Humans ; Child ; Retrospective Studies ; Thrombocytosis/etiology*

OBJECTIVETo investigate the viral etiology in hospitalized children with acute lower respiratory tract infections (ALRTI) plus platelet disorders.

METHODSA total of 255 children with ALRTI plus platelet disorders and 442 children with ALRTI and normal platelets, all of whom were hospitalized between March 2010 and February 2011, were included in the study. Their nasopharyngeal aspirate samples were collected, and RT-PCR or PCR was performed to detect 14 viruses.

RESULTSOf 255 ALRTI patients with platelet disorders, thrombocytosis was found in 253 cases (99.2%) and thrombocytopenia in 2 cases (0.8%). Among ALRTI patients with platelet disorders, 173 (67.8%) were infected with at least one virus, with human rhinovirus as the most common one, followed by parainfluenza virus type 3 (PIV3) and respiratory syncytial virus (RSV). The detection rate of PIV3 in the abnormal platelet group was significantly higher than in the normal platelet group (P<0.05). In contrast, the detection rate of influenza virus B (IFVB) in the abonormal platelet group was significantly lower than in the normal platelet group (P<0.05). The age distribution showed significant difference between the abnormal and normal platelet groups (P<0.01). Platelet disorders were mainly found in children under one year of age (P<0.01).

CONCLUSIONSThrombocytosis is often found in children with ALRTI caused by viruses, especially PIV3, but infection with IFVB seldom causes platelet disorders. Hospitalized children with ALRTI under one year tend to develop platelet disorders.

Acute Disease ; Adolescent ; Age Factors ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Infant, Newborn ; Male ; Respiratory Tract Infections ; blood ; complications ; virology ; Thrombocytopenia ; etiology ; Thrombocytosis ; etiology

No abstract available.
Aged ; Bone Marrow/pathology ; Genome, Human ; Humans ; Isochromosomes/*genetics ; Karyotyping ; Leukemia, Myeloid, Acute/complications/*diagnosis/genetics ; *Loss of Heterozygosity ; Male ; Oligonucleotide Array Sequence Analysis ; Thrombocytosis/*etiology

Kawasaki disease (KD) is an acute febrile illness of infancy and early childhood. In spite of extensive studies, the cause of KD is not known. Interleukin 6 (IL-6) has manyfold biological functions involved in the immune or inflammatory responses of the host to various stimuli. Here the author investigated whether IL-6 might be responsible for manifestations of KD, such as immunoglobulin hypersecretion, lymphocyte activation and systemic vasculitis. Serum IL-6 levels in KD were determined by ELISA. Usually sera from healthy children contained only negligible levels of IL-6. Serum IL-6 was markedly elevated in all patients with acute KD, which gradually decreased during the course of the disease. Serum IL-6 correlated with serum concentration of C-reactive protein and with serum soluble interleukin-2 receptor level, but did not show any correlation with peak platelet count during subacute phase of the disease. Increased serum IL-6 level did not show any relation to development of coronary aneurysms and dilatation. Further studies will be needed to examine the source and the pathogenetic roles of increased serum IL-6 in KD.
Child ; Child, Preschool ; Female ; Human ; Infant ; Interleukin-6/*blood ; Male ; Mucocutaneous Lymph Node Syndrome/*blood ; Receptors, Interleukin-2/analysis ; Thrombocytosis/etiology

The incidence of acute hepatitis in syphilis patient is rare. First of all, our patient presented with hepatitis comorbid with thrombocytosis. To our knowledge, this is only the second report of syphilitic hepatitis with thrombocytosis. The 42-yr-old male complained of flulike symptoms and skin eruptions on his palms and soles. Laboratory findings suggested an acute hepatitis and thrombocytosis. Serologic test results were positive for VDRL. He recovered from his symptoms and elevated liver related enzymes with treatment. Because syphilitic hepatitis can present without any typical signs of accompanying syphilis, syphilis should be considered as a possible cause in acute hepatitis patients.
Acute Disease ; Adult ; Alkaline Phosphatase/blood ; Bilirubin/blood ; Epidermis/pathology ; Hepatitis/*diagnosis/etiology/pathology ; Humans ; Jaundice ; Male ; Penicillin G Benzathine/therapeutic use ; Syphilis/*complications ; Syphilis Serodiagnosis ; Thrombocytosis/*etiology ; Tomography, X-Ray Computed

OBJECTIVES: To study the role and mechanism of platelet-derived growth factor BB (PDGF-BB) on platelet production in Kawasaki disease (KD) mice and human megakaryocytic Dami cells through in vitro and invivo experiments. METHODS: ELISA was used to measure the expression of PDGF in the serum of 40 children with KD and 40 healthy children. C57BL/6 mice were used to establish a model of KD and were then randomly divided into a normal group, a KD group, and an imatinib group (30 mice in each group). Routine blood test was performed for each group, and the expression of PDGF-BB, megakaryocyte colony forming unit (CFU-MK), and the megakaryocyte marker CD41 were measured. CCK-8, flow cytometry, quantitative real-time PCR, and Western blot were used to analyze the role and mechanism of PDGF-BB in platelet production in Dami cells. RESULTS: PDGF-BB was highly expressed in the serum of KD children (P<0.001). The KD group had a higher expression level of PDGF-BB in serum (P<0.05) and significant increases in the expression of CFU-MK and CD41 (P<0.001), and the imatinib group had significant reductions in the expression of CFU-MK and CD41 (P<0.001). In vitro experiments showed that PDGF-BB promoted Dami cell proliferation, platelet production, mRNA expression of PDGFR-β, and protein expression of p-Akt (P<0.05). Compared with the PDGF-BB group, the combination group (PDGF-BB 25 ng/mL + imatinib 20 μmol/L) had significantly lower levels of platelet production, mRNA expression of PDGFR-β, and protein expression of p-Akt (P<0.05). CONCLUSIONS PDGF-BB may promote megakaryocyte proliferation, differentiation, and platelet production by binding to PDGFR-β and activating the PI3K/Akt pathway, and the PDGFR-β inhibitor imatinib can reduce platelet production, which provides a new strategy for the treatment of thrombocytosis in KD.
Child ; Humans ; Animals ; Mice ; Mice, Inbred C57BL ; Becaplermin ; Imatinib Mesylate/therapeutic use* ; Mucocutaneous Lymph Node Syndrome/drug therapy* ; Phosphatidylinositol 3-Kinases ; Proto-Oncogene Proteins c-akt ; Thrombocytosis/etiology* ; RNA, Messenger

No abstract available.
Aged ; Antineoplastic Agents/therapeutic use ; Bone Marrow/pathology ; Fusion Proteins, bcr-abl/genetics/metabolism ; Humans ; Imatinib Mesylate/therapeutic use ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/complications/*diagnosis/drug therapy ; Leukocyte Count ; Male ; Multiple Myeloma/complications/*diagnosis/drug therapy ; Platelet Count ; Polymerase Chain Reaction ; Thrombocytosis/etiology