Showing papers on "Monocytosis published in 1993"

A review on the acute phase response in major depression.

Abstract: There is some evidence that major depression is characterized by systemic immune activation with involvement of phagocytic cells, T cell activation, B cell proliferation and increased autoantibody production This paper reviews that major depression may be accompanied by higher concentrations of positive and lower concentrations of negative acute phase proteins (APPs) The most prominent abnormalities of APPs in major depression are increased haptoglobin (Hp) plasma levels The latter are significantly and positively correlated with interleukin (IL)-6 production, various indices of systemic immune activation (eg monocytosis, neutrophilia, T cell activation) and with the vegetative symptoms of depression (eg anorexia, weight loss, psychomotor retardation, sleep disorders, anergy) Major depression is characterized by an altered distribution of Hp phenotypes and genes suggesting that genetic variation on chromosome 16 may be associated with this illness It is concluded that increased production of IL-6 and IL-1 in major depression may underlie both immune activation and the "acute" phase response in that illness, and that disorders in Hp may be related to the pathophysiology and pathogenesis of major depression

Feline Immunodeficiency Virus Infection Clinicopathologic Findings in 90 Naturally Occurring Cases

Abstract: In 90 cats with naturally occurring feline immunodeficiency virus (FIV) infection, the clinicopathologic changes seen at the time of first diagnosis of FIV infection included lymphopenia (29%), neutrophilia (27%), monocytosis (23%), anemia (18%), leukocytosis (13%), leukopenia (13%), neutropenia (11%), hyperproteinemia (38%), and hyperglobulinemia (25%). Forty-nine (54%) of the cats showed multiple hematologic abnormalities, and a further 24 (17%) had a single abnormality. The most consistent changes in serum protein electrophoretic patterns were increases in the concentrations of alpha 2 globulin and gammaglobulin subfractions. Although there is no established system for staging the degree of immunosuppression in cats infected with FIV, cytopenias appeared to be more common in cats with advanced clinical signs of disease.

Specific skin manifestations in acute leukemia with monocytic differentiation a morphologic and immunohistochemical study of 11 cases

Abstract: Background. Monocytic differentiation is present in the myelomonocytic (M4) and monocytic (M5) type of acute myeloblastic leukemia. Infiltration of the skin in acute myelomonocytic leukemia occurs in 10–20% of patients, the skin lesions occasionally being the first symptom, even preceding monocytosis. Methods. Eleven patients with myelomonocytic (n = 2) and monocytic leukemia (n = 9) were studied who had skin manifestations. Results and Conclusions. Clinically, all patients showed disseminated papules or nodules that corresponded histologically to nodular or diffuse infiltrates of monocytoid cells, occasionally displaying a whorled pattern. The currently available antibodies for paraffin-embedded sections (lysozyme), elastase, leukocyte common antigen (CD45), MT1 (CD43), Leu-Mi (CD15), LN2 (CD74), MB2, MB1 (CD45RA), LN1 (w75), Mac387, L26 (CD20), UCHL1 (CDR0), MT2 (CD45RA), and KP-1 (CD68)) and chloracetate–esterase are not more helpful in diagnosis than are the histologic findings. By contrast, the antibodies used on frozen sections (Leu-4 (CD3), Leu-3a (CD4), BA1 (CD24), B4 (CD19), Leu-M5 (CD11c), Vim12 (CD11b), VimD5 (CD15), KiM6 (CD68), KIM7 (CD68), My7 (CD13), and My9 (CD33) allow the definition of a reaction pattern that is diagnostic for acute myeloid leukemia with monocytic differentiation. Cancer 1993; 71:124-32.

Comparisons between microvascular changes in cerebral and non-cerebral malaria in mice, using the retinal whole-mount technique

Abstract: CBA/T6 mice inoculated with Plasmodium berghei ANKA strain (PbA) exhibited cerebral symptoms and died from cerebral malaria 6–8 days p.i. whereas DBA/2J mice developed (around days 6–9) a non-fatal cerebral malaria, with milder cerebral symptoms, and died between days 15 and 22 from other malaria-related complications. When inoculated with P. berghei K173 (Pb) these mouse strains did not develop cerebral malaria. These mouse/parasite strain combinations were used, in conjunction with the retinal whole-mount technique, to elucidate factors critical in the pathology of murine cerebral malaria. CBA/T6 mice infected with PbA (PbA-CBA mice) demonstrated mild changes in vascular permeability as early as days 2–3, prior to the appearance on day 5 of cerebral symptoms, whereas mice with non-cerebral malaria did not show any vascular permeability changes until the very late stage of the disease (days 14–22). In the PbA infections, progressive deterioration of endothelial barrier properties, demonstrated by Evans' Blue leakage both generally and from specific focal areas, as well as a developing monocytosis and adherence of mononuclear cells to the endothelium of the retinal vessels continued until death (in CBA/T6 mice) or resolution (in DBA/2J mice). Adherent monocytes, particularly in PbA-CBA mice, were associated with reduced Hoechst staining of individual endothelial cells and a banking up proximally of both parasitized and non-parasitized blood cells in the small blood vessels, often with accompanying focal leakage of Evans' Blue from the retinal vessels. The occurrence and severity of these early changes in the microcirculation correlated with the subsequent development of cerebral symptoms. Monocyte margination appeared to be the most significant factor associated with the development of cerebral symptoms.

Early pathogenesis of disease caused by SIVsmmPBj14 molecular clone 1.9 in macaques.

Abstract: We have studied the early pathogenesis of infection by molecular clone 1.9 of SIVsmmPBj14 in pig-tailed and cynomolgus macaques. Like the uncloned PBj14 parent, SIVsmmPBj14-1.9 consistently induced an acute clinical syndrome characterized by behavioral depression, fever, profuse diarrhea, dehydration, lymphadenopathy, splenomegaly, and mucocutaneous exanthema that began at 7 days postinfection (DPI). The acute clinical disease coincided with a marked cell-associated and cell-free viremia, during which SIV p27 was demonstrated in 4 to 68% of circulating mononuclear leukocytes between 4 and 17 DPI. Also characteristic were monocytosis and reductions in CD4+ and CD8+ T lymphocytes, as well as CD20+ B lymphocytes. The most profound depletion occurred in the CD44hi subset of CD4+ T cells. Unlike animals infected previously with uncloned or biologically cloned PBj14, however, all SIVsmmPBj14-1.9-infected macaques survived the acute-phase disease to progress to a chronic, largely asymptomatic phase of infection. Recovery from the acute-phase disease correlated with down modulation of virus replication and the appearance of antibodies to SIV Env and Gag proteins. Similar to the PBj14 parent, PBj14-1.9 targeted to intestine, spleen, bone marrow, lymph node, and cerebellum. Saliva contained substantial quantities of infectious virus and no viral antibodies during the early phase of infection. By contrast, saliva from chronically infected animals usually contained antibodies but no virus. This study extends previous work demonstrating that the acute clinical syndrome produced by SIVsmmPBj14 in pig-tailed macaques represents a unique model of lentiviral pathogenesis.

Alterations of cell-mediated immune response following cardiac surgery.

Abstract: Nosocomial infections in patients following cardiac surgery are frequently associated with opportunistic microorganisms indicating a dysregulation of cell-mediated immune response. The objective of this prospective randomized trial, therefore, was to investigate the mechanisms of dysregulation and the counterregulatory effects of immunomodulation. Twenty patients underwent conventional postoperative therapy, another 20 patients received indomethacin, which inhibits synthesis of the down-regulating mediator prostaglandin E2, and a further 20 patients were given thymopentin in addition to indomethacin, thereby augmenting activation and differentiation of the T-lymphocytes. The immunologic parameters studied included T-lymphocytes and monocytes as well as interleucin (IL)-1 and IL-6 synthesis by monocytes, and IL-2 and IL-6 synthesis by T-lymphocytes. Following cardiac surgery a significant, persistent reduction of T-lymphocytes and IL-2 synthesis as well as significant monocytosis could be observed. Indomethacin treatment resulted in a normalization of the cellular imbalance at the end of the first postoperative week, but IL-2 synthesis remained significantly reduced during the entire observation period. Conversely, with combined indomethacin and thymopentin treatment restoration of cellular distribution as well as protection of IL-2 synthesis could be achieved. These results indicate a quantitative and functional impairment of the forward regulation of cell-mediated immunity. It was shown for the first time that combined indomethacin and thymopentin treatment could successfully counteract these immunomechanistic alterations.

Intrathecal administration of interleukin-2 for meningeal carcinomatosis due to malignant melanoma : sequential evaluation of intracranial pressure, cerebrospinal fluid cytology, and cytokine induction

Abstract: A patient with interleukin (IL)-2 responsive metastatic melanoma developed meningeal carcinomatosis. Treatment was attempted with intrathecal (i.t.) IL-2 (5 weekly doses of 3-6 x 10(6) IU) without glucocorticosteroids. Marked increases in cerebrospinal fluid (CSF) pressure occurred 5-10 h following each IL-2 dose, resulting in reversible abnormalities of neurologic function. IL-2 clearance from the CSF ranged from 21 to 85 ml/h, with an apparent first order rate constant of 0.08-0.23 hr-1. These values were consistent with clearance by bulk flow mechanisms. Clearance also correlated directly with peak CSF pressure. Progressive increases in CSF tumor necrosis factor (TNF)-alpha and IL-6 levels, but not Il-1 alpha, were also noted over successive treatment cycles. Increasing neutrophilia (peaking at 12 h postdose) and a delayed lymphocytosis and monocytosis (at 20-30 h) were observed with each successive i.t. IL-2 dose. Activated lymphocytes were not observed in the CSF, however, suggesting that an exogenous source of activated lymphokine-activated killer (LAK) cells may be helpful in obtaining effective antitumor responses.

Myelodysplastic syndrome associated with relapsing polychondritis: unusual transformation from refractory anemia to chronic myelomonocytic leukemia.

Abstract: The authors report an unusual case of myelodysplastic syndrome (MDS) associated with relapsing polychondritis (RP), which developed at almost the same time as MDS. The initial diagnosis was MDS, refractory anemia (RA) subtype, according to the FAB classification [3]. Symptoms of RP were apparently controlled by oral administration of prednisolone (PSL), although MDS was not. Within 1 month after the diagnosis, monocytosis and thrombocytopenia without excess of blasts became prominent and transformation from RA to chronic myelomonocytic leukemia (CMML) was recognized. Combination chemotherapy including daunorubicin (DNR) and cytosine arabinoside (ara-c) did not subdue the progressive monocytosis and thrombocytopenia. Finally, the patient died of pulmonary hemorrhage 3 months after the onset of the disease. The prognosis of MDS may be poorly influenced by association with RP.

Urinary neopterin as a predictive marker of coronary artery abnormalities in Kawasaki syndrome.

Abstract: We investigated whether urinary neopterin concentrations respond to the pathological conditions (especially coronary artery dilatation) of Kawasaki syndrome. All of 29 children with Kawasaki syndrome had very high urinary neopterin concentrations. Increased urinary neopterin concentrations coincided with fever and with monocytosis in peripheral blood. The urinary neopterin excretion peaking within the first 8 days after onset correlated with the development of coronary artery dilatation. Increased urinary neopterin concentrations indicate that cell-mediated immunity is activated in patients with Kawasaki syndrome. Endogenous interferon-gamma and activation of monocytes/macrophages may play a role in the pathogenesis of Kawasaki syndrome. Not only do neopterin concentrations correlate with symptoms in the acute phase of Kawasaki syndrome, they also act as a predictive marker of coronary artery abnormalities in affected patients.

Juvenile chronic myelogenous leukemia: report of the Italian Registry. Associazione Italiana di Ematologia Oncologia Pediatrica (AIEOP).

Abstract: BACKGROUND Since juvenile chronic myeloid leukemia (JCML) represents no more than 2% of leukemia in children, clinical and investigative experience of this disorder has been limited. In order to evaluate the diagnostic criteria currently applied, to provide centralized facilities for blood culture and to collect data on treatment, and to propose a uniform treatment protocol in our country, a National Registry for JCML was recently established in the "Associazione Italiana di Ematologia Oncologia Pediatrica" (AIEOP). PATIENTS Out of the 24 cases reported from 9/35 centres, 22 were considered sufficiently documented and were enrolled in the Registry. Clonogenic assay on marrow and peripheral blood cells was performed in all available cases. RESULTS Common features were non-specific clinical (fever, splenomegaly, hepatomegaly, lymphadenomegaly) and hematologic alterations (anemia, thrombocytopenia, leukocytosis usually < 50 x 10(9)/l, monocytosis, circulating immature granulocytes, increased HbF, normal karyotype). In 11 out of 11 cases, in vitro blood cultures showed the spontaneous growth of CFU-C in the absence of any exogenous source of colony-stimulating activity. Twelve of the 22 patients (55%) are alive (probability of survival 47.7%); most patients were treated according to an acute myeloid leukemia-directed schedule; 5/7 children treated with interferon were alive with disease after a median time of 29 months from diagnosis (range 8-95 months); 4/5 children who underwent bone marrow transplantation were alive in complete remission 10, 24, 42 and 118 months, after the diagnosis. Age < 1 year at presentation was the most significant prognostic factor in terms of probability of survival (80% vs 28%; p = 0.0024). CONCLUSIONS JCML must be considered in young children for whom acute leukemia has been suspected but ruled out; in vitro cultures should be considered mandatory to confirm the diagnosis. Age less than one year at the presentation was associated with prolonged survival. Only bone marrow transplantation was followed by prolonged disease-free survival, whereas intensive chemotherapy seemed not very effective and potentially associated with life-threatening complications. Interferon therapy appears to be a promising alternative to chemotherapy while the value of unrelated marrow donor is explored.

Falciparum malaria in naturally infected human patients: IV--Ultrastructural changes in peripheral white blood cells.

Abstract: Ultrastructure of white blood cells (WBC) were studied in peripheral venous blood from Saudi patients with acute falciparum malaria (AFM) and compared with their counterparts in same patients 2 weeks after chloroquine treatment and full recovery. A counting system was incorporated to determine the rate of abnormal to normal cell type in plastic thick sections during the course of the disease. Neutrophilia, monocytosis, eosinopenia and lymphocytosis were associated with various ultrastructural abnormalities including: (1) Knobby phagocytic polymorphonuclear neutrophils (PMN) and promyelocytes, and PMN with highly vacuolated cytoplasm. (2) Irregularly outlined electron-dense nuclei in non-functional monocytes. (3) Unusual distribution of nuclear chromatin in resting B-lymphocytes, while others possess highly vacuolated cytoplasm and knobby surfaces. (4) Absence of granules in granular lymphocytes containing the known diagnostic paratubular crystalline arrays. (5) Plasmablasts containing electron-dense granules and swollen mitochondria. These abnormalities were suggested to be due to the high level of parasitaemia producing some toxic soluble products. They may also be attributed to alteration of bone marrow macrophages as a sequence of their interaction with soluble parasite products or their phagocytic parasitized red cells and debris released during the rupture of schizonts. This study showed that the number of abnormal WBC increases in patients with high level of parasitaemia; plasmablasts have the lowest rate of abnormalities, while monocytes have the highest; old patients present with lower degree of parasitaemia than young patients due to a less mature immune system; and the AFM may have independent effects on the structure of human WBC.