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PubMed1991

Absent neutrophil alkaline phosphatase in the eosinophilia myalgia syndrome associated with L-tryptophan use.

The clinical constellation of leukocytosis, thrombocytosis, and low or absent stainable neutrophil alkaline phosphatase (NAP) is considered characteristic of chronic myelogenous leukemia (CML). CML with eosinophilic differentiation (eosinophilic leukemia) is well described, and leukemia and other clonal hematologic malignancies are associated with the syndrome of eosinophilic fasciitis. We describe leukocytosis, thrombocytosis, eosinophilia, mild basophilia, and absent stainable NAP, initially suggesting the diagnosis of CML in a patient with the eosinophilia myalgia syndrome associated with L-tryptophan use, a condition resembling eosinophilic fasciitis. Cytogenetic and molecular genetic studies failed to demonstrate a clonal proliferation of eosinophils.

Adult↗
PubMedDate not supplied

A prospective evaluation of bacteremic patients with chronic liver disease.

We prospectively studied 51 consecutive bacteremic patients with chronic liver disease in order to evaluate their clinical presentation and to assess the relationship of various clinical parameters to mortality. Forty-two patients had alcoholic liver disease and 40 were in Class C, by the Pugh modification of Child's criteria. Soft tissue infections were the most common source of bacteremia, followed by pneumonia, spontaneous bacterial peritonitis and urinary tract infection. Gram positive organisms were isolated in 69% of cases, and Gram negative ones in 31%. In nine patients, no source of bacteremia was detected. Leukocytosis occurred in 59% of patients and bandemia in only 41%. Although appropriate antibiotic therapy was begun in all cases on admission, 17 patients (33%) died in the hospital. Of 38 clinical parameters evaluated, multivariate analysis revealed that the three variables contributing the most independent information toward predicting in-hospital mortality were the absence of a history of fever, an elevated serum creatinine and marked leukocytosis. Improved understanding of the pathophysiologic relationship between these parameters and patient outcome may enable us to improve the therapy of bacteremic patients with chronic liver disease.

Chronic Disease↗
PubMed1985

CSF producing gall bladder cancer: case report and characteristics of the CSF produced by tumor cells.

Due to an increase in mature neutrophils, a 72-year-old female with gall bladder cancer showed leukocytosis of up to 1.32 X 10(11)/l; hypercalcemia was up to 7.7 mEq/l in her terminal stage. Leukocyte counts and calcium values increased as the tumor progressed. There was no sign of infection or bone marrow metastasis. Cultured cells from the tumor tissue produced high colony-stimulating factor (CSF) activity into the supernatant. The tumor cell-conditioned medium stimulated exclusively granulocytic colonies. The study of this patient shows that leukocytosis was caused by the CSF produced by tumor cells. Approximately 90% of CSF activity was lost by heat treatment at 60 degrees C for 30 min. The CSF was stable over a pH range of 3-11 and was inactivated by treatment with proteolytic enzymes, but was not affected by treatment with DNase or neuraminidase. Molecular weight of the CSF, demonstrated by fractionation using Sephacryl S-200, was approximately 27,000 to 30,000.

Adenocarcinoma↗
PubMed1988

Haematology and serum biochemistry in the racing greyhound following intraperitoneal povidone-iodine.

Povidone-iodine caused peritonitis with neutrophilic leukocytosis and a minimal left shift at the dosage rate of 3.5 ml/kg body weight. A dosage rate of 2 ml/kg only caused slight neutrophilic leukocytosis. There was a significant increase in the levels of creatinine (p = 0.049) and BUN (p = 0.020) in dogs that received the higher dose rate. Two dogs died from povidone-iodine toxicity with a marked increase in ALT, AP, SDH and conjugated bilirubin. It is concluded that povidone-iodine is unsafe for use in the peritoneal cavity of dogs.

Animals↗
PubMed1975

[Possible errors in leukocyte count caused by carryover in the Coulter counter S].

In 163 samples of venous blood with significant leukocytosis (20 000 to 172000 cells pro mm-3) a carryover of 400 to 22000 leukocytes up to the third count of the following specimens (200 to 9300 cells/mm-3) could be observed. Even after 41 specimens of normal leukocyte range and low leukocytosis (6700 to 17700 cells/mm-3) in cases of extreme leukopenias (less than 2000 cells/mm-3) the correct result was exceeded by 500 to 1000 cells. In four additional machines of other laboratories a carryover of different extent could be reproduced. In comparison to samples of venous blood only a very small carryover into subsequent samples of isotonic solution was found. The considerable spreading of the coefficient of variation between 1.7 and 16.2% (arithmetic mean 7.1%) prohibited a mathematical correction of error. Erroneously too high numbers of leukocytes could be absolutely avoided by at least two repeated counts.

Humans↗
PubMed1993

In vivo anti inflammatory effects of the M20 IL-1 inhibitor: I. Effects on acute inflammatory parameters.

Previous studies have described an IL-1 Inhibitor produced by a myelomonocytic line developed in our laboratory (Eur J Immunol 1986; 16: 1449). This IL-1 Inhibitor was secreted by the M20 line constitutively in addition to IL-1, from which it could be separated. We have recently shown that the M20 IL-1 Inhibitor is distinct from the IL-1ra. In vitro this factor inhibited IL-1 induced proliferative responses as well as PGE2 secretion by IL-1 induced fibroblasts. We also showed for the first time (Lymphokine Research 1988; 7(3): 268) that an IL-1 inhibitor can reduce IL-1 induced inflammatory effects. This study describes the specific effect of the M20 IL-1 Inhibitor on IL-1 induced parameters of inflammation: fever, leukocytosis and local foot pad swelling or lymph node enlargement. Purified preparations of the IL-1 Inhibitor, when injected together with IL-1, or before the IL-1, reduced fever, leukocytosis, foot pad swelling and lymph node enlargement caused by IL-1. Similar responses were obtained by injection of IL-6 or TNF, but were unaffected by the IL-1 Inhibitor, when injected together. These results indicate that the M20 IL-1 Inhibitor acts specifically on IL-1 induced responses in vivo. The potential importance of this factor as an anti-inflammatory and immune regulatory factor, is supported by the findings of this study.

Animals↗
PubMed2005

Gastric adenosquamous carcinoma producing granulocyte-colony stimulating factor.

We report a case of adenosquamous carcinoma of the stomach that produced granulocyte-colony stimulating factor (G-CSF). The patient, who had an admission diagnosis of advanced gastric cancer, had marked leukocytosis without evidence of infection. After leukemia and metastatic leukemoid reaction were excluded by bone marrow examination, a G-CSF-producing cancer was suspected as the cause of the abnormally elevated serum G-CSF level. The resected stomach tumor was histologically diagnosed as adenosquamous carcinoma; positive expression of G-CSF by tumor cells was shown with immunohistochemical detection, which confirmed the preoperative diagnosis. Recurrent disease in the liver and lymph nodes, accompanied by leukocytosis and re-elevation of serum G-CSF, developed just 3 months after the curative gastrectomy and adjuvant chemotherapy. All of the recurrent disease was resected, restoring normal levels of serum G-CSF. The patient survived for almost 2 years after the initial surgery with extensive chemotherapy, including weekly treatment with paclitaxel, before finally succumbing to liver failure secondary to extensive liver metastasis.

Carcinoma, Adenosquamous↗
PubMed1987

Comparison of potential cytoprotective action of sucralfate and cimetidine. Studies with experimental feline esophagitis.

The potential mucosal protective effects of a liquid sucralfate preparation and the histamine (H2)-antagonist cimetidine on acid-induced esophagitis were studied. Esophagitis was induced in adult cats using a constant infusion of 0.1 N hydrochloric acid at 1 ml/minute for 20 minutes. Mucosal lesions were evaluated by blinded investigators using both fiber-optic endoscopy and light microscopy. Histology was scored for basal cell hyperplasia, intraepithelial leukocytosis, and subepithelial leukocytosis. Liquid sucralfate given prior to acid infusion consistently prevented acid-induced lesions, demonstrated by quantitative histologic scoring. Although cimetidine did not show the same degree of protection as sucralfate, the results did show a trend towards a cytoprotective effect.

Animals↗
PubMed1993

Liver damage in patients with colony-stimulating factor-producing tumors.

PURPOSE: We have demonstrated that colony-stimulating factor (CSF)-producing tumor cell lines produce not only CSF but also interleukin-1 (IL-1) and interleukin-6 (IL-6). Clinically, we have observed that patients bearing such tumors present with liver dysfunction and fever in addition to marked leukocytosis. The purpose of this study was to determine whether or not the liver damage was specifically related to CSF-producing tumors. PATIENTS AND METHODS: Clinicopathologic examinations were performed in six autopsied patients with CSF-producing tumors. We also transplanted two tumor cell lines (KHC287 and CHU-2), which produce granulocyte (G)-CSF, IL-1, and IL-6, to nude mice. RESULTS: Of the six patients, five had G-CSF- and one had granulocyte/macrophage (GM)-CSF-producing tumors. IL-1 and IL-6 concentrations in plasma or culture supernatant were elevated in these patients. Biochemical examinations revealed high serum enzyme levels of the biliary system in contrast to normal or slight increases in transaminase levels in all patients studied. Serum direct bilirubin was elevated in five of the six patients. Three common pathologic changes of the liver were found: (1) focal necrosis associated with neutrophil infiltration in the centrilobular zones, (2) fibrous change and enlargement of the portal area associated with neutrophil infiltration, and (3) intrahepatic cholestasis. The same pathologic changes, except for cholestasis, were reproduced in the liver of mice transplanted with KHC287 or CHU-2. CONCLUSION: These results indicate that patients with CSF-producing tumors have characteristic liver damage, and suggest a new paraneoplastic syndrome of leukocytosis and liver damage.

Aged↗
PubMed1987

Effects of drugs and metabolic inhibitors on the acute toxicity of T-2 toxin in mice.

The antidotal effects of antiinflammatory agents, inhibitors of bioamine syntheses, an opioid antagonist and other pharmacological agents on lethal toxicity, leukocytosis and ear inflammation, were investigated in mice subcutaneously administered or topically exposed to T-2 toxin, a trichothecene mycotoxin of Fusarium species. The acute lethal toxicity of T-2 toxin was reduced by administration of the steroidal anti-inflammatory agents, prednisolone and dexamethasone, and prolongation of survival times was demonstrated with an antihistaminic agent, diphenhydramine, and an opioid antagonist, naloxone. Prednisolone also antagonized leukocytosis and the increment of ear weight caused by T-2 toxin. These findings suggest that the action site(s) of steroidal anti-inflammatory agents is involved in the development of the toxic actions of T-2 toxin, and the implications of the results with bioamines and opioids are also discussed.

Animals↗
PubMed1993

Leukemogenesis-associated antigen in HTLV-I-transformed rabbit cells.

The presence of a leukemogenesis-associated antigen was investigated in an experimental model of adult T-cell leukemia in (B/J x Chbb:HM)F1 rabbits, where adult rabbits develop leukemia within 1-2 weeks following inoculation with HTLV-I-transformed syngeneic cell lines. Leukemogenic activity was found in some but not all HTLV-I-transformed cell lines, and was associated with leukocytosis-inducing activity which was assayed by inoculating these cells into adult rabbits of the parental Chbb:HM strain. The leukemogenic cell line diminished or lost the leukemogenic and leukocytosis-inducing activities during prolonged culture in vitro. A mouse mAb was raised which recognized an antigen uniquely expressed on the cell surface of the leukemogenic cell lines. This antigen was present, however, in all HTLV-I-transformed cells examined and the mAb immunoprecipitated the same 65 kD glycoproteins from both leukemogenic and non-leukemogenic cell lines. Taken together, the antigenic epitope seemed to be expressed on the cell surface in such a manner as to be accessible to the mAb in leukemogenic but not non-leukemogenic cells. The analyses of various cell lines revealed that this antigen was an endogenous antigen and not a viral antigen. The antibody was cytotoxic in vitro against leukemogenic cell lines in the presence of complement, and administration of this antibody to leukemic rabbits resulted in an abrupt decrease in the peripheral blood leukocyte number, leading to remission of the disease.

Animals↗
PubMed1995

Confirmation of spurious hypoxemia using continuous blood gas analysis in a patient with chronic myelogenous leukemia.

Patients with extreme leukocytosis or thrombocytosis who have hypoxemia on arterial blood gas analysis may demonstrate normal oxygen saturation using pulse oximetry. The most commonly invoked explanation for this phenomenon is oxygen consumption in the blood gas sample prior to analysis. However, others have challenged the premise that the hypoxemia is spurious. We describe a patient with extreme leukocytosis and hypoxemia in whom normoxia was confirmed by continuous blood gas analysis.

Adult↗
PubMed1993

Assessment of acute iron poisoning by laboratory and clinical observations.

A survey of medical records at a tertiary children's medical center was performed to determine whether selected laboratory and clinical observations and the serum iron concentration exceeding the total iron-binding capacity serve as indicators of acute iron poisoning. Patients were hospitalized for treatment of iron poisoning during January 1976 through June 1992. A total of 128 patients were identified; 92 met selection criteria and 65 had a serum iron concentration and total iron-binding capacity obtained simultaneously. The present study was unable to confirm that vomiting, diarrhea, leukocytosis, hyperglycemia, and radiopacities were associated with a serum iron concentration in excess of 300 micrograms/dL (54 mumol/L); only one observation, coma, was associated (P < .02) with a serum iron greater than 500 micrograms/dL (90 mumol/L). Coma, radiopacities, leukocytosis, and an elevated anion gap will be concurrently present (predictive value positive = 100%) when the serum iron concentration is greater than 500 micrograms/dL; moreover, they will be absent collectively (predictive value negative = 95%) when the serum iron concentration is below 500 micrograms/dL. Individually, these signs and symptoms have a low positive predictive value, but the absence of any one of these variables is likely to be associated with serum iron concentrations less than 500 micrograms/dL (predictive value negative > or = 93%). The ratio of serum iron concentration to the total iron-binding capacity was not associated with symptoms of systemic iron toxicity or presence of vin rosé urine after parenteral deferoxamine administration. A serum iron concentration in excess of the total iron-binding capacity may not identify patients with serious iron poisoning.

Acute Disease↗
PubMed2004

The relationship between partial splenectomy and peripheral leukocyte count.

BACKGROUND: Partial splenectomy is accepted as a treatment modality for hypersplenism permitting preservation of the spleen functions. Since a prominent leukocytosis is a marked event after total splenectomy, it was the aim of the present study to compare the peripheral white blood cell counts (PWBC) and immune response in mice following partial and total splenectomy. MATERIALS AND METHODS: Four groups of animals were included in the study: mice in which 70% of the spleen was removed, animals that underwent total splenectomy, mice with sham operation, and a group of mice that served as controls. The proliferative response of peripheral blood mononuclear cells, peritoneal cells, and splenocytes was examined using concavalin (Con) A. RESULTS: In distinction from marked leukocytosis observed in mice after total splenectomy, in partially splenectomized mice the PWBC counts did not show any significant increase during a follow-up period of up to 2 months after surgery. The mitogen response of the mononuclear cells to Con A in partially splenectomized mice was similar to that of controls, while in animals after total splenectomy, it was increased in cells from the peripheral blood and decreased in those from the peritoneum. CONCLUSIONS: The results indicate that removal of as much as about 70% of the spleen in mice is sufficient to maintain a normal PWBC count, suggesting a regulatory role of the spleen remnant on the PWBC production. The normal mitogen response of the cells to Con A indicates that the spleen rudiment preserves at least a part of the immune activity of the intact spleen.

Animals↗
PubMed2005

Analysis of FLT3 internal tandem duplication and D835 mutations in Chinese acute leukemia patients.

Genomic aberrations of Fms-like tyrosine kinase 3 (FLT3), including internal tandem duplication (ITD) and point mutations, have been demonstrated in 25-30% of adults acute myeloid leukemia (AML) and are markers of poor prognosis. FLT3/ITD and D835 mutations were analyzed in 194 Chinese patients with acute leukemia and myelodysplastic syndromes (MDS) by polymerase chain reaction (PCR). FLT3/ITDs and D835 mutations were found in 25.9 and 6.3% of 143 AML patients, respectively. Two patients showed both ITD and point mutations. Among the FAB subtypes of AML, the rate of FLT3 aberration was significantly higher in M3 and M5. However, neither aberrations was found in 25 patients with acute lymphoblastic leukemia (ALL), 2 acute hybrid leukemia, 17 MDS and 7 chronic myeloid leukemia in blast crisis (CML-BC). FLT3/ITD was associated to leukocytosis and lower complete remission (CR) rate, and was more prevalent in patients with normal karyotype. In contrast, D835 mutation was not associated with leukocytosis or low CR rate. Our results confirm that FLT3 activating mutations also occur in a significant percentage in Chinese AML patients. FLT3/ITD(+) patients treated with standard induction regimen could achieve lower complete remission rates compared with patients not harboring this defect. Early detection of FLT3 mutations and an intensification of induction therapy might thus be useful for this group of patients to overcome the poor prognosis.

Acute Disease↗
PubMed2001

Murine gammaherpesvirus-68 infection causes multi-organ fibrosis and alters leukocyte trafficking in interferon-gamma receptor knockout mice.

Murine gammaherpesvirus-68 (MHV-68) infection in interferon-gamma receptor knockout mice (IFN-gammaR(-)/(-)) results in splenic fibrosis and excessive loss of splenocytes. In our present study we found that MHV-68 infection in IFN-gammaR(-)/(-) mice also resulted in fibrosis and atrophy of the mediastinal lymph nodes, interstitial pulmonary fibrosis and fibrotic changes in the liver. Atrophy and cellular depletion of the spleen in IFN-gammaR(-)/(-) was not the result of increased cell death. The loss of splenocytes in IFN-gammaR(-)/(-) mice, which was most evident on day 23 after infection, correlated with an increase in the number of leukocytes in peripheral blood. At the peak of leukocytosis, on day 23 after infection, peripheral blood cells from infected IFN-gammaR(-)/(-) mice were unable to traffic through the fibrosed spleens of IFN-gammaR(-)/(-) mice but were able to enter the spleens of wild-type mice. This indicates that leukocytosis was in part the result of emigration of cells from the spleen and their subsequent exclusion of re-entry at the height of fibrosis. Significant cytokine and chemokine changes were observed in spleens of IFN-gammaR(-)/(-) mice. IFN-gamma, tumor necrosis factor-alpha (TNF-alpha ), TNF-beta, interleukin-1beta (IL-1beta), transforming growth factor-beta1 (TGF-beta1), lymphotactin, and MIP-1beta were elevated on day 14 after infection whereas chemokines IP-10 and MIG were significantly reduced. These changes suggest a role for dysregulated cytokines and chemokines in severe organ-specific fibrosis with implications for immune-mediated fibrotic disorders.

Animals↗
PubMed1995

Characteristics of blood hemostatic markers in a patient with ovarian hyperstimulation syndrome who actually developed thromboembolism.

OBJECTIVE: To investigate whether a patient with ovarian hyperstimulation syndrome (OHSS) demonstrated characteristic changes in the blood hemostatic markers before she developed thromboembolism. DESIGN: Patients with OHSS had blood drawn to determine hemostatic markers and related factors. PATIENTS: Twenty-three OHSS patients, including a case complicated with thromboembolism. SETTING: The IVF-ET program of the Department of Obstetrics and Gynecology, The University of Akita, School of Medicine. MAIN OUTCOME MEASURES: Blood hemostatic markers and related factors. RESULTS: The patient with thromboembolism demonstrated marked leukocytosis and higher levels of activation in the blood markers related to fibrinolytic system, such as alpha 2 plasmin inhibitor, plasmin-alpha 2 antiplasmin complexes, and D-dimers, before the onset of this episode. CONCLUSION: Marked leukocytosis and higher levels of activation of the fibrinolytic system may be the signs of imminent thromboembolism in OHSS patients.

Adult↗
PubMed1993

Bladder carcinoma producing granulocyte colony-stimulating factor: a case report.

A 67-year-old man with squamous cell bladder carcinoma showed remarkable leukocytosis (maximum 50,300 per microliter.) for 4 months while the neoplasm recurred and metastasis progressed. The patient died of systemic metastasis within 9 months after cystectomy. Enzyme immunoassay of the serum demonstrated remarkably high levels of granulocyte colony-stimulating factor (4,928 pg./ml.). Immunohistochemical examination with anti-granulocyte colony-stimulating factor monoclonal antibody demonstrated granulocyte colony-stimulating factor production in the metastatic cancer cells in the liver. The expression of the granulocyte colony-stimulating factor gene in the tumor specimens was examined by standard Northern blot analysis. Specific granulocyte colony-stimulating factor transcript was identified in the total ribonucleic acid fraction extracted from a tumor specimen of the peritoneal metastatic lesion. These results indicated that the autonomous production of granulocyte colony-stimulating factor in this bladder carcinoma induced paraneoplastic leukocytosis.

Aged↗