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PubMed1995

Squamous cell carcinoma of the ureter with marked leukocytosis producing granulocyte colony-stimulating factor.

This paper describes a case of squamous cell carcinoma (SCC) of the ureter which showed marked leukocytosis without any evidence of infection and hematologic malignancies. The level of serum granulocyte colony-stimulating factor (G-CSF) assayed by enzyme immunoassay increased and the immunohistochemical staining of the ureter tumor showed the presence of G-CSF in tumor cells. These findings indicate that SCC of the ureter produced G-CSF which stimulated leukocyte production in bone marrow and resulted in leukocytosis. To our knowledge, this is the first report of ureter tumor with leukocytosis producing G-CSF.

Aged↗
PubMed1991

Occurrence of hypercalcemia and leukocytosis with cachexia in a human squamous cell carcinoma of the maxilla in athymic nude mice: a novel experimental model of three concomitant paraneoplastic syndromes.

Hypercalcemia and leukocytosis may occur in conjunction as paraneoplastic syndromes associated with malignant disease. Here we describe a human squamous cell carcinoma of the maxilla that was associated with hypercalcemia and leukocytosis, and also cachexia. The primary tumor was surgically removed and established in permanent cell culture. When either primary tumors or cultured tumor cells were inoculated into nude mice, the nude mice developed the same paraneoplastic syndromes as those which occurred in the patient from whom the tumor was originally derived. The plasma calcium was increased two and one-half-fold and the WBC count 30-fold, and the body weight was decreased by 45% in tumor-bearing animals. Each of these paraneoplastic syndromes was alleviated by surgical excision of the tumor, indicating that the paraneoplastic syndromes were due to a factor or factors produced by the primary tumor. The development of each of these paraneoplastic syndromes in nude mice correlated positively with the other two syndromes. We examined the organs of tumor-bearing mice and found striking histopathologic abnormalities in the bones, spleen, and liver, but no infiltration with tumor cells. The bones showed marked evidence of osteoclastic bone resorption. This model of a human tumor associated with the hypercalcemia-leukocytosis paraneoplastic syndrome, together with cachexia, should make it possible to determine the mechanisms responsible for these paraneoplastic syndromes and their relationship to each other.

Animals↗
PubMed1975

Accelerated host metabolism of L-thyroxine during acute infection: role of the leukocyte and peripheral leukocytosis.

Metabolism of thyroid hormones is accelerated during acute infection in man and in experimental animals. The pathogenetic mechanisms mediating this phenomenon are uncertain, but activated leukocytes of the infected host have been implicated as potentially important sites of hormone degradation. The present studies were conducted in an attempt to assess the in vivo contribution of leukocytes and peripheral leukocytosis to the enhancement of L-thyroxine (T4) clearance seen during infection, and to evaluate further the possible roles of fever and of changes in the extracellular binding of T4. In 10 rhesus monkeys inoculated with virulent yellow fever (YF) virus, peripheral disposal of T4 was significantly accelerated (2-fold) during the febrile phase of the illness. This experimental viral infection was not accompanied by neutrophilic leukocytosis nor by detectable changes in serum free T4 levels, suggesting that neither an increased circulating neutrophil mass nor diminished extracellular binding of T4 contributed appreciably to the increase in metabolism of T4. A pathogenetic role for fever in the enhancement of T4 degradation was not specifically excluded in these infected monkeys. However, the failure of T4 turnover to increase during other febrile infections, such as that which followed inoculation of monkeys with Venezuelan equine encephalitis virus, indicates that the acceleration of peripheral disposal of T4 seen in infection is not a simple concomitant of fever. In monkeys with bacterial sepsis and in those inoculated iv with zymosan particles, T4 turnover was similarly accelerated in the absence of detectable changes in serum free T4 levels, suggesting a pathogenetic role for enhances cellular uptake and metabolism of hormone. However, in these monkeys deiodination of T4 by leukocytes did not appear to account for the increase in T4 disposal. During sepsis and following zymosan administration, T4 turnover was markedly increased in both intact monkeys with a neutrophilic leukocytosis and in those with irradiation-induced neutropenia. Therefore, the cellular sites of increased T4 degradation during infection remain uncertain. Fixed tissue macrophages serve as the major site of clearance of YF virus, circulating bacteria and zymosan particles. Accordingly, a relationship between activation of these phagocytic cells and the acceleration of T4 metabolism seemed possible but was not established by our studies.

Acute Disease↗
PubMedDate not supplied

A case of a gallbladder cancer with marked hypercalcemia and leukocytosis.

Hypercalcemia and leukocytosis of malignancy have been highlighted over a decade. We report a case of a gallbladder cancer with marked hypercalcemia and leukocytosis. A 54-year-old woman was admitted to the hospital because of remittent fever and left hypochondric pain. The computed tomographic scan of the abdomen revealed the cancer of the gallbladder with liver metastases. The patient's medical condition deteriorated as the tumor was rapidly growing up. Her medical course was marked by hypercalcemia and an increase in mature neutrophils. Medical therapy with normal saline, furosemide, indomethacin, prednisolone, and calcitonin failed to ameliorate hypercalcemia. On the twenty-ninth hospital day the serum calcium was elevated to 17.6 mg/dl which responded to 1000 micrograms of mithramycin while leucocytosis continued. Despite the chemotherapy with doxorubicin and tegafur, the tumor continued to grow. Leukocytosis was attributed to the elevated colony-stimulating factor activity which was two-fold of control. The parathyroid hormone and nephrogeneous cyclic AMP levels were normal with low vitamin D levels. Hypercalcemia was attributed to a parathyroid hormone-like substance because of a decrease in %TRP in the presence of normal renal function and the normal parathyroid hormone level. Autopsy revealed an undifferentiated adenocarcinoma of the gallbladder with multiple liver metastases, and bone resorption in the vertebral column and sternum without evident bone metastasis.

Adenocarcinoma↗
PubMed1996

[An autopsy case of systemic lupus erythematosus complicating leukocytosis, amegakaryocytic thrombocytopenia, interstitial pneumonitis, and pleulitis].

A 52-year-old female was admitted to our hospital in August 1988, for evaluation of purpura and gingival bleeding. Hematologic examination showed mild leukocytosis (12,400/microliter) and severe thrombocytopenia (1,000/microliter). On bone marrow examination, megakaryocyte count was normal and the number of myeloblasts was increased (7.2%). Serological examination was positive for anti-nuclear antibody and anti-DNA antibody. She was diagnosed as having idiopathic or autoimmune thrombocytopenia, and received thrombocyte transfusion and gamma-globulin administration. Hematologic values improved temporarily, but leukocytosis and thrombocytopenia recurred. On the 22nd hospital day, leukocytes increased to 49,300/microliter and thrombocytes decreased to 10,000/microliter. Bone marrow myeloblasts were also increased to 18.8%, and she was suspected of having myelodysplastic syndrome. Then, hematologic values improved simultaneously, and she was discharged in November 1988. After the discharge, leukocyte count ranged from 6,000 to 16,500/microliter, but the number of bone marrow myeloblasts was normal. However, transient thrombocytopenia appeared in association with decrease or absence of bone marrow megakaryocytes and rise of platelet associated-IgG, (PA-IgG) to 99.6 ng/10(7) cells. From September to December 1989, she complained of fever, morning stiffness, multiple arthralgia, and oral ulcer. On serological findings, she was positive for LE cell. Therefore, she was diagnosed as having systemic lupus erythematosus (SLE). In January 1990, she had a high grade fever and dyspnea. Bilateral pleuritis and interstitial pneumonitis were shown on the chest roentgenogram. She received gamma-globulin administration, methylprednisolone pulse therapy, and mechanical ventilation. However, hypoxia developed rapidly, and she died of respiratory failure. Autopsy revealed severe interstitial pneumonitis, fibrinous pleuritis, fibrinous pericarditis, and vasculitis in the arcuate artery of the kidney. This is the first report of SLE complicating thrombocytopenia associated with decrease of megakaryocytes and rise of the PA-IgG, and severe leukocytosis associated with increased bone marrow myeloblasts.

Fatal Outcome↗
PubMed1994

Erythropoietin-independent colonies of red blood cells and leukocytosis in a worker exposed to low levels of benzene.

BACKGROUND: Exposure to high levels of benzene commonly results in the suppression of hemopoiesis, although cases of leukocytosis and leukocytosis with thrombocytosis have been reported. No hematologic abnormalities have generally been found with exposure to low levels of benzene. METHODS: A pipe fitter exposed to low levels of benzene (time-weighted average 0.9 ppm) developed leukocytosis. His blood counts and growth of erythroid burst forming units (BFU-E) was followed with and without the addition of erythropoietin. RESULTS: Erythropoietin-independent BFU-E colonies were increased to 40 per 4 x 10(4) cells (normal < 3 per 4 x 10(4) cells). Both the leukocyte count and the number of erythropoietin-independent BFU-E colonies decreased when exposure to benzene was terminated. On reexposure the white blood count again increased. After the work was terminated, the white blood count returned to normal, as did the number of erythropoietin-independent BFU-E colonies, over a period of 12 months. CONCLUSIONS: Our findings suggest that even low levels of benzene can result in perturbations of the hemopoietic system. Further studies are warranted to determine whether these findings are idiosyncratic, coincidental, or a more general phenomenon.

Adult↗
PubMed1975

Leukocytosis and fibrinolytic activity of the blood in leukemic patients.

The relation between the levels of leukemic leukocytosis and blood fibrinolytic activity was studied in 58 patients with acute leukemia, 58 with chronic granulocytic leukemia, and 60 with chronic lymphocytic leukemia. In all these groups, high levels of leukemic leukocytosis were associated with increased blood fibrinolytic activity. Differences between patients with high and low values of leukocytosis were statistically significant.

Adult↗
PubMed2000

Leukocytosis: basics of clinical assessment.

Leukocytosis, a common laboratory finding, is most often due to relatively benign conditions (infections or inflammatory processes). Much less common but more serious causes include primary bone marrow disorders. The normal reaction of bone marrow to infection or inflammation leads to an increase in the number of white blood cells, predominantly polymorphonuclear leukocytes and less mature cell forms (the "left shift"). Physical stress (e.g., from seizures, anesthesia or overexertion) and emotional stress can also elevate white blood cell counts. Medications commonly associated with leukocytosis include corticosteroids, lithium and beta agonists. Increased eosinophil or basophil counts, resulting from a variety of infections, allergic reactions and other causes, can lead to leukocytosis in some patients. Primary bone marrow disorders should be suspected in patients who present with extremely elevated white blood cell counts or concurrent abnormalities in red blood cell or platelet counts. Weight loss, bleeding or bruising, liver, spleen or lymph node enlargement, and immunosuppression also increase suspicion for a marrow disorder. The most common bone marrow disorders can be grouped into acute leukemias, chronic leukemias and myeloproliferative disorders. Patients with an acute leukemia are more likely to be ill at presentation, whereas those with a chronic leukemia are often diagnosed incidentally because of abnormal blood cell counts. White blood cell counts above 100,000 per mm3 (100 x 10(9) per L) represent a medical emergency because of the risk of brain infarction and hemorrhage.

Bone Marrow Diseases↗
PubMed1992

Neutrophil chemotactic factors promote leukocytosis. A common mechanism for cellular recruitment from bone marrow.

We investigated cellular responses in a rabbit to i.v. administration of five established chemotactic factors (leukotriene B4 (LTB4), platelet-activating factor (PAF), C5a, N-Formyl-Met-Leu-Phe (F-MLF), and IL-8), and each exerted a characteristic effect on circulating white blood cell levels. All five factors induced a rapid and transient leukopenia. The blood was nearly devoid of circulating neutrophils 5 min after administration of each chemotactic factor. Other leukocytes were also variably depleted during the leukopenic phase, including eosinophils, basophils, monocytes, and lymphocytes. The lymphocyte numbers remained significantly depressed (approximately 30%) for as long as 3 h after administration of PAF or f-MLF. Each chemotactic factor produced a marked neutrophilia (i.e., 250-400% of baseline levels) after the initial leukopenia. Eosinophil numbers were elevated along with the neutrophil response in the C5a- and LTB4-treated animals. Basophil levels were significantly elevated only in LTB4-treated animals. The cellular response to PAF, f-MLF, and IL-8 appeared to be specific for the neutrophils. The kinetic profiles of the neutrophilia induced by PAF (10 micrograms/kg) or f-MLF (2.5 micrograms/kg) were similar, with maximal responses occurring 3 to 4 h after administration. In contrast, LTB4 (10 micrograms/kg), IL-8 (2.5 micrograms/kg), and C5a (5 micrograms/kg) induced a more rapid neutrophilia, with peak responses occurring 1 to 1.5 h after injection, and remaining elevated for 3 to 4 h. In all animals the neutrophilia was accompanied by a relative increase in the number of nonsegmented neutrophils (bands), suggesting that a major component of leukocytosis is caused by the release of bone marrow reserves. Phenidone (10 mg/kg), a dual cyclooxygenase/5-lipoxygenase inhibitor, affected neither the neutropenia nor the neutrophilia induced by C5a, f-MLF, or PAF. The protein synthesis inhibitor actinomycin D also failed to suppress neutrophil responses induced by either C5a or PAF. These results suggest that leukocytosis is a common response induced by all neutrophil chemotactic factors. Leukocytosis appears to be a direct result of the dynamic adaptive response of neutrophils to chemotactic factor stimulation without involvement of a secondary mediator system.

Animals↗
PubMed1975

[Leukocytosis and polynucleosis in infectious disease].

During bacterial infections, the intensity of the polymorphonuclear leukocytosis depends on the bacterium but also on the mechanism and extent of the infection. Polymorphonuclear leukocytosis is greater during pyogenic and anaerobic infections. It is due to deep suppuration, septicemia of thrombophlebitic origin, acute endocarditis, purulent meningitis and pneumonia. The increase in the number of polymorphonuclear cells is, on the other hand, less marked in sub-acute bacterial endocarditis. Apart from bacterial infections, a polymorphonuclear leukocytosis is common in inflammatory disease, such as tissue necrosis and several malignant diseases. It may also be due to drug allergy.

Bacterial Infections↗
PubMed1990

Synovial leukocytosis in infectious arthritis.

The clinical presentation of 41 adult patients with infectious arthritis has been reviewed with special emphasis on initial synovial fluid leukocytosis. Fifty percent of the patients with culture-proven joint-space infections had synovial fluid leukocyte counts below 28,000/mm3. Comparison of this investigation with previous studies of similar magnitude demonstrates a striking difference in the mean and median synovial fluid white cell counts. The population reviewed had a higher incidence of patients with potentially immunocompromising medical conditions than previous reports. Similarities between this and previous reports include predisposing conditions, the spectrum of pathogens cultured, associated clinical findings on admission, hospital course, and mortality. The data presented here document the magnitude of potential overlap between the synovial fluid leukocytosis in infected joints and in joints afflicted with other forms of inflammatory arthropathy. Three patients populations (malignant neoplasms, steroid use, and intravenous drug abuse) with positive cultures from synovial fluid aspirates but initial synovial fluid white cell counts averaging below 50,000 cells/mm3 were identified. Patients with moderate synovial fluid leukocytosis, especially those potentially immunocompromised, must be considered to have infectious arthritis unless other causes of inflammatory arthropathies are demonstrated.

Adult↗
PubMed1989

[A case report of thyroid papillary cancer that manifested leukocytosis and hypercalcemia after radiotherapy in bone metastasis].

Bone metastasis from a thyroid papillary cancer of a 59-year-old woman had been successfully treated with radiotherapy (6,000 rad) and iodine-131 (120 mCi). One year later, the patient developed leukocytosis (maximum 143,000/mm3) and hypercalcemia (16.0 mg/dl). A colony stimulating factor (CSF) was detectable in her plasma, and nude mice that had been given metastatic tissues similarly developed leukocytosis and hypercalcemia. Leukocytosis and hypercalcemia seemed to have been caused by the CSF produced in the bone metastasized tissues of this thyroid cancer.

Bone Neoplasms↗
PubMed1988

Hematuria and extreme neutrophilic leukocytosis in a dog with renal tubular carcinoma.

Renal tubular carcinoma was believed responsible for hematuria and extreme leukocytosis in a dog. Other paraneoplastic syndromes possibly associated with this neoplasm included fever, thoracolumbar hyperesthesia, and anemia attributable to myelophthisis. All clinical and clinicopathologic abnormalities resolved after unilateral nephrectomy. Neutrophil cytochemical stains were used to differentiate leukemoid reaction from myelocytic leukemia as the cause of the leukocytosis. The extreme leukocytosis in this dog may have been leukemoid reaction caused by production of colony-stimulating factor by the renal tubular carcinoma.

Adenocarcinoma↗
PubMed1987

Recombinant human GM-CSF induces leukocytosis and activates peripheral blood polymorphonuclear neutrophils in nonhuman primates.

The in vivo efficacy of glycosylated and nonglycosylated recombinant human granulocyte macrophage colony-stimulating factor (rh GM-CSF) expressed in Chinese hamster ovary cells and Escherichia coli respectively was studied in rhesus monkeys following a daily subcutaneous (SC; three times) or intravenous (IV; over six hours) dose for seven consecutive days. The monkeys responded to the rh GM-CSF with a prompt (within 24 hours) rise in circulating white blood cells (WBCs). Thereafter the total cell counts increased steadily in a dose-dependent manner with repeated dosing to numbers six times over the pretreatment levels. Overall, granulocyte counts increased fivefold, lymphocytes twofold to fourfold, and monocytes threefold to fourfold. Platelets and erythrocytes were unaffected. Within 1 week after the end of treatment the leukocytosis had disappeared. Of the two routes of treatment, SC (three times daily)-administered rh GM-CSF was more effective than the same dose given by a six-hour IV infusion. In addition to inducing leukocytosis, parenterally administered rh GM-CSF primed mature circulating granulocytes for enhanced oxidative metabolism and killing of an E coli strain. These results show that exogenously administered glycosylated or nonglycosylated rh GM-CSF is both an effective stimulator of leukocytosis and a potent activator of the phagocytic function of mature granulocytes in monkeys.

Animals↗
PubMed1987

[Interspecies similarity of the trajectory of reactive leukocytosis].

Reactive leukocytosis was studied in 60 patients after appendectomy by daily test for 8 days. Reactive leukocytosis trajectory in these patients was compared to the analogous trajectory in 87 dogs with experimentally induced inflammation. The similarity of reactive leukocytosis trajectory in humans and animals has been established and a uniform period of leukocyte blood count changes equal to 48 h has been determined.

Adult↗
PubMed1980

Carbamazepine-induced leukocytosis.

An apparent case of carbamazepine-induced leukocytosis in a 26-year-old woman is presented. When admitted for psychiatric evaluation, the patient had been receiving carbamazepine for seizures for some time. A hemogram revealed a white blood cell (WBC) count of 21.2 x 10(3)/cu mm. Five days after the patient's medication was changed from carbamazepine (600 mg/day) to phenytoin (400 mg/day) and phenobarbital (120 mg/day), her WBC count was within normal range. When she experienced dizziness and ataxia, the phenytoin and phenobarbital were replaced with carbamazepine (600 mg/day). WBC counts performed 11 and 13 days after resumption of carbamazepine therapy again were significantly elevated. Other drugs administered during hospitalization included chlorpromazine, acetaminophen, and codeine. The possible causes of and pathophysiology of leukocytosis are reviewed. The changes in WBC that occurred with the rechallenge of carbamazepine indicate that the drug was the probable cause of the leukocytosis.

Adult↗
PubMed1994

Early mortality and the retinoic acid syndrome in acute promyelocytic leukemia: impact of leukocytosis, low-dose chemotherapy, PMN/RAR-alpha isoform, and CD13 expression in patients treated with all-trans retinoic acid.

All-trans retinoic acid (RA) has proven a major advance in the treatment of acute promyelocytic leukemia (APL). However, the proper management of patients who present with or develop leukocytosis during remission induction with all-trans RA is not established, nor is there a clear relation between leukocytosis and the development of the retinoic acid syndrome. We reviewed the course of our patients who underwent induction with all-trans RA to identify potential factors that might predict for the development of this syndrome and to identify which patients, if any, might specifically benefit from additional treatment with cytotoxic chemotherapy. Seventy-eight courses of all-trans RA therapy were administered to patients with a molecular diagnosis of APL. Initial and peak leukocyte counts, their rate of rise, leukocyte count criteria developed in Europe, and cell surface marker expression were all analyzed relative to subsequent development of both the RA syndrome as well as all causes of early mortality. The outcome of patients who received specific treatment for retinoid-induced leukocytosis was also examined. No factor was found to consistently predict for the development of the RA syndrome. Although the occurrence of the syndrome was positively associated with the peak value of the peripheral blood leukocyte count (P = .001), neither the initial leukocyte count nor the rate of rise in leukocyte counts on days preceding onset of the syndrome were sufficiently well-correlated to be clinically useful (P = .21). The leukocyte count criteria developed in Europe had a sensitivity of 62%, a specificity of 69%, and a positive predictive value that ranged from only 44% to 72%. However, we unexpectedly found that basal expression of CD13 (aminopeptidase N), a cell surface enzyme previously linked to tumor cell invasion and an inferior outcome in patients with acute myeloid leukemia, was highly associated with both development of the syndrome (P < .05) as well as an elevated leukocyte count (P = .006). Neither low-dose chemotherapy nor leukapheresis prevented development of the syndrome nor ameliorated its effects. In fact, 9 of 11 patients who received these interventions sustained fatal or near-fatal events, most of which were due to hemorrhage. However, early treatment with a short-course of high-dose corticosteroids halted progression of the syndrome in most cases. Finally, we found that expression of the type "A" isoform of PML/RAR-alpha (also known as bcr3 or "short") was associated with a significantly shorter duration of relapse-free and overall survival (P = .005).(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Cortex Hormones↗
PubMed1996

Abnormal organisation of the splenic marginal zone and the correlated leukocytosis in lymphotoxin-alpha and tumor necrosis factor alpha double deficient mice.

In this study we further characterized the phenotype at the homeostasis of mice genetically deficient in Tumor Necrosis Factor-alpha and Lymphotoxin-alpha (LT-alpha TNF-alpha -/-). As initially observed in LT-alpha -/- mice, these mice are devoid of lymph nodes and Peyer's patches, while in their spleen the white and red pulp domains are no more detectable. In the blood the leukocytosis dominated by lymphocytosis is not solely due to the absence of lymph nodes. Indeed, this abnormality was shown to be correctable by the transfer of wild type bone marrow in the absence of lymph node. We now report that the metallophilic macrophages of the marginal zone are no more detectable with an antibody reactive to sialoadhesin, a macrophage restricted transmembrane molecule known to bind myeloid and lymphoid cells. The absence of sialoadhesin within the marginal zone, a critical domain for lymphocyte trafficking towards the white pulp suggests a possible cellular basis for the observed blood leukocytosis. In addition, in the peritoneal cavity of LT-alpha TNF-alpha-/- mice, the size of the resident leukocyte population is increased. By their amplitudes these leukocytosis are similar within the blood and the peritoneal compartments.

Animals↗