Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Valacyclovir”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources
PubMed2005

A case of Epstein-Barr virus infection complicated with Guillain-Barré syndrome involving several cranial nerves.

This report presents a case of infectious mononucleosis with severe neurological complications in a previously healthy young female. Both peripheral and cranial nerves were affected causing paralysis and need for assisted ventilation. There was a clear correlation between the symptoms and the serological findings, indicating that the causative agent was Epstein-Barr virus. The patient was treated with acyclovir, methylprednisolone and immunoglobulins. Two months later she had recovered completely. Epstein-Barr virus infection must be considered among the possible causes in patients with cranial nerve affection or Guillain-Barré syndrome.

Acyclovir↗
PubMed1998

Complete histological regression of Kaposi's sarcoma following treatment with protease inhibitors despite persistence of HHV-8 in lesions.

There is no current curative treatment for HIV-related Kaposi's sarcoma. The identification of human herpesvirus-8 as a possible aetiological agent suggests potential efficacy of anti-viral agents. We report here on the complete histological remission of Kaposi's sarcoma following treatment with protease inhibitors, even in patients with limited virological response and persistence of HHV-8.

Acyclovir↗
PubMed1999

Successful treatment of generalized primary herpes simplex type 2 infection during pregnancy.

Generalized herpes simplex virus infections constitute a severe threat to mother and child during pregnancy. Before antiviral treatments were available, both mother and foetus had a high mortality rate. The following case illustrates a successful outcome after long-term antiviral treatment. It is of great importance to suspect, diagnose and treat patients with HSV 2 early, especially during pregnancy.

Acyclovir↗
PubMedDate not supplied

Early therapy with valaciclovir or famciclovir reduces but does not abrogate herpes simplex virus neuronal latency.

Mice were infected via the ear pinna using a recombinant strain of HSV-1 expressing the beta-gal gene under the LAT promoter. Mice were treated continuously with valaciclovir or famciclovir, from 1 day before or 1 day after virus inoculation for 10 days. Ipsilateral and contralateral trigeminal and cervical ganglia were later assessed by co-cultivation or for X-Gal-positive or LAT-positive neurons. Latency was markedly reduced by early therapy, however, a basal level of HSV-1-positive neurons was detected in all mice.

2-Aminopurine↗
PubMed2004

Assessing bioequivalence using genomic data.

For approval of a generic drug product, the assessment of bioequivalence in drug absorption is usually considered as a surrogate for evaluation of drug efficacy and safety in clinical studies. For some drug products, the United States Food and Drug Administration indicates that the assessment of similarity between dissolution profiles may be used as a surrogate for assessment of bioequivalence. Along this line, we propose assessing bioequivalence using genomic data collected from the same individuals, assuming that there is an established relationship between pharmacokinetic and genomic data. Because there may be a bias in the prediction of pharmacokinetic data using genomic data and the variations in these two types of data are different, we propose to assess bioequivalence based on sensitivity analysis of prediction bias and variation difference within some predetermined limits. Our methods are derived for average, population, and individual bioequivalence.

Acyclovir↗
PubMed2002

Prevention of cytomegalovirus disease in hematopoietic stem cell transplantation.

Prevention of cytomegalovirus (CMV) infection after hematopoietic stem cell transplantation (HSCT) generally involves preemptive treatment of recognized infection before the onset of overt CMV-associated disease. The success of this method depends on efficient recognition of infection and intervention before the disease progresses. Reliable tests for such diagnosis include blood culture, antigenemia assays, polymerase chain reaction assays, and other DNA sequence- or RNA sequence-based assays. For selected high-risk patients, such as patients receiving T cell-depleted hematopoietic stem cell transplants, prophylactic use of antiviral agents before the onset of CMV infection is recommended. The ability to monitor the immunological status of the patient relative to CMV-specific immunity is increasing in importance. Ultimately, the solution to the problem of efficient prevention of CMV infection in this population will require combined antiviral chemotherapy and improved reconstitution of CMV immunity.

Acyclovir↗
PubMed2002

Understanding pain in herpes zoster: an essential for optimizing treatment.

After herpes zoster, immunocompetent persons frequently experience chronic pain and considerable suffering. Zoster-associated pain has a complex pathophysiology that begins with viral damage and increased sensitization of peripheral sensory neurons. The enhanced afferent barrage from these neurons sensitizes spinal neurons and leads to loss of synapses from descending inhibitory fibers, resulting in central neuropathic pain and allodynia. Antiviral therapy of acute zoster limits this sequence of pathophysiologic mechanisms. There is no clear consensus regarding the optimal means of determining the benefits of antiviral therapy in the management of pain of herpes zoster. A novel statistical approach utilizing rates of disappearance of pain of differing pathophysiologic mechanisms is proposed.

2-Aminopurine↗
PubMed2002

Beta-herpesvirus challenges in the transplant recipient.

Cytomegalovirus (CMV) has major consequences after allogeneic stem cell and solid organ transplantation. CMV may cause significant morbidity and mortality, and monitoring to detect reactivation to reduce disease or management of end organ disease is associated with increased resource utilization. Two other members of the beta-herpesvirus family, human herpesvirus (HHV) type 6 and HHV-7, are increasingly recognized as important pathogens in transplant recipients, either by direct infection (e.g., encephalitis, hepatitis, or pneumonitis) or via interaction with CMV. In addition to direct effects of CMV infection, such indirect effects as an increased risk for bacterial and fungal infections or impaired graft acceptance and function are important research topics. Diagnosis and treatment of CMV infection is currently more advanced than for HHV-6 and HHV-7.

Acyclovir↗
PubMed2002

Recommendations for prevention of and therapy for exposure to B virus (cercopithecine herpesvirus 1).

B virus (Cercopithecine herpesvirus 1) is a zoonotic agent that can cause fatal encephalomyelitis in humans. The virus naturally infects macaque monkeys, resulting in disease that is similar to herpes simplex virus infection in humans. Although B virus infection generally is asymptomatic or mild in macaques, it can be fatal in humans. Previously reported cases of B virus disease in humans usually have been attributed to animal bites, scratches, or percutaneous inoculation with infected materials; however, the first fatal case of B virus infection due to mucosal splash exposure was reported in 1998. This case prompted the Centers for Disease Control and Prevention (Atlanta, Georgia) to convene a working group in 1999 to reconsider the prior recommendations for prevention and treatment of B virus exposure. The present report updates previous recommendations for the prevention, evaluation, and treatment of B virus infection in humans and considers the role of newer antiviral agents in postexposure prophylaxis.

Acyclovir↗
PubMed2004

Effect of Epstein-Barr virus replication on Langerhans cells in pathogenesis of oral hairy leukoplakia.

Epstein-Barr virus (EBV) replicates productively in oral hairy leukoplakia (HLP). One characteristic of human immunodeficiency virus (HIV)-associated HLP is a decreased oral epithelial Langerhans cell count. This prospective study tested the hypothesis that oral epithelial EBV replication decreases oral Langerhans cell counts. EBV replication in HLP was highly correlated with decreased oral Langerhans cell counts. Inhibition of EBV replication restored oral Langerhans cell counts to normal control levels, and the return of EBV replication after treatment resulted in a recurrent decline in oral Langerhans cell counts. Decreased oral Langerhans cell counts occurred independently of HIV infection, as demonstrated in HLP of otherwise healthy HIV-seronegative individuals. These results support the tested hypothesis and suggest that EBV manipulates and evades the mucosal immune response in oral epithelial infection. This novel EBV strategy for eliminating oral Langerhans cells may facilitate the persistence of oral epithelial EBV and may contribute to the pathogenesis of HLP.

AIDS-Related Opportunistic Infections↗
PubMed2004

Expression of Epstein-Barr virus latent genes in oral epithelium: determinants of the pathogenesis of oral hairy leukoplakia.

This retrospective study examined expression of Epstein-Barr virus (EBV) latent genes in oral epithelium from human immunodeficiency virus-seropositive subjects, to identify genes associated with the pathogenesis of oral hairy leukoplakia (HLP). Transcription of EBV latent genes was detected in tissues with productive EBV replication and, also, in normal oral epithelial tissues without EBV replication. Expression of the EBV EBNA-2 open-reading frame in oral epithelium was identified as an important cofactor associated with the pathogenesis of HLP. In vitro experiments suggested that a recombinant variant of the EBNA-2 gene may play a role in the pathogenesis of HLP, through modulation of EBNA-2 protein function.

Acyclovir↗
PubMed2005

A case of Ramsay Hunt-like syndrome caused by herpes simplex virus type 2.

We report an immunocompetent patient with recurrent auricular and facial vesicles associated with painful paresthesias and facial paralysis, consistent with Ramsay Hunt syndrome, due to herpes simplex virus (HSV) type 2. Clinical and laboratory-proven acyclovir resistance developed during therapy. Immunologic assays revealed normal reactivity to HSV-2.

Acyclovir↗
PubMed1998

A randomized, double-blind trial of valaciclovir prophylaxis for cytomegalovirus disease in patients with advanced human immunodeficiency virus infection. AIDS Clinical Trials Group Protocol 204/Glaxo Wellcome 123-014 International CMV Prophylaxis Study Group.

Cytomegalovirus (CMV) disease is a common complication of advanced human immunodeficiency virus (HIV) infection. Administration of oral valaciclovir, a valine ester of acyclovir, achieves sufficient plasma acyclovir levels to inhibit many clinical isolates. Acyclovir has been associated with enhanced survival in AIDS but not with CMV disease prevention. CMV-seropositive patients (1227) with CD4 cell counts <100/mm3 were enrolled in a randomized, double-blind trial. Valaciclovir, 8 g/day, was compared with acyclovir, 3.2 or 0.8 g/day, for CMV prevention; all three arms were compared for survival. The confirmed CMV disease rate was 11.7% among valaciclovir recipients and 17.5% in the pooled acyclovir arms, a 33% reduction in risk. Time to confirmed CMV disease was significantly longer for the valaciclovir group (P = .03). A trend toward earlier mortality for valaciclovir recipients was seen (P = .06). Toxicity and earlier medication discontinuation were more common in this group. Valaciclovir significantly reduces the risk of CMV disease. Further exploration of a better-tolerated dose is warranted.

AIDS-Related Opportunistic Infections↗
PubMed1998

The effect of valaciclovir on cytomegalovirus viremia and viruria detected by polymerase chain reaction in patients with advanced human immunodeficiency virus disease. AIDS Clinical Trials Group Protocol 204/Glaxo Wellcome 123-014 International CMV Prophylaxis Study Group.

Samples of blood and urine were collected at baseline, week 4, and week 8 and then every 8 weeks from 310 patients entering a controlled trial of prophylaxis with valaciclovir versus acyclovir. Samples were tested under code by polymerase chain reaction (PCR) in one laboratory. The median number of samples collected from each patient was 5 for blood (range, 0-15) and 5 for urine (range, 0-15). Both baseline PCR viremia and PCR viruria were significantly associated with future cytomegalovirus (CMV) disease (P = .002 and P = .02, respectively). The greatest effect of valaciclovir on CMV disease was seen in patients who were PCR-positive in blood at baseline (P = .002), although a significant effect was also seen in those who were PCR-negative in urine (P = .02). Thus, PCR viremia provides prognostic information about CMV disease in AIDS patients, and valaciclovir showed activity as both a preemptive and prophylactic agent.

AIDS-Related Opportunistic Infections↗