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PubMed1990

The role of cytokines in the generation of inflammation and tissue damage in experimental gram-positive meningitis.

Cytokines mediate many host responses to bacterial infections. We determined the inflammatory activities of five cytokines in the central nervous system: TNF-alpha, IL-1 alpha, IL-1 beta, macrophage inflammatory protein 1 (MIP-1), and macrophage inflammatory protein 2 (MIP-2). Using a rabbit model of meningeal inflammation, each cytokine (except IL-1 beta) induced enhanced blood brain barrier permeability, leukocytosis in cerebrospinal fluid, and brain edema. Homologous antibodies to each mediator inhibited leukocytosis and brain edema, and moderately decreased blood brain barrier permeability. In rabbits treated with anti-CD-18 antibody to render neutrophils dysfunctional for adhesion, each cytokine studied lost the ability to cause leukocytosis and brain edema. After intracisternal challenge with pneumococci, antibodies to TNF or IL-1 prevented inflammation, while anti-MIP-1 or anti-MIP-2 caused only a 2-h delay in the onset of inflammation. We suggest these cytokines have multiple inflammatory activities in the central nervous system and contribute to tissue damage during pneumococcal meningitis.

Animals↗
PubMed1992

Bacterial components and the pathophysiology of injury to the blood-brain barrier: does cell wall add to the effects of endotoxin in gram-negative meningitis?

In animal models, the lipopolysaccharide (LPS) from Haemophilus influenzae contributes to all the signs of meningitis associated with living bacteria. However, when tested in vitro, the amount of LPS in cerebrospinal fluid (CSF) in natural disease shows much greater effects on leukocytes than on endothelial permeability. To investigate whether other bacterial components act with LPS to incite meningeal inflammation, animals were challenged intracisternally with H. influenzae lysates. Upon neutralization of endotoxin, leukocytosis was greatly attenuated, but protein accumulation in CSF persisted. Cell wall from H. influenzae induced meningeal inflammation in a pattern opposite to that of LPS. Its ability to induce blood-brain barrier permeability greatly exceeded its ability to induce leukocytosis in vivo. Thus, cell wall, by acting on endothelia, and LPS, by inducing leukocytosis, may cooperate to induce inflammation in H. influenzae meningitis. Optimal reduction of inflammation and tissue damage in meningitis may require agents directed against cell wall as well as LPS.

Animals↗
PubMed1998

Visceral larva migrans and the hypereosinophilia syndrome.

This is a case of visceral larva migrans and hypereosinophilia syndrome with persistently elevated white blood cell count despite adequate medical therapy in a 4-year-old boy with leukocytosis and splenomegaly. Medical history included reactive airway disease and geophagia (pica). Serology for Toxocara canis revealed elevated IgG and IgM titers. Ophthalmologic evaluation ruled out ocular larva migrans. After 5 days of thiabendazole therapy, leukocytosis persisted, and a second course of anthelmintics was prescribed. Two weeks later, a decrease in leukocytosis was noted. Thiabendazole therapy was continued for 15 more days. Repeated serology for T canis revealed a decreased IgM titer and a further elevated IgG titer. Follow-up showed increased physical activity, improved respiratory status, and resolution of splenomegaly.

Animals↗
PubMedDate not supplied

Hematologic changes after splenectomy for cytoreduction: implications for predicting infection and effects on chemotherapy.

Postsplenectomy leukocytosis and thrombocytosis are common findings in trauma patients. The intent of this study is to describe postsplenectomy hematologic changes in gynecological oncology surgery and subsequent chemotherapy. We performed a retrospective record review of gynecological oncology patients at our institutions. Postsurgical hematologic changes, infectious morbidity, and pre- and post-chemotherapy hematologic changes were noted. Data were analyzed using repeated measures analysis of variance. We identified 27 patients who underwent cytoreductive surgery with splenectomy. Thirteen patients with splenectomy had postoperative chemotherapy data available, and we matched these patients with 13 control patients who underwent cytoreduction surgery without splenectomy and postoperative chemotherapy. Nine of the 27 splenectomy patients had documented infectious morbidity. There was a significant difference in postoperative platelet counts between the infected and the noninfected splenectomy patients (P= 0.037), and a significant difference between splenectomy and control patients for white blood cell (WBC) counts (P = 0.007). Patients with splenectomy had higher precycle WBC, absolute neutrophil count (ANC), platelet counts, and higher postcycle nadir levels in all cycles compared to control patients. There was a significant overall difference between splenectomy patients and controls with regard to WBC (P = 0.001), ANC (P = 0.005), and platelet counts (P = 0.016) during chemotherapy cycles. Median postchemotherapy nadir WBC was 4.4 (range: 3.4-4.8) for the splenectomy group versus 2.8 (range: 2.5-3.0) for the control group. Median postchemotherapy nadir ANC was 1800 (range: 1320-2450) for the splenectomy group and 1001 (range: 864-1064) for the control group. Median postchemotherapy nadir platelet count was 222 (range: 181-277) for the splenectomy patients and 169 (range 164-215) for the control patients. In conclusion, the patients who undergo splenectomy as part of cytoreductive surgeries have a statistically significant leukocytosis and insignificant thrombocytosis relative to the control patients. Leukocytosis alone is not an accurate indicator of infection. Splenectomy is not associated with an increased risk of chemotherapy-related neutropenia and thrombocytopenia.

Adult↗
PubMed1984

Serum antibody responses to the outer membrane proteins of Bordetella pertussis.

The serum antibody responses to the outer membrane proteins, purified filamentous hemagglutinin, and leukocytosis-promoting factor of Bordetella pertussis were examined in mice and children immunized with pertussis whole-cell vaccine. It was found that, although there were many similarities in the responses of mice and children, there were important differences. Sera from vaccinated mice reacted strongly with purified filamentous hemagglutinin and gave weak or undetectable responses to the components of purified leukocytosis-promoting factor. The converse was found with sera from vaccinated children. Antibodies to leukocytosis-promoting factor may thus be of importance in protecting children against pertussis, although they appear to play no role in the active mouse protection test for vaccine efficacy. These results cast doubt on the value of the mouse as an animal model for the potency testing of extracted acellular pertussis vaccines.

Animals↗
PubMed1984

Lymphocytosis-promoting factor of Bordetella pertussis alters mononuclear phagocyte circulation and response to inflammation.

Previous results from our laboratory demonstrated that purified lymphocytosis-promoting factor (LPF), a protein toxin from Bordetella pertussis, inhibited the migration of murine macrophages in vitro. The current study examined the in vivo effects of LPF on mononuclear phagocyte circulation and response to an inflammatory stimulus. Intravenous injection of mice with 200 ng of LPF produced a prolonged monocytosis which peaked with a fivefold increase on day 5 after injection. LPF (200 ng) also inhibited by more than 75% the increase in peritoneal inflammatory macrophages induced by intraperitoneal injection of thioglycolate broth, phytohemagglutinin, or paraffin oil. The inhibition was significant when thioglycolate was given 1 h or 2 or 4 days after LPF but not when thioglycolate was given 2 or 4 days before LPF. The LPF-induced monocytosis on day 5 after injections was not altered by the intraperitoneal injection of thioglycolate broth. The leukocytosis-promoting and macrophage-inhibiting properties of LPF were the same in N:NIH(S) and C3H/HeJ mice. Treatments of LPF that reduced the leukocytosis-promoting effect of LPF also reduced the ability of LPF to inhibit the macrophage response. LPF doses sufficient to induce leukocytosis (greater than or equal to 25 ng) significantly inhibited the thioglycolate-induced increase in peritoneal macrophages. The results indicate that coincident with an LPF-induced monocytosis is a reduction in the number of mononuclear phagocytes at a site of inflammation. An in vivo inhibition of mononuclear phagocyte migration would explain both effects of LPF and is consistent with the in vitro inhibition of macrophage migration by LPF.

Animals↗
PubMed2005

Therapeutic angiogenesis with intramuscular injection of low-dose recombinant granulocyte-colony stimulating factor.

OBJECTIVE: In vivo administration of granulocyte colony-stimulating factor (G-CSF) has been shown to facilitate regeneration of cardiovascular tissues. However, G-CSF causes marked leukocytosis that potentially induces adverse cardiovascular events. Earlier studies showed that G-CSF had direct stimulatory actions on mature endothelial cells, resulting in promotion of angiogenesis. We thus examined whether low doses of recombinant human G-CSF (rhG-CSF) locally injected into ischemic tissues would stimulate angiogenesis without inducing severe leukocytosis. METHODS AND RESULTS: Reverse-transcription polymerase chain reaction (PCR) revealed expression of G-CSF receptor in human umbilical vein endothelial cells (HUVECs). rhG-CSF (100 ng/mL) enhanced migration and tube formation but not proliferation of HUVECs in vitro. We then examined the effects of rhG-CSF on angiogenesis in a rat model of hindlimb ischemia. Nude rats received in their ischemic skeletal muscles either rhG-CSF (2, 10, 20 microg/kg per day) or saline (control) for 6 days. Laser Doppler blood flowmetry (LDBF) revealed an augmented ischemic/normal limb LDBF ratio and an increased capillary density in the rhG-CSF-treated groups compared with the control at days 14, 21, and 28 (P<0.05). These doses of rhG-CSF induced only mild leukocytosis ( approximately 1.4-fold increases versus baseline). CONCLUSIONS: rhG-CSF promoted endothelial migration and tube formation in vitro. Local injection of low doses rhG-CSF effectively augmented ischemia-induced angiogenesis in vivo. This treatment regimen of low-dose rhG-CSF may become a new and safe modality for therapeutic angiogenesis.

Animals↗
PubMed2006

Clinical and radiological recurrence after childhood arterial ischemic stroke.

BACKGROUND: Data on rates and risk factors for clinical and radiological recurrence of childhood arterial ischemic stroke (AIS) might inform secondary prevention strategies. METHODS AND RESULTS: Consecutive Great Ormond Street Hospital patients with first AIS were identified retrospectively (1978-1990) and prospectively (1990-2000). Patients underwent repeat neuroimaging at the time of clinical recurrence or, if asymptomatic, at least 1 year after AIS. Cox and logistic regression analyses were used to explore the relationships between risk factors and clinical and radiological recurrence, respectively. A total of 212 patients were identified, of whom 97 had another prior diagnosis. Seventy-nine children had a clinical recurrence (29 strokes, 46 transient ischemic attacks [TIAs], 4 deaths with reinfarction 1 day to 11.5 years (median 267 days) later); after 5 years, 59% (95% confidence interval, 51% to 67%) were recurrence free. Moyamoya on angiography and low birth weight were independently associated with clinical recurrence in the whole group. Genetic thrombophilia was associated with clinical recurrence in previously healthy patients, independent of the presence of moyamoya. Sixty of 179 patients who had repeat neuroimaging had radiological reinfarction, which was clinically silent in 20. Previous TIA, bilateral infarction, prior diagnosis (specifically immunodeficiency), and leukocytosis were independently associated with reinfarction. Previous TIA and leukocytosis were also independently associated with clinically silent reinfarction. CONCLUSIONS: Clinical and radiological recurrence are common after childhood AIS. The risk of clinical recurrence is increased in children with moyamoya and, in previously healthy patients, in those with genetic thrombophilia. Preexisting pathology, including immunodeficiency, and persistent leukocytosis are risk factors for radiological recurrence, which suggests a potential role for chronic infection.

Adolescent↗
PubMed1993

A structure-activity relationship for induction of meningeal inflammation by muramyl peptides.

Components of bacterial peptidoglycans have potent biological activities, including adjuvant effects, cytotoxicity, and induction of sleep. Mixtures of peptidoglycan components also induce inflammation in the lung, subarachnoid space, and joint, but the structural requirements for activity are unknown. Using a rabbit model for meningitis, we determined the biological activities of 14 individual muramyl peptides constituting > 90% of the peptidoglycan of the gram-negative pediatric pathogen Haemophilus influenzae. Upon intracisternal inoculation, most of the muropeptides induced leukocytosis in cerebrospinal fluid (CSF), influx of protein into CSF, or brain edema, alone or in combination. The disaccharide-tetrapeptide, the major component of all gram-negative peptidoglycans, induced CSF leukocytosis and protein influx at doses as low as 0.4 microgram (0.42 nM). Modification of the N-acetyl muramic acid or substitution of the alanine at position four in the peptide side chain decreased leukocytosis but enhanced brain edema. As the size of the muropeptide increased, the inflammatory activity decreased. Muropeptide carrying the diaminopimelyl-diaminopimelic acid cross-link specifically induced cytotoxic brain edema. These findings significantly expand the spectrum of biological activities of natural muramyl peptides and provide the basis for a structure-activity relationship for the inflammatory properties of bacterial muropeptides.

Amino Acid Sequence↗
PubMed1989

Peripheral white blood cells and HPA axis neurohormones in major depression.

Alterations in peripheral blood leukocyte distribution in major depression, including leukocytosis, neurotrophilia and lymphopenia, have been described. To assess peripheral white blood cells and the hypothalamic-pituitary (HP) axis in drug-free patients with major depression, we measured the total white blood cell count (WBC), and percentage of lymphocytes, and the plasma levels of cortisol, adrenocorticotropic hormone (ACTH), growth hormone (GH) and prolactin (PRL). Twenty male patients with major depression had relative lymphopenia and leukocytosis when compared with 20 age, sex and racematched control subjects. Elevated Beck and Hamilton depression scores correlated with a decreased percentage of lymphocytes, in a group of all subjects combined. There was a weak tendency for elevated growth hormone to correlate with relative lymphopenia in the control subjects only. Relative lymphopenia and leukocytosis may be a part of the psychobiology of major depression.

Adrenocorticotropic Hormone↗
PubMed2000

Retinoic acid syndrome induced by arsenic trioxide in treating recurrent all-trans retinoic acid resistant acute promyelocytic leukemia.

Arsenic Trioxide (As2O3) is an effective agent for treating acute promyelocytic leukemia achieving a complete remission rate of about 60% to 90%. It is similar to all-trans retinoic acid (ATRA) when treating acute promyelocytic leukemia (APL), because both agents have limited side effects compared to conventional chemotherapy, although the treatment period is more prolonged. During treatment, both agents may induce leukocytosis, and in patients taking ATRA, leukocytosis appears to be related to the development of retinoic acid syndrome (RAS). We report here a case of APL treated with ATRA in combination with chemotherapy 3 years earlier. During treatment, an episode of RAS with fever, edema, pericardiac effusion etc. was encountered. Recently, she had a relapse of leukemia, and As2O3 therapy was used. Leukocytosis developed again, and symptoms of fever, skin rash, edema resembling a RAS also developed, which was quickly relieved by steroid administration in a manner resembling response to RAS.

Adult↗
PubMed1995

Collagenous colitis: mucosal biopsies and association with fecal leukocytes.

OBJECTIVE: To determine the frequency of patchy colonic involvement, fecal leukocytosis, and association with celiac sprue in a large cohort of patients with collagenous colitis. DESIGN: We conducted a retrospective review of the medical records of 172 consecutive Mayo Clinic patients in whom collagenous colitis had been diagnosed between 1982 and 1993. METHODS: For each of the 172 patients, the medical record was reviewed to determine the frequency of (1) fecal leukocytosis; (2) characteristic histologic findings in the rectum and the sigmoid, descending, and ascending colon; and (3) small bowel biopsy findings consistent with celiac sprue. RESULTS: The presence of fecal leukocytes was noted in 64 of 116 patients (55%) who had undergone assessment for fecal leukocytosis. On analysis of histologic findings, 113 of 123 rectal, 116 of 121 sigmoid, and 68 of 70 descending colon biopsy specimens were diagnostic of collagenous colitis. Small bowel biopsies were performed in 45 patients who did not have a history of small intestinal disease: 1 had celiac sprue and 44 had normal findings. Two other patients had previously diagnosed celiac sprue. CONCLUSION: The finding of fecal leukocytes in 55% of patients with collagenous colitis confirms the inflammatory basis of this disease. Biopsy specimens obtained by flexible sigmoidoscopy seem sufficient to establish the diagnosis in most patients, and colonoscopic biopsy of the more proximal area of the colon is usually unnecessary. Celiac sprue infrequently accompanies collagenous colitis; thus, routine small bowel biopsy is not warranted.

Adolescent↗
PubMed2006

Essential thrombocythemia beyond the first decade: life expectancy, long-term complication rates, and prognostic factors.

OBJECTIVE: To describe the long-term natural history of essential thrombocythemia (ET) in terms of life expectancy, risk of disease transformation Into a more aggressive myeloid disorder, and prognostic factors for both survival and disease complications. PATIENTS AND METHODS: The study population consisted of a consecutive cohort of patients seen at the Mayo Clinic In Rochester, Minn, in whom a diagnosis of ET was established before 1992, thus allowing a minimum of 10 years of potential follow-up. The conventional criteria-based diagnosis was confirmed by bone marrow biopsy in all Instances. RESULTS: A total of 322 patients were studied (median age, 54 years; median follow-up, 13.6 years). With a median survival time of 18.9 years, survival in the first decade of disease was similar to that of the control population (risk ratio, 0.72; 95% confidence interval, 0.50-0.99) but became significantly worse thereafter (risk ratio, 2.21; 95% confidence Interval, 1.74-2.76). Multivariable analysis identified age at diagnosis of 60 years or older, leukocytosis, tobacco use, and diabetes mellitus as Independent predictors of poor survival. A 2-variable model based on an age cutoff of 60 years and leukocyte count of 15 x 10(9)/L resulted in 3 risk groups with significant difference in survival. In addition, age at diagnosis of 60 years or older, leukocytosis, and history of thrombosis were independent predictors of major thrombotic events. The risk of leukemic or any myeloid disease transformation was low in the first 10 years (1.4% and 9.1%, respectively) but increased substantially in the second (8.1% and 28.3%, respectively) and third (24.0% and 58.5%, respectively) decades of the disease. CONCLUSION: Life expectancy in patients with ET is significantly worse than that of the control population. Leukocytosis is identified as a novel independent risk factor for both inferior survival and thrombotic events.

Adolescent↗
PubMed1993

[A case of bladder carcinoma representing leukemoid reaction].

A 60-year-old male with locally invasive bladder carcinoma (pT4 pNo Mo) had a remarkable leukocytosis of 64,900/mm3 in the peripheral blood count without any findings of inflammatory disease. The grade 3 transitional cell carcinoma (TCC) measuring 60 by 58 mm involved the prostate, but radiological examinations including abdominal CT scan and isotopic bone scan failed to prove distant metastasis. Serum calcium level was within normal level. Negative bone marrow finding for leukemia strongly suggested a leukemoid reaction by the bladder carcinoma. Preoperative arterial chemoembolization utilizing mitomycin C microcapsules and cisplatin infused into the tumor feeding arteries provided a normalization of leukocyte count (8,200/mm3) in association with a substantial tumor reduction, and was followed by radical cystoprostatectomy. Although the leukocyte count maintained a normal range for 2 months postoperatively, leukocytosis recurred and rapidly progressed to a leukocyte count of 51,300/mm3. CT scan revealed intrapelvic tumor recurrence, and serum analysis for granulocyte colony stimulating factor (G-CSF) demonstrated an elevated value of 130.9 pg/ml (normal, less than 30 pg/ml). The patient is now on systemic chemotherapy. The laboratory data and the response to the treatments would indicate that the leukocytosis in this patient is a leukemoid reaction due to the bladder carcinoma which may release G-CSF. Ten cases of bladder tumor representing leukemoid reaction have been reported in the literature.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1989

Effects of bacterially synthesized recombinant human granulocyte-macrophage colony-stimulating factor in patients with advanced malignancy.

STUDY OBJECTIVE: To define the clinical and hematologic effects of subcutaneously administered bacterially synthesized recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF). DESIGN: Single arm nonrandomized dose escalation study. PATIENTS: Twenty-one patients with advanced malignancy who were not receiving concurrent myelosuppressive therapy. INTERVENTIONS: Subcutaneous administration of rhGM-CSF by once-daily injection to groups of two to four patients at doses of 0.3 to 30 micrograms/kg body weight.d for 10 consecutive days. Some patients received a second 10-day period of daily rhGM-CSF treatment after a 10-day nontreatment interval followed by alternate-day treatment. Clinical status and hematologic values were monitored frequently. MEASUREMENTS AND MAIN RESULTS: All doses of rhGM-CSF caused an immediate transient fall of 84% to 99% in circulating neutrophils, eosinophils, and monocytes. Continued daily dosing caused a leukocytosis of up to 10-fold with increases in numbers of circulating neutrophils, eosinophils, monocytes, and lymphocytes. There appeared to be a plateau in the increase in neutrophils in the dose range 3 to 15 micrograms/kg.d. Marrow aspirates showed increased proportions of promyelocytes and myelocytes. Alternate-day injection of 15 micrograms/kg maintained a leukocytosis. At doses up to 15 micrograms/kg.d, rhGM-CSF was well tolerated but adverse effects included bone pains, myalgias, rashes, and liver dysfunction. At doses exceeding 15 micrograms/kg.d, pericarditis was a dose-limiting toxicity. Idiopathic thrombocytopenic purpura was reactivated by rhGM-CSF in one patient. CONCLUSIONS: Bacterially synthesized rhGM-CSF induces a leukocytosis in the dose range of 3 to 15 micrograms/kg.d. These doses are appropriate for phase II studies.

Adult↗
PubMed2000

[Toxocariasis with liver involvement].

We are reporting 16 cases of toxocariasis found in a two year period. Mean age was 2 years and 9 months. Sex distribution was 1:1. Thirteen (81%) children presented pica, 8 (50%) had pets at home, 10 (62.5%) presented anemia and long standing fever, and all eosinophilic leukocytosis. Fundoscopy was normal in all. Toxocara antibodies (Through ELISA) were increased in all of them. High resolution ultrasonography revealed hypoechoic areas in the liver in 50% of the cases. Therapeutic response was good, the clinical signs and symptoms disappearing at the end of treatment. The eosinophilic leukocytosis, ELISA serum positivity for toxocara and ultrasound findings persisted approximately for a year. Toxocariasis is a common parasitosis in our setting. It must be regarded as the first diagnosis when confronted with eosinophilic leukocytosis and abnormal liver findings by ultrasound.

Antibodies, Helminth↗
PubMed2000

[Progression of refractory thrombocytopenia to chronic myelomonocytic leukemia accompanied by various inflammatory reactions].

A 51-year-old man was admitted for treatment of severe thrombocytopenia in May 1997. A diagnosis of MDS RA (refractory thrombocytopenia; RTC) was made by bone marrow examination, which revealed mild marrow hypoplasia and a reduced number of megakaryocytes accompanied by micromegakaryocytes and hypolobular megakaryocytes. Chromosome analysis demonstrated 46, XY, t(5;7) (q31;q22) in all 20 cells examined. The patient received only supportive therapy including platelet transfusion, until leukocytosis and monocytosis gradually developed in November 1998. In view of a marked increase in the number of monocytes (more than 3,000/microliter), a diagnosis of CMML was made in December 1998. As the leukocytosis progressed, various inflammatory symptoms such as facial erythema and endophthalmitis developed. Administration of interferon alpha (IFN alpha) unexpectedly worsened the leukocytosis and monocytosis, suggesting abnormal responses of these cells to IFN alpha. Detailed molecular analysis of these cells might reveal a novel mechanism of leukemogenesis associated with 5q31.

Disease Progression↗
PubMed2000

[Pyogenic and non-pyogenic vertebral osteomyelitis: descriptive and comparative study of a series of 40 cases].

BACKGROUND: To describe the features of vertebral osteomyelitis (VO) in our area, and to compare pyogenic VO (PVO) and non-pyogenic VO (NPVO). METHODS: Retrospective study of patients with VO diagnosed in our hospital between january 1992 and december 1998. RESULTS: We identify 40 patients with VO: 17 (42.5%) with tuberculous VO, 12 (30%) with PVO, 10 (25%) with brucellar VO and 1 (2.5%) with a VO caused by Candida albicans. The mean age was 52.9 years, and 75% of patients were male. Only a 20% of cases had a known immunosuppression. Fever/febricule was present in 55% of patients and vertebral pain in 95%. The more frequent locations were lumbar (67.5%) and dorsal (27.5%). One or more paravertebral or epidural abscesses were present in 67.5% of cases and spinal cord compression was present in 27.5%. An elevated erythrocyte sedimentation rate (ESR) was present in 40% and leukocytosis in 27.5%. Sequelae after complete treatment occurred in 40% of patients, with residual vertebral pain in 37.5%. There was a shorter clinical course and a higher frequency of fever/febricule and leukocytosis in PVO than in NPVO. CONCLUSIONS: In our area the more frequent etiology of VO is tuberculosis. VO occurs predominantly in males older than 50 years, without known immunosuppression, and almost exclusively with lumbar or dorsal locations. The absence of fever/febricule, leukocytosis or elevated ESR do not exclude the diagnosis of VO. Sequelae after complete treatment are relatively frequent, fundamentally residual vertebral pain. There are some differences in the features between PVO and NPVO, which may aid in the differential diagnosis of both entities.

Adolescent↗