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PubMed2004

Leukocytosis occurs in response to resistance exercise in men.

The purpose of this study was to determine the effects of a single bout of resistance exercise on immune cell numbers of moderately active men. Subjects were 16 male volunteers (mean +/- standard deviation [SD] age 30 +/- 7 years, height 180.1 +/- 7.0 cm, mass 83.97 +/- 10.33 kg); 8 were randomly assigned to treatment and 8 to control groups. Treatment was a common resistance training routine (3 sets of 8-10 repetitions at 75% of 1 repetition maximum) of 8 large muscle mass exercises using resistance machines. Blood samples were drawn before exercise and at 0 minutes (P0), 15 minutes (P15), and 30 minutes (P30) postexercise. Control subjects sat quietly in the training facility; blood was drawn at the same intervals as treatment. Leukocyte and lymphocyte (LY) subpopulation numbers were determined. Statistical analysis was analysis of variance (ANOVA) (repeated measures, p < or = 0.050) and multiple comparisons (Dunn method) to isolate variability. All leukocyte subpopulations, except basophils (BA) and eosinophils (EO), increased and counts declined by P15 and P30. Only neutrophils (NE) did not return to preexercise levels by P30. The majority of resistance exercise induced leukocytosis was due to an increase in circulating LY (natural killer cells increased most, CD4+/CD8+ ratio unchanged) and monocytes (MO). The transient, inconsequential immune cell population responses to resistance exercise are similar to those during aerobic activity. The lack of large alterations in and rapid recovery from cell number changes suggests that resistance exercise is not immunosuppressive.

Adult↗
PubMed1992

Thrombocytopenia and leukocytosis induced by single intravenous injections of cadmium-saturated metallothioneins-I and -II in rats.

To comparably investigate hemotoxic potentials of CdCl2, cadmium-saturated metallothioneins-I (Cd-MT-I) and -II (Cd-MT-II), rats received single intravenous injections of one of those dissolved in saline with equivalent concentrations of Cd (0, 0.1, 0.3 and 1.0 mg Cd/kg body weight), and blood for hematological examinations was sampled at 1 and 5 days (Days 1 and 5) after the administrations. The counts of white blood cells showed dose-dependent increments in the 0.3 and 1.0 mg Cd/kg groups in Cd-MT-I and Cd-MT-II at Day 1, and returned to the normal levels at Day 5. The counts of platelets showed dose-dependent decrements in the three-doses groups of Cd-MT-I and Cd-MT-II at Day 1, and did a returning- and further increasing tendency at Day 5. The counts of red blood cells, values of hematocrit, hemoglobin, mean corpuscular volume, mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration, showed only slight and sporadic changes at Days 1 and 5. As to that thrombocytopenia and leukocytosis were dose-dependently brought by Cd-MTs and not by CdCl2, and as to that CdCl2 and Cd-MTs hardly affected erythrocytes regarding their counts, sizes, hemoglobin contents etc., etiological mechanism (s) remains to be explored. However, our findings should be clinically emphasized in relation to Itai-Itai disease and Cd-intoxication.

Animals↗
PubMed2002

PTHrP-producing tumor: squamous cell carcinoma of the liver accompanied by humoral hypercalcemia of malignancy, increased IL-6 and leukocytosis.

A 77-year-old man was admitted to our hospital showing symptoms of general fatigue and appetite loss. He had leukocytosis, thrombocytosis and hypercalcemia with elevated serum levels of parathyroid hormone related peptide (PTHrP) and interleukin-6 (IL-6). An increase in tumor markers SCC and CYFURA21-1 was observed. The liver contained a huge tumor, which was proved to be PTHrP producing squamous cell carcinoma by immuno-histochemical analysis. Since the tumor did not express IL-6, it was assumed to be induced by PTHrP in osteoblasts. This is the first report of PTHrP producing squamous cell carcinoma of the liver.

Aged↗
PubMed2006

Prognostic value of leukocytosis in acute coronary syndromes: the cinderella of the inflammatory markers.

In recent years, numerous studies have validated the role of inflammation in the pathogenesis of atherosclerosis. Several of such studies have produced compelling evidence that inflammation participates in both, the initiation and perpetuation of the atherosclerotic process. Furthermore, epidemiological observations have found basal white blood cell (WBC) count is strongly associated with future cardiovascular disease (CVD), highlighting the participation of leukocytes in the pathogenesis of the ischemic damage that occurred during an acute coronary event, in particularly during the acute myocardial infarction (MI). Fundamentally, an acute MI triggers a systemic response to a necrotic insult characterized by leukocytosis and acute-phase protein synthesis. In this setting, elevated WBC count plays a central role in the reparative process that takes place to replace the necrotic tissue for collagen. In addition to be a proxy for the intensity of the peri-infarction inflammatory response, recent evidence has also shown that an elevated WBC counts, measured during the acute phase of MI, to be associated with adverse outcomes. This relationship holds true even when adjusting for classical prognostic variables some of which are surrogates for the extension of the infarcted-area. WBC count prognostic value in absence of necrosis marker elevation (like unstable angina), however, remains unclear and controversial. Additionally, and essentially due to its simplicity, cost-effectiveness and wide availability, WBC count has drawn the attention of researchers as a potential stratification tool in acute coronary syndromes (ACS). However, a formal comparison is needed between WBC count with other inflammatory markers such high-sensitive C-reactive protein to fully characterize its diagnostic accuracy.

Biomarkers↗
PubMed2005

Peripheral total and differential leukocyte count in diabetic nephropathy: the relationship of plasma leptin to leukocytosis.

OBJECTIVE: Because of increasing evidence that white blood cells (WBCs) play a role in the development and progression of diabetes complications, this study aimed to investigate the relation of circulating total and differential leukocyte counts to nephropathy in patients with type 2 diabetes. Plasma leptin levels were also measured to investigate their role in peripheral leukocytosis. RESEARCH DESIGN AND METHODS: For this study, 1,480 subjects with type 2 diabetes who were enrolled in a disease management program were stratified according to urinary microalbumin and serum creatinine measurements. The total and differential leukocyte profiles of peripheral blood were measured and plasma leptin was examined by enzyme-linked immunosorbent assay. Demographic and potential metabolic confounding factors were analyzed with linear and logistic regression to calculate the effects of leukocyte count on diabetic nephropathy. RESULTS: The peripheral total WBC, monocyte, and neutrophil counts increased in parallel with the advancement of diabetic nephropathy. In contrast, the lymphocyte count decreased. When WBC counts were analyzed per quartile and as continuous variables after adjusting for age, sex, and other known risk factors with multiple regression analysis, peripheral total WBC, monocyte, neutrophil, and lymphocyte counts were independently and significantly associated with diabetic nephropathy. Plasma leptin levels increased in patients with nephropathy and correlated significantly with total WBC count (r = 0.194, P = 0.014). CONCLUSIONS: Because leukocytes are activated and secrete cytokines in the diabetic state and leptin stimulates leukocyte proliferation and differentiation, our results suggest that circulating leukocytes contribute to the development and progression of nephropathy, partially through the effects of leptin, in patients with type 2 diabetes.

Albuminuria↗
PubMed1981

Endotoxin dose-related leukocytosis in milk of guinea pigs.

Objectives were to determine minimum and maximum doses of Escherichia coli endotoxin that would stimulate leukocytosis in the mammary gland of the guinea pig. Endotoxin concentrations of .005, .05, .5, 5.0, and 50.0 microgram/ml in 1 ml were used to stimulate migration of polymorphonuclear leukocytes in milk of guinea pigs at five times (2, 4, 6, 8, and 12 h postinjection with endotoxin). There were three animals in each experimental group per endotoxin concentration. Each animal served as its own control by having sterile saline injected into one mammary gland and endotoxin into the other. A control group of three animals had no saline or endotoxin injected. Guinea pigs were milked with a modified milking apparatus. Leukocyte numbers in the uninjected mammary gland did not differ from those in saline injected glands. The difference in mean leukocyte numbers between saline injected and .005 microgram/ml endotoxin injected glands approached significance at 5%. There was no difference between mean numbers recruited by the 5.0 and 50.0 microgram/ml endotoxin doses at 4, 6, 8, and 12 h. The chemotactic effect and, therefore, the rate of polymorphonuclear leukocyte recruitment was maximal at the 5 microgram/ml endotoxin dose.

Animals↗
PubMed2003

Leukocytosis as an independent risk factor for cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

OBJECT: The identification of patients at an increased risk for cerebral vasospasm after subarachnoid hemorrhage (SAH) may allow for more aggressive treatment and improved patient outcomes. Note, however, that blood clot size on admission remains the only factor consistently demonstrated to increase the risk of cerebral vasospasm after SAH. The goal of this study was to assess whether clinical, radiographic, or serological variables could be used to identify patients at an increased risk for cerebral vasospasm. METHODS: A retrospective review was conducted in all patients with aneurysmal or spontaneous nonaneurysmal SAH who were admitted to the authors' institution between 1995 and 2001. Underlying vascular diseases (hypertension or chronic diabetes mellitus), Hunt and Hess and Fisher grades, patient age, aneurysm location, craniotomy compared with endovascular aneurysm stabilization, medications on admission, postoperative steroid agent use, and the occurrence of fever, hydrocephalus, or leukocytosis were assessed as predictors of vasospasm. Two hundred twenty-four patients were treated for SAH during the review period. One hundred one patients (45%) developed symptomatic vasospasm. Peak vasospasm occurred 5.8 +/- 3 days after SAH. There were four independent predictors of vasospasm: Fisher Grade 3 SAH (odds ratio [OR] 7.5, 95% confidence interval [CI] 3.5-15.8), peak serum leukocyte count (OR 1.09, 95% CI 1.02-1.16), rupture of a posterior cerebral artery (PCA) aneurysm (OR 0.05, 95% CI 0.01-0.41), and spontaneous nonaneurysmal SAH (OR 0.14, 95% CI 0.04-0.45). A serum leukocyte count greater than 15 x 10(9)/L was independently associated with a 3.3-fold increase in the likelihood of developing vasospasm (OR 3.33, 95% CI 1.74-6.38). CONCLUSIONS: During this 7-year period, spontaneous nonaneurysmal SAH and ruptured PCA aneurysms decreased the odds of developing vasospasm sevenfold and 20-fold, respectively. The presence of Fisher Grade 3 SAH on admission or a peak leukocyte count greater than 15 x 10(9)/L increased the odds of vasospasm sevenfold and threefold, respectively. Monitoring of the serum leukocyte count may allow for early diagnosis and treatment of vasospasm.

Aneurysm, Ruptured↗
PubMed2004

Murine gamma-herpesvirus-68-induced IL-12 contributes to the control of latent viral burden, but also contributes to viral-mediated leukocytosis.

Early IFN-alpha/beta production, followed by the development of a viral-specific CTL response, are critical factors in limiting the level of murine gamma-herpesvirus-68 (gammaHV-68) infection. Development of a long-lived CTL response requires T cell help, and these CTLs most likely function to limit the extent of infection following reactivation. The importance of IL-12 in the development and/or activity of Th1 cells and CTLs is well documented, and we investigated the kinetics and magnitude of gammaHV-68-induced IL-12 production. Following intranasal infection, IL-12 and IL-23 mRNA expression was up-regulated in lung and spleen and lung, respectively, followed by increased levels of IL-12p40 in lung homogenates and sera. Exposure of cultured macrophages or dendritic cells to gammaHV-68 induced secretion of IL-12, suggesting that these cells might be responsible for IL-12 production in vivo. gammaHV-68 infection of mice made genetically deficient in IL-12p40 expression (IL-12p40(-/-)) resulted in a leukocytosis and splenomegaly that was significantly less than that observed in syngeneic C57BL/6 mice. IL-12p40(-/-) mice showed increased levels of infectious virus in the lung, but only at day 9 postinfection. Increased levels of latent virus in the spleen at day 15 postinfection were also observed in IL-12p40(-/-) mice when compared with syngeneic C57BL/6 mice. An overall reduction in gammaHV-68-induced IFN-gamma production was observed in IL-12p40(-/-) mice, suggesting that most of the viral-induced IFN-gamma in C57BL/6 mice was IL-12 dependent. Taken together, these results suggest that gammaHV-68-induced IL-12 contributes to the pathophysiology of viral infection while also functioning to limit viral burden.

Acute Disease↗
PubMed1999

[B cell acute lymphocytic leukemia with marked leukocytosis and t(3;15)(q27;q2?2)].

We report on a 16-year-old boy with B cell acute lymphocytic leukemia presenting marked leukocytosis (388,000/microliter) and resistance to multidrug chemotherapy. Karyotypical analysis revealed a novel t(3;15)(q27;q2?2) chromosomal abnormality. Because 3q27 is known to be a locus of the bcl-6 gene, which is frequently involved in B cell malignancies, molecular biological analyses were performed. Although no rearrangement was detected in 5 genes including bcl-6 on 3q27 and 2 genes on 15q2, reverse transcriptase-polymerase chain reaction procedures detected relatively strong mRNA expression of the bcl-6, smrp, dvl3, and tpml genes. These results indicate that immature leukemic cells with CD10 and CD34 positivity and rearrangement of the T cell receptor beta gene may coexist with relatively mature subpopulations that are positive for CD19 and CD20 surface markers, bcl-6 expression, and rearrangement of the gene for immunoglobulin kappa.

Adolescent↗
PubMed2000

Leukocytosis is proportional to HELLP syndrome severity: evidence for an inflammatory form of preeclampsia.

BACKGROUND: We investigated the possibility that HELLP syndrome is in part a systemic inflammatory response. METHODS: We evaluated total white blood cell (WBC) counts of all patients with severe preeclampsia with and without HELLP syndrome admitted to our hospital between 1995 and 1997. Patients were grouped by diagnosis and timing of platelet nadir. Analysis of variance and regression analysis were used for data analysis. RESULTS: Of 177 patients, 91 had HELLP syndrome, and 86 had severe preeclampsia alone. The WBC counts were significantly higher in patients with HELLP syndrome (12.5 +/- .442 x 10(9)/L) than in patients with severe preeclampsia (10.3 +/- .288 x 10(9)/L). Regression analysis showed that platelet counts varied inversely with WBC counts. Also, patients with class I HELLP syndrome had significantly higher WBC counts than patients with other classes of HELLP syndrome. CONCLUSION: The finding of an association between increasing leukocytosis and worsening thrombocytopenia early in the course of HELLP syndrome supports the hypothesis that it may represent an inflammatory process.

Analysis of Variance↗
PubMed2000

[A case of adenocarcinoma complicated with massive leukocytosis and hypercalcemia].

A 66-year-old man was admitted to our hospital complaining of non-productive cough and low-grade fever. Chest X-ray examination revealed a mass shadow in the right hilum. Transbronchial lung biopsy of the tumor mass yielded a diagnosis of adenocarcinoma. Despite repeated chemotherapy using CDDP and VDS, metastasis to the right adrenal gland and right femur occurred, and was accompanied by hypercalcemia and hypophosphatemia. Serological study revealed elevated levels of PTH-rP and G-CSF. Six months after adenocarcinoma was diagnosed, multiple skin metastases of the cancer were observed. Immunohistochemical staining for PTH-rP and G-CSF indicated that production of cytokines had caused a paraneoplastic syndrome including hypercalcemia and leukocytosis. It appeared that the elevation of G-CSF was induced by IL-6 produced from PTH-rP in cancer tissue. Documentation of similar cases is required.

Adenocarcinoma↗
PubMed1975

Pseudohyperkalemia and extreme leukocytosis.

Two patients with chronic lymphocytic leukemia and pseudolhyperkalemia are described. Both patients had white blood cell counts exceeding 600,000 per cubic millimeter. Routine determinations of serum potassium were elevated while normal values were obtained when plasma and serum were separated within 30 minutes of venipuncture. Incubation of clotted and heparinized specimens for 6 hours was accompanied by a marked increase of potassium levels. This study indicates that extreme leukocytosis alone can give rise to apparent hyperkalemiamtrue values can be obtained if the determinations are performed quickly after venipuncture.

Aged↗
PubMed1999

The relationship between the levels of granulocyte colony-stimulating factor and leukocytosis induced by all-trans retinoic acid in acute promyelocytic leukemia.

OBJECTIVE: To explore the mechanism of leukocytosis. METHODS: Enzyme linked immunosorbent assay (ELISA) method was used for detecting levels of serum granulocyte colony-stimulating factor (G-CSF) in 47 cases of acute promyelocytic leukemia (APL) during the treatment with all-trans retinoic acid (ATRA). RESULTS: The peak of increased serum G-CSF level occurred on the 9th day, and WBC number was the highest on the 11th day. After ATRA treatment, both serum G-CSF level and WBC number increased in 68.1% of the cases. In 19.2% of the cases treated, serum G-CSF level was increased but without obvious change in WBC number, and the reverse was true in 12.7% of the cases. CONCLUSION: Serum G-CSF level was statistically correlated to the number of WBC, promyelocytes and its late stage by Spearman's rank-order correlation coefficient.

Adolescent↗
PubMed2002

Leflunomide induced fevers, thrombocytosis, and leukocytosis in a patient with relapsing polychondritis.

The most common adverse events reported with the use of leflunomide are hypertension, infections, alopecia, and various gastrointestinal complaints. No fatal adverse hematologic events have been reported in humans, although anemia and leukopenia have been described in animals receiving 20 mg/kg/day. We describe a patient with relapsing polychondritis, in whom treatment failure with glucocorticoids, methotrexate, hydroxychloroquine, and azathioprine led to the institution of therapy with leflunomide at a maintenance dose of 20 mg/day. Two months after the dose of leflunomide had been increased to 30 mg daily, the patient developed high fevers, photophobia, thrombocytosis, and leukocytosis that returned to normal following treatment with cholestyramine and discontinuation of leflunomide. Rechallenge with leflunomide was not attempted and the syndrome did not recur during 14 month followup.

Anti-Inflammatory Agents↗
PubMed1977

Leukemic reticuloendotheliosis: "hairy cell leukemia," functional and structural features of the abnormal cell in a patient with profound leukocytosis.

The development of profound leukocytosis in a patient with leukemic reticuloendotheliosis (LRE) enabled us to obtain purified LRE cells for the investigation of their structural and functional characteristics. The LRE cells of our patient bore surface immunoglobulin and had complement receptors but did not bear Fc receptors and did not form rosettes with sheep erythrocytes. By electron microscopy, the cells were observed to contain typical ribosome lamella structures and to phagocytize both 0.81 micron latex particles and complement-coated zymosan particles. They were adherent to both glass and nylon wool fibers. The mitogenic response to erythroagglutinating phytohemagglutinin was normal to magnitude but delayed chronologically. The binding of 125I-labeled plant lectins was used to characterize the surface topography of LRE cells. Results of these studies indicated that the LRE cell surface differed significantly from the surface of normal T and B lymphocytes and chronic lymphatic leukemia cells. The LRE cells were capable of both stimulating and responding in a one-way mixed lymphocyte culture. However, the LRE cells were not active as effector cells of either cell-mediated lympholysis, a T cell function, or antibody-dependent cellular cytotoxicity, a null cell function. In contrast, they were effector cells of lectin-induced cellular cytotoxicity showing that they did possess the capacity to function as cytotoxic effector cells. These data indicated that the LRE cells in our patient had surface and functional characteristics of both lymphocytes and monocytes.

Binding Sites↗
PubMed1992

Paraneoplastic leukocytosis associated with a rectal adenomatous polyp in a dog.

A dog with a rectal adenomatous polyp had extreme neutrophilic leukocytosis, monocytosis, and eosinophilia consistent with a paraneoplastic syndrome. Resolution of the leukogram abnormalities after tumor excision supported this belief. Except for a lack of circulating myeloblasts, the dog had leukogram findings consistent with a neutrophilic leukemoid reaction.

Animals↗
PubMed2004

[A case of large-cell lung cancer with marked leukocytosis successfully treated with chemoradiotherapy].

A 45-year-old woman was transferred to our hospital for further examination of a persistent fever, marked leukocytosis and abnormal shadow on chest CT scan. At the time of admission, her leukocyte count was 48,800/microliter and her chest CT scan showed a solitary nodule in the right upper lobe with hilar and mediastinal lymphadenopathy. A US-guided biopsy revealed a large-cell carcinoma. She was given radiation (total 60 Gy) and 4 courses of chemotherapy with paclitaxel (150 mg/m2) in combination with carboplatin (AUC = 5). The primary tumor and swollen lymph nodes disappeared and leukocyte count normalized. Although 3 years have passed, no recurrence has been observed.

Antineoplastic Combined Chemotherapy Protocols↗