RESUMO
BACKGROUND: To investigate the clinical features of Kikuchi-Fujimoto disease (KFD) in children, and place an emphasis on the therapeutic effects of hydroxychloroquine as monotherapy. METHODS: We retrospectively reviewed the medical records of all children diagnosed with KFD during the period January 1992 to September 2016 at a tertiary medical center in Taiwan. RESULTS: 40 patients were histopathologically confirmed as KFD, and the mean age of the patients was 13.9 ± 3.1 years. The male to female ratio was 1:1. The lymph node involvements were often cervical (95%) with features of unilateral predisposition (75%), polyadenopathy (84.4%) and tenderness (56.3%). Fever, cough, rhinorrhea, and tonsillitis were other common presentations. Laboratory findings included leukopenia (56.5%), monocytosis (63.6%), with positive results of EB-VCA IgG (88.9%), EB-VCA IgM (22.2%), EBEA IgG (22.2%) and EBNA IgG (88.9%). The univariate analyses of prolonged fever with lymphopenia, monocytosis, thrombocytopenia and necrotizing type in histopathology were disclosed as statistically significant (P < 0.05). Corticosteroids and hydroxychloroquine were administered in 15.6% of patients respectively, along with symptomatic treatments for the rest. Recurrence occurred in 13.0% of patients without corticosteroids or hydroxychloroquine treatment. There were neither recurrences nor relevant major adverse effects in all the five KFD cases treated with hydroxychloroquine. CONCLUSION: KFD should be suspected in children with febrile cervical lymphadenopathy, especially when concomitant with leukopenia and monocytosis. Lymphopenia, monocytosis, thrombocytopenia and necrotizing type in histopathology are reliable predictors for prolonged fever. Hydroxychloroquine may be an alternative choice to corticosteroids for its favorable effects and safety.
Assuntos
Linfadenite Histiocítica Necrosante/tratamento farmacológico , Linfadenite Histiocítica Necrosante/patologia , Hidroxicloroquina/uso terapêutico , Adolescente , Corticosteroides/uso terapêutico , Biópsia , Criança , Diagnóstico Diferencial , Feminino , Linfadenite Histiocítica Necrosante/diagnóstico , Humanos , Linfonodos/patologia , Masculino , Recidiva , Estudos Retrospectivos , Taiwan , Resultado do TratamentoRESUMO
Low-molecular-weight Fucoidan (Oligo-Fucoidan) is a sulfated polysaccharide that has a variety of biological effects and has also been shown to have beneficial health effects. However, the molecular mechanisms underlying the therapeutic effects of Oligo-Fucoidan in patients with cancer remain unclear. Using human colorectal cancer HCT116 cells with (p53+/+) or without (p53-/-) normal p53 expression, we found that Oligo-Fucoidan treatment reduces the occurrence of spontaneous DNA lesions. Etoposide induces double strand DNA breaks. Subsequent administration of Oligo-Fucoidan to etoposide-treated cells promotes p53 accumulation, p21 expression and significant decreases in ataxia-telangiectasia-mutated (ATM), checkpoint kinase 1 (Chk1) and γ-H2AX phosphorylation in p53+/+ cells compared with p53-/- cells. Similarly, co-administration of Oligo-Fucoidan with etoposide inhibits ATM, Chk1 and γ-H2AX phosphorylation, particularly in the presence of p53. Furthermore, Oligo-Fucoidan supplementation increases cancer cell death and attenuates the adverse effects induced by etoposide that decreases production of the pro-inflammatory cytokine IL-6 and chemokine CCL2/MCP-1. Importantly, Oligo-Fucoidan decreases the tumor-promoting M2 macrophages in microenvironment as well as collaborates with p53 and works in combination with etoposide to prevent HCT116 tumorigenicity. Our results first demonstrate that p53 enables Oligo-Fucoidan to effectively inhibit tumor progression, and Oligo-Fucoidan minimizes the side effects of chemotherapy and alters tumor microenvironment.
Assuntos
Proteínas Mutadas de Ataxia Telangiectasia/metabolismo , Quimiocina CCL2/biossíntese , Interleucina-6/biossíntese , Neoplasias Experimentais/metabolismo , Oligossacarídeos/farmacologia , Polissacarídeos/farmacologia , Transdução de Sinais/efeitos dos fármacos , Proteína Supressora de Tumor p53/metabolismo , Animais , Proteínas Mutadas de Ataxia Telangiectasia/genética , Quimiocina CCL2/genética , Células HCT116 , Humanos , Interleucina-6/genética , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Neoplasias Experimentais/tratamento farmacológico , Neoplasias Experimentais/genética , Neoplasias Experimentais/patologia , Transdução de Sinais/genética , Células THP-1 , Proteína Supressora de Tumor p53/genéticaRESUMO
Z-K8 (2), the racemic form of isochaihulactone (1), previously showed significant antitumor effects in A549 and LNCaP tumor-bearing mice. In the present study, 17 derivatives of 2, were designed, synthesized and evaluated for anti-proliferative activity against four human tumor cell lines. All new derivatives exhibited high potency against A549 and P-glycoprotein (P-gp)-overexpressing KBvin. One of our new derivative exhibited greater activity against three tested tumor cells (A549, KB, and KB-VIN) than 2, and induced cell cycle arrest in the G2/M phase. Moreover, SAR conclusions were first established for this series of compounds. Our study clearly identified a structural feature that should be retained for good activity and also a moiety that can tolerate various modifications and, thus, is ideal for further changes.
RESUMO
BACKGROUND: Lower respiratory tract infections (LRTIs) play an important role in pediatric diseases; however, there are limited data about LRTIs in Southern Taiwan. This study aimed to investigate the clinical and epidemiological data of LRTIs in this area. METHODS: Children aged under 5 years who were hospitalized at a medical center in Southern Taiwan with acute LRTIs from July 2010 to October 2010 (summer) and from March 2011 to May 2011 (spring) were prospectively enrolled. Nasopharyngeal aspirates were obtained and sent for viral cultures, multiplex polymerase chain reaction (PCR), and traditional quick tests. The clinical features, laboratory data, and imaging findings were recorded and analyzed. RESULTS: A total of 90 children were enrolled, 70 of whom had detectable pathogens. The positive rate of conventional viral and bacterial cultures was 25.6%, which increased to 77.77% after combining with the two multiplex PCR methods. Adenovirus and enterovirus were the most common viral etiologies identified (26.5% of cases) and Streptococcus pneumoniae was the leading bacterial etiology (46.4%). The seasonal trend of viral infections in Southern Taiwan was different from Northern Taiwan. There were no differences in demographic data, severity of disease, or hospital stay between single and mixed infections. A similar result was found between nonpneumococcal and pneumococcal infections. CONCLUSION: Viral infections were the main etiologies of LRTIs in young children. Multiplex PCR methods are rapid assays that can increase the diagnostic yield rate. Mixed infections do not seem to affect the severity of disease. Early detection may aid clinicians in appropriate decision-making and treatment.
Assuntos
Infecções Pneumocócicas/epidemiologia , Infecções Respiratórias/diagnóstico , Infecções Respiratórias/epidemiologia , Viroses/epidemiologia , Adenoviridae/isolamento & purificação , Pré-Escolar , Enterovirus/isolamento & purificação , Feminino , Hospitalização , Humanos , Lactente , Masculino , Reação em Cadeia da Polimerase Multiplex , Infecções Pneumocócicas/microbiologia , Estudos Prospectivos , Infecções Respiratórias/microbiologia , Infecções Respiratórias/virologia , Estações do Ano , Streptococcus pneumoniae/isolamento & purificação , Taiwan/epidemiologia , Viroses/virologiaRESUMO
BACKGROUND: Infective endocarditis (IE) due to Pseudomonas aeruginosa is rare and accounts for only about 3% of all patients with this disease. Most infections are associated with the use of intravenous drugs. Patients with P. aeruginosa-related IE who do not use intravenous drugs are extremely rare. We carried out a review of the literature to identify the nature and risk factors of this disease. METHODS: Patients with IE reported between 1993 and 2013 were reviewed by searching the Medline database using the keywords "endocarditis" and "Pseudomonas aeruginosa". All of the patients included met the definition of the modified Duke criteria. RESULTS: Twenty-seven patients in 22 reports were reviewed. IE associated with health care accounted for 20 patients (74%). The mean age of the patients was 53.4 years and there was a predominance of men (81.5%). Native valve endocarditis was seen in 20 (74.1%) patients. Surgery for infection control was performed in 15 (55.6%) patients and the mortality rate in patients who underwent surgery was 33.3% (five patients). A relapse of IE after adequate treatment was seen in nine (33.3%) patients. The mortality rate in all 27 patients was 28.6% (2/7) for those with community-acquired IE and 40% (8/20) for those with IE associated with health care. Univariate analysis showed a higher mortality rate in patients aged >60 years and in those whose source of endocarditis was related to a prosthetic device. CONCLUSION: P. aeruginosa endocarditis has substantial morbidity and mortality. It is characterized by easy relapse and is highly associated with prosthetic devices.
Assuntos
Endocardite Bacteriana/mortalidade , Pseudomonas aeruginosa/patogenicidade , Endocardite Bacteriana/microbiologia , Endocardite Bacteriana/cirurgia , Mortalidade Hospitalar , Humanos , Pessoa de Meia-Idade , Infecções Relacionadas à Prótese/microbiologia , Fatores de Risco , Resultado do TratamentoRESUMO
BACKGROUND: The androgen receptor (AR) is a main therapeutic target for treatment of prostate cancer (PCa). The natural compound isochaihulactone (K8), which has a chiral center ring and two racemic forms (E-K8 and Z-K8), has anti-tumor effects on multiple cancer types both in vitro and in vivo. Here, we determined which form of K8 contains significant tumor cytotoxicity and examined how this form regulates AR expression in PCa cells and xenografts. METHODS: We chose the androgen-dependent human PCa cell line LNCaP and the androgen-independent cell lines DU145 and PC-3 to study the anti-tumor potency and AR regulation mediated by Z-K8. We measured cell viability and used flow cytometry, RT-PCR, and Western blotting. Growth inhibition in vivo was evaluated with an LNCaP xenograft animal model. RESULTS: In LNCaP cells, Z-K8 significantly repressed cell proliferation, induced apoptosis, repressed AR mRNA and protein expression in a time-dependent manner, and induced JNK phosphorylation. Furthermore, treatment with a JNK inhibitor significantly abolished Z-K8-induced AR downregulation. Z-K8 did not significantly inhibit reporter gene expression of constructs containing the AR promoter when it contained a mutated Sp1 binding site. Z-K8 also showed anti-tumor effects in the xenograft animal model. CONCLUSION: Z-K8 not only induced LNCaP apoptosis but also reduced AR expression. These results indicate that Z-K8 may be a potential anti-tumor drug for PCa therapy.
Assuntos
4-Butirolactona/análogos & derivados , Benzodioxóis/farmacologia , Sistema de Sinalização das MAP Quinases/fisiologia , Neoplasias da Próstata/tratamento farmacológico , Receptores Androgênicos/genética , 4-Butirolactona/química , 4-Butirolactona/farmacologia , Animais , Antineoplásicos/química , Antineoplásicos/farmacologia , Apoptose/efeitos dos fármacos , Benzodioxóis/química , Linhagem Celular Tumoral , Citotoxinas/farmacologia , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Proteínas de Fluorescência Verde/genética , Humanos , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Neoplasias da Próstata/genética , Neoplasias da Próstata/metabolismo , Receptores Androgênicos/metabolismo , Transcrição Gênica/efeitos dos fármacos , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
In spite of numerous advances, the 5-year survival rate for head and neck squamous cell cancer has remained largely stagnant and few new anti-tumor drugs have been developed. PCH4, a derivative of n-butylidenephthalide, has been investigated for its anti-tumor effects on oral squamous cell carcinoma (OSCC). The aim of this study was to investigate the anti-tumor mechanism of a potential target gene, Nur77, in OSCC cells, which can be induced by PCH4 treatment. Data show that PCH4 promoted Nur77 translocation from the nucleus to the cytoplasm and induced cell apoptosis in OSCC cells. When Nur77 translocation was blocked, the degree of tumor apoptosis caused by PCH4 was significantly inhibited (p < 0.05). Within the MAPK pathway, PCH4 only induced JNK phosphorylation. Furthermore, treatment with a JNK inhibitor significantly reduced PCH4-induced apoptosis (p < 0.05) and decreased PCH4-induced Nur77 expression (p < 0.05). In a xenograft animal model, administration of PCH4 also showed anti-tumor effects. We have demonstrated that OSCC cells are sensitive to PCH4 and that Nur77 protein translocation from the nucleus to the cytoplasm might be associated with the induction of apoptosis by PCH4. These results indicate that PCH4 may serve as a potential anti-tumor drug for OSCC therapy.
Assuntos
Antineoplásicos/farmacologia , Apoptose/efeitos dos fármacos , Benzofuranos/farmacologia , Carcinoma de Células Escamosas/tratamento farmacológico , Proliferação de Células/efeitos dos fármacos , Etilaminas/farmacologia , Neoplasias Bucais/tratamento farmacológico , Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo , Anidridos Ftálicos/farmacologia , Transporte Ativo do Núcleo Celular , Animais , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/metabolismo , Carcinoma de Células Escamosas/patologia , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Relação Dose-Resposta a Droga , Feminino , Humanos , Proteínas Quinases JNK Ativadas por Mitógeno/antagonistas & inibidores , Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Neoplasias Bucais/genética , Neoplasias Bucais/metabolismo , Neoplasias Bucais/patologia , Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/genética , Fosforilação , Inibidores de Proteínas Quinases/farmacologia , RNA Mensageiro/metabolismo , Fatores de Tempo , Carga Tumoral/efeitos dos fármacos , Regulação para Cima , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
BACKGROUND: Telomerase is widely expressed in most human cancers, but is almost undetectable in normal somatic cells and is therefore a potential drug target. Using the human telomerase promoter platform, the naturally occurring compound butylidenephthalide (BP) was selected for subsequent investigation of antitumor activity in vitro and in vivo. METHODS: We treated human glioblastoma cells with BP and found a dose-dependent decrease in human telomerase reverse transcriptase (hTERT) mRNA expression and a concomitant increase in p16 and p21 expression. Because c-Myc and Sp1 are involved in transcriptional regulation of hTERT, the effect of BP on c-Myc and Sp1 expression was examined. RESULTS: Using electrophoretic mobility shift assays and western blotting, we showed that BP represses hTERT transcriptional activity via downregulation of Sp1 expression. Using the telomerase repeat amplification protocol, an association between BP concentration and suppression of telomerase activity, induction of human glioblastoma senescence, and inhibition of cellular proliferation was identified. This was supported by a mouse xenograft model, in which BP repressed telomerase and inhibited tumor proliferation, resulting in tumor senescence. Overexpression of hTERT restored telomerase activity in human glioblastoma cells and overcame replicative senescence. CONCLUSIONS: These findings suggest that BP inhibits proliferation and induces senescence in human glioblastomas by downregulating hTERT expression and consequently telomerase activity. This is the first study to describe regulation of telomerase activity by BP in human glioblastomas.
Assuntos
Neoplasias Encefálicas/enzimologia , Proliferação de Células/efeitos dos fármacos , Regulação Neoplásica da Expressão Gênica , Glioblastoma/enzimologia , Anidridos Ftálicos/farmacologia , Proteínas Proto-Oncogênicas c-myc/metabolismo , Telomerase/metabolismo , Animais , Western Blotting , Neoplasias Encefálicas/tratamento farmacológico , Neoplasias Encefálicas/patologia , Senescência Celular/efeitos dos fármacos , Inibidor de Quinase Dependente de Ciclina p21/genética , Inibidor de Quinase Dependente de Ciclina p21/metabolismo , Ensaio de Desvio de Mobilidade Eletroforética , Citometria de Fluxo , Genes p16 , Glioblastoma/tratamento farmacológico , Glioblastoma/patologia , Humanos , Técnicas Imunoenzimáticas , Camundongos , Camundongos Nus , Regiões Promotoras Genéticas/genética , Proteínas Proto-Oncogênicas c-myc/genética , RNA Mensageiro/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Telomerase/antagonistas & inibidores , Telomerase/genética , Transcrição Gênica , Células Tumorais CultivadasRESUMO
We have shown that the natural compound z-butylidenephthalide (Bdph), isolated from the chloroform extract of Angelica sinensis, has antitumor effects. Because of the limitation of the blood-brain barrier, the Bdph dosage required for treatment of glioma is relatively high. To solve this problem, we developed a local-release system with Bdph incorporated into a biodegradable polyanhydride material, p(CPP-SA; Bdph-Wafer), and investigated its antitumor effects. On the basis of in vitro release kinetics, we demonstrated that the Bdph-Wafer released 50% of the available Bdph by the sixth day, and the release reached a plateau phase (90% of Bdph) by the 30th day. To investigate the in situ antitumor effects of the Bdph-Wafer on glioblastoma multiforme (GBM), we used 2 xenograft animal models-F344 rats (for rat GBM) and nude mice (for human GBM)-which were injected with RG2 and DBTRG-05MG cells, respectively, for tumor formation and subsequently treated subcutaneously with Bdph-Wafers. We observed a significant inhibitory effect on tumor growth, with no significant adverse effects on the rodents. Moreover, we demonstrated that the antitumor effect of Bdph on RG2 cells was via the PKC pathway, which upregulated Nurr77 and promoted its translocation from the nucleus to the cytoplasm. Finally, to study the effect of the interstitial administration of Bdph in cranial brain tumor, Bdph-Wafers were surgically placed in FGF-SV40 transgenic mice. Our Bdph-Wafer significantly reduced tumor size in a dose-dependent manner. In summary, our study showed that p(CPP-SA) containing Bdph delivered a sufficient concentration of Bdph to the tumor site and effectively inhibited the tumor growth in the glioma.
Assuntos
Angelica sinensis/química , Neoplasias Encefálicas/tratamento farmacológico , Glioma/tratamento farmacológico , Anidridos Ftálicos/administração & dosagem , Polímeros/química , Animais , Barreira Hematoencefálica , Linhagem Celular Tumoral , Fatores de Transcrição Forkhead/fisiologia , Humanos , Cinética , Masculino , Camundongos , Camundongos Nus , Camundongos Transgênicos , Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo , Anidridos Ftálicos/farmacocinética , Ratos , Ratos Endogâmicos F344 , Distribuição TecidualRESUMO
BACKGROUND: In previous study, n-butylidenephthalide (BP), a natural compound from Angelica sinensis, has anti-glioblastoma multiform (GBM) cell effects. In this study, we modified BP structure to increase anti-GBM cell effects. The anti-GBM cell effects of one derivative of BP, (Z)-N-(2-(dimethylamino)ethyl)-2-(3-((3-oxoisobenzofuran-1(3H)-ylidene)methyl)phenoxy)acetamide (PCH4) were tested in vitro and in vivo. METHODS: MTT assay and PI/Annexin V assay were performed to evaluate the anti-GBM effects of PCH4. The Nur77 expression and translocation were assayed by RT-PCR and Western blot. The Nur77 siRNA was used to downregulate the Nur77 expression. The JNK inhibitor (SP600125) was used to block the JNK pathway. RESULTS: The anti-GBM effect of PCH4 is four times more than BP. The IC(50) of PCH4 on DBTRG-05MG cells was 50 µg/ml. Nur77 expression and translocation from the nucleus to the cytoplasm were important in PCH4-induced apoptosis. Furthermore, the downregulation of PCH4-induced Nur77 expression by Nur77 siRNA reduced PCH4-induced apoptosis. In addition, PCH4-induced apoptosis was associated with the JNK pathway. The JNK inhibitor, SP600125, inhibited Nur77 mRNA expression and reduced PCH4-induced apoptosis. CONCLUSIONS: In conclusion, PCH4, a derivative of BP, induced Nur77-mediated apoptosis via the JNK pathway and this mechanism, which is different from that of BP, may explain the increase in the anti-tumor effects on GBM.
Assuntos
Apoptose/efeitos dos fármacos , Benzofuranos/farmacologia , Neoplasias Encefálicas/tratamento farmacológico , Proliferação de Células/efeitos dos fármacos , Etilaminas/farmacologia , Glioblastoma/tratamento farmacológico , Glioblastoma/patologia , Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo , Transporte Proteico/efeitos dos fármacos , Angelica sinensis/química , Animais , Western Blotting , Neoplasias Encefálicas/metabolismo , Neoplasias Encefálicas/patologia , Proteínas de Ligação a DNA/antagonistas & inibidores , Proteínas de Ligação a DNA/genética , Proteínas de Ligação a DNA/metabolismo , Citometria de Fluxo , Glioblastoma/metabolismo , Humanos , Luciferases/metabolismo , MAP Quinase Quinase 4/antagonistas & inibidores , MAP Quinase Quinase 4/metabolismo , Camundongos , Camundongos Nus , Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/antagonistas & inibidores , Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/genética , Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/antagonistas & inibidores , Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/genética , Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo , Anidridos Ftálicos/química , Anidridos Ftálicos/farmacologia , RNA Mensageiro/genética , RNA Interferente Pequeno/genética , Receptores de Esteroides/antagonistas & inibidores , Receptores de Esteroides/genética , Receptores de Esteroides/metabolismo , Receptores dos Hormônios Tireóideos/antagonistas & inibidores , Receptores dos Hormônios Tireóideos/genética , Receptores dos Hormônios Tireóideos/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Transdução de Sinais , Células Tumorais Cultivadas , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
The potential to generate virtually any differentiated cell type from stem cells offers the possibility of creating new sources of cells for regenerative medicine. To realize this potential, it will be essential to control stem cell differentiation. Chinese herbal medicine is a major aspect of traditional Chinese medicine and is a rich source of unique chemicals. As such, individual herbs or extracts may play a role in the proliferation and differentiation of stem cells. In this review, we discuss some of the Chinese herbal medicines that are used to treat human diseases such as neuronal degenerative diseases, cardiovascular diseases, and osteoporosis. We also describe the relationship between Chinese herbal medicines and stem cell regulation.
Assuntos
Medicamentos de Ervas Chinesas/uso terapêutico , Células-Tronco Neurais/citologia , Doenças Ósseas Metabólicas/terapia , Constrição Patológica/terapia , Humanos , Infarto do Miocárdio/terapia , Células-Tronco Neurais/transplante , Doenças Neurodegenerativas/terapia , Neurogênese , Medicina RegenerativaRESUMO
BACKGROUND AND PURPOSE: To determine the frequency, risk factors, associated pathogens, and outcomes of ventilator-associated pneumonia (VAP) after pediatric cardiac surgery. METHODS: This was a retrospective review of the medical records of patients younger than 18 years with congenital heart disease (CHD) who underwent cardiac surgery from January 2005 to December 2007. Patients were categorized into 2 groups: with and without VAP. RESULTS: Of 100 patients, 13% acquired VAP. Most patients (85%) who developed VAP were infants younger than 1 year. Patients with complex CHD were more likely to develop VAP than patients with simple CHD (chi(2) = 7.69; p < 0.03). Two independent and modifiable risk factors were identified: prolonged use of mechanical ventilation (adjusted odds ratio [AOR], 15.196; 95% confidence interval [CI], 2.158-107.2) and prolonged use of a central venous catheter (AOR, 7.342; 95% CI, 1.054-51.140). The cardiopulmonary bypass time and duration of chest tube drainage were not risk factors. The development of VAP increased pediatric intensive care unit duration of stay (p < 0.006), duration of hospital stay (p < 0.001), and mortality rate (p < 0.001). Pseudomonas aeruginosa and methicillin-resistant Staphylococcus aureus were the most common pathogens isolated from endotracheal aspirate. CONCLUSIONS: VAP is common after congenital heart surgery. Physicians must pay special attention to infants with complex CHD because they are at high risk for the development of VAP after congenital heart surgery. Shortening the duration of mechanical ventilation and central venous catheter placement are critical factors for reducing the risk for VAP.