[A family associated outbreak of Mycoplasma pneumoniae infection in a hospital ward].

OBJECTIVE: To describe the epidemiological and serological features on a family associated outbreak caused by Mycoplasma pneumoniae (MP) infection occurred in Beijing in August 2007. METHODS: Mutual exposure of the family members was investigated and retrospective medical record was reviewed for the hospitalized patients. Serum antibodies to MP were measured and chest X-rays were taken for all the family members. RESULTS: This family consisted of 5 members, with fixed members as the boy (13 years old), his father (43 years old) and mother (44 years old), grandmother (64 years old) and uncle (32 years old) who was involved in taking care of the sick boy and his father. During 23 days of the event, four of all the five family members were ill. Three (boy, father and uncle) had radiographic pneumonia, whose paired sera all showed a ≥ fourfold increase in antibody titer, and two of them were confirmed by chest X-ray on day 2 after onset of fever. The grandmother suffered from bronchitis, with positive (PA) serum antibody to MP. Serum MP-IgG from the father and uncle was positive, 3 days and 2 days after the onset of fever. The chances of contact between grandmother with the boy and uncle with the father were both only in the hospital wards. Only the mother remained asymptomatic, with her serum MP-IgM(-) and MP-IgG(+) for which the blood sample was collected 37 days after close contact with the boy. The longest time of exposure to the patients was between mother and the boy but only the mother did not increase her total workload or feeling for fatigue. RESULTS: of MP-IgG from post-infection did not completely defend against the repeated MP infection. Combined risk factors as index patients with severe cough, prolonged close contact, poorly ventilation of the environment, and family members with excessive fatigue might work as the causes of this family MP outbreak.

[Clinical features and prognosis of decompensated hepatitis C virus related cirrhosis].

OBJECTIVE: To study the clinical features and prognosis of hepatitis C virus (HCV)-related cirrhosis after the first occurrence of complications. METHODS: The clinical data of 89 decompensated HCV-related cirrhosis patients were analyzed. Univariate and multivariate analyses of the factors influencing the clinical decompensation were conducted. RESULTS: Ascites was the most frequent first decompensation (44.9%), followed by upper gastrointestinal bleeding (23.6%), and self-originated peritonitis (20.2%), and hepatic encephalopathy (11.2%). During the follow-up of 62 months (60-66 months) ascites was the most frequent first decompensation (47. 2%), followed by self-originated peritonitis (18.0%), upper gastrointestinal bleeding (15.7%), and hepatic encephalopathy (7.9%). The 5-year survival rates after of the patients with hepatic encephalopathy, ascites, upper gastrointestinal bleeding and self-originated peritonitis as the first decompensated complications were 64.5%, 85.0%, 75.0%, and 83.3% respectively. Multivariate regression analysis showed that esophageal and gastro varices and bilirubin were independently correlated with survival. CONCLUSION: Hepatitis C is a slowly progressing disease. Decompensation occurring in hepatitis C is significantly correlated with survival.

[An integrated biological model for interferon signaling pathway and its gene polymorphisms].

To construct a systemic structural model for interferon (IFN) signaling pathways with gene's single nucleotide polymorphisms (SNPs) information, it is visual to investigate the effects of gene-gene interaction on IFN signaling path-ways. The genes function information was retrieved from Pubmed and Embase database. The IFN signaling pathways were constructed by applying Teranode Design Suite (TDS) biological software. The SNPs information of genes in pathways was retrieved by using SNP Trawler biological software. The biological systemic structural model for IFN signaling pathways, involving in genetic information, particularly their SNPs information, was constructed successfully. It contained JAK-STAT, MAPK-p38 and PI3K pathways, through which IFNs play variable biological roles. Type-I-IFN makes an important role in against viral infection, cell proliferation and immunoregulation by these three pathways. However, the biological activities of type-II-IFN are through JAK-STAT and MAPK-p38 pathways, and type-III-IFN is only through PI3K pathway. These pathways contained 98 genes and 19 693 SNPs information, which consist of a complicate gene-gene interactional network. In conclusion, this software model not only helps us intensively research the effects of SNPs on IFN biological roles and predict IFN therapeutic effect, but also set up a good foundation for translational medicine, discovering new target of drugs and developing new drugs.

Encephalic large arteries narrowness and peripheral neuropathy in a patient with adult-onset Still's disease.

Adult-onset Still's disease (AOSD) is a rare, systemic inflammatory disorder, characterized by spiking high fever, fever-associated evanescent rash, arthritis, myalgia, serositis and hepatosplenomegaly. White blood cell count, neutrophilic cell count, and serum ferritin level are markedly elevated in the active stage of the disease. Neurological complications of AOSD commonly were cranial nerve palsies, seizures, aseptic meningoencephalitis, peripheral neuropathy and Miller-Fisher syndrome. We report a previously healthy 60-year-old Chinese man who fulfilled the criteria for AOSD and had a combination of focal and peripheral neurological symptoms. Magnetic resonance angiography (MRA) and transcranial Doppler ultrasonography (TCD) showed narrowness of cerebral blood vessel. Peripheral neuropathy was confirmed by electromyography and sural nerve biopsy. His generalized neuropathy and other symptoms were rapidly improved by receiving glucocorticoid therapy. We do a literature review about neurological manifestations observed in AOSD patients.

[An analysis of clinical characteristics and risk factors of cirrhosis-related hepatocellular carcinomas in patients with hepatitis C virus infection].

OBJECTIVE: To study the epidemiological and clinical characteristics and risk factors of cirrhosis-related hepatocellular carcinomas (HCC) in patients with hepatitis C virus (HCV) infection. METHODS: Eighty-nine compensated and decompensated HCV cirrhosis patients were analyzed and followed-up. The main clinical and laboratory variables were analyzed as incidence factors of HCC with univariate analysis and multivariate analysis regression models. RESULTS: The patients were followed-up for 86 months. Thirty-five of the 89 patients had HCC during the 86 months follow-up. Their five and ten-year cumulative incidences were 16.9% and 40.4% respectively. Of the 35 HCC patients, 4 had a family history of hepatitis C, 12 had a familial history of HCC, and 7 had a history of alcohol ingestion. Five and ten-year cumulative incidences of HCC in patients with hepatic steatosis were 24.6% and 51.0% respectively. Five-year and ten-year cumulative incidences of HCC in patients with non-hepatic steatosis were 8.7% and 26.2% respectively, and the difference in the cumulative incidences between them was significant (P < 0.05). Hepatic steatosis severity was associated with the severity of the cirrhosis. ALT and TBil levels were higher in the HCC group than in the non-HCC group, ALB was lower in the HCC group than in the non-HCC group, and the differences between them were significant (P < 0.05). Child-Pugh score and the severity of the hepatic steatosis during follow-up were independently correlated with HCC. CONCLUSION: HCC is the most important and frequent outcome of chronic hepatitis C cirrhosis. Child-Pugh score and the severity of the hepatic steatosis are related to the risk factors. History of alcohol ingestion and family history of hepatitis C are also related to liver cancer.

[The histopathologic and clinical analysis of viral chronic hepatitis patients with negative serological viral markers].

OBJECTIVE: To analyze the histopathological and clinical features of viral chronic hepatitis patients with negative serological viral markers. METHODS: 62 hepatitis patients with negative serological markers were assayed with serological viral hepatitis markers, liver function test and liver biopsies were enrolled in the study. Serum HBV DNA of HBV cases was analyzed by PCR. Liver specimens were examined by immunohistochemistry for HBsAg and HBcAg. RESULTS: The fit rate of histopathological diagnosis with clinical diagnosis is 53.2%, the fit rate is 69.1% in moderate chronic hepatitis group. The immunohistochemistry showed that HBsAg and/or HBeAg positive rate was 45.2%, 53.6% had moderate chronic hepatitis and 25% had mild hepatitis. 13 (46.4%) had G1 hepatitis, 10 (35.7%) had G2 hepatitis, 3 (10.8%) had G3 hepatitis and 2 (7.1%) had G4 hepatitis, and serum HBV DNA positive rate was 35.7%. There were no differences in HBV DNA levels between different hepatitis group and fibrosis stage group (P > 0.05). There were no differences in all indexes between HBV DNA negative group and HBV DNA positive group (P > 0.05). There were no differences in all indexes between HBV patients and other patients (P > 0.05). CONCLUSION: Occult HBV infection may account for a high proportion of the cases with chronic hepatitis of unknown etiology. Most patients are chronic mild hepatitis, but they still have HBV replication and can progress to liver cirrhosis. Serum PCR test, liver biopsy and immunohistochemistry are helpful for the diagnosis.

[An analysis of the pathohistology of liver tissues, clinical features and prognostic factors of chronic hepatitis B virus carriers].

OBJECTIVE: To study the correlations between clinical features and liver pathohistological changes of chronic hepatitis B virus (HBV) carriers and to discuss the factors which may influence the prognosis. METHODS: Ninety HBV carriers who had liver biopsies were enrolled in this study. RESULTS: (1) The mean follow-up period of the patients was 118 weeks. (2) Fifty-four patients (60.0%) had G1 hepatitis and 21 (23.3%) had G2 hepatitis. The fibrosis stages were graded as S1(42) and S2(21). (3) There were significant age differences among S0, S1 and S2. (4) There were significant differences in aminotransferase levels between patients who had a normal liver histology and those who had mild hepatitis. (5) The grades of liver inflammation were not correlated with the titers of HBeAg and HBV DNA in sera. The stages of liver fibrosis were not correlated with the titers of HBVDNA in sera. Most of the HBeAg negative patients progressed to S2. (6) There were significant differences in spleen dimensions measured by ultrasonography between S0, S1 and S2 patients. (7) During the follow-up period serum aminotransferase (ALT) levels remained normal in 60 patients (group A); 22 patients had transient elevations (group B), and 8 patients had persistent increases (group C). There were significant differences of the ratios of S0 and S2 cases among patients in groups A, B and C. (8) Age and fibrosis stages were predictive factors of liver cirrhosis. CONCLUSIONS: Most chronic HBV carriers had mild inflammatory histological changes in their livers and also had different degrees of liver fibrosis. This follow-up study shows that some of those carriers should have had antiviral therapy.

[Serum autoantibodies of patients with chronic hepatitis C and the significance thereof in infection of hepatitis C virus].

OBJECTIVE: To investigate the serum autoantibodies in patients with chronic hepatitis C and to investigate the significance of autoimmune reaction in hepatitis C virus (HCV) infected patients. METHODS: Peripheral blood samples were collected from 69 patients with chronic hepatitis C, 69 patients with chronic hepatitis B (HB), and 69 patients with autoimmune hepatitis (AIH). Indirect immunofluorescence technique was used to detect the serum anti nuclear antibody (ANA), anti-mitochondrial antibody (AMA), anti-smooth muscle antibody (anti-SMA), and anti-liver-kidney antibody (anti-LKM). HCV RNA was detected by PCR. The biochemical indices: alanine transaminase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), and gamma-globulin were detected. The relations of autoantibodies to virus load, HCV genotype, cirrhosis, age, sex, and liver function were analyzed. RESULTS: (1) Twenty of the HCV patients were positive in autoantibodies, most being at a low titer, 11 of them being positive in ANA, 7 in anti-SMA, 1 in anti-AMA, and 1 in anti-LKM, with a positive rate of 28.9%, significantly higher than that of the HB patients (4.3%, P < 0.05), and significantly lower than that of the AIH patients (100%, P < 0.05). (2) There were no significant differences between the autoantibody positive group and autoantibody negative group in virus load and HCV genotype. (3) Fourteen of the 18 patients positive in autoantibodies responded to the anti-virus treatment with alpha-interferon with a response rate of 77.8%, significantly higher than that of the autoantibody negative group (53%, P < 0.05). (4) The average age of the autoantibody positive group was 47 +/- 18 years, significantly higher than that of the autoantibody negative group (39 +/- 12 years, P < 0.05). The positive autoantibody rate of the patients aged >or= 40 was 23.1%, significantly higher than that of the patients aged < 40 (5.8%, P < 0.05). There was no significant difference in the autoantibody rate between males and females. (5) The cirrhosis prevalence rate of the autoantibody positive group was 80%, significantly higher than that of the autoantibody negative group (46.9%, P < 0.05). (6) The serum ALT, AST, TBIL and gamma-globulin of the autoantibody positive group were 191 U/L +/- 89 U/L, 169 U/L +/- 80 U/L, 78 micromol/L +/- 50 micromol/L, and 200 g/L +/- 80 g/L respectively, all significantly higher than those of the autoantibody negative group (113 U/L +/- 69 U/L, 98 U/L +/- 62 U/L, 51 micromol/L +/- 30 micromol/L, and 160 g/L +/- 70 g/L respectively, all P < 0.05). (7) There were no significant differences in HCV RNA load and HCV genotype between the autoantibody positive group and the autoantibody negative group (both P > 0.05). CONCLUSION: HCV infection induces the autoimmune reaction resulting in production of autoantibodies. Positive autoantibody rate is related with cirrhosis and age. Titer and type of autoantibody serve as important indices in the diagnosis and treatment of HCV.

[Significance of serum carnitine in patients with liver diseases].

OBJECTIVE: To determine serum carnitine levels in patients with liver diseases and to investigate their significance. METHODS: 25 patients with acute viral hepatitis, 34 with chronic viral hepatitis, 22 with post hepatitis cirrhosis with normal renal function, 9 with post hepatitis cirrhosis but with renal disfunction, and 40 healthy subjects (serving as controls) were enrolled in this study. An enzymatic cycling method was used to determine the serum free carnitine levels. RESULTS: The serum free carnitine level was (48.3+/-10.2)micromol/L in the healthy control group. It was (35.2+/-13.2)micromol/L in the acute viral hepatitis group, (36.5+/-9.9)micromol/L in the chronic viral hepatitis group, (45.0+/-11.0)micromol/L in the post hepatitis cirrhosis with normal renal function group, and (83.6+/-50.4)micromol/L in the post hepatitis cirrhosis with renal dysfunction group. Serum free carnitine levels in the acute viral hepatitis and chronic viral hepatitis groups were significantly lower than those in the healthy controls. There were no significant differences in serum free carnitine levels of the post hepatitis cirrhosis group and the normal control group. CONCLUSIONS: Patients with liver diseases can have carnitine metabolism errors. One of the secondary carnitine lack causes is liver disease.

[Significance of blood HCV RNA screening in the prevention of post-transfusion hepatitis C].

BACKGROUND: To investigate the significance of blood HCV RNA screening in the prevention of post-transfusion hepatitis C. METHODS: Totally 56,400 anti-HCV negative blood samples collected from Jan. 2000 to Dec. 2003 were tested for HCV RNA by RT-PCR, and the patients who received the HCV RNA negative blood were followed up. RESULTS: The HCV RNA positive rate was 2.5 per thousand (146/56,000) and none of the patients followed up suffered from HCV infection. CONCLUSION: HCV RNA screening for the anti-HCV negative blood samples is very effective and feasible for prevention of post-transfusion hepatitis C.

[Serum HBV-DNA level can predict treatment effectiveness in patients with chronic hepatitis B using interferon-alpha-2a].

OBJECTIVE: To evaluate the correlation between the efficacy of interferon-alpha-2a and the kinetics of viral load in serum. METHODS: The authors conducted a trial including 58 patients with chronic hepatitis B. Patients were treated with interferon-alpha-2a three times a week for 6 months. Viral kinetics were assessed by serial quantitive measurements of HBV-DNA. RESULTS: A significant decline of serum HBV-DNA was seen after interferon-alpha-2a administration for 1 month, the decreases were (2.50 +/- 0.44) log10, (1.62 +/- 1.12) log10 and (1.05 +/- 1.35) log10 for complete responders, partial responders and no-responders, respectively. After 1 month of treatment, HBV-DNA level was (3.99 +/- 0.91) log10 for complete responders versus (5.63 +/- 1.31) log10 for partial responders, and (6.69 +/- 1.42) log10 for no-responders (P < 0.05). Multivariate analysis suggested that undetectable serum HBV-DNA after 1 month of interferon-alpha-2a treatment was associated with better efficacy; higher baseline ALT or/and no family history were also correlated with better treatment outcomes. CONCLUSION: Kinetics of HBV-DNA level under interferon-alpha-2a treatment are highly predictive of therapeutic response.

[Therapeutic effect of levamisole plus HBV vaccine and dipyridamole on patients chronically infected by HBV with precore mutation].

OBJECTIVE: To evaluate the incidence of precore mutation in HBeAg negative HBV infected patients and the therapeutic effect of the immune therapy (levamisole + HBV vaccine + dipyridamole) on patients chronically infected by HBV with precore mutation. METHODS: The precore region of HBV from the HBeAg (-) chronic hepatitis patients was sequenced and the patients suffered from HBV with precore mutation were treated with immune therapy. RESULTS: The precore mutation rate was 10/12. The therapeutic effect of the immune therapy on the precore mutation patients (5/7) was better than that on the HBsAg(+), HBeAg(+) patients (2/11), P less than 0.05. CONCLUSION: The precore mutation rate was quite high in the HBsAg(+), HBeAg(-) patients we studied. The immune-therapy has some therapeutic effects on the patients with precore mutation. But the number of cases was too small, further study is needed.

[Differential clinical diagnostic parameters of acute hepatitis B and flare of chronic HBV infection].

OBJECTIVE: To evaluate useful clinical diagnostic parameters for differentiating acute hepatitis B and flare of chronic HBV infection. METHODS: Using PCR method to detect viral level in the patient's serum, HBV marker was detected by ELISA kit. Liver function was also detected. RESULTS: The patient can be diagnosed as acute hepatitis B if a patient has one of the following parameters: (1)HBV-DNA negative on admission. (2) When the patient's ALT was lower than 400 IU/L, HBV-DNA was negative or HBsAg became negative or HBeAg/HBeAb seroconverted. CONCLUSION: The viral DNA level, HBV marker and ALT can help differentiate acute hepatitis B and flare of chronic HBV infection.

[Dynamics of HBV-DNA level in acute hepatitis B].

OBJECTIVE: To verify the mechanism of the hepatitis B viral clearance using clinical data. METHODS: Viral level and HBV marker in serum were analyzed in 12 patients with acute hepatitis B. RESULTS: The clearance of hepatitis B virus occurred before the patients were hospitalized in 66.7% of patients. The viral level and the A value of HBsAg;HBeAg declined gradually during hospitalization. CONCLUSIONS: In most of patients with acute hepatitis B in the study, the virus was cleared without destruction of infected cells.