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PubMed1996

The effect of decalcification and choice of fixative on histiocytic iron in bone marrow core biopsies.

IRon stains are often used for bone marrow core biopsies obtained by needle biopsy of the iliac crest. Because bone must be decalcified by brief treatment with acid, it is possible that an undetermined amount of stainable histiocytic iron may be lost. A study was carried out to determine whether decalcification results in loss of histiocytic iron and the effects of fixatives and the recovery of histiocytic iron in decalcified bone marrow tissue. Aspirates of bone marrow were stained for iron with Prussian blue. Because aspirate material does not require decalcification, it served as a control for the study. One hundred bone marrow biopsies and accompanying aspirates from 100 adult subjects were evaluated. Fifty bone marrow biopsies were fixed using a fixative containing mercuric chloride (B-5) and the remaining 50 were fixed in zinc-formalin. Histiocytic iron was graded as minimal, moderate or marked depending on whether less than 5, 6-10, or more than 10 iron positive histiocytes, respectively, were observed. When histiocytic iron was markedly present in aspirate material, at least moderate amounts of stainable iron were found in 22 of 25 B-5 fixed and 21 of 25 zinc-formalin fixed decalcified bone marrow. When aspirate histiocytic iron was minimal or moderate, 14 of 25 B-5 fixed and 7 of 25 zinc-formalin fixed decalcified bone marrow specimens revealed histiocytic iron. Decalcification results in decreased recovery of stainable iron, and where histiocytic iron is minimally or moderately present, B-5 fixation results in greater postdecalcification recovery. There was no significant difference in recovery when larger quantities of histiocytic iron were present prior to the decalcification step.

Adult↗

PubMed1992

[Evaluation of clinical features, cytopathological findings and prognosis of histiocyte proliferative disorders].

Clinicopathological analysis was performed in 19 patients diagnosed clinically with malignant histiocytosis. Ultimately, 9 patients died and 10 are still alive. All 19 had fever of unknown origin. Among the 10 surviving patients, 6 recovered with only supportive therapy such as antibiotic treatment. One recovered with steroid therapy and 2 with VP (vincristine and prednisolone) therapy. Complications due to immunodeficiency were detected in one surviving patient and 2 who died. All 9 patients who died had anemia, and 8 had thrombocytopenia. However, among survivors, only one had anemia and only 2 had thrombocytopenia. Chromosomal abnormality was detected in one patient who died. Histiocytic cells were classified morphologically into 3 types: immature, intermediate and mature. In 4 patients who died, histiocytic cells were immature, but in 4 others mature histiocytic cells were detected. In 5 of the 10 surviving patients, histiocytic cells were of the immature type. Immuno-histochemical analysis of the origin of histiocytic cells in 8 deceased patients showed T-zone histiocytes in one, T cells in one, monocyte phagocytic system (MPS) in 5, and histiocytes of unknown origin in one. Thus, malignant histiocytosis is a heterogenous entity including reactive histiocytic disorder, lymphocytic neoplasm and true histiocytic neoplasm. In histiocyte proliferative disorders, red blood cell counts and platelet counts are useful for assessing prognosis, while cytological findings only confuse this evaluation.

Adult↗

PubMed1963

STUDIES OF TUBERCLE BACILLUS-HISTIOCYTE RELATIONSHIPS. VII. HOMOLOGOUS AND HETEROLOGOUS TRANSFER OF CELLULAR RESISTANCE.

Immunization of mice or guinea pigs with BCG rendered all or most of the histiocytes of these animals resistant to necrotization by virulent H37Rv; this cellular resistance was mediated by immune serum. Immune mouse histiocytes (from BCG-immunized animals) were able to induce cellular resistance in normal homologous and heterologous (rabbit) animal species; mouse histiocytic ribosomes were also tested in the homologous species and found to be active. Immune guinea pig histiocytes (from BCG-immunized guinea pigs) were ineffective in transferring cellular resistance to either homologous or heterologous (mouse and rabbit) animal species. Immune rabbit histiocytes were capable of inducing cellular resistance in mice and guinea pigs; rabbit histiocytic ribosomes were also tested in normal mice and found to be active in induction of cellular resistance. Recipient guinea pig histiocytes (from guinea pigs inoculated with immune rabbit histiocytes) were capable of inducing cellular resistance in normal guinea pigs and rabbits. Cultivation of lysed immune histiocytes of all three animal species on glycerol-blood agar medium failed to reveal any viable BCG; this provided one additional bit of evidence against the idea that induction of cellular resistance is due to viable bacilli.

Animals↗

PubMed2006

Evaluation of dysregulation of the receptor tyrosine kinases Kit, Flt3, and Met in histiocytic sarcomas of dogs.

OBJECTIVE: To evaluate canine histiocytic sarcoma cell lines and tumor samples for dysregulation of the Kit/stem-cell factor (SCF), Flt3/Flt3 ligand (Flt3L), and Met/hepatocyte growth factor (HGF) receptor tyrosine kinase signaling pathways, as these are known to contribute to the differentiation and survival of normal dendritic cells as well as malignant transformation of dendritic cells in mouse models. SAMPLE POPULATION: 4 histiocytic sarcoma tumor cell lines and 35 formalin-fixed histiocytic sarcoma specimens obtained from dogs. PROCEDURE: Histiocytic sarcoma cell lines were evaluated for expression of Kit/SCF, Flt3/Flt3L, and Met/HGF by use of reverse transcriptase-PCR procedures. Histiocytic sarcoma cell lines and tumor samples were evaluated for mutations in Kit, Flt3, and Met by use of PCR analysis of genomic DNA, followed by both sequencing and fluorescent PAGE for deletions or internal tandem duplications. The ability of the multi-targeted split-kinase inhibitor SU11654 to block proliferation and induce apoptosis of histiocytic sarcoma cell lines was also evaluated. RESULTS: No mutations in Kit, Flt3, and Met were identified in any of the cell lines or tumor samples evaluated. Furthermore, SU11654 did not induce cell-cycle arrest or apoptosis of histiocytic sarcoma lines, even at supratherapeutic doses. CONCLUSIONS AND CLINICAL RELEVANCE: These data suggest that dysregulation of Kit/SCF, Flt3/Flt3L, and Met/HGF signaling pathways is unlikely to occur in histiocytic sarcomas of dogs and that inhibitors of the Kit, Flt3, and Met pathways are unlikely to provide clinical benefit to dogs with histiocytic sarcomas.

Animals↗

PubMed1984

The application of the metalophil method for the demonstration of histiocytes.

The metalophil method has been performed on 250 sections of a wide variety of inflammatory and neoplastic lesions in which different types of histiocytes might be encountered. In lymph nodes, dendritic histiocytes related to the B-lymphocyte system were consistently metalophil. They appeared as small cells with slender extensions in lymph nodes with follicular hyperplasia and/or sinus histiocytosis and in some cases of Hodgkin's lymphomas or as larger pleomorphic cells in primary or secondary malignancies of lymph nodes. Small, rounded cells were seen in some cases of marked paracortical reaction, in dermatopathic lymphadenitis and in some cases of mycosis fungoides. These cells most probably represented Langerhans cells and interdigitating reticulum cells, which are related to the T-lymphocyte system. Interdigitating cells become metalophil when they are activated or proliferating. Epithelioid cells in different benign and malignant lesions were metalophil like the sinus histiocytes of the lymph nodes, the Kupffer cells of the liver and the alveolar histiocytes in the lung. Foreign-body giant cells in lymph nodes after lymphography were also metalophil. The sinus lining cells lymph nodes were also well-delineated. Histiocytes of malignant histiocytic proliferations were sometimes metalophil as were the so-called histiocytes in malignant fibrous histiocytomas. Epithelial cells, particularly the basal cells of squamous epithelium often take up the silver. Carcinoma cells were sometimes metalophil and the method appeared not to be of value in the differentiation between metastatic carcinomas and lymphomas. The most promising application seems to be the study of the distribution of dendritic histiocytes in malignant proliferations of B-lymphocytes.

Carcinoma, Squamous Cell↗

PubMed1983

Immunohistochemical differentiation between histiocytic and lymphoid neoplasms.

Lysozyme has, until recently, been accepted as the only reliable immunohistochemical marker of benign and malignant histiocytes. Using this marker, very few lymphoreticular neoplasms of histiocytic origin are recognized and more recently alpha-1-anti-trypsin has been shown to be a better marker of malignant histiocytes. By immunizing rabbits with highly purified human blood monocytes we have obtained an antiserum (S22) which stains histiocytes and neutrophils in paraffin sections with a high degree of specificity. Using this antiserum and antisera to lysozyme and alpha-1-anti-trypsin we have stained paraffin sections of tissues containing reactive histiocytes, histiocytic proliferations, leukaemic infiltrates and lymphoreticular tumours of histiocytic and T-cell origin. Our results show that alpha-1-anti-trypsin is the most reliable marker of malignant histiocytes but that the as yet uncharacterized antigen defined by S22 may offer a promising alternative.

Animals↗

PubMed1996

Small, freshly arrived histiocytes in cutaneous and mucosal herpetic lesions.

We report on the predominance of a special type of small histiocyte in the inflammatory infiltrate accompanying herpetic bullae. These histiocytes, which have previously been taken to be neutrophils, are freshly arrived cells with a hitherto unknown function. Until now, they have been found only in Sweet's syndrome and erythema nodosum where they form Miesscher's radial granulomas. Similar small histiocytes were found in half of those herpetic lesions with intact bullae, and in over two-thirds of ulcerated lesions in which these cells formed a palisade in the fibrinoid material covering the floor of the ulcerated vesicles. Small histiocytes, admixed with neutrophils, were in close proximity to virally infected keratinocytes. Immunohistochemical analysis confirmed their histiocytic nature. With the exception of ecthyma contagiosum (orf), similar small histiocytes were not found in other viral infections or in nonspecific ulcers of the skin. In cases of herpetic folliculitis, small histiocytes showed massive epidermotropism towards hair follicle epithelium. We conclude that cutaneous and oral herpetic infections represent yet another disease in which small, freshly arrived histiocytes occur. They may be involved in antigen presentation, or in killing of infected keratinocytes.

Antigens, CD↗

PubMed1962

Studies on tubercle bacillus-histiocyte relationship. V. Passive transfer of cellular resistance.

Studies of passive transfer of cellular resistance, as manifested by refractoriness to necrotization with virulent tubercle bacilli, have shown that immune histiocytes or immune lymphocytes were effective transferring agents; immune polymorphonuclear leucocytes and immune serum as well as comparable cells from normal animals lacked this capacity. Comparisons of immune histiocytes and immune lymphocytes showed that the former cells were more efficient; this was indicated by (a) the smaller numbers of immune histiocytes needed for passive transfer, (b) the longer duration of cellular resistance in recipients given histiocytes than in those given lymphocytes, (c) the greater capacity of histiocytes to effect serial passive transfer, and (d) the ability of histiocytic but not lymphocytic lysates to transfer cellular resistance. Experiments to establish the mechanism of passive transfer of cellular resistance showed that there was no active induction of resistance in recipients through transfer of bacillary antigens contained in immune histiocytes; in fact, the results of serial passive transfers with immune histiocytes suggested an active replication of the "cell resistance factor."

Animals↗

PubMed2004

Histiocytic subpopulations in the gastrointestinal tract: distribution and possible relationship to function.

The distribution of specific histiocyte subsets within the human gastrointestinal tract has not been extensively characterized. Our goal was to immunohistochemically evaluate the distribution and location of CD1a-positive, CD68-positive, and Factor XIIIa (FXIIIa)-positive histiocyte subsets within the normal gastrointestinal tract and attempt to relate distribution to possible function. Twenty-nine samples of normal esophagus, stomach, small bowel, large bowel, and anus were routinely processed and immunohistochemically stained with antibodies to CD68, CD1a, and FXIIIa. The distribution and histologic location of histiocyte subsets were qualitatively analyzed. CD1a-positive cells were seen exclusively within anal and esophageal squamous mucosa. CD68 positive histiocytes were present in lamina propria and submucosa throughout the gastrointestinal tract and in Peyer patches. FXIIIa-positive histiocytes were also abundant in lamina propria and submucosa throughout the gastrointestinal tract, particularly around pericryptal sheaths and in parafollicular regions surrounding Peyer patches. Our results showed that there are distinct subpopulations of gastrointestinal histiocytes, and that distribution varies according to both cell type and site. Because Langerhans cells are epidermal antigen processing/presentation cells, their exclusive presence in squamous mucosa suggests an analogous function there. The prominence of both CD68 and FXIIIa-positive cells surrounding glandular pericryptal sheaths suggests that they are important to immune function at this mucosal interface and may play a role in communication between glands and lamina propria. In addition, the presence of specific histiocyte subsets within Peyer patches and para-follicular regions suggests that they are involved in different aspects of antigen processing associated with gut lymphoid tissue. Further studies are needed to explore the relation between specific histiocyte subsets and gastrointestinal disease processes.

Antigens, CD↗

PubMedDate not supplied

Value of histiocyte detection in Pap smears for predicting endometrial pathology. An institutional experience.

OBJECTIVE: To determine the clinical implications of the finding of histiocytes in Pap smears in 1 patient population. STUDY DESIGN: The medical records and Pap smears which the presence of histiocytes was mentioned in the diagnosis between August 1996 and August 2001 were reviewed in conjunction with follow-up surgical findings. The positive predictive value (PPV) for significant endometrial pathology for the isolated finding of histiocytes on Pap smear was determined. RESULTS: Of the 238,225 women screened over a 60-month period, 325 were reported to have histiocytes in their Pap smears. Of them, 238 (73.2%) had subsequent endometrial sampling, hysterectomy or both, and follow-up Pap smears. Two hundred seven smears (87%) failed to disclose endometrial pathology. Thirty-one cases (13%) resulted in significant histopathologic findings, including 12 uterine malignancies, 8 endocervical polyps, 7 endometrial polyps, 2 submucosal leiomyomata, 1 simple hyperplasia without atypia and 1 case of tamoxifen-related changes. Upon review of the clinical records, 58% (18/31) of those patients had other significant clinical and/or cytologic findings. Five of the 18 patients (27.8%) had associated postmenopausal bleeding, 11 had additional abnormal Pap smear findings (atypical glandular cells, 6/18, or 33.3%; endometrial cells, 5/18, or 27.8%), and another 2 had both postmenopausal bleeding and atypical glandular cells (2/18, or 11.1%). The PPV for significant uterine pathology for women with the isolated finding of histiocytes on a Pap smear was 5.5% and 60% with additional clinical and/or Pap smear findings. The PPV for endometrial cancer was 1.3% in women with the isolated finding of histiocytes on a Pap smear but 20% for women with histiocytes and additional clinical/or Pap smear findings. CONCLUSION: Based on the findings of this study and recently published data, we conclude that the isolated finding of increased histiocytes in the absence of postmenopausal bleeding, endometrial cells or atypical glandular cells on a Pap smear is a poor indicator of uterine disease.

Adenocarcinoma↗

PubMed2002

Localized and disseminated histiocytic sarcoma of dendritic cell origin in dogs.

Canine histiocytic proliferative disorders include a wide spectrum of diseases characterized by different biologic behaviors. The etiology and pathogenesis of these diseases are largely unknown. The clinicopathologic, morphologic and immunophenotypic characteristics of canine localized and disseminated histiocytic sarcoma were examined in 39 dogs. Rottweilers, Bernese Mountain Dogs, and retrievers were most commonly affected (79%). Localized histiocytic sarcomas (19 dogs) arose from a single site, and metastatic lesions were observed in draining lymph nodes. Predilection sites were subcutis and underlying tissues on extremities, but tumors occurred in other locations, including spleen, lung, brain, nasal cavity, and bone marrow. Disseminated histiocytic sarcomas (20 dogs), a multisystem disease previously described as malignant histiocytosis, primarily affected spleen, lungs, bone marrow, liver, and lymph nodes. Both localized and disseminated canine histiocytic sarcomas were composed of pleomorphic tumor cell populations. CD1+, CD4-, CD11c+, CD11d-, MHC II+, ICAM-1 +, Thy-1 +/- tumor cells were identified in all snap-frozen samples (31 dogs). This phenotype is characteristic for myeloid dendritic antigen-presenting cell lineage. Hence, canine localized and disseminated histiocytic sarcomas are likely myeloid dendritic cell sarcomas. Dendritic antigen-presenting cells are a heterogeneous cell population with regards to their ontogeny, phenotype, function, and localization. The exact sublineage of the proliferating dendritic antigen-presenting cells involved in canine histiocytic sarcomas remains to be determined. Phenotypic analysis of formalin-fixed tissues from eight dogs was limited by available markers. Morphologic features and the phenotype CD18+, CD3-, and CD79a- were the most useful criteria to indicate likely histiocytic origin.

Animals↗

PubMed1986

Phenotypes and phorbol ester-induced differentiation of human histiocytic lymphoma cell lines (U-937 and SU-DHL-1) and Reed-Sternberg cells.

Hodgkin's mononuclear cells, Reed-Sternberg (H-RS) cells, and U-937 and SU-DHL-1 histocytic cell lines were induced to differentiate by phorbol ester in cultures. The phenotypes of cells were determined by a panel of antibodies specific for monocytes, histiocytes, and interdigitating reticulum cells. Before induction, SU-DHL-1 cells and H-RS cells expressed similar markers, such as HeFi-1, 2H9, 1A2, and 1E9. In addition, SU-DHL-1 cells were also stained by Tac and Leu M5. Other monocyte markers, including OK M1, Co Mo2, BRL Mo1, BRL Mo2, and Leu M3 were consistently negative in both types of cells. After induction, SU-DHL-1 cells conserved the same phenotype, but H-RS cells became negative for HeFi-1, 1A2, and 2H9. The U-937 cells expressed Leu M1 and Co Mo2 and became positive for Leu M5, OK M1, Co Mo2, BRL Mo2, 2H9, and 1E9 after phorbol ester induction. The U-937 cells did not express HeFi-1 or 1A2. The marker expression of H-RS cells, SU-DHL-1 cells, and U-937 cells were compared with those of histiocytes or interdigitating reticulum cells in lymphoid tissues and with neoplastic cells in true histiocytic lymphoma and malignant histiocytosis. It is concluded that SU-DHL-1, U-937, and H-RS cells are derived from or most closely related to fixed histiocytes, free histiocytes, and interdigitating reticulum cells, respectively. Our study further confirms the diagnosis of SU-DHL-1 as true histiocytic lymphoma but reveals that U-937 is a case of malignant histiocytosis rather than the previously diagnosed histiocytic lymphoma. The phenotypes and induction properties of SU-DHL-1 cells are quite different from those of U-937 cells, which suggests that true histiocytic lymphoma and malignant histiocytosis are two distinct disease entities.

Antibodies, Monoclonal↗

PubMed1995

Transformation of chronic lymphocytic leukemia to lymphoma of true histiocytic type.

BACKGROUND: Chronic lymphocytic leukemia (CLL) may evolve into large cell lymphoma (Richter's syndrome), prolymphocytic leukemia, acute lymphoblastic leukemia, and myeloma. METHODS: A patient with CLL that transformed into a lymphoma of true histiocytic type is described, and the literature on the association of these two disorders is reviewed. RESULTS: Lymphomas of true histiocytic type developing as an aggressive terminal phase of CLL previously have been reported in nine patients. Fever and rapidly increasing lymphadenopathy and splenomegaly were the most common signs and symptoms. As with de novo lymphoma of true histiocytic type, extranodal involvement of the soft tissue, gastrointestinal tract, kidneys, bone marrow, liver, and lungs was documented among the 10 patients with lymphoma of true histiocytic type transformed from CLL. The median interval between diagnosis of CLL and the evolution to lymphoma of true histiocytic type was 25.5 months. Patients with lymphomas of true histiocytic type after CLL were treated with fludarabine and various other combination chemotherapy regimens with only short-lived responses. The median time to death after transformation was only 33 days (range, 10 days to 5 months). CONCLUSION: Lymphomas of true histiocytic type appear to represent an additional, though uncommon, form of transformation in CLL. Although their presentation is reminiscent of other intermediate to high grade lymphomas, they can be distinguished based on their morphologic and immunophenotypic features. In the patients described in this study to date, transformation of CLL to lymphomas of true histiocytic type is a poor prognostic sign, with survival generally of only days to weeks.

Bone Marrow↗

PubMed1982

Immunohistochemical investigations of tumors of supposed fibroblastic-histiocytic origin.

The aim of this study was to localize alpha 1-antitrypsin, ferritin, and lysozyme by means of the indirect immunoperoxidase technique and to evaluate the significance of these antigens as markers of histiocytic differentiation in tumors of a supposed dual fibroblastic-histiocytic origin. The series comprised 31 malignant fibrous histiocytomas (MFH) of the pleomorphic, spindle cell, and myxoid types, four cutaneous fibrous histiocytomas, and four atypical fibroxanthomas, four dermatofibrosarcoma protuberans, and two osteoclastomas of bone. For comparison, 15 soft tissue sarcomas of various other types were examined. Of the MFHs of the pleomorphic type, 18 of 22 (82 per cent) were positively stained for alpha 1-antitrypsin and 12 of 22 (54 per cent) were positively stained for ferritin. Of the five MFHs of the spindle cell type, none was positively stained for alpha 1-antitrypsin, three were positive for ferritin, and one was positive for lysozyme. None of the myxoid variants (corresponding to grade I-II myxofibrosarcoma) was positively stained for either of the antigens. These results and the observations made on the cutaneous fibrous histiocytomas, atypical fibroxanthomas, dermatofibrosarcoma protuberans, and the various soft tissue sarcomas indicated that 1) alpha 1-antitrypsin is a valuable marker of histiocytic differentiation in both benign and malignant fibrous histiocytomas, 2) ferritin can be visualized in more than half of these fibroblastic-histiocytic tumors, and the presence of ferritin distinguishes the spindle cells of these tumors from fibroblasts of connective tissue and most fibrosarcomas, and 3) lysozyme, although a good marker of histiocytic differentiation in ordinary histiocytes and benign fibrous histiocytomas, is a poor marker of neoplastic histiocytes of malignant tumors. The results further support the concept that MFH is a tumor of a dual fibroblastic-histiocytic origin.

Ferritins↗

PubMed1986

Monoclonal antibodies against SU-DHL-1 cells stain the neoplastic cells in true histiocytic lymphoma, malignant histiocytosis, and Hodgkin's disease.

Three murine monoclonal antibodies, named 2H9, 1E9 and 1A2, were produced after immunization of BALB/c mice with cells of the SU-DHL-1 cell line from a true histiocytic lymphoma. In frozen sections from various lymphomas, 2H9 and 1A2 selectively stained the cell membranes of neoplastic cells in true histiocytic lymphoma and Hodgkin's disease. Antibody 1E9 stained the nuclear membranes of the tumor cells in true histiocytic lymphoma and malignant histiocytosis. No staining was seen in 56 cases of B and T cell lymphoma. Several tissue culture cell lines, including T cell acute lymphoblastic leukemia and pre-B cell lines, were not stained. With 2H9, however, a positive reaction was noted for two Epstein-Barr virus (EBV)-positive African Burkitt's lymphoma cell lines (Daudi and P3HRI), one human T cell lymphoma/leukemia-virus-positive cell line (HUT 102), and one EBV-transformed normal B lymphoblastoid cell line (RPMI 8057). In normal lymphoid tissues, 2H9 and 1E9 reacted with the nuclear membranes of histiocytes and interdigitating reticulum cells, whereas 1A2 stained only rare cells of an unknown type. All three antibodies failed to react with B or T cells in frozen tissue sections of normal lymphoid tissues. The use of these three antibodies should facilitate the diagnosis of histiocyte and interdigitating reticulum (IR) cell-related neoplasms, namely, true histiocytic lymphoma, malignant histiocytosis, and Hodgkin's disease. True histiocytic lymphoma and Hodgkin's disease exhibit similar reactivities with these three and with two other monoclonal antibodies (HeFi-1 and Tac), suggesting that these two types of lymphoma are related. In contrast, malignant histiocytosis was negative for 2H9, 1A2, Tac, and HeFi-1. The difference in the phenotypic expression of true histiocytic lymphoma and malignant histiocytosis indicates that they are two different disease entities.

Animals↗

PubMedDate not supplied

Cerebrospinal fluid cytology in histiocytic proliferative disorders.

Morphologically atypical histiocytes were observed in the cerebrospinal fluid (CSF) of five patients with histiocytic proliferative disorders, including one each classified as Letterer-Siwe disease and Hand-Schüller-Christian disease and three as malignant histiocytosis. In all of these patients except the one with Letterer-Siwe disease, neurologic examination, CSF leukocyte count and protein and glucose concentrations were normal. Necropsy studies in the three fatal cases (one patient with Letterer-Siwe disease and two with malignant histiocytosis) demonstrated leptomeningeal involvement by atypical histiocytes in all three and brain involvement in the patient with Letterer-Siwe disease. These observations suggest that cytologic examination of CSF is warranted in patients with histiocytic proliferative disorders and may be reliable in documenting central nervous system, particularly leptomeningeal, involvement. The atypicality of the histiocytes in the CSF, however, was not indicative of the classification of the histiocytic proliferative disorder. Because the patient with Hand-Schüller-Christian disease continues to have a normal neurologic examination seven years after abnormal histiocytes were initially detected in his CSF, we believe that the clinical condition of the patient and classification of the histiocytic proliferative disorder are of primary importance for initiating aggressive therapy directed at the central nervous system.

Adolescent↗

PubMed1996

Storage histiocytes and hemophagocytosis: a common finding in the bone marrow of patients with active systemic lupus erythematosus.

We report the frequency of the finding of storage and hemophagocytic histiocytes in the bone marrow of patients with systemic lupus erythematosus with one or more hemocytopenias. The study was performed on bone marrows of ten patients with systemic lupus erythematosus during an episode of hemocytopenia. Four patients were not receiving any treatment and six had been taking oral prednisone (3.5 +/- 1.5 mg/day) for the previous 6 months. Hemocytopenias found were lymphocytopenia in five, thrombocytopenia in three, and neutropenia and anemia in two each. The bone marrow had variable cell content; megakaryocytes, the myeloid:erythroid ratio, as well as lymphocyte, plasma cell, and reticular cell contents were usually increased. Seven bone marrow samples showed storage histiocytes (sea-blue histiocytes and other histiocytes that contained unidentified intracytoplasmic material). These same samples revealed histiocytes phagocytosing erythoblasts, erythrocytes, polymorphonuclear neutrophils, lymphocytes or platelets. The presence of these histiocytes in all seven patients was related to a decrease in serum complement and with lupus disease activity as measured with the SLEDAI index (mean +/- SD = 2.1 +/- 1.5). The SLEDAI score of the remaining three patients, who had no histiocytes in their bone marrow, was 0, 0, and 1, respectively. The present study reveals that the bone marrow in patients with systemic lupus erythematosus and peripheral hemocytopenia contains storage and hemophagocytic histiocytes and the significance of these cells is discussed.

Adult↗

PubMed1983

Concanavalin A binding histiocytes in Hodgkin's disease and their relation to clinicopathologic features of the disease.

The occurrence and staining patterns of Concanavalin A (Con A) binding histiocytes were studied in diagnostic lymph node specimens of 133 patients with Hodgkin's disease. Varying numbers of Con A binding histiocytes were present in all tumors. Two distinct cytoplasmic staining patterns of the Con A binding histiocytes were noted: diffuse, and a pattern termed "globular" which represents a dense, solitary paranuclear aggregate of binding sites. The diffuse binding pattern was seen in the majority of histiocytes with no apparent nuclear atypia, but was also occasionally seen in Reed-Sternberg cells. Globular binding was present in both benign and malignant-looking histiocytes, including rare Reed-Sternberg cells. Based on the number of histiocytes in which globular binding of Con A (G-cells) was observed, tumors were grouped in the following three categories: Group 1: tumors with large numbers of G-cells (42 cases); Group 2: tumors with a small number of G-cells (16); and Group 3: tumors with rare or no G-cells (75). Tumors with large numbers of G-cells were seen more frequently in patients with disseminated disease than in those with localized (69.0% versus 31.0%; P less than or equal to 0.002), and more often in patients with B-symptoms than in those without (73.8% versus 26.2%; P less than or equal to 0.001). Large numbers of G-cells were present in most tumors of the lymphocyte depletion type (14/16), whereas rare or no G-cells were seen in the majority of the nodular sclerosis type (46/59). These observations suggest that the G-cells may represent an abnormal variant of histiocytes, the occurrence of which is associated with unfavorable clinical and pathologic features of Hodgkin's disease.

Adolescent↗