (40%) RN cases, respectively. PG-M1 staining intensity (1.6 +/- 0.13) was slightly higher than that of KP-1 (1.4 +/- 0.18) (p = 0.27) and significantly higher than that of lysozyme (0.4 +/- 0.13) (p < 0.0001). CONCLUSIONS: PG-M1 is consistently and strongly expressed by the histiocytic population of GA and RN, being more sensitive and reliable than other histiocytic markers. We recommend its use in difficult cases in which the histiocytic nature of the lesion needs to be confirmed.

Antibodies, Monoclonal↗

PubMed1998

Perforin and Fas pathways of cytotoxic T-cells in histiocytic necrotizing lymphadenitis.

AIMS: Cell death can be divided into necrosis and apoptosis. In histiocytic necrotizing lymphadenitis (HNL), apoptosis is the main form of cell death. Two molecular mechanisms of T-cell-mediated cytotoxicity, one perforin-based and the other Fas-based, have been demonstrated, and both systems induce apoptosis of the target cells. This study was designed to investigate the Fas and perforin pathways in HNL. METHODS AND RESULTS: Twelve cases of HNL were analysed using immunohistochemical staining. The Fas and/or FasL-positive cells, including lymphocytes and histiocytes, were frequently encountered in the necrotizing lesions, however, they were rare in the nonpathological regions. The perforin and/or granzyme-positive cells were also confined in the necrotizing lesions. In double staining, CD8-positive lymphocytes occasionally expressed Fas and/or FasL, and histiocytes also expressed FasL and/or Fas. However, CD4-positive lymphocytes rarely expressed FasL and/or Fas. In a flow cytometric analysis, most of the cytotoxic T-cells, which were recognized by cytolytic granules of TIA-1 and considered to be CD8-positive lymphocytes, expressed FasL and Fas. The perforin-positive lymphocytes also expressed FasL and Fas. CONCLUSION: In our previous study, the apoptotic cells were T-cells, especially CD8-positive cells rather than CD4-positive cells. Based on these findings, in Fas and perforin pathways, the CD8-positive cells were considered to be effector and target cells, while histiocytes could possibly be enhancers. As a result, both pathways seemed to induce an abundance of apoptosis and thus induce necrotizing lesions.

Adolescent↗

PubMed2003

Lack of human herpesvirus 8 and Epstein-Barr virus in Kikuchi's histiocytic necrotizing lymphadenitis.

Kikuchi's histiocytic necrotizing lymphadenitis is a self-limited disorder that typically involves the cervical lymph nodes of young women. Although a viral etiology has been postulated, a definitive viral agent has not been identified. Recent reports have suggested that human herpesvirus 8 (HHV 8) or Epstein-Barr virus (EBV) may play an etiologic role. We investigated the presence of HHV 8 and EBV in archival tissue from 34 cases of Kikuchi's histiocytic necrotizing lymphadenitis. We examined 29 cases for HHV 8 using a nested polymerase chain reaction (PCR) on paraffin-embedded or frozen tissue, and 24 cases for EBV RNA using in situ hybridization (ISH) for EBER1. Controls included reactive lymph nodes from 8 adult women presenting with cervical or axillary lymphadenopathy. The study patients included 7 men and 27 women with a mean age of 28 years. All patients were previously healthy without evidence of immunocompromise and presented with cervical, axillary, or inguinal lymphadenopathy. Two cases exhibited EBV RNA by ISH; this was confirmed by PCR for EBV DNA. HHV 8 DNA was not amplified by nested PCR in any of the cases of Kikuchi's histiocytic necrotizing lymphadenitis or reactive lymph nodes; control PCR demonstrated the presence of amplifiable DNA in all cases. These findings suggest that HHV 8 and EBV do not play causative roles in Kikuchi's histiocytic necrotizing lymphadenitis.

Adolescent↗

PubMed1999

Phenotypic characterization of histiocytes infiltrating a leiomyofibrosarcoma.

We described previously a unique cutaneous tumour in a young pig, which was characterized by several criteria as a histiocytic leiomyofibrosarcoma. The lipid-laden macrophages (histiocytes) which permeated the tumour were CD2+/CD18+/CD49d+ but MAC387 (L1 antigen) and CD15 negative. The present study compared the phenotypes of histiocytes in tumour metastases in the liver with resident liver macrophages, revealing differential expression of certain macrophage activation markers. After repeated subcutaneous passage of the tumour in athymic (nu/nu) mice, flow cytometry demonstrated a rapid loss of porcine MHC Class II, but a more prolonged expression of porcine MHC Class I, consistent with our immunohistological observations. Mouse macrophages (CD2+/F4.80+) infiltrated the later-passage tumours, suggesting that the histiocytes were not of neoplastic origin.

Animals↗

PubMed2003

Primary histiocytic sarcoma of the spleen associated with erythrophagocytic histiocytosis.

We report an exceptional case of a histiocytic sarcoma presenting as a primary isolated spleen tumor in a 71-year-old woman. The neoplastic cells in the cords and sinuses of the red pulp formed multiple lobulated tumors, which were detected in vivo by ultrasound scan. The medium cells, large cells and the giant cells expressed CD68, a histiocyte-associated marker, lysozyme and S100 protein. All these cells were negative for B- and T-cell markers, cytokeratins, melanosome markers (HMB45) and CD1a (Langerhans' cells). Many tumor cells displayed strong erythrophagocytosis and sometimes lymphocytophagocytosis. In addition, numerous histiocytes with morphology indistinguishable from reactive macrophages also exhibited a strong erythrophagocytosis, and were found in the tumor as well as in the normal splenic parenchyma. Despite multi-agent chemotherapy, the patient suffered from a relapse in the liver, with a rapid fatal outcome. A literature review showed that such a primary splenic presentation with multiple tumors is rare. In contrast, in systemic malignant histiocytosis, secondary spleen involvement occurs more frequently but with diffuse infiltration. The association with a reactive histiocytosis with erythrophagocytosis corresponds to "histiocytic medullary reticulosis", as previously described by Scott and Robb-Smith.

Aged↗

PubMed2002

Interferon-gamma, interleukin-18, monokine induced by interferon-gamma and interferon-gamma-inducible protein-10 in histiocytic necrotizing lymphadenitis.

Apoptosis of histiocytes is a characteristic feature of necrotizing lymphadenitis (HNL). Recent studies have indicated that Fas and perforin-based pathways are involved in the apoptotic process of HNL. Elevated levels of serum interferon (IFN)-gamma are reported in HNL. The CXC chemokine interferon-gamma-inducible protein-10 (IP-10) and monokine induced by interferon-gamma (MIG) cause tissue necrosis, and interleukin (IL)-18 induces the expression of IFN-gamma and Fas ligand (FasL) by T and natural killer (NK) cells. This study was designed to determine the expression of IFN-gamma, IL-18, MIG and IP-10 in HNL. Ten cases of HNL were analyzed by using immunohistochemical staining and/or reverse transcriptase-polymerase chain reaction (RT-PCR). As a control, we included four cases of non-specific lymphadenitis. MIG and IP-10 proteins, which enhance the release of granzyme, showed a similar distribution pattern in viable tissues surrounding dead tissue, mostly within histiocytes, and lymphocytes in HNL. IL-18 was located within histiocytes, especially phagocytic histiocytes, but not within lymphocytes. In addition, IFN-gamma-positive lymphocytes were frequently detected in the surrounding dead tissue, and the lymphocytes in the same area were frequently positive for CXCR3, a specific receptor of MIG and IP-10. In non-specific lymphadenitis, MIG, IP-10 and IL-18 positive cells were detected, but their numbers were relatively small compared with HNL, while IFN-gamma positive cells were rarely encountered. Our findings suggest that the cytokine and chemokine pathways of IFN-gamma, IL-18, MIG and IP-10 play an important role in the pathogenesis of apoptosis associated with HNL.

Adolescent↗