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At least 19 recordsLinked to original sources
PubMed1981

Prednisone-induced leukocytosis. Influence of dosage, method and duration of administration on the degree of leukocytosis.

The long-term pattern of prednisone-induced leukocytosis was examined in 80 patients. Our results disclosed an extremely variable leukocytic responses, in which the white blood cell count surpassed 20,000/mm3 as early as the first day of treatment, an increase that persisted for the duration of therapy. Although the degree of leukocytosis was related to the dosage administered, it did appear sooner with higher doses. Leukocytosis reached maximal values within two weeks in most cases, after which the white blood cell count decreased, albeit not to pretreatment levels. The leukocytosis was attributed predominantly to a rise in the polymorphonuclear white blood cells, a phenomenon that coincided with monocytosis, eosinopenia and a variable degree of lymphopenia. It can be concluded that even small doses of prednisone, administered over a prolonged period of time, can induce extreme and persistent leukocytosis. This observation is of consequence especially when infection is suspected, particularly in an immunocompromised host. However, a shift to the left in the peripheral white blood cells, i.e., more than 6 percent band forms, and the appearance of toxic granulation may assist in the differential diagnosis between infection, in which the latter are observed, and corticosteroid-induced leukocytosis, in which they are rare.

Dose-Response Relationship, Drug↗
PubMed1992

Histamine leukocytosis. II. Source of histamine leukocytosis.

Leukocytes were labelled by intravenous injection of tritiated thymidine (3H-thymidine) in dogs to discover the source of the increased number of neutrophils in the circulating blood after injection of histamine in beeswax. Dogs with normal hemograms were given 1.0 mCi/kg of 3H-thymidine alone, and in different sequences, with histamine in beeswax. When 3H-thymidine was given during maintained histamine leukocytosis, labelled granulocytes appeared in and disappeared from the blood earlier than in control tests and the number of labelled cells was greater in the histamine-treated animals. Administration of histamine in beeswax 3 days after injection of 3H-thymidine also induced the premature appearance and disappearance of labelled neutrophils in the circulating blood. It was concluded that leukocytosis induced by the chronic action of histamine is due to 1) stimulated proliferation and differentiation of neutrophil precursor cells in the bone marrow and 2) the release of mature leukocytes from the bone marrow.

Animals↗
PubMed1998

Causes of leukocytosis in liver transplant recipients: relevance in clinical practice.

BACKGROUND: Leukocytosis without a recognizable etiology often poses a diagnostic and therapeutic dilemma in transplant recipients. METHODS: Fifty consecutive episodes of leukocytosis in 47 liver transplant recipients were prospectively assessed. RESULTS: Leukocytosis was documented in 70% (33/47) of the patients, whereas 30% (14/47) of the patients never developed leukocytosis. Three distinctive etiologies accounted for 82% of the episodes. Thirty-two percent (16/50) of the episodes occurred between 1 and 3 days after transplantation, were unaccompanied by fever, and resolved spontaneously within 2 days. Infections accounted for 28% (14/50) of the episodes of leukocytosis; median time to onset was 25 days after transplantation, and fever occurred in 57%. In 22% (11/50) of the episodes, a characteristic leukocytosis occurred 7-14 days after transplantation (in the absence of documented infections or rejection) that was unaccompanied by fever, and resolved spontaneously without antibiotics; the platelet count of these patients was significantly higher than those of postoperative (P < 0.01) or infectious leukocytosis (P < 0.05). Resolution of pretransplant hypersplenism, with the release of sequestered splenic granulocytes and platelets, was the likely cause. Rejection and corticosteroid boluses accounted for 4% and 8% of the episodes, respectively. CONCLUSIONS: Timing of onset and awareness of the patterns of leukocytosis can be valuable in the evaluation of posttransplant leukocytosis. Stable patients with leukocytosis, but without fever or documented infections, in the immediate postoperative period and between 7 and 14 days after transplantation, need not be empirically treated with antibiotics.

Adult↗
PubMed1990

[Studies on the pathophysiology of paraneoplastic syndromes: both cancer cells and host immune cells are responsible for the pathophysiology of leukocytosis associated with oral cancer].

Leukocytosis associated with malignant disease has been known as a paraneoplastic syndrome and occurs occasionally in patients with oral malignancies. In this study, mechanisms underlying leukocytosis associated with malignancy was investigated, using a squamous cell carcinoma of the maxilla from a patient who manifested marked leukocytosis. When the patient's tumor was inoculated into nude mice, it formed squamous cell carcinoma (MH85) and induced leukocytosis and splenomegaly. Leukocytosis and splenomegaly paralleled tumor growth. Surgical excision of MH85 tumor resulted in a dramatic reduction of leukocyte count and spleen weight, indicating an involvement of humoral mediators released by MH85. MH85 cells conditioned medium (MH85CM) were shown to contain granulocyte-colony stimulating factor (G-CSF) activity, which is a potent growth factor specific for granulocytes. These results suggest G-CSF or G-CSF like substance secreted by MH85 cells is responsible for leukocytosis in MH85 bearing nude mice (MH85 mice) and in the patient. MH85 cell growth was stimulated by G-CSF and inhibited by anti-G-CSF antibody, thus suggesting that G-CSF like substance is a autocrine growth factor for MH85 cells. Splenectomized MH85 mice developed less severe leukocytosis than did non-splenectomized mice. This finding indicated that not only G-CSF like substance secreted by MH85 cells but other humoral factors released by the hyperplastic spleen contribute to the development of leukocytosis. Splenic monocytes derived from MH85 mice and MH85CM-stimulated splenic monocytes showed increased secretion of tumor necrosis factor (TNF) and interleukin-1 (IL-1), both of which have been reported to induce neutrophilia in animals. Moreover, injection of anti-TNF-antibody into neutrophilic MH85 mice significantly, although not completely, decreased leukocyte count. Thus, it seemed likely that increased secretion of TNF and IL-1 by spleen cells that are stimulated by humoral factors released from MH85 also contributes to the progression of leukocytosis. In splenectomized mice, enlargement of MH85 tumor was retarded and metastases were impaired compared these in nonsplenectomized mice. Coculture of splenocytes from MH85 mice with normal spleen cells, inhibited blastogenesis in response to mitogen. The result suggests that splenocytes from MH85 mice played as immune suppressive cells. MH85CM conferred immune suppressive activity on normal spleen cells. This suppressor cell-inducing factor (SCIF) in MH85CM was found to have an apparent molecular weight of approximately 25kd, and its biological activity was neutralized by anti-G-CSF antibody. Therefore, SCIF secreted by MH85 cells was likely to be G-CSF like substance.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Leukocytosis in non hematological malignancies--a possible tumor-associated marker.

Leukocytosis (WBC counts 10,000/mm3) was detected in 77 out of 252 patients (30%) with ten different types of nonhematological malignancy (NHM) at the time of diagnosis. A full search including serological and bacteriological screening was performed to exclude other possible causes of leukocytosis. Among the different tumors, carcinomas of the lung and colorectum were the most prevalently associated with leukocytosis. Absolute monocytosis was found in 25% of the patients and absolute eosinophilia in only 4.8%. The leukocytosis was attributed mainly to an increase in the mature polymorphonuclears, suggesting a release mechanism of WBC from storage pools by factors secreted or induced by the tumor. Neither the age nor the sex of the patients affected the incidence or magnitude of leukocytosis. However, the presence of metastases was associated with a significantly higher incidence of leukocytosis (p less than 0.05). The associated leukocytosis may be regarded as a poor prognostic sign, and was associated with a significantly (p less than 0.007) shorter survival time. In contrast, absolute lymphocytosis may have a positive effect on the survival time (p = 0.01). Tumor-associated leukocytosis may be an additional tumor-associated marker, of value in assessing and monitoring patients with NHMs.

Female↗
PubMed2000

Effect of leukocytosis at initial examination on prognosis in patients with primary unstable angina.

BACKGROUND: Leukocytosis with acute myocardial infarction at initial examination predicts adverse prognosis, but it is unknown whether it predicts outcome in patients with primary unstable angina. METHODS AND RESULTS: We studied 414 consecutive patients with unstable angina admitted through the emergency department to telemetry and intensive care units of an urban academic hospital. To study primary unstable angina, we excluded 134 patients with precipitants (eg, urosepsis, pneumonia) that may cause leukocytosis. Of 280 patients, 96 (34%) had leukocytosis (leukocyte count >10,000 per microL) at initial examination. A total of 30 patients (11%) died and 47 (17%) died or had nonfatal myocardial infarction within 12 months of initial examination. In a univariate Cox model, patients with leukocytosis had a hazard ratio (HR) of 2.6 (95% confidence interval [CI] 1.3-5.4) for death by 1 year. In a multivariate Cox model the only significant predictors of 1-year death were congestive heart failure at initial examination (HR 7.8; 95% CI 2.8-22) and elevated creatinine (HR 2.7; 95% CI 1.3-5.7); in this model, the relation between leukocytosis and prognosis was markedly attenuated (HR 1.4; 95% CI 0.6-2.9). The adjusted HR for leukocytosis was 1.3 (95% CI 0. 7-2.3) for death or nonfatal MI by 1 year. CONCLUSIONS: Leukocytosis at initial examination is associated with adverse prognosis in patients with primary unstable angina. However, the association is confounded by other important predictors of prognosis. Leukocytosis may be a marker of stress associated with more severe cases of unstable angina or comorbid conditions.

Adult↗
PubMed2003

Clostridium difficile infection in patients with unexplained leukocytosis.

PURPOSE: To determine whether unrecognized Clostridium difficile infection is responsible for a substantial proportion of cases of unexplained leukocytosis in a tertiary care hospital setting. METHODS: We prospectively identified 60 patients who had unexplained leukocytosis (white blood cell count > or =15,000/mm3). Fecal specimens were tested for C. difficile toxin using an enzyme immunosorbent assay. We compared the clinical features of patients who had positive or negative assay results, as well as of 26 hospitalized control patients who did not have unexplained leukocytosis. RESULTS: Thirty-five (58%) of the patients with unexplained leukocytosis had C. difficile toxin in at least one fecal specimen as compared with 3 (12%) of the controls (P <0.001). Symptoms of colitis were often mild or absent at the time the white blood cell count was first elevated or, if present, had not been recognized by the attending physicians. Leukocytosis resolved promptly in most patients who were treated with metronidazole. In the 25 patients (42%) who had a negative test for C. difficile toxin, leukocytosis also tended to resolve during empiric therapy with metronidazole; some of these patients may have had C. difficile infection. CONCLUSION: The majority of patients in our hospital who had unexplained leukocytosis had C. difficile infection. Unexplained leukocytosis in hospitalized patients should prompt a search for symptoms and signs consistent with C. difficile infection and a study to detect C. difficile. Empiric therapy with metronidazole may be effective in the appropriate epidemiologic setting.

Anti-Infective Agents↗
PubMed2000

Implications of asymptomatic endocervical leukocytosis in infertility.

Genital tract infection is a known cause of male and female infertility. In this retrospective study, we investigated the effect of treatment of asymptomatic cervical leukocytosis on pregnancy rates. Twenty-five infertile women with asymptomatic cervical leukocytosis received broad-spectrum antibiotic treatment (100 mg doxycycline, 200 mg ofloxacin, and 500 mg metronidazole twice a day for 7-10 days). Pregnancy rates and resolution of leukocytosis were evaluated 6 months after treatment. Eleven patients (44%) had persistent cervical leukocytosis and 16 (64%) had become pregnant within 6 months after treatment. Successful treatment of cervical leukocytosis resulted in an increase in the pregnancy rate: 13 of the 14 patients (93%) who were cured of leukocytosis became pregnant, while 3 of the 11 (27%) who did not become pregnant were cured (p = 0.002). Patients who did not achieve pregnancy were older (p = 0. 002) than those who did. Patients who were not cured were also older than those who were (p = 0.014). Our findings suggest that the treatment for cervical leukocytosis is less effective for older patients than for younger patients. However, treatment of asymptomatic cervical leukocytosis appears to help preserve the fertility of patients with this disease.

Anti-Bacterial Agents↗
PubMed2000

Leukocytosis and the retinoic acid syndrome in patients with acute promyelocytic leukemia treated with arsenic trioxide.

PURPOSE: Arsenic trioxide, like all-trans-retinoic acid (RA), induces differentiation of acute promyelocytic leukemia (APL) cells in vivo. Treatment of APL patients with all-trans RA is commonly associated with leukocytosis, and approximately 50% of patients develop the RA syndrome. We reviewed our clinical experience with arsenic trioxide to determine the incidence of these two phenomena. PATIENTS AND METHODS: Twenty-six patients with relapsed or refractory APL were treated with arsenic trioxide for remission induction at daily doses that ranged from 0.06 to 0.17 mg/kg. RESULTS: Twenty-three patients (88%) achieved complete remission. Leukocytosis was observed in 15 patients (58%). The median baseline leukocyte count for patients with leukocytosis was 3,900 cells/microL (range, 1,200 to 72,300 cells/microL), which was higher than that for patients who did not develop leukocytosis (2,100 cells/microL; range, 500 to 5,400 cells/microL; P =.01). No other cytotoxic therapy was administered, and the leukocytosis resolved in all cases. The RA syndrome was observed in eight patients (31%). Patients who developed leukocytosis were significantly more likely to develop the RA syndrome (P <.001), and no patient without a peak leukocyte count greater than 10,000 cells/microL developed the syndrome. Among the patients with leukocytosis, there was no observed relation between the leukocyte peak and the probability of developing the syndrome (P =.37). CONCLUSION: Induction therapy of APL with all-trans RA and arsenic trioxide is associated with leukocytosis and the RA syndrome. These clinical effects seem to be intrinsically related to the biologic responsiveness and the differentiation process induced by these new agents.

Antineoplastic Agents↗
PubMed2001

Correlation between leukocytosis and necropsy findings in dogs with immune-mediated hemolytic anemia: 34 cases (1994-1999).

OBJECTIVE: To determine whether severity of leukocytosis correlates with severity of postmortem lesions in dogs with immune-mediated hemolytic anemia (IMHA). DESIGN: Retrospective study. ANIMALS: 34 dogs with IMHA that had CBC performed within 48 hours prior to death and complete necropsy examinations. PROCEDURE: Dogs were independently assigned to 4 leukocytosis groups (within reference range; mild leukocytosis, moderate leukocytosis, marked leukocytosis) and 3 lesion severity groups (mild lesions, moderate lesions, severe lesions). RESULTS: Moderate to marked leukocytosis correlated with moderate to severe postmortem lesions. Ischemic necrosis within liver, kidney, heart, lung, and spleen attributable to thromboembolic disease or anemic hypoxia were the most common important lesions found at necropsy. None of the dogs with mild lesions had moderate or marked leukocytosis. Four of 14 severely affected dogs had WBC counts within reference range, but all 4 had neutrophilic left shifts. Three of these 4 dogs had toxic change in neutrophils. CONCLUSION AND CLINICAL RELEVANCE: Moderate to marked leukocytosis, neutrophilic left shift, and toxic change in neutrophils in dogs with IMHA should alert clinicians to the potential for moderate to severe tissue injury, which could complicate treatment and worsen prognosis. Lesions appear to be secondary to anemic hypoxia, thromboembolic disease, or both; therefore, treatment objectives should focus on improving blood oxygen-carrying capacity and monitoring for thromboembolic disease.

Anemia, Hemolytic, Autoimmune↗
PubMed1996

Presence of fever and leukocytosis in acute cholecystitis.

STUDY OBJECTIVE: To determine the frequency of fever and leukocytosis in patients presenting to the emergency department with acute cholecystitis (AC). METHODS: We carried out a retrospective review of charts from 1990 to 1993 at a university-affiliated hospital. Our subjects were ED patients with hepato-iminodiacetic acid (HIDA) scans interpreted as showing AC and who had undergone cholecystectomy during hospitalization. Final diagnosis was determined on the basis of the pathology report. Fever was defined as an oral temperature of 100 degrees F (37.7 degrees C) or greater or a rectal temperature of 100.4 degrees F (38.0 degrees C) or greater. Leukocytosis was defined as a WBC count of 11,000/mm3 or greater. RESULTS: Of the 198 cases studied, the pathologic diagnosis of nongangrenous AC was made in 103 (52%), gangrenous AC was diagnosed in 51 (26%), and chronic cholecystitis was diagnosed in 44 (22%). In patients with nongangrenous AC, 71% were afebrile, 32% lacked leukocytosis, and 28% lacked fever and leukocytosis. In patients with gangrenous AC, 59% were afebrile, 27% lacked leukocytosis, and 16% lacked fever and leukocytosis. CONCLUSION: We found that patients with AC diagnosed in the ED frequently lacked fever or leukocytosis. The clinician should not rely on the presence of these signs in making the diagnosis of acute cholecystitis.

Acute Disease↗
PubMedDate not supplied

Leukocytosis in rabbits with diet-induced atherosclerosis.

In cholesterol-fed rabbits the extent of monocyte involvement in atherogenesis may be influenced by the level of circulating leukocytes during hypercholesterolemia. We characterized the leukocytosis in rabbits fed either a 0.25% or a 0.1% cholesterol-enriched diet (0.25% or 0.1% rabbits, respectively). Circulating leukocytes were elevated by 1 week of feeding, and the elevation was sustained for at least 30 weeks. Differential counts were unchanged. Immature leukocytes were not seen, indicating that the leukocytosis was not due to premature release of bone marrow cells. Animals were free of bacterial or parasitic disease; selected rabbits with leukocytosis had normal body temperatures. Spleen weights averaged at least 100% higher in 0.25% rabbits but did not show histological evidence for hematopoiesis that could account for the leukocytosis. At approximately 22 weeks there was a second rise in leukocytosis in bilirubinemic 0.25% rabbits, suggesting that in the late stages of hypercholesterolemia, leukocytosis is related to liver failure. Cholesterol-fed rabbits also showed thrombocytosis. Existing leukocytosis and hypercholesterolemia were reversed to pretreatment levels by switching the rabbits to chow diets. In bone marrow from 0.25% rabbits, the mean number of cells per gram was greater (p less than 0.05) than that from normocholesterolemic rabbits. In 0.25% rabbits, the fraction of blood mononuclear cells showing phagocytosis of immunoglobulin G-coated red blood cells did not differ from that of controls, suggesting an unchanged population of these cells with regard to Fc and phagocytic function during hypercholesterolemia. These data suggest an effect (direct or indirect) of hypercholesterolemia on the production of leukocytes in the bone marrow and/or on the circulation kinetics of leukocytes in the blood.

Animals↗
PubMed1999

Leukocytosis in acute pulmonary embolism.

PURPOSE: The purpose of this investigation is to assess the level of leukocytosis in acute pulmonary embolism (PE). BACKGROUND: Limited data exist regarding leukocytosis in acute PE. One reason that the prevalence of leukocytosis in acute PE is unknown, despite an extensive number of investigations of PE, may relate to the fact that acute PE is usually associated with other conditions that themselves may cause leukocytosis. METHODS: Hospital records of 386 patients with a diagnosis of acute PE were reviewed retrospectively. Patients with no other possible or definite cause of leukocytosis were analyzed separately. A diagnosis of PE was made by a high-probability interpretation of the ventilation/perfusion lung scan or pulmonary angiogram. RESULTS: Among patients with PE in whom other possible or defined causes for leukocytosis were eliminated, 52 of 266 (20%) had a WBC count > 10,000/mm3. None had a WBC count that was > or = 20,000/mm3. Patients with the pulmonary hemorrhage/infarction syndrome had an increased WBC count in 32 of 183 (17%) vs 20 of 83 (24%) in patients who did not have pulmonary hemorrhage/infarction syndrome (not significant). CONCLUSION: A modest leukocytosis may accompany (and possibly be caused by) PE. Its presence should not dissuade the clinician from objectively pursuing the diagnosis of PE.

Acute Disease↗
PubMed1991

Frequency of the hypercalcemia-leukocytosis syndrome in oral malignancies.

There have been a number of reports over the last 15 years of patients with cancer who develop both leukocytosis and hypercalcemia, particularly in patients with cancers of the oral cavity. In this study, the authors report the frequency of hypercalcemia and leukocytosis in 225 patients with oral malignancies. Ten patients (4.4%) had hypercalcemia, 11 patients (4.9%) had leukocytosis, and five (2.2%) had both hypercalcemia and leukocytosis. The occurrence of these two distinct paraneoplastic syndromes in the same patients was greater than could have been expected from chance alone (chi-square = 45.8, P less than 0.0001). This study demonstrates that although hypercalcemia and leukocytosis are relatively uncommon in oral cancers, when they do occur they are frequently associated. To the knowledge of the authors, this is the first report in which the frequency of the association hypercalcemia and leukocytosis is studied in detail in large numbers of patients with oral cancer.

Adenocarcinoma↗