OBJECTIVETo explore the changes in HBsAg titer and HBV DNA load and their correlation in patients with chronic hepatitis B (CHB) and HBV-related liver cirrhosis (HBV-LC).

METHODSForty-six patients with mild to moderate CHB (CHB-LM), 24 patients with severe CHB (CHB-S), and 28 patients with HBV-LC at admission, and 51 patients with HBV-LC at 4.08 ± 3.06 months during antiviral treatment were tested for serum HBsAg titer and HBV DNA load using Abbott chemiluminescence and fluorescence quantitative PCR, respectively.

RESULTSThe serum HBsAg titer and HBV DNA load gradually decreased with increased disease severity (from CHB-LM, CHB-S to HBV-LC; χ(2)=12.537 and 8.381, respectively, P<0.05). HBsAg titer and HBV DNA load were significantly higher in CHB-LM and CHB-S groups than in HBV-LC group (P<0.05), but comparable between CHB-LM and CHB-S groups (Z=-0.649 and 0.032, respectively, P>0.05). Among HBeAg-positive patients, HBsAg titer and HBV DNA load tended to decrease with increased disease severity (from CHB-LM, CHB-S to HBV-LC; χ(2)=6.146, P=0.046 and χ(2)=1.017, P>0.05; respectively), and CHB-LM group had significantly higher HBsAg titer than HBV-LC group (Z=-2.247, P=0.025). Among the HBeAg-negative patients, serum HBsAg and HBV DNA load gradually declined with the disease severity (χ(2)=8.660 and 13.581, respectively, P<0.05), and were obviously higher in CHB-LM and CHB-S groups than in HBV-LC group (P<0.05). Positive correlations were found between serum HBsAg and HBV DNA levels in CHB-LM (r=0.389, P=0.009) and HBV-LC groups (r=0.431, P=0.022), but not in CHB-S group (r=0.348, P=0.104). After antiviral therapy, the serum HBsAg titer was slightly decreased (Z=-1.050, P=0.294) while HBV DNA load markedly reduced (Z=-5.415, P<0.001), showing no correlation between them (r=0.241, P=0.111) or between the measurements before and after treatment (r=0.257, P=0.085).

CONCLUSIONSerum HBsAg titer and HBV DNA load decreases progressively from CHB-LM to CHB-S and HBV-LC in both HBeAg- positive and -negative patients. The serum HBsAg titer is positively correlated with HBV DNA load, but their levels are not consistently parallel.

Antiviral Agents ; therapeutic use ; DNA, Viral ; blood ; Hepatitis B Surface Antigens ; blood ; Hepatitis B, Chronic ; blood ; Humans ; Liver Cirrhosis ; blood ; virology ; Viral Load

Objective To explore the changes in HBsAg titer and HBV DNA load and their correlation in patients with chronic hepatitis B (CHB) and HBV-related liver cirrhosis (HBV-LC). Methods Forty-six patients with mild to moderate CHB (CHB-LM), 24 patients with severe CHB (CHB-S), and 28 patients with HBV-LC at admission, and 51 patients with HBV-LC at 4.08± 3.06 months during antiviral treatment were tested for serum HBsAg titer and HBV DNA load using Abbott chemiluminescence and fluorescence quantitative PCR, respectively. Results The serum HBsAg titer and HBV DNA load gradually decreased with increased disease severity (from CHB-LM, CHB-S to HBV-LC;χ2=12.537 and 8.381, respectively, P<0.05). HBsAg titer and HBV DNA load were significantly higher in CHB-LM and CHB-S groups than in HBV-LC group (P<0.05), but comparable between CHB-LM and CHB-S groups (Z=-0.649 and 0.032, respectively, P>0.05). Among HBeAg-positive patients, HBsAg titer and HBV DNA load tended to decrease with increased disease severity (from CHB-LM, CHB-S to HBV-LC;χ2=6.146, P=0.046 andχ2=1.017, P>0.05;respectively), and CHB-LM group had significantly higher HBsAg titer than HBV-LC group (Z=-2.247, P=0.025). Among the HBeAg-negative patients, serum HBsAg and HBV DNA load gradually declined with the disease severity (χ2=8.660 and 13.581, respectively, P<0.05), and were obviously higher in CHB-LM and CHB-S groups than in HBV-LC group (P<0.05). Positive correlations were found between serum HBsAg and HBV DNA levels in CHB-LM (r=0.389, P=0.009) and HBV-LC groups (r=0.431, P=0.022), but not in CHB-S group (r=0.348, P=0.104). After antiviral therapy, the serum HBsAg titer was slightly decreased (Z=-1.050, P=0.294) while HBV DNA load markedly reduced (Z=-5.415, P<0.001), showing no correlation between them (r=0.241, P=0.111) or between the measurements before and after treatment (r=0.257, P=0.085). Conclusion Serum HBsAg titer and HBV DNA load decreases progressively from CHB-LM to CHB-S and HBV-LC in both HBeAg- positive and-negative patients. The serum HBsAg titer is positively correlated with HBV DNA load, but their levels are not consistently parallel.

Objective To explore the changes in HBsAg titer and HBV DNA load and their correlation in patients with chronic hepatitis B (CHB) and HBV-related liver cirrhosis (HBV-LC). Methods Forty-six patients with mild to moderate CHB (CHB-LM), 24 patients with severe CHB (CHB-S), and 28 patients with HBV-LC at admission, and 51 patients with HBV-LC at 4.08± 3.06 months during antiviral treatment were tested for serum HBsAg titer and HBV DNA load using Abbott chemiluminescence and fluorescence quantitative PCR, respectively. Results The serum HBsAg titer and HBV DNA load gradually decreased with increased disease severity (from CHB-LM, CHB-S to HBV-LC;χ2=12.537 and 8.381, respectively, P<0.05). HBsAg titer and HBV DNA load were significantly higher in CHB-LM and CHB-S groups than in HBV-LC group (P<0.05), but comparable between CHB-LM and CHB-S groups (Z=-0.649 and 0.032, respectively, P>0.05). Among HBeAg-positive patients, HBsAg titer and HBV DNA load tended to decrease with increased disease severity (from CHB-LM, CHB-S to HBV-LC;χ2=6.146, P=0.046 andχ2=1.017, P>0.05;respectively), and CHB-LM group had significantly higher HBsAg titer than HBV-LC group (Z=-2.247, P=0.025). Among the HBeAg-negative patients, serum HBsAg and HBV DNA load gradually declined with the disease severity (χ2=8.660 and 13.581, respectively, P<0.05), and were obviously higher in CHB-LM and CHB-S groups than in HBV-LC group (P<0.05). Positive correlations were found between serum HBsAg and HBV DNA levels in CHB-LM (r=0.389, P=0.009) and HBV-LC groups (r=0.431, P=0.022), but not in CHB-S group (r=0.348, P=0.104). After antiviral therapy, the serum HBsAg titer was slightly decreased (Z=-1.050, P=0.294) while HBV DNA load markedly reduced (Z=-5.415, P<0.001), showing no correlation between them (r=0.241, P=0.111) or between the measurements before and after treatment (r=0.257, P=0.085). Conclusion Serum HBsAg titer and HBV DNA load decreases progressively from CHB-LM to CHB-S and HBV-LC in both HBeAg- positive and-negative patients. The serum HBsAg titer is positively correlated with HBV DNA load, but their levels are not consistently parallel.

Objective:To summarize the clinical characteristics and laboratory diagnostic methods of infant botulism caused by Clostridium botulinum type B. Methods:Clinical data of 3 infants with type B botulism who were admitted to Children′s Hospital Affiliated to Capital Institute of Pediatrics from May to November 2018 were retrospectively analyzed. Botulinum toxin was detected in fecal samples or fecal enrichment solution of the patients, and Clostridium botulinum was cultured and isolated from fecal samples. Results:The age of onset of the patients (two boys and one girl) was 3, 3 and 8 months old, respectively. Two cases had the onset in May and one case had the onset in November. There were two cases with mixed feeding and one case with breast feeding. One case′s family members engaged in meat processing. All of them were previously healthy. All the children presented with acute flaccid paralysis, cranial nerve involvement and difficult defecation. Two cases had secondary urinary tract infection. Electromyograms of two cases showed that action potential amplitude of the motor nerve were lower than those of their peers. After treatments including intravenous human immunoglobulin, respiratory tract management, urethral catheterization, nasal feeding, etc., three cases recovered completely 2 to 4 months later. Type B botulinum toxin was detected in the fecal diluent of one patient, and the TPGYT enrichment solution and cooked meet medium of the feces of 3 patients, respectively. Clostridium botulinum B was identified from the feces of 3 infants after culture, isolation and purification. Conclusions:Combined with typical clinical manifestations including acute flaccid paralysis, cranial nerve involvement symptoms and difficult defecation examination, infant botulism can be clinically diagnosed. The detection of fecal botulinum toxin and the culture and isolation of Clostridium botulinum are helpful for the diagnosis.