m.ehime-u.ac.jp

OBJECTIVE: To investigate the therapeutic effects of acyclovir and prednisolone in relation to the timing of treatment in Bell's palsy. STUDY DESIGN: This was a retrospective study of 480 Bell's palsy patients who were treated with oral acyclovir and prednisolone (94 cases) or prednisolone alone (386 cases). PATIENTS: Patients met the after criteria: (1) severe or complete Bell's palsy with a score lower than 20 on the 40-point Yanagihara facial score and (2) treatment started within 7 days after onset. The patients were treated with oral prednisolone (60-40 mg/day) with or without oral acyclovir (2,000 mg/day). MAIN OUTCOME MEASURE: Rate of recovery, which was defined as a facial score of 36 or more, and the absence of contracture with synkinesis. RESULTS: The overall recovery rate of patients treated with acyclovir and prednisolone was 95.7 percent, which was better than that of patients treated with prednisolone alone (88.6%). The recovery rate in patients who began the combined therapy within 3 days of the onset of palsy was 100 percent and early treatment resulted in early remission. In contrast, the recovery rate in patients who started the combined therapy more than 4 days after onset was 86.2 percent. CONCLUSION: These results suggest that early diagnosis and treatment within 3 days of the onset of paralysis are necessary for maximal efficacy of combined acyclovir and prednisolone therapy for Bell's palsy.

Online pharmacy ref source - acyclovir: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14600480&dopt=Abstract acyclovir Zovirax




J Pharmacol Exp Ther. 2003 Nov 14 [Epub ahead of print]
Transport of Amino acid-based Prodrugs by the Na+- and Cl-- coupled Amino Acid Transporter ATB0,+ and Expression of the Transporter in Tissues Amenable for Drug Delivery.

Hatanaka T, Haramura M, Fei YJ, Miyauchi S, Bridges CC, Ganapathy PS, Smith SB, Ganapathy V, Ganapathy ME.

Medical College of Georgia.

We evaluated the potential of the Na(+)- and Cl(-) -coupled amino acid transporter ATB(0,+) as a delivery system for amino acid- based prodrugs. Immunofluorescence analysis indicated that ATB(0,+) is expressed abundantly on the luminal surface of cells lining the lumen of the large intestine and the airways of the lung and in various ocular tissues including the conjunctival epithelium, the tissues easily amenable for drug delivery. We screened a variety of beta-carboxyl derivatives of aspartate and gamma-carboxyl derivatives of glutamate as potential substrates for this transporter using heterologous expression systems. In mammalian cells expressing the cloned ATB(0,+), several of the aspartate and glutamate derivatives inhibited glycine transport via ATB(0,+). Direct evidence for ATB(0,+)- mediated transport of these derivatives was obtained in X. laevis oocytes using electrophysiological methods. Exposure of oocytes, which express ATB(0,+) heterologously, to aspartate beta- benzyl ester as a model derivative induced inward currents in a Na(+)- and Cl(-) - dependent manner with a Na(+):Cl(- ):aspartate beta-benzyl ester stoichiometry of 2:1:1. ATB(0,+) transported not only the beta- carboxyl derivatives of aspartate and the gamma- carboxyl derivatives of glutamate but also valacyclovir which is an alpha-carboxyl ester of acyclovir with valine. The transport of valacyclovir via ATB(0,+) was demonstrable in both heterologous expression systems. This process was dependent on Na(+) and Cl(-). The ability of ATB(0,+) to transport valacyclovir was comparable to that of the peptide transporter PEPT1. These findings suggest that ATB(0,+) has significant potential as a delivery system for amino acid- based drugs and prodrugs.

Online pharmacy ref source - acyclovir: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14617696&dopt=Abstract acyclovir Zovirax[PubMed - as supplied by publisher]

hunterdonhealthcare.org

OBJECTIVE: To report a case of neurotoxicity and aseptic meningitis in a patient receiving valacyclovir.CASE SUMMARY: An 86-year-old white man had started valacyclovir 1 g 3 times a day for a herpetic rash along the left side of his face. He subsequently presented with balance difficulties, constant frontal headaches, and a seizure 1 day prior to admission. Cerebral spinal fluid (CSF) analysis revealed 162 white cells/mm(3), 1 red blood cell/mm(3), glucose 56 mg/dL, and protein 144 mg/dL, with a negative Gram stain. Further laboratory examination failed to demonstrate other causes for the patient's clinical picture. After discontinuation of valacyclovir and supportive care, the patient symptomatically improved.DISCUSSION: As of the third week of September 2003, only 1 other case of valacyclovir-related aseptic meningitis was published describing a patient with characteristics similar to those of our patient. Our patient's neurologic symptoms may have been due to acyclovir toxicity, but acyclovir-toxic patients present with normal CSF findings. Several drug classes, including nonsteroidal antiinflammatory drugs, antibiotics, and intravenous immunoglobulins, can induce aseptic meningitis. Other reasons for the patient's symptoms or causes of meningitis were excluded, although viral meningitis remains a possibility. Valacyclovir-induced aseptic meningitis was considered to be possible according to the Naranjo probability scale.CONCLUSIONS: Healthcare providers should be aware of valacyclovir as a possible cause of drug-induced aseptic meningitis.

Online pharmacy ref source - acyclovir: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14632597&dopt=Abstract acyclovir Zovirax[PubMed - in process]

swosu.edu

OBJECTIVE: To evaluate the literature regarding short-course oral therapy for recurrent genital herpes.DATA SOURCES: Literature was accessed through MEDLINE (1966-March 2003), IOWA Drug Information Service (1966-March 2003), and International Pharmaceutical Abstracts (1966-March 2003).DATA SYNTHESIS: Data are available describing short-course (2 or 3 d) therapy with acyclovir and valacyclovir. Short-course acyclovir therapy was superior to placebo. Three- and 5-day regimens of valacyclovir were equivalent. Early initiation of therapy may be more important than duration of therapy.CONCLUSIONS: More head-to-head studies are needed to determine the most efficacious and cost-effective short-course regimens for recurrent genital herpes.

Online pharmacy ref source - acyclovir: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14632601&dopt=Abstract acyclovir Zovirax[PubMed - in process]




J Med Virol. 2004 Jan;72(1):112-20.
Suppression of generation and replication of acyclovir-resistant herpes simplex virus by a sensitive virus.

Okuda T, Kurokawa M, Matsuo K, Honda M, Niimura M, Shiraki K.

Department of Virology, Toyama Medical and Pharmaceutical University, Sugitani, Toyama, Japan.

The role of acyclovir-sensitive herpes simplex virus (HSV) was analyzed in the process of its replacement by a resistant virus in vitro and in vivo in the aspect of acyclovir therapy. The mode of replacement of acyclovir-sensitive HSV with acyclovir-resistant HSV was examined by the passages of acyclovir-sensitive wild type HSV in Vero cells under acyclovir-treatment. The development of resistance was monitored more adequately by counting the number of acyclovir-resistant viruses in 10,000 plaque forming units than by the conventional susceptibility assay. The resistance increased with the proportion of thymidine kinase-deficient (TK(-)) viruses, when the susceptibilities of acyclovir-treated HSV population to 5'-iodo-2'deoxyuridine and phosphonoacetic acid were examined. The increased resistance was due to the increased proportion of acyclovir-resistant virus but not intermediately resistant virus. Infection with mixtures of TK(-) and acyclovir-sensitive strains rendered TK(-) sensitive to acyclovir, and virus yields were reduced to the levels of acyclovir-sensitive virus in Vero cells. Their yield reduction depended on the proportion of acyclovir-sensitive viruses and induction of TK activity. This reduction in virus yields of the mixture of TK(-) and acyclovir-sensitive strains was confirmed by acyclovir treatment in the skin of mice with cutaneous infection. Acyclovir treatment combined with superinfection of acyclovir-sensitive virus delayed the development of herpetic skin lesions due to acyclovir-resistant virus and reduced virus yields in the infected skin. Acyclovir-sensitive virus plays an important role in suppressing the generation and replication of acyclovir-resistant virus during acyclovir therapy. Copyright 2004 Wiley-Liss, Inc.

Online pharmacy ref source - acyclovir: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14635018&dopt=Abstract acyclovir Zovirax