Home About us Contact
|
Home About us Contact | ||
|
|
||
Occult Infection (occult + infection)
Selected AbstractsRole of Chronic Infection and Inflammation in the Gastrointestinal Tract in the Etiology and Pathogenesis of Idiopathic ParkinsonismHELICOBACTER, Issue 4 2005Part 1: Eradication of Helicobacter in the Cachexia of Idiopathic Parkinsonism ABSTRACT Background., Neuronal damage in idiopathic parkinsonism may be in response to ubiquitous occult infection. Since peptic ulceration is prodromal, Helicobacter is a prime candidate. Aim., To consider the candidature of Helicobacter in parkinsonism with cachexia. Methods., We explore the relationship between being underweight and inflammatory products in 124 subjects with idiopathic parkinsonism and 195 controls, and present the first case-series evidence of efficacy of Helicobacter eradication, in parkinsonism advanced to the stage of cachexia. Results., Association of a low body mass index with circulating interleukin-6 was specific to parkinsonism (p = .002), unlike that with antibodies against Helicobacter vacuolating-toxin and cytotoxicity-associated gene product (p < .04). Marked reversibility in both cachexia and disability of idiopathic parkinsonism followed Helicobacter heilmannii eradication in one case, Helicobacter pylori eradication in another, follow-up being , 3.5 years. The latter presented with postprandial bloating, and persistent nausea: following eradication, radioisotope gastric-emptying returned towards normal, and upper abdominal symptoms regressed. Reversibility of their cachexia/disability contrasts with the outcome of anti- Helicobacter therapy where eradication repeatedly failed (one case), and in non- Helicobacter gastritis (three cases). Anti-parkinsonian medication remained constant. Intestinal absorption and barrier function were normal in all. Conclusion., Categorization, according to presence or absence of Helicobacter infection, was a useful therapeutic tool in late idiopathic parkinsonism. [source] The paradox of normal serum albumin in anorexia nervosa: A case reportINTERNATIONAL JOURNAL OF EATING DISORDERS, Issue 3 2005Mori J. Krantz MD Abstract Objective Anorexia nervosa (AN) is associated with marked decreases in caloric intake and a corresponding reduction in body weight due to abnormal self body image. Although counterintuitive, hypoalbuminemia and vitamin deficiencies are not expected consequences of this disorder. Etiologic considerations for hypoalbuminemia are discussed. Method The case report of a patient with AN and marked hypoalbuminemia is presented and a focused literature review is reported. Results Hypoalbuminemia was initially attributed to starvation. However, occult infection was ultimately responsible. Serum albumin concentration normalized with antibiotic therapy despite minimal restoration of body weight. Discussion Hypoalbuminemia should not be considered a characteristic feature of AN even in the setting of progressive weight loss. The presence of other potentially life-threatening conditions should be sought, as reduced serum albumin concentration is a marker of inflammation in AN. © 2005 by Wiley Periodicals, Inc. [source] Occult hepatitis B virus infection and lamivudine-resistant mutations in isolates from renal patients undergoing hemodialysisJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 1 2010Jorge S. Motta Abstract Background and Aims:, Patients undergoing hemodialysis are at risk of infection with both hepatitis B virus (HBV) and hepatitis C virus (HCV). Occult HBV infection is usually associated with low levels of HBV and is frequently detected in HCV-infected patients. The aims of the present study were to compare the prevalence of occult HBV infection among anti-HCV-positive and anti-HCV-negative patients undergoing hemodialysis, and characterize the molecular patterns of HBV isolates from patients with occult infection. Methods:, Serum samples from 100 patients negative for hepatitis B surface antigen undergoing hemodialysis, half of whom were positive for anti-HCV antibodies, were tested for the presence of HBV-DNA using semi-nested polymerase chain reaction (PCR). PCR products of the S gene were directly sequenced. Results:, HBV-DNA was detected in 15 samples. There were no significant differences in HCV status, sex, age, time of dialysis, alanine aminotransferase levels or HBV serological markers between patients with or without occult HBV infection, with the exception of antibody to hepatitis B core antigen (anti-HBc)-only serological marker (P = 0.003). All six HBV isolates that could be sequenced were of genotype A/subgenotype A1. Four of these six HBV isolates contained mutations associated with lamivudine resistance in the DNA polymerase (two with L180M/M204V and two with rt173V/180M/204V) and a specific substitution (Y100C) in the HBV small surface protein. Conclusions:, HBV isolates with the identified substitutions have the potential to spread silently by nosocomial transmission within the hemodialysis unit. These results have potential implications for the management of patients with occult HBV infection undergoing hemodialysis. [source] Can the serological status of "anti-HBc alone" be considered a sentinel marker for detection of "occult" HBV infection?JOURNAL OF MEDICAL VIROLOGY, Issue 4 2008Francesco Vitale Abstract Some individuals have "occult" infection with hepatitis B virus (HBV), defined as presence of HBV genome in the serum or liver tissue without HBV surface antigen (HBsAg) in the serum. The aim of this study was to investigate whether serum antibodies against HBV core antigen in isolation ("anti-HBc alone") are a useful marker of "occult" HBV in patients with or without hepatitis C virus (HCV) infection. "Anti-HBc alone" was detected in the sera of 119/6,544 (1.8%) asymptomatic outpatients referred to the diagnostic laboratory for routine testing for viral hepatitis, 62/607 (10.2%) drug users, and 42/195 (21.5%) patients with hepatocellular carcinoma. Using three in-house nested-PCR amplification assays to detect HBV preS-S (S), precore-core (C), and Pol viral regions, respectively, "occult" HBV sequences were found in 9 of the 223 sera (4.0%) with "anti-HBc alone." The highest prevalence of "occult" HBV sequences (5.9%) was detected in "anti-HBV alone" sera of individuals referred to the diagnostic laboratory without HCV antibodies. Direct sequencing of all PCR products confirmed the specificity of the PCR reactions and revealed the predominance of HBV genotype D. The data presented in this study suggest that detection of "anti-HBc alone" could reflect unrecognized "occult" HBV infection and that physicians should consider investigating such patients with HBV molecular tests. J. Med. Virol. 80:577,582, 2008. © 2008 Wiley-Liss, Inc. [source] Sequencing of human-viral DNA junctions in hepatocellular carcinoma from patients with HCV and occult HBV infectionJOURNAL OF MEDICAL VIROLOGY, Issue 4 2003Akihiro Tamori Abstract DNA of free hepatitis B viruses (HBV) has been detected in the liver of patients infected with hepatitis C virus (HCV). It is unknown whether HBV DNA is integrated into such livers; if so, it may affect hepatocarcinogenesis. Hepatocellular carcinomas (HCCs) from 34 patients without HBV surface antigen (HBsAg) and with anti-HCV, and from 7 patients with HBsAg and without anti-HCV as controls, were examined, using the cassette-ligation,mediated polymerase chain reaction and primers based on HBV DNA sequence. In the controls, HBV DNA had been integrated into human DNA of all HCCs. On the basis of HBV DNA in tumor tissue, 23 of the 34 patients with anti-HCV had occult infection. Junctions between human DNA and HBV DNA were detected in 10 of the 34 patients without HBsAg and with anti-HCV. HBV DNA was integrated into chromosome 11q in 4 of the 10 HCCs with junctions. The DNA to either side of the human-viral junctions was sequenced. Clinically, the mean tumor size of these 10 HCCs was 39 mm; that of the 24 HCCs without integrated HBV was 25 mm. The surrounding tissue was cirrhotic in 2 of the 10 former HCCs and in 16 of the latter 24 HCCs. In conclusion, integrated HBV was detected in some patients with HCV infection; in these patients, the integrated DNA was associated with accelerated hepatocarcinogenesis. J. Med. Virol. 69:475,481, 2003. © 2003 Wiley-Liss, Inc. [source] Chronic hepatitis C and persistent occult hepatitis C virus infection are characterized by distinct immune cell cytokine expression profilesJOURNAL OF VIRAL HEPATITIS, Issue 8 2009T. N. Q. Pham Summary., Hepatitis C virus (HCV) replicates in immune cells in both chronic hepatitis C (CHC) and occult HCV infection, but the extent of virus replication in this compartment in these opposing infection forms varies greatly. It was unknown whether this could be linked to HCV genotype or to differences in host gene expression shaping the immune response, and whether HCV replication in immune cells is sensitive to endogenous antiviral cytokines. In this study, we uncovered that significantly greater HCV load in peripheral blood mononuclear cells (PBMC), but not in plasma, coincided with HCV genotypes 2 and 3 in CHC, but with genotype 1 in residual occult infection after clinical resolution of hepatitis C. Moreover, PBMC from individuals with occult infection transcribed significantly greater levels of IFN-,, IFN-, and TNF-,, but less interleukin (IL)-10 than those from CHC. In CHC, PBMC with low HCV load expressed significantly more IFN-, but less IL-12 than did cells with high virus content. In occult infection, HCV RNA detection in PBMC was associated with much lower IFN-, and IL-12 expression. Further, HCV replication in T lymphocytes could be completely eliminated by activation of endogenous IFN-, in CHC, but of IFN-, in occult infection. In conclusion, CHC and persistent occult HCV infection are characterized by clearly different profiles of antiviral cytokine response in circulating immune cells which are also different from those of healthy individuals. Higher expression of IL-10, combined with lower transcription of IFN-,, IFN-, and TNF-,, is associated with a more robust HCV replication in immune cells. [source] Antagonistic expression of hepatitis C virus and alpha interferon in lymphoid cells during persistent occult infectionJOURNAL OF VIRAL HEPATITIS, Issue 8 2007T. N. Q. Pham Summary., Detection of residual HCV in individuals with SVR after treatment of CHC can be significantly heightened by analyzing ex vivo mitogen-activated T and B lymphocytes and applying sensitive nucleic acid amplification assays. However, it remained unknown if synergistic activation of lymphocytes and monocytes would further augment HCV detection, if viral replication becomes universally upregulated in treated cells, and if examining sequential sera and lymphoid cells would improve detection of occult infection. Using paired sera and lymphoid cells collected 1 year apart from 17 individuals with normal liver enzymes for up to 72 months after SVR, it was found that simultaneous activation of lymphocytes and monocytes enhanced identification of silent HCV infection and revealed that in some cases monocytes were the principal immune cell type where HCV persisted. Testing of serial samples further increased detection of occult infection. Ultimately, by combining the above two approaches, all individuals with SVR were found to be silent carriers of HCV. Clonal sequencing revealed HCV variations in sera and lymphoid cells and evolution of viral genomes confirming ongoing virus replication. Surprisingly, similar to those with CHC, naive lymphoid cells from some individuals carried ,103 HCV copies/,g total RNA. HCV loads in naive lymphoid cells predetermined the outcome of ex vivo stimulation with respect to upregulation or inhibition of HCV replication. HCV RNA levels in occult infection were inversely proportional to the expression of IFN, and IFN-inducible MxA, but not to IFN, or tumour necrosis factor , in naive and mitogen-treated lymphoid cells. [source] Cytomegalovirus infection in the brain of liver transplant recipients: Do pathologically occult infections matter clinically?LIVER TRANSPLANTATION, Issue 3 2003Raymund R. Razonable MD Cytomegalovirus (CMV) infection remains a highly prevalent systemic complication following orthotopic liver transplantation (LT), accounting for a significant increase in morbidity and affiliated costs. However, unlike other immunosuppressed groups of population, CMV infection of the central nervous system in LT is rarely diagnosed, either clinically or postmortem. Furthermore, in 20% of the LT patients who develop preterminal neurological complications, the etiology remains undetermined. With the hypothesis that at least some of these cases could be related to an occult CMV infection, we examined brain tissue from 83 unselected autopsies of LT patients by morphological, immunohistochemical (IHC), in situ hybridization (ISH), and nested polymerase chain reaction (nested PCR) techniques. Microglial nodules were observed in 17 brains of the LT group (20.4%) but in none of the 36 controls. Isolated positive cells by either IHC, ISH, or both techniques, were identified in 11 LT patients (13.2%) and in 2 controls (5.5%). CMV DNA amplification was obtained from paraffin embedded tissues in 41 of 81 LT cases (50.6%), and in 5 controls (13.8%) (P=0.00017). Viral inclusion bodies, inflammatory infiltrates, or necrotizing changes were not identified in any case. Our findings indicate an increased susceptibility of the brain of LT patients to occult infection by CMV and suggest that a latent or low-grade infection of the central nervous system could operate as a reservoir of the CMV and play a role in some of the unexplained neurological symptoms that appear in the postoperative period. [source] | ||||||||||