ABSTRACT
OBJECTIVE: To study the effects of hemoperfusion treatment on serum interleukin-17 (IL-17) and IL-23 levels in children with Henoch-Schönlein purpura (HSP). METHODS: Eighty-seven children who were diagnosed with HSP and who had received hemoperfusion treatment between January 2011 and December 2012 were enrolled. Twenty-seven sex- and age-matched healthy children were recruited as normal controls. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum concentrations of IL-17 and IL-23. RESULTS: The serum IL-23 and IL-17 levels in the HSP group were significantly higher than in the control group (P<0.05). After hemoperfusion treatment, the serum IL-23 and IL-17 levels in the HSP group were significantly reduced to the levels of the control group. Serum serum IL-17 level was positively correlated with serum IL-23 level (P<0.05) in children with HSP. CONCLUSIONS: Hemoperfusion treatment can reduce serum IL-23 and IL-17 levels in children with HSP, suggesting that the treatment may be effective for HSP.
Subject(s)
Hemoperfusion , IgA Vasculitis/therapy , Interleukin-17/blood , Interleukin-23/blood , Child , Child, Preschool , Female , Humans , IgA Vasculitis/immunology , Interleukin-17/physiology , Interleukin-23/physiology , MaleABSTRACT
OBJECTIVE: To explore the method for early diagnosis and pathogenesis of MYH9-related syndrome through analysis of the clinical manifestation and gene mutation of a Chinese family with MYH9-related syndrome. METHODS: Peripheral blood samples were collected from a three-generation Chinese family with MYH9-related syndrome (11 individuals, including 3 patients) and 100 healthy individuals. Polymerase chain reaction (PCR) amplification and direct sequencing of DNA were performed to analyze mutations of MYH9 gene. RESULTS: Thrombocytopenia, increased volume of platelet, and granulocyte inclusion bodies were found in the patients with MYH9-related syndrome via a peripheral blood test. A missense mutation of a base pair (G-A) in exon 30 was revealed by PCR amplification and direct sequencing of MYH9 of the proband. That lead to Asp-Asn substitution at position 1424 (D1424N mutation). The mutation was the same as in other patients with MYH9-related syndrome. It was not found in healthy people from the Chinese family or in the other 100 healthy individuals. CONCLUSIONS: Patients with MYH9-related syndrome show diverse symptoms. Mutation of MYH9 gene may be the molecular mechanism of MYH9-related syndrome, and D1424N mutation of MYH9 has not been reported in Chinese people. Early diagnosis of MYH9-related syndrome can be carried out by investigating family history and making early examinations.