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PubMed1988

Mepacrine impairs neutrophil response after acute lung injury in rats. Effects on neutrophil migration.

Intraalveolar leukocytosis is integral in initiating and perpetuating airspace inflammatory reactions. We used intratracheal instillation of silica suspensions in adult male rats to cause neutrophil flux (32% increase over saline controls) without creating a protein leak, so simulating an early inflammatory response. We examined the in vivo effects of a known phospholipase A2 inhibitor (mepacrine) and the two mast cell active agents (cyproheptadine and reserpine) on lung lavage fluid chemotactic capability, alveolar macrophage (AM) production of chemotactic factor(s), and neutrophil diapedesis. Only mepacrine significantly depressed the leukocytosis (from 32% to 8% of total cells), with a similar diminution in AM chemotaxin production. Separate in vitro experiments using mepacrine-pretreated neutrophils and macrophages gave evidence that mepacrine: (1) diminishes neutrophil response to chemotaxin(s), (2) inhibits spontaneous, random neutrophil movement, and (3) diminishes macrophage-derived chemotactic factor production. These observations suggest that the earliest events in alveolar inflammatory reactions probably involve local production of chemotactic factors by AM, and that mepacrine's anti-inflammatory action results from inhibitory influences on both macrophage and neutrophil populations.

Acute Disease↗
PubMed1976

Homozygous human C3 deficiency. The role of C3 in antibody production, C-1s-induced vasopermeability, and cobra venom-induced passive hemolysis.

Studies of the family of a patient with marked deficiency of the third component of complement (C3) demonstrated that the patient was homozygous for a blank allele at the C3 locus, C3-. Metabolic studies with purified radiolabeled C3 in the patient revealed a mildly elevated fractional catabolic rate and a markedly reduced synthesis rate, consistent with a lack of C3 synthesis as the patient's primary defect. There was also a mild increase in the rate of conversion of purified C3 added to her serum and incubated at 37 degrees C in vitro. Major blood group-compatible erythrocytes from a patient with paroxysmal nocturnal hemoglobinuria had the same shortened survival in the C3-deficient patient as in a normal control. Although no leukocytosis developed in the patient in spontaneous infection by pyogenic organisms, there was a normal leukocytosis in response to the injection of thyphoid vaccine. The intradermal injection of C-1s, which produces a marked increase in vasopermeability in the skin of normal subjects, produced no definite change in the patient, possibly implicating C3 or a protein in the alternative pathway as the normal mediator of this response. The patient's serum exhibited near-normal immune adherence activity, confirming the lack of requirement of C3 for this function. C5 inactivation and passive hemolysis of unsensitized guinea pig erythrocytes occurred normally in C3-deficient serum on incubation with cobra venom factor, indicating that C3 is not required for these reactions. The patient's humoral antibody response to both protein and carbohydrate antigens was entirely normal, making it unlikely that C3 is required for antigen processing.

Alleles↗
PubMed1994

The clinical characteristics and infectious outcomes of febrile infants aged 8 to 12 weeks.

We reviewed 356 consecutive cases of febrile infants aged 8 to 12 weeks who received outpatient evaluation for sepsis over 4 years. Thirty-three infants (9.3%) had a serious bacterial infection (SBI), including bacterial meningitis, bacteremia, urinary tract infection (UTI), and Salmonella enteritis. The SBI rate, which was directly proportional to fever height, was significantly greater for infants with hyperpyrexia (35%) than those with lesser degrees of fever (7.7%) and for infants with peripheral blood leukocytosis (total WBC count > or = 15,000/mm3; 25%) than those with lesser total WBC counts (5.8%). An attending-level physician judged that 67% of infants with SBI appeared to be "well," including five or eight cases (63%) of bacteremia, 14 of 17 cases (82%) of UTI, and all three cases of Salmonella enteritis, whereas all five patients with bacterial meningitis appeared to be "ill." Urinalysis abnormalities indicative of UTI were present in 15 of 17 infants (88%) who had this infection. SBIs are not uncommon in febrile infants aged 8 to 12 weeks and occur significantly more often in those with either hyperpyrexia or peripheral blood leukocytosis.

Bacterial Infections↗
PubMed2005

Acute appendicitis: the reliability of diagnosis by clinical assessment alone.

BACKGROUND AND AIMS: This prospective study aimed to review the trustworthiness of the initial clinical assessment in acute appendicitis without employment of imaging modalities, laparoscopy or any other adjunct diagnostic test. PATIENTS AND METHODS: 717 patients were operated on for appendicitis by six different surgeons. Initial clinical and laboratory examination were evaluated in relation to the intraoperative and the pathological appreciation of the appendiceal inflammation. RESULTS: 598 patients were found to have appendicitis, 34 a different condition, 41 had both appendicitis and an additional condition and 44 no pathology. 6% of the laparotomies and 11% of the appendectomies were unnecessary. The severity of the inflammation correlated significantly with periumbilical pain, pain migrating to right lower quadrant, loss of appetite, fever, rebound tenderness, local rigidity, polymorphonuclear predominance on deferential, polymorhonucleosis and leukocytosis. Leukocytosis was less frequent in aged patients. All the six surgeons were found to be equally reliable, although they all underestimated the setting compared to the pathologists. Patients with a long duration of symptoms had milder forms of inflammation and increased percentage of unanticipated abdominal conditions. CONCLUSIONS: Appendicitis can be reliably diagnosed clinically without employment of adjunct tests. These can be reserved for equivocal cases.

Acute Disease↗
PubMed2001

Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies.

Mutations of receptor tyrosine kinases are implicated in the constitutive activation and development of human malignancy. An internal tandem duplication (ITD) of the juxtamembrane (JM) domain-coding sequence of the FLT3 gene (FLT3/ITD) is found in 20% of patients with acute myeloid leukemia (AML) and is strongly associated with leukocytosis and a poor prognosis. On the other hand, mutations of the c-KIT gene, which have been found in mast cell leukemia and AML, are clustered in 2 distinct regions, the JM domain and D816 within the activation loop. This study was designed to analyze the mutation of D835 of FLT3, which corresponds to D816 of c-KIT, in a large series of human hematologic malignancies. Several kinds of missense mutations were found in 30 of the 429 (7.0%) AML cases, 1 of the 29 (3.4%) myelodysplastic syndrome (MDS) cases, and 1 of the 36 (2.8%) acute lymphocytic leukemia patients. The D835Y mutation was most frequently found (22 of the 32 D835 mutations), followed by the D835V (5), and D835H (1), D835E (1), and D835N (1) mutations. Of note is that D835 mutations occurred independently of FLT3/ITD. An analysis in the 201 patients newly diagnosed with AML (excluding M3) revealed that, in contrast to the FLT3/ITD mutation (n = 46), D835 mutations (n = 8) were not significantly related to the leukocytosis, but tended to worsen disease-free survival. All D835-mutant FLT3 were constitutively tyrosine-phosphorylated and transformed 32D cells, suggesting these mutations were constitutively active. These results demonstrate that the FLT3 gene is the target most frequently mutated to become constitutively active in AML.

Acute Disease↗
PubMed2004

Resting tachycardia, a warning sign in anorexia nervosa: case report.

BACKGROUND: Among psychiatric disorders, anorexia nervosa has the highest mortality rate. During an exacerbation of this illness, patients frequently present with nonspecific symptoms. Upon hospitalization, anorexia nervosa patients are often markedly bradycardic, which may be an adaptive response to progressive weight loss and negative energy balance. When anorexia nervosa patients manifest tachycardia, even heart rates in the 80-90 bpm range, a supervening acute illness should be suspected. CASE PRESENTATION: A 52-year old woman with longstanding anorexia nervosa was hospitalized due to progressive leg pain, weakness, and fatigue accompanied by marked weight loss. On physical examination she was cachectic but in no apparent distress. She had fine lanugo-type hair over her face and arms with an erythematous rash noted on her palms and left lower extremity. Her blood pressure was 96/50 mm Hg and resting heart rate was 106 bpm though she appeared euvolemic. Laboratory tests revealed anemia, mild leukocytosis, and hypoalbuminemia. She was initially treated with enteral feedings for an exacerbation of anorexia nervosa, but increasing leukocytosis without fever and worsening left leg pain prompted the diagnosis of an indolent left lower extremity cellulitis. With antibiotic therapy her heart rate decreased to 45 bpm despite minimal restoration of body weight. CONCLUSIONS: Bradycardia is a characteristic feature of anorexia nervosa particularly with significant weight loss. When anorexia nervosa patients present with nonspecific symptoms, resting tachycardia should prompt a search for potentially life-threatening conditions.

Anorexia Nervosa↗
PubMed2003

Nicotine induces human neutrophils to produce IL-8 through the generation of peroxynitrite and subsequent activation of NF-kappaB.

Leukocytosis in tobacco smokers has been well recognized; however, the exact cause has not been elucidated. To test the hypothesis that tobacco nicotine stimulates neutrophils in the respiratory tract to produce IL-8, which causes neutrophilia in vivo, we examined whether nicotine induces neutrophil-IL-8 production in vitro; the causative role of NF-kappaB in its production, in association with the possible production of reactive oxygen intermediates that activate NF-kappaB; and the nicotinic acetylcholine receptors (nAChRs) involved in IL-8 production. Nicotine stimulated neutrophils to produce IL-8 in both time- and concentration-dependent manners with a 50% effective concentration of 1.89 mM. A degradation of IkappaB-alpha/beta proteins and an activity of NF-kappaB p65 and p50 were enhanced following nicotine treatment. The synthesis of superoxide and the oxidation of dihydrorhodamine 123 (DHR) were also enhanced. The NOS inhibitor, nomega-Nitro-l-arginine methyl ester, prevented nicotine-induced IL-8 production, with an entire abrogation of DHR oxidation, IkappaB degradation, and NF-kappaB activity. Neutrophils spontaneously produced NO whose production was not increased, but rather decreased by nicotine stimulation, suggesting that superoxide, produced by nicotine, generates peroxynitrite by reacting with preformed NO, which enhances the NF-kappaB activity, thereby producing IL-8. The nAChRs seemed to be involved in IL-8 production. In smokers, blood IL-8 levels were significantly higher than those in nonsmokers. In conclusion, nicotine stimulates neutrophil-IL-8 production via nAChR by generating peroxynitrite and subsequent NF-kappaB activation, and the IL-8 appears to contribute to leukocytosis in tobacco smokers.

Humans↗
PubMed1986

Neuroleptic malignant syndrome complicating closed head injury.

Lethargy, hyperpyrexia, tremor, and rigidity associated with leukocytosis and elevation of the creatine kinase level occurred in a patient with a closed head injury who was being treated with haloperidol for control of agitation. This constellation of symptoms, known as the neuroleptic malignant syndrome (NMS), partially improved when the neuroleptic medication was stopped, but complete resolution of the syndrome did not occur until the patient was treated with bromocriptine. Because haloperidol is the most widely used medication for the agitation that develops in patients with significant closed head injuries, neurosurgeons should be aware of the NMS. The NMS is caused by neuroleptic medications and may initially present with unexplained hyperpyrexia, leukocytosis, and elevated creatine kinase levels. Halting the neuroleptic, supportive care, and the use of dantrolene sodium and bromocriptine are the treatment modalities of choice for this syndrome, which has a mortality rate of 20 to 30% and may be linked to malignant hyperthermia.

Adult↗
PubMed1993

Effects of recombinant human granulocyte-macrophage colony stimulating factor on hematopoiesis in normal cynomolgus monkeys.

The in vivo efficacy of nonglycosylated recombinant human granulocyte-macrophage colony stimulating factor (rh GM-CSF) expressed in Escherichia coli was studied in cynomolgus monkeys (Macaca fascicularis). A single intravenous (IV) administration of rh GM-CSF (100 micrograms/kg) resulted in a two-fold increase in peripheral white blood cell (WBC) count with a predominance of neutrophils after 12 hr. The increased WBC count returned to the initial level within 48 hr after administration. In a study with consecutive IV administrations for 10 days, animals treated with 20 micrograms/kg/day rh GM-CSF underwent marked leukocytosis (four fold) and thrombocytosis (two fold). The increase in WBC count was due to increased number of neutrophils, eosinophils, lymphocytes, monocytes and basophils. Red blood cell count was unaffected. The leukocytosis resolved within one week after the termination of administration. A lower mean platelet volume compared to the pre-treatment level was observed in rh GM-CSF treated animals receiving 20 micrograms/kg/day for 20 days. This coincided with the elevation in platelet count.

Animals↗
PubMed1995

Thyroid anaplastic carcinoma producing granulocyte-colony-stimulating factor and parathyroid hormone-related protein.

A 65-year-old woman noticed a rapidly enlarging neck mass with tenderness and complained of dyspnea. She was diagnosed as having anaplastic thyroid carcinoma. She died of respiratory failure 14 days after admission. Marked leukocytosis and hypercalcemia were observed in the clinical course. Both serum granulocyte-colony-stimulating factor and parathyroid hormone-related protein levels were elevated. The cancerous tissue was also immunohistochemically stained for both peptides. We conclude that the leukocytosis and hypercalcemia of this patient were induced by these two factors produced by the tumor.

Aged↗
PubMedDate not supplied

Stevens-Johnson syndrome presenting as intravenous line sepsis.

A 25-year-old Hispanic female with insulin dependent diabetes mellitus (IDDM) and endstage renal disease on chronic hemodialysis was hospitalized with paroxysms of fever and chills for a day. A day after starting piperacillin for presumed intravascular line infection, she developed a maculopapular dermatitis and abnormal liver function tests, at which point the drug was discontinued. However, the rash persisted for 10 days, after which it progressively worsened. She continued to have high fevers, abnormal liver function tests, and marked leukocytosis, despite multiple negative cultures and other nondiagnostic examinations. She was treated as a patient with sepsis of unknown etiology and received multiple antibiotics on an empiric basis without response. A diagnosis of Stevens-Johnson syndrome was then made based on the triad of cutaneous dermatitis, mucosal, and hepatic involvement. She received high dose corticosteroids and her fever, dermatitis, mucosal lesions, leukocytosis, and abnormal liver function tests improved dramatically.

Adult↗
PubMed1986

Are white blood cell count, platelet count, erythrocyte sedimentation rate and C-reactive protein useful in the diagnosis of septicaemia and endocarditis?

In 851 predominantly adult patients with septicaemia or endocarditis data regarding white blood cell (WBC) count, platelet count, ESR and C-reactive protein (CRP) obtained within 3 days of admission were analyzed retrospectively. Among 232 patients with complete laboratory data none had the combination of normal ESR, negative CRP and lack of both leukocytosis and thrombocytopenia. CRP was positive (greater than 10 mg/l) in 93%, ESR was elevated (greater than 20 mm/h) in 90%, leukocytosis (WBC greater than 9 X 10(9)/l) was present in 60% and thrombocytopenia (platelets less than 150 X 10(9)/l) in 35% of the patients. Patients with pneumococcal infection had generally higher ESR and CRP values and WBC counts than patients with other infections.

Blood Sedimentation↗
PubMed1995

Synovial fluid L-lactic acid in acute arthritis of the adult knee joint.

Determination of synovial fluid (SF) lactic acid has been suggested to be an unspecific indicator of SF leukocytosis, and it is not recommended for differential diagnosis of bacterial arthritis. We analyzed the L-lactic acid content by enzymatic UV-method in 65 SF samples obtained from adult patients with acute knee arthritides. The concentration of L-lactic acid was not high in any SFs with intensive leukocytosis. The mean concentration of L-lactic acid was 13.5 mmol/l (95% confidence intervals 9.4; 17.6 mmol/l) in the synovial-fluid samples from culture-positive arthritis and 5.5 mmol/l (4.9; 6.2 mmol/l) in the synovial-fluid samples from culture-negative arthritis. Determination of SF L-lactic acid is an important part of the diagnostic setup for acute arthritis. Values > 9 mmol/l strongly support occurrence of bacterial arthritis and indicates an immediate onset of the treatment.

Acute Disease↗
PubMedDate not supplied

Infection-associated hemophagocytic syndrome complicated by infectious lymphoproliferation: a case report.

The case of a 7-year-old boy with virus-associated hemophagocytic syndrome (VAHS) and serologically proven parvovirus B-19 infection is described. The patient with VAHS presented with fever, hepatosplenomegaly, pancytopenia, and hyperlipidemia type IV. After induction therapy with VP-16 and prednisone, partial remission was achieved. Despite maintenance therapy, reinductions, and the addition of cyclosporine A for 3 months, several relapses occurred. The therapy was stopped because of life-threatening complications (Klebsiella sepsis, neutropenic enterocolitis, and stercoral peritonitis). The complications were treated successfully. The patient status was stabilized after splenectomy. However, hepatomegaly progressed slowly and the hyperlipidemia endured. Ten months after the diagnosis leukocytosis with absolute T lymphocytosis appeared. Reactivation of VAHS was suspected and intravenous immunoglobin and then antilymphocyte immunoglobulin ALG therapy were started. The resultant decrease in leukocytosis was prompt, but lymphopenia did not occur. Virostatic treatment with foscarnet was introduced based on human herpesvirus-6 seroconversion. Twenty-six months after the diagnosis, the patient is well, without any sign of VAHS or lymphoproliferation.

Bone Marrow↗
PubMedDate not supplied

Cutaneous infiltration by leukemic cells in acute promyelocytic leukemia of a child after treatment with all-trans retinoic acid.

We describe here the first case of childhood acute promyelocytic leukemia (APL) with cutaneous infiltration of leukemic cells following treatment with all-trans retinoic acid (ATRA) confirmed by immunostaining and polymerase chain reaction for PML/RAR alpha. An 11-year-old girl was diagnosed as having APL. Chromosomal analysis demonstrated the characteristic karyotype of t(15;17). ATRA therapy was begun at a dose of 45 mg/m2 daily. During ATRA therapy, leukocytosis and retinoic acid syndrome were observed but were resolved by dexamethasone. Two months after commencement of ATRA therapy, complete remission was achieved. During the course of consolidation chemotherapy, however, multiple cutaneous nodules developed in her trunk, the size and number of which increased despite intensive chemotherapy. Histological and immunological studies of the cutaneous nodules showed infiltration of leukemic cells. PML/RAR alpha mRNA was detected in both the cutaneous nodules and bone marrow by means of polymerase chain reaction. ATRA treatment for APL may be associated with an increased incidence of extramedullary disease such as cutaneous lesions. The best available therapy for APL may be a combination of ATRA and chemotherapy, especially when a marked leukocytosis occurs during ATRA therapy.

Antineoplastic Agents↗
PubMed1996

[An elderly patient with Ph1-positive chronic myelomonocytic leukemia].

An 80-year-old man with leukocytosis was admitted to our hospital on February 20, 1995. There were no blasts in the peripheral blood, but leukocytosis, associated with marked monocytosis, anemia, and thrombocytopenia was observed. The bone marrow was hyperplastic and there was a slight decrease in megakaryocytes. The myelogram showed 5.6% blasts + promyelocytes, and there was no basophilia. Mild dysplasia of third-line cells was observed. Chromosome analysis yielded 47, XY, +8, t (9;22) (q34;q11), and the Philadelphia (Ph1) chromosome and trisomy 8 were detected. Fluorescence in-situ hybridization revealed a large ber. Because the French-American-British (FAB) cooperative group diagnostic criteria for chronic myelomonocytic leukemia (CMMoL) were fulfilled and the Ph1 chromosome was detected, a diagnosis of Ph1-positive CMMoL was made. Hydroxyurea was given for cytoreduction and the patient has been followed with no evidence of acute transformation for about one year. CMMoL is classified as a myelodysplastic syndrome. However, it is rare to find the Ph1 chromosome in patients with these syndromes, and there have been very few reports of its detection in CMMoL. CMMoL may not be a single disease entity, and it may be useful to investigate more cases like the present one, to reassess this disease.

Aged↗
PubMed1989

Effect of steroidal anti-inflammatory drugs on Escherichia coli endotoxin-induced mastitis in the cow.

Effects of intramammary infusion of prednisolone (40 mg) or intramuscular injection of dexamethasone (30 mg) or flumethasone (5 mg) on local and systemic signs in Escherichia coli endotoxin-induced mastitis were studied. The effect of varying intervals (0, 2, and 4 h) between intramammary infusion of endotoxin and prednisolone in the same quarter was determined. Intramammary infusion of endotoxin (.01 mg lipopolysaccharide of E. coli) produced inflammation of the infused quarter, fever, tachycardia, and leukopenia followed by a neutrophilic leukocytosis in the blood and a decrease in plasma zinc and iron concentrations. All corticosteroid treatments, except intramammary administration of prednisolone 4 h after endotoxin infusion, enhanced leukocytosis and diminished local signs of inflammation. Intramuscular injection of dexamethasone or flumethasone together with intramammary infusion of endotoxin and intramammary administration of prednisolone 2 h after lipopolysaccharide infusion completely abolished the febrile response. Abolishment of fever and attenuation of several hematologic and blood biochemical changes may be explained by diminished synthesis of endogenous mediators within the inflamed quarters due to glucocorticosteroid action.

Animals↗
PubMed1997

Cerebrospinal fluid interleukin-1 receptor antagonist and tumor necrosis factor-alpha following subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) causes an inflammatory reaction and may lead to ischemic brain damage. Experimental ischemia has been shown to be connected with the alarm-reaction cytokines interleukin-1 receptor antagonist (IL-1Ra) and tumor necrosis factor-alpha (TNF alpha). Increased levels of these cytokines, however, have not been detected thus far in patients following an SAH event. For this reason daily cerebrospinal fluid (CSF) samples were collected from 22 consecutively enrolled patients with SAH and from 10 non-SAH patients (controls). The CSF samples were studied using immunoassays for IL-1Ra and TNF alpha to investigate whether an SAH caused increased cytokine levels. The mean IL-1Ra levels were significantly higher in patients with SAH who were in poor clinical condition on admission than in those who were in good condition (318 pg/ml vs. 82 pg/ml, p < 0.02). The IL-1Ra levels increased during delayed ischemic episodes and after surgery in patients who were in poor clinical condition. Significant increases in IL-1Ra and TNF alpha were detected during Days 4 through 10 in patients suffering from SAH who eventually had a poor outcome (p < 0.05). Patients with good outcomes and control patients had low levels of these cytokines. The levels of IL-1Ra increased after surgery in patients with Hunt and Hess Grades III through V, but not in those with Grade I or II. This finding indicates that patients in poor clinical condition have a labile biochemical state in the brain that is reflected in increased cytokine levels following the surgical trauma. Both IL-1Ra and TNF alpha are known to induce fever, malaise, leukocytosis, and nitric oxide synthesis and to mediate ischemic and traumatic brain injuries. The present study shows that levels of these cytokines increase after SAH occurs and that high cytokine levels correlate with brain damage. It is therefore likely that fever, leukocytosis, and nitric oxide synthesis are also mediated by IL-1 in patients suffering from SAH and it is probable that the inflammatory mediators contribute to brain damage.

Adult↗