The Incidence and Risk Factors of Extrapulmonary Manifestations in Mycoplasma Pneumoniae Pneumonia

Abstract

Background: Mycoplasma pneumoniae pneumonia (MP) is a major cause of community acquired pneumonia (CAP) in children and it is known to be associated with extrapulmonary manifestations (EPM). The incidence and risk factors of EPM in children are not known.Methods: This is a retrospective study involving 65,243 pediatric CAP patients between 2010 and 2015 at 23 nationwide hospitals was conducted in South Korea. The medical records were reviewed to collect the information regarding the clinical characteristics, radiological results, and laboratory findings. In total, 9,190 children with MP were identified and included in the analysis. Logistic regression with multivariable analysis was performed to evaluate the risk factors associated with EPM in MP.Results: The mean age of the enrolled patients with MP was 64.3±39.8 months, and the proportion of male patients was 49.5%. The incidence of EPM was 23.9% and included elevation of liver enzymes (18.1%), mucocutaneous manifestations (4.4%), proteinuria (4.1%), cardiovascular and neurologic manifestation (0.4%), hematologic manifestation (0.2%) and arthritis (0.2%). Statistical analysis showed that mucocutaneous manifestations were significantly increased with elevated alanine aminotransferase (adjusted odds ratio [aOR] 3.623, 95% confidence intervals [CI] 1.933-6.790) and atopic sensitization (aOR 2.973, 95% CI 1.615-5.475) and decreased with respiratory virus co-infection (aOR 0.273, 95% CI 0.084-0.887). Elevated liver enzymes was significantly associated with the elevation of lactate dehydrogenase (aOR 3.055, 95% CI 2.257-4.137) and presence of pleural effusion (aOR 2.635, 95% CI 1.767-3.930) and proteinuria with respiratory virus co-infection (aOR 2.245, 95% CI 1.113-4.527). Conclusions: About 24% of pediatric MP patients were identified with various EPM. Since risk factors associated with each EPM was different, it is necessary to evaluate the various clinical aspects and findings of MP to predict and prepare for the occurrence of EPM.

Anaplastic thyroid cancer: genome-based search for new targeted therapy options

“…[2] The presence of the aberrant fusion protein results in abnormal signaling that provokes increased cell growth, proliferation and survival. [4] Crizotinib is indicated for the treatment of such cases but the presence of ALK kinase domain mutations confer resistance to the treatment. Thus, brigatinib is indicated for the treatment of patients with ALK+ NSCLC with intolerance to Crizotinib.…”

“…Upon internalization, the calicheamicin derivative is released inside the lysosomes of the myeloid cell. The released calicheamicin derivative binds to DNA in the minor groove resulting in site-specific DNA double strand breaks via formation of a p-benzene diradical [4]. Eventually, cell death is induced.…”

“…Gilteritinib is a potent selective inhibitor of both of the mutations, internal tandem duplication (ITD) and tyrosine kinase domain (TKD), of the FLT3 receptor.2 In the same note, gilteritinib also inhibits AXL and ALK tyrosine kinases.3 FLT3 and AXL are molecules involved in the growth of cancer cells. 4 The activity of gilteritinib permits an inhibition of the phosphorylation of FLT3 and its downstream targets such as STAT5, ERK and AKT. 6 The interest in FLT3 transmembrane tyrosine kinases was raised when studies reported that approximately 30% of the patients with acute myeloid leukemia presented a mutationally activated isoform.1 As well, the mutation ITD is associated with poor patient outcomes while the mutation TKD produces a resistance mechanism to FLT3 tyrosine kinase inhibitors and the AXL tyrosine kinase tends to produce a resistance mechanism to chemotherapies.…”

“…6 The interest in FLT3 transmembrane tyrosine kinases was raised when studies reported that approximately 30% of the patients with acute myeloid leukemia presented a mutationally activated isoform.1 As well, the mutation ITD is associated with poor patient outcomes while the mutation TKD produces a resistance mechanism to FLT3 tyrosine kinase inhibitors and the AXL tyrosine kinase tends to produce a resistance mechanism to chemotherapies. 4 Gilteritinib is indicated for the treatment of adult patients who have relapsed or refractory acute myeloid leukemia with an FLT3 mutation detected by an FDA-approved test. The Fab segment of the antibody targets the CD20 epitope on B-cells, allowing the radioactive yttrium to destroy the cell via production of beta particles.…”

“…Median overall survival (OS) for patients treated with targeted therapy, regardless of their grouping, was 15.7 months compared with 7.6 months in patients not having received any targeted therapy (3). In another single-institution retrospective study with 120 Korean ATC patients, tyrosine kinase inhibition (TKI) was also associated with favorable OS in a multivariate analysis (4).…”