Dwindled serum IgG levels of Rubella, Diphtheria toxin, Hepatitis B virus and Tetanus Toxoid after chemotherapy; a report from Iranian children with malignancy

Author(s):  
Kazem Ghaffari ◽  
Simin Sarlak ◽  
Abdorrahim Absalan ◽  
Roghayeh Rahimi Afzal ◽  
Aygin Eghbali ◽  
...  

Backgrounds: Epigenetic regulation such as DNA methylation plays a major role in chromatin organization Background: Chemotherapy suppresses immunoglobulin production as a result of cell toxicity. Decreased immunoglobulin levels can result in the onset of opportunistic infections. The aim of the current study is to compare the immunoglobulin G (IgG) levels of the selected vaccine-preventable disease (VPD) before and six months after chemotherapy in a group of Iranian children with malignancies. Materials and Methods: In this interventional study, serum levels of Rubella, Diphtheria toxin, Hepatitis B virus (HBV), Tetanus Toxoid, Mumps, and Measles IgG were measured in 30 children with malignancy and previously vaccinated for these diseases. Six months after chemotherapy, serum IgG levels were reassessed and compared with their corresponding pre-chemotherapy levels. Results: In this study, 17 (56.7%) male and 13 (43.3%) female were included. The mean age was 7.69±3.09 years. After chemotherapy, Rubella IgG levels dropped from 73.88±85.11 to 56.59±72.84 IU/mL (P<0.05; r= 0.956; 33.4% become serum negative (SN)). Diphtheria toxin IgG was diminished from 0.683±0.454 to 0.174±0.248 IU/mL (P<0.05; r=0.601; 26.7% SN). Anti-HBV IgG showed a reduction from 46.26±101.56 to 25.56±80.49 IU/mL (p<0.05; r= 0.524; 60% SN) and Anti-Tetanus Toxoid IgG fell down from 1.031±0.582 to 0.321±0.408 IU/mL (p<0.05; r= 0.365; 33.4% SN). Anti-Measles and Anti-Mumps IgGs showed no significant change (p>0.05). Conclusion: Pediatric chemotherapy was associated with dropped serum IgG levels of most VPDs. A good correlation was also observed between serum levels of IgG before and six months after chemotherapy. Revaccination of children with malignancies may be necessary upon declined serum IgG titers.

2019 ◽  
Author(s):  
Caixia Xia ◽  
Wei Zhu ◽  
Chunhong Huang ◽  
Guohua Lou ◽  
Bingjue Ye ◽  
...  

Abstract Background Interleukin-6 (IL-6) plays an important role in chronic inflammation. Thus, we aimed to investigate the effects of IL-6 polymorphisms in predicting the progression of hepatitis B virus (HBV) -related liver cirrhosis. Methods A cross-sectional study was conducted to analysis IL-6 polymorphisms and serum levels of IL-6 in HBV-infected patients of different clinical phases and in healthy controls. IL-6 polymorphisms were detected by Taqman PCR method and plasma IL-6 levels were assessed by ELISA. Results Our analysis included 182 chronic hepatitis B (CHB) patients, 190 HBV-infected liver cirrhosis cases, 125 inactive HBsAg carriers, and 246 healthy controls. Seven SNPs in IL-6 including rs10499563, rs17147230, rs1800796, rs2069837, rs1524107, rs2066992, rs2069852 were analyzed. In haplotype analysis between HBV-infected liver cirrhosis cases with CHB patients, inactive HBV-carriers or healthy controls, haplotype CT in block 1 and haplotype GGCGG in block 2 were associated with liver cirrhosis (P<0.05). What’s more, the genotype or allele frequencies were significantly different in IL-6 rs10499563 and rs2069837 when HBV-infected liver cirrhosis patients compared with CHB patients, inactive HBV-carriers or healthy controls. A further study found that compared with the controls or CHB patients, plasma IL-6 was elevated in HBV-infected liver cirrhosis patients (P<0.05). Conclusion In conclusion, the polymorphisms of the IL-6 rs10499563 and rs2069837 are associated with the susceptibility of liver cirrhosis may through their effects on IL-6 expressions and these two single nucleotide polymorphisms can be used as potential predicting markers for prognosis of HBV-infected liver cirrhosis.


1989 ◽  
Vol 24 (6) ◽  
pp. 646-654 ◽  
Author(s):  
Hiroshi Ikeda ◽  
Kazuharu Matsuura ◽  
Takao Tsuji

1996 ◽  
Vol 103 (1) ◽  
pp. 105-110 ◽  
Author(s):  
G. FATTOVICH ◽  
F. VINANTE ◽  
G. GIUSTINA ◽  
L. MOROSATO ◽  
A. ALBERTI ◽  
...  

2007 ◽  
Vol 4 (1) ◽  
pp. 93 ◽  
Author(s):  
Min Lian ◽  
Xu Zhou ◽  
Lai Wei ◽  
Shihong Qiu ◽  
Tong Zhou ◽  
...  

Hepatology ◽  
1987 ◽  
Vol 7 (4) ◽  
pp. 704-708 ◽  
Author(s):  
Georg Hess ◽  
Wolfram Gerlich ◽  
Guido Gerken ◽  
Michael Manns ◽  
Thomas H. Hütteroth ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-7
Author(s):  
Chengliang Zhu ◽  
Huan Han ◽  
Jie Li ◽  
Limin Xu ◽  
Fang Liu ◽  
...  

Objective. Hepatitis B virus (HBV) causes inflammation of the liver and is the leading cause of both liver cirrhosis (LC) and hepatocellular carcinoma (HCC). Serine protease inhibitor Kazal type 1 (SPINK1) is an acute-phase response protein that is overexpressed in liver cancer tissue. This study investigated the clinical value of SPINK1 with regard to the diagnosis of HBV-related diseases and its regulatory mechanism. Methods. Serum levels of SPINK1 in HBV-infected patients and healthy participants were detected by enzyme-linked immunosorbent assay (ELISA). Reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) and western blotting were used to detect differential expression of SPINK1 mRNA and protein in HepG2 and HepG2.2.15 cells. The HBV infectious clone pHBV1.3 and its individual genes were cotransfected into HepG2 cells with the SPINK1 promoter coupled to a luciferase reporter; luciferase activity was measured, and the expression levels of SPINK1 were examined. Results. Serum SPINK1 levels of HBV-infected patients were significantly higher than those of healthy participants, and the serum levels of SPINK1 in patients who tested positive for HBeAg were significantly higher than those in patients who tested negative for HBeAg. The serum SPINK1 levels of patients with LC or HCC were markedly higher than those of patients with chronic hepatitis. The HBV X protein (HBx) activated the SPINK1 promoter to upregulate expression of SPINK1 at both mRNA and protein levels. Conclusions. HBV enhances expression of SPINK1 through X. SPINK1 levels are increased during progression of HBV-related diseases and might be utilized as a biomarker for the diagnosis of HBV-related diseases.


2020 ◽  
Vol 23 (07) ◽  
pp. 303-317
Author(s):  
Farah T. Hasan ◽  
Hassan M. Naif ◽  
Zaid H Taha ◽  
Safaa A. Abdul-Razzak

2017 ◽  
Vol 11 (9) ◽  
pp. 733-740 ◽  
Author(s):  
Wenfeng Gao ◽  
Rui Wang ◽  
Xiaojun Wang ◽  
Hao Wu ◽  
Yang Wang ◽  
...  

2015 ◽  
Vol 22 (5) ◽  
pp. 484-492 ◽  
Author(s):  
Xueping Yu ◽  
Ruyi Guo ◽  
Desong Ming ◽  
Yong Deng ◽  
Milong Su ◽  
...  

ABSTRACTThe transforming growth factor β1/interleukin-31 (TGF-β1/IL-31) pathway plays an important role in the process of cell injury and inflammation. The purpose of this work was to explore the role of the TGF-β1/IL-31 pathway in the cytopathic process of hepatitis B virus (HBV)-related acute-on-chronic liver failure (ACLF). The quantitative serum levels of TGF-β1, IL-9, IL-10, IL-17, IL-22, IL-23, IL-31, IL-33, and IL-35 were analyzed among chronic hepatitis B (CHB) patients (n= 17), ACLF patients (n= 18), and normal control (NC) subjects (n= 18). Disease severity in patients with ACLF was assessed using the model for end-stage liver disease (MELD) and Child-Pugh scores. Serum TGF-β1 levels were strongly positively correlated with IL-31 in all subjects, and both of them were positively correlated with IL-17, IL-22, and IL-33. In CHB and ACLF patients, serum levels of TGF-β1 and IL-31 were both increased significantly compared with those in NC subjects and positively correlated with total bilirubin (TBil) and alpha-fetoprotein (AFP) levels. ACLF patients showed the highest levels of TGF-β1 and IL-31, which were positively correlated with Child-Pugh scores. Furthermore, the recovery from the liver injury in CHB was accompanied by decreased TGF-β1 and IL-31 levels. More importantly, serum levels of TGF-β1 and IL-31 were markedly upregulated in ACLF nonsurvivors, and IL-31 displayed the highest sensitivity and specificity (85.7% and 100.0%, respectively) in predicting nonsurvival of ACLF patients. Increasing activity of the TGF-β1/IL-31 pathway is well correlated with the extent of liver injury, disease severity, and nonsurvival of ACLF patients, while reducing activity is detected along the recovery from liver injury in CHB, suggesting its potential role in the pathogenesis of liver injury during chronic HBV infection.


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