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1.
Fetal Pediatr Pathol ; 42(3): 376-384, 2023 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-36484731

RESUMO

OBJECTIVE: We compared the immunologic characteristics of mycoplasma pneumoniae-triggered Kawasaki disease (MP-KD) with Kawasaki disease (KD) not associated with mycoplasma pneumoniae (MP), with mycoplasma pneumoniae-triggered Henoch-Schönlein purpura (MP-HSP), and with healthy controls. METHODS: Complement levels, cellular and humoral immunity were assessed in KD, in MP-KD, in MP-HSP, and in healthy children. RESULTS: Of 622 children with KD, 74 had MP-KD. Complement C3 and CD4/CD8 ratio were significantly increased in MP-KD compared to KD. C3, C4, and the ratio of CD4/CD8 in the MP-KD group were higher than those in the MP-HSP group. IgA and CD56 were lower in the MP-KD group than the MP-HSP group. CONCLUSIONS: Both C3 and polyclonal CD4+ T lymphocytes may be activated in the patients with MP-KD.


Assuntos
Vasculite por IgA , Síndrome de Linfonodos Mucocutâneos , Pneumonia por Mycoplasma , Criança , Humanos , Síndrome de Linfonodos Mucocutâneos/complicações , Pneumonia por Mycoplasma/complicações , Vasculite por IgA/complicações
2.
Fetal Pediatr Pathol ; 41(6): 954-961, 2022 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-34978251

RESUMO

Objectives The objectives of present study were to analyze the association of the streptococcal infection with childhood Henoch-Schönlein purpura (HSP) in China. Methods: We performed a case-control study over a period of five years to evaluate the epidemiology and clinical characteristics of group A ß-hemolytic streptococcal (GABHS) triggered HSP. Results: 1. The frequency of GABHS-triggered HSP was 15.1%, while that of GABHS infection developing HSP in children was 4.7%. 2.The epidemiological characteristics of HSP with streptococcal infection were similar to those of HSP alone. 3. The GABHS-triggered HSP cases had a significantly higher frequency of renal involvement than the noninfectious group. 4. IgA and IgG were significantly increased in the streptococcal infection group than in the noninfectious group, while the levels of C3 and C4 decreased significantly. Conclusions: GABHS infection is the most frequent agent in HSP children, and may aggravate the immune dysfunction and prolong the course of HSP.


Assuntos
Vasculite por IgA , Infecções Estreptocócicas , Criança , Humanos , Vasculite por IgA/complicações , Vasculite por IgA/epidemiologia , Estudos de Casos e Controles , Infecções Estreptocócicas/complicações , Infecções Estreptocócicas/epidemiologia , China/epidemiologia
3.
Mediterr J Hematol Infect Dis ; 13(1): e2021064, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34804438

RESUMO

BACKGROUND: Henoch-Schönlein purpura (HSP) is an immune-mediated vasculitis, and the formation of immune complexes may be triggered by exposure to Epstein-Barr virus (EBV) infection. METHODS: We performed a five-year case-control study to evaluate the epidemiology and clinical characteristics of HSP associated with EBV infection. RESULTS: The incidence of EBV-triggered HSP was 4.2%, while EBV infection in children with HSP was 0.9%; The EBV-triggered HSP cases had a significantly higher frequency of abdominal pain than the Mycoplasma Pneumoniae (MP)-triggered HSP group (χ2 = 8.024, p = 0.005); Significant differences were observed in the duration of abdominal pain (Z = -1.935, p = 0.027) between the two groups; C3 (t = 9.709, p < 0.001), IgA (t = 20.39, p < 0.001) and IgG (t = 6.407, p < 0.001) were significantly increased in the EBV infection group than those in the healthy control group. Notably, significantly higher proportion of CD19 (t = 6.773, p < 0.001) and lower proportion of CD56 (t = 11.13, p < 0.001) was found in EBV infection group compared with healthy control group. The IgA level was higher than that of the non-infectious group (t = 2.162, p = 0.032), but their CD4/CD8 ratio (t = 10.070, p < 0.001) and CD56 proportion (t = 2.096, p = 0.037) were significantly lower. CONCLUSIONS: Both cellular and humoral immunity were involved in the pathogenesis of EBV-triggered HSP, leading to increased production of inflammatory mediators and immunoglobulins. Those events may cause or promote the development of systemic vessel vasculitis.

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